Examination Notes in Psychiatry

Examination Notes in Psychiatry

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Examination Notes in Psychiatry

4th edition PETER BUCKLEY MD MRCPsych Professor and Chairman, Department of Psychiatry, Medical College of Georgia, Augusta, Georgia, USA DEL PREWETTE MD Child and Adolescent Psychiatry Fellow, Palmetto Health/University of South Carolina School of Medicine, Columbia, South Carolina, USA JONATHAN BIRD BSc MB ChB FRCPsych Consultant Neuropsychiatrist, The Burden Centre for Neuropsychiatry, Bristol, and Honorary Senior Lecturer, Division of Psychiatry, University of Bristol, Bristol, UK GLYNN HARRISON MD FRCPsych Norah Cooke Hurle Professor of Mental Health, University of Bristol, Bristol, UK

Hodder Arnold A MEMBER OF THE HODDER HEADLINE GROUP LONDON

First published in Great Britain in 2005 by Hodder Education, a member of the Hodder Headline Group, 338 Euston Road, London NW1 3BH www.hoddereducation.co.uk Distributed in the United States of America by Oxford University Press Inc., 198 Madison Avenue, New York, NY10016 Oxford is a registered trademark of Oxford University Press © 2005 Peter Buckley, Del Prewette, Jonathan Bird and Glynn Harrison All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronically or mechanically, including photocopying, recording or any information storage or retrieval system, without either prior permission in writing from the publisher, or a licence permitting restricted copying. In the United Kingdom such licences are issued by the Copyright Licensing Agency: 90 Tottenham Court Road, London W1T 4LP. Whilst the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. In particular, (but without limiting the generality of the preceding disclaimer) every effort has been made to check drug dosages; however it is still possible that errors have been missed. Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons the reader is strongly urged to consult the drug companies’ printed instructions before administering any of the drugs recommended in this book. British Library Cataloguing in Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging-in-Publication Data A catalog record for this book is available from the Library of Congress ISBN-10: 0 340 81003 3 ISBN-13: 978 0 340 81003 3 1 2 3 4 5 6 7 8 9 10 Commissioning Editor: Serena Bureau Development Editor: Layla Vandenbergh Production Controller: Jane Lawrence Cover Design: Nichola Smith Typeset in 9/11pt Minion by Charon Tec Pvt. Ltd, Chennai, India www.charontec.com Printed and bound in Malta

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Contents Preface 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27

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Research methodology and statistics Descriptive psychopathology Schizophrenia Affective disorders Neurotic disorders Personality: development and disorders Eating disorders Human sexuality Alcohol dependence Drug dependence and gambling Suicide and non-fatal deliberate self-harm Uncommon psychiatric syndromes Organic psychiatry Psychiatric aspects of epilepsy and sleep disorders EEG and brain imaging in psychiatry Psychophysiological, somatoform, dissociative and related disorders Psychogeriatrics Forensic psychiatry Child psychiatry Mental retardation Drug therapy Physical treatments Psychotherapy Community-orientated psychiatry Specific psychiatric problems of women Transcultural psychiatry Psychiatry and the Internet

1 13 24 43 60 77 86 96 109 123 134 144 150 175 185 195 205 215 233 253 266 289 297 312 318 328 333

Index

337


Preface As with any subject worthy of human study and endeavour, pshychiatry develops, understandings change, new facts emerge or old ones are seen in a new light. Since the first edition of this book some 20 years ago there have been tremendous advances in neuroscience and, as a result, major new insights into the functioning of the brain have emerged. Yet, at the same time, major changes are also taking place in the organization and delivery of mental health services throughout the world. We hope that the fourth edition of this widely read text will prove even more useful to mental health trainees of various disciplines (psychiatrists, psychologists, nurses and other professionals), to interested medical students, and to mental health clinicians wishing to prepare lectures or brush up on the main essentials of psychiatry. This edition has been almost totally revised and, inevitably, expanded. Almost every subject has been revisited in the light of the most current knowledge and theories. ‘New’ conditions (e.g. Internet addiction) and new investigations (e.g. functional MRI) sit beside all the old favourites. References are included where these are considered to be ‘key’ papers or reviews which could be quoted and which readers should look up for themselves. There are also suggestions for further reading. Finally, we would reiterate what we have written in previous prefaces, that this book is not intended as a substitute for wider reading or experience, but as a detailed and comprehensive aide-mémoire. In order to gain fluency in the subject, readers might carry it with them, rehearse its content, follow up its references, debate its currently received wisdom and enjoy the fruits of their labours by achieving the success that their endeavours deserve. Peter Buckley Del Prewette Jonathan Bird Glynn Harrison

Acknowledgements Material in Tables 3.1, 3.3, 4.1, 5.1, 6.1, 7.3, 7.4, 8.1, 16.1, 18.1 and 19.1 is reproduced, with permission from: The ICD-10 classification of Mental and Behavioural Disorders: Diagnostic Criteria for Research. Geneva, World Health Organization, 1993. Material in Tables 3.2, 3.8, 7.3, 7.4 and 18.1 is reproduced, with permission from: The Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American Psychiatric Association.


Research methodology and statistics

1

PHILOSOPHY OF SCIENCE Science is only one approach to understanding the world. According to Popper, it involves:

• • • • • •

Hypothesis formulation. Observation based on the hypothesis. Attempts to falsify the hypothesis. Control of variables. Predictions based on the hypothesis. Replication of results.

HOW TO DO RESEARCH 1 2 3 4 5 6 7 8 9 10

Find a problem – from everyday practice, past research or theory. Formulate a testable hypothesis on the basis of observation and a literature search. Define the variables to be studied. Design an experiment to measure the variables and thus to test the hypothesis. Run a pilot experiment to explore difficulties. Seek funding. Redesign the experiment as necessary. Run the main experiment. Collect and analyse the data. Publish so as to allow for replication.

PLANNING RESEARCH Write a protocol:

• •

Title Introduction – survey of background information and reasons for doing the research

2

RESEARCH METHODOLOGY AND STATISTICS

• •

Statement of hypotheses to be tested Description of method: – Sample and target populations – Method of sample selection – Information to be gathered – Methods of gathering information – Design of study – Discussion of reliability and validity – Statistical methods to be used and power calculation Facilities and resources required: – Personnel – Equipment – Space – Time – Costs Ethical aspects and responsibility for the experiment Anticipated problems.

•

• •

BASIC DEFINITIONS VARIABLES Variables are any constructs or events which research studies.

• • • • •

Independent variable – the antecedent condition manipulated by the experimenter (e.g. drug levels). Dependent variable – the variable used to measure the effect of the independent variable (e.g. recovery rates). Confounding variable – any extraneous variable whose potential influence on the dependent variable has not been controlled for; a source of error (e.g. age or sex imbalances). Controlled variable – a variable whose influence is kept constant by the experimenter (e.g. other medications). Uncontrolled variable – a variable which is not manipulated or held constant, though it may be measured (e.g. life events).

RESEARCH DESIGN Simple designs may be:

• •

Cross-sectional in time Longitudinal in time.

They may also be:

• • •

Between-group Within-group Within-individual.

BASIC DEFINITIONS

3

Designs may also be:

• • • •

Cross-over – patients used as their own controls. Longitudinal – in time. Double-blind – observer and patient are unaware of independent variables when assessing dependent variables. Latin square – variables are allocated randomly to subjects and longitudinally in time.

Longitudinal designs may be:

• • •

Retrospective – observations in the present to elicit information about past events; may be methodologically unsatisfactory owing to information bias. Prospective (cohort study) – ongoing gathering of information after the event studied; may be difficult and expensive but methodologically sounder. Mixed – retrospective study to elicit desired group of subjects, then prospective follow-up.

Research may be:

• • •

Normothetic – information derived from classifying a number of events and experiences. Ideographic – information derived from a single event or individual. Operationally defined – precise definition of terms used, in measurable quantities or attributes; these are essential for effective research and communication.

RELIABILITY Reliability is the extent to which there is repeatability of an individual’s score or other test result.

• • • •

Test–retest reliability – high correlation between scores on the same test given on two occasions. Alternate-form reliability – high correlation between two forms of the same test. Split-half reliability – high correlation between two halves of the same test. Inter-rater reliability – high correlation between results of two or more raters of the same test.

Inter- or intra-reliability is measured using intraclass correlation coefficient (ICC – range 0–1; ICC of ⭓0.7 is acceptable). VALIDITY Validity is the extent to which a test measures what it is designed to measure.

• • •

Predictive validity – ability of the test to predict outcome. Content validity – whether the test selects a representative sample of the total tests for that variable. Construct validity – how well the experiment tests the hypothesis underlying it.

The ‘reliability paradox’ is that a very reliable test may have low validity precisely because its results do not change; i.e. it does not measure true changes.

4


SAMPLE SELECTION (see also Chapter 21)

• • • • • • •

Target population – the whole population from whom information could be gathered (e.g. all chronic schizophrenics). This is studied in a census. Sample population – the subsection of a target population which is actually under study (e.g. the chronic schizophrenics in one area). This is studied in a survey. A sample population should be selected in such a way that generalized inferences may be made. Such inferences are always statements of probability. Bias – the difference between the sample population result and the true target population result. Bias is caused by inaccurate sampling. Random sampling – selection of a sample population such that each member of the target population has a calculable, non-zero and usually equal probability of being selected. Stratified sampling – the target population is divided into a number of strata (e.g. age groups) and sampling occurs within each stratum. Multiphase sampling – some information is gathered from the whole sample population, but additional information is gathered from subsamples. Multistage sampling – further information is gathered at a later date from the original sample population.

A control group is used to hold constant or eliminate any possible confounding variables. It is a sample population which receives no treatment or some standard treatment, as a comparison with the population which does receive the experimental treatment or manipulation.

MEASUREMENT IN PSYCHIATRIC RESEARCH QUESTIONNAIRES, INTERVIEWS AND CASE-NOTE STUDIES Aims may be:

• • •

To identify psychiatric cases To diagnose psychiatric disorder accurately To assess severity and change in severity.

Collect information by:

• • • •

Document studies – case notes, which are retrospective, not written with research in mind; journal articles; official studies, e.g. census. Mail questionnaires – cheap and easy but low response rate, hence sampling bias. Self-rating questionnaires – cheap, easy, sensitive to changes, but may be answered inaccurately due to misunderstanding; cannot be complex. Observer-rater interview – may be structured, semi-structured or informal; allow great flexibility and accuracy but are expensive and require training. See Table 1.1.

SOURCES OF ERROR

• •

Response set – subject always tends either to agree or to disagree with questions. Bias towards centre – subject tends to choose the middle response and shun extremes.

MEASUREMENT IN PSYCHIATRIC RESEARCH

Table 1.1 Commonly used psychiatric instruments Evaluation

Scale

Comments

General health

General Health Questionnaire (GHQ) Clinical Global Impressions (CGI)

Commonly used screening, used in primary care and general population studies. Global observation of severity of psychiatric illness, 7-point scale. Very commonly used observational scale, mostly used for inpatients with psychosis. Evaluates social functioning and severity of symptoms. 90-item checklist of 9 symptom dimensions, with 3 global indices of distress. Generates Research Diagnostic Criteria diagnosis. Generates RDC or DSM-III-R diagnosis of psychotic disorders. Incorporates Present Status Examination 10 with an updated CATEGO program. Evaluates different time periods – primary and secondary and lifetime. Generates both ICD-10 and DSM – IV diagnoses. Generates DSM-III-R diagnosis.

Global assessment/screening

Nurses Observation Scale for Inpatient Evaluation (NOSIE) Global Assessment Scale (GAS)

Structured interview schedules

Hopkins Symptom Checklist (SCL-90) NIMH Diagnostic Interview (DIS) Schedule for Affective Disorders and Schizophrenia (SADS) Schedule for Clinical Assessment in Neuropsychiatry (SCAN)

Schizophrenia

Depression

Mania Anxiety

Obsessive–compulsive disorder

Psychosomatic/eating disorders

Personality

Structured Clinical Interview for DSM-III-R (SCID) Brief Psychiatric Rating Scale (BPRS)

Widely used measure of psychotic symptoms (not just schizophrenia) and psychopathology, 18 items. Comprehensive Assessment of Evaluates major psychoses re: symptoms, past Symptoms and History (CASH) history, premorbid function and cognitive status. Schedule for the Assessment of Details hallucinations, delusions, bizarre Positive Symptoms (SAPS) behaviour, formal thought disorder. Schedule for the Assessment of Details alogia, affective blunting, avolition, Negative Symptoms (SANS) asociality, attentional impairment. Positive and Negative Symptoms Developed from BPRS, more detailed, more Scale (PANSS) structured, includes general psychopathology section. Beck Depression Inventory (BDI) Self-rating, 21 items. Hamilton Depression Scale (HamD) Observer rating, 17 items and severity dimension, widely used in depression research. Zung Depression Scale Self-rating, 20 items. Young Mania Scale 11-item observer scale. Hamilton Anxiety Rating Scale 14-item observer scale covering psychic and (HARS) somatic dimensions. Zung Anxiety Scale Combined observer and brief report formats, 20 items. Maudsley Obsessional– Self-report, 30 items. Compulsive Inventory (MOCI) Yale-Brown Obsessive– Observer scale, 19 items. Compulsive Scale (YBOCS) Eating Attitudes Test (EAT) Self-report on eating behaviour. McGill Pain Questionnaire Detailed self-report. Psychosocial Adjustment to Self-report and interview – based on adjustment Illness Scale (PAIS) to (chronic) illness. Eysenck Personality 90-item questionnaire yielding sub-scales of Questionnaire (EPQ) neuroticism, extroversion, psychoticism, lie score. (Continued)

5

6


Table 1.1 Continued Evaluation

•

Self-rating questionnaire, validated on psychiatric patients not normally given ‘personality profile’. Produces 5 diagnostic categories plus dimensional trait scores. Cut down on drinking; annoyed by others criticizing; guilty over drinking; eye-opener. 25-item interview or 10-item self-report formats.

Substance abuse

Child disorders

Michigan Alcoholism Screening Test (MAST) Severity of Alcohol Dependency Questionnaire (Stockwell Questionnaire) Child Behaviour Checklist (CBCL)

Mental retardation

•

Comments

Minnesota Multiphasic Personality Inventory (MMPI) Personality Assessment Scale (PAS) CAGE

Geriatric disorders

•

Scale

Child Assessment Schedule Mini Mental Status Examination (MMSE) Katz Activity of Daily Living Index Adaptive Behaviour Scales (ABS)

Measures impact of alcoholism.

Many versions according to child’s age, self-report/parent/teacher informant. Semistructured interview schedule. Very widely used 19-item test. 6-item observer scale for staff and/or family members. 110-item observer scale of social life, symptoms and behaviour.

Social acceptability – subject chooses the acceptable answer rather than the true one. Halo effect – answers are chosen to ‘fit’ with previously chosen answers; responses become what is expected by the observer. Hawthorne effect – researchers alter the situation by their presence.

PSYCHOMETRIC TESTING Psychological tests must be:

• • •

Standardized – as regards both the procedure (i.e. it is repeatable) and the scores produced (i.e. it is related to normative data). Reliable. Valid.

Psychological tests may assess general intelligence, personality or neuropsychological status:

•

General intelligence, e.g.: – Stanford–Binet – in which mental age is assessed as a ratio of chronological age, giving a mean IQ of 100. – Wechsler Adult Intelligence Scale – a series of subtests of verbal and performance aspects of intelligence allows more detailed breakdown of scores and assessment of discrepancies.

STATISTICS

•

•

7

Personality, e.g.: – Minnesota Multiphasic Personality Inventory – Eysenck Personality Inventory – Projective tests – which analyse fantasy material (e.g. Rorschach Ink Blot Test, Thematic Apperception Test). Neuropsychological status: – Usually aimed at assessing whether diffuse or focal brain change is present, whether localization of pathology is possible, and what rehabilitation measures might help. – Screening tests used include Bender Gestalt, Benton Visual Retention Test, Trail Making Task, Memory for Designs, WAIS, Wechsler Memory Scale. – Batteries of tests are often used – e.g. the Halstead–Reitan and Luria–Nebraska batteries.

Also assess interests, aptitudes and attitudes.

PSYCHOPHYSIOLOGICAL TECHNIQUES These are the quantification of biological events as they relate to psychological variables.

• • •

Tend to measure non-specific arousal. Measure base levels, degree of response and habituation (the reduction of response with repeated stimuli). Measures taken include: – Sweat gland activity – galvanic skin response (GSR) – Forearm blood flow – Electromyography – Electroencephalography – Pulse – Blood pressure – Salivation – Pupil size.

STATISTICS DESCRIPTIVE STATISTICS These simply summarize the data. MEASURES OF CENTRAL TENDENCY

• • •

Mode – the most commonly occurring score. Mean – sum of scores divided by number of scores. Median – the middle score, i.e. the score below which 50% of scores fall.

8


MEASURES OF DISPERSION

• • • • • • •

Range – from largest to smallest score. Variance – a measure of the dispersion of data about the mean; the average squared deviation from mean. Standard deviation – 64% of scores in a normal distribution fall within one standard deviation either side of the mean; square-root of the variance. Standard error – an estimate of the discrepancy between sample mean and true population mean; standard deviation divided by square-root of number of cases. Z score – number of standard deviations on each side of the mean. Skewness – measures deviation from the normal distribution curve. Kurtosis – measures peakedness or flatness of curve.

INFERENTIAL STATISTICS These assess the meaning of the data.

• • • • • • • • • •

Null hypothesis – The first step in the decision-involving process. The hypothesis that there is no significant difference between comparison groups or any difference is only due to chance. P (probability) value ⫽ 0.01 says there is a one-in-a-hundred chance of finding any given difference. Type I error – null hypothesis is erroneously rejected (i.e. there is no difference but an apparent one is shown). Multiple comparisons (‘throwing the dice’) increase the risk of type I error; this may be taken into account by resetting the probability level using a Bonferroni correction test. Type II error – null hypothesis is erroneously accepted (i.e. a true difference is not shown). Small sample sizes predispose to type II errors. The power of a study to detect differences (␣ value) is related to sample size. Correlation coefficient (CC) – measures the statistical relationship between two variables, without assuming that either is dependent or independent; i.e. no causality is assumed (CC ⫽ 1.0 implies exact similarity; CC ⫽ 0.0 implies no relationship). Pearson’s product moment correlation – the most widely used parametric test of correlation (r ⫽ ⫺1 implies inverse relationship; r ⫽ ⫹1 implies positive relationship; r ⫽ 0 implies no relationship). Spearman’s rank correlation (rs) – non-parametric equivalent test to Pearson’s, for ordinal data. Regression coefficient (R) – measures strength of dependency of one variable on the independent variable; R2 describes the amount of shared variance between these variables. Regression analysis – determines the predictive power of each successive variable upon the outcome variable; uses multivariate statistical tests (e.g. MANOVA), with each variable independently entered into a regression equation or model. Parametric statistics – assume a normal distribution (see Table 1.2). Non-parametric statistics – do not assume a normal distribution; less powerful, less dependent upon sample size (see Table 1.2).

STATISTICS

9

Table 1.2 Parametric and non-parametric tests Parametric tests

Non-parametric tests

(Student’s) t-test Analysis of variance (F test/ANOVA) Analysis of covariance (ANCOVA)

Chi-squared (␹2) Analysis of variance Mann–Whitney U test Kruskal–Wallis analysis of covariance (ANCOVA)

Student’s t-test can use paired or non-paired relationships between variables, so that either within-subject or between-subject comparisons can be studied. ANOVA may be one- or two-way ANOVA (takes multiple relationships into account). ANCOVA ‘partials out’ an observed effect that may contribute to group difference (e.g. gender, educational status).

• • •

Factor analysis – segregates data into the minimum number of dimensions that define a group (e.g. principal component analysis, principal factor analysis, eigenvalue determination, verimax factor rotation). It is used, e.g., to generate positive, negative and disorganization syndromes in schizophrenia (see Liddle, 1987). Cluster analysis – segregates data into groups, but with some overlap; e.g. Pakel’s classification of depression (see Chapter 4). Meta-analysis – statistical technique in which related data from numerous studies on a topic are pooled to determine the size and strength of a proposed association; e.g. treatment response in schizophrenia and dose of atypical antipsychotics (see Leucht et al., 2003).

THE PLACEBO EFFECT A placebo is any therapeutic procedure (or that component of a therapeutic procedure) which is given deliberately to have an effect, or which unknowingly has an effect on the patient’s symptom, disease or syndrome, but which is objectively without specific activity for the condition treated. The placebo is also used to describe an adequate control in experimental studies. A placebo effect is defined as the changes produced by placebo. The placebo effect is influenced by:

• • • •

Expectations of the patient – general characteristics of placebo responders are: younger patients of lower intelligence, higher levels of anxiety, extraversion, and possibly more females than male. Status and attitude of the person prescribing. Nature of the placebo – tablet size, shape, colour, etc. (e.g. smaller tablets viewed as more potent). Condition being treated – possibly more effective in acute complaints, including headache, sickness, postoperative pain.

Modes of action are not understood. It is unlikely that it works purely by suggestion, as patients with hysterical conversion symptoms respond poorly. Side-effects are often reported: frequently dry mouth, headache, nausea and drowsiness. More severe reactions have been reported, including hypersensitivity reactions and withdrawal phenomena.

10


DESIGNING A TRIAL See Freeman and Tyrer (1992). Patient selection Specify inclusion and exclusion criteria, source of recruitment, diagnostic criteria (operationally defined). Treatment Prepare active drug in a form identical to the placebo or to a comparison drug. Ensure that new drug and standard drug have similar bio-availability. Compliance should be assessed in outpatients at least by a tablet count. Plasma drug level may also be monitored. Control group Important variables influencing response must be spread across the treatment and control groups (i.e. age, sex, duration of symptoms). Randomization must be ensured. Crossover designs, where patients receive two or more treatments one after the other, should ensure ‘order effect’. Ensure adequate ‘washout’ to avoid overlapping of patients, and exclude rapid placebo responders. Evaluation Each outcome variable should be precisely defined, objective and reliably detected. Use standardized rating scales with training of observers for inter-rater reliability. Ensure ‘blindness’ as far as possible. Trial size The number of subjects needed should be calculated from the proportion of patients expected to respond, and the smallest difference between treatments considered worth measuring. Power analysis should be part of the initial protocol. Analysis and presenting results Explain all patient withdrawals. Present each patient’s responses, where possible, to demonstrate variations. For treatment studies with missing data points, survival analysis or ‘intent-to-treat’ statistical approaches as appropriate. Subject data to statistical analysis ensuring correct methods are used in view of numbers of patients, spread of data, etc. Remember that the more significance tests used, the more likely are some false positives to appear by chance (type 1 error) unless a ‘multiple contrast’ adjustment is used. Consult a statistician at time of trial design, not after conclusion. Conclusions should present a balanced appraisal of evidence. Avoid illustrations and diagrams which exaggerate treatment differences.

REVIEWING A RESEARCH PUBLICATION

• •

Title and abstract – should be interesting, informative. Introduction – should provide review of topic, contain key references and provide a clear rationale as to why study was performed.

REFERENCES AND FURTHER READING

• • • •

11

Methods – ideally, readers should be able to perform study on the basis of the depth of description. Sample should be appropriate in selection and size; also, wellmatched with controls. Results – clearly stated, no excess of analyses (Bonferroni correction, if needed). Tables and figures enhance clarity and interpretation of results. Discussion – major findings should be explicitly stated; should not be overinterpreted. Methodological constraints should be acknowledged. References – should be scholarly. Other relevant work of the authors cited; not under/over-referenced. Readers need to know some background of topic to judge merit of the study, its importance – breaking new ground or replication?

EVIDENCE-BASED MEDICINE (EBM) AND PSYCHIATRY

• • • •

EBM is the integration of the best research evidence with the expertise of the clinician in delivering care to individual patients (Sacket et al., 2000). Swift access to the latest published scientific data is available from numerous commercial, as well as free, Internet sites (see Chapter 26). EBM allows guidelines to be formulated that aid the clinician in making an accurate diagnosis and prescribing the most effective treatment. The central limitation of EBM involves the reliability of the scientific evidence. In psychiatry, EBM is further encumbered by the relative lack of neuropathology with many psychiatric illnesses and the complexity of psychosocial aspects of individuals.

REFERENCES AND FURTHER READING Bech P, Malt UF, Dencker SJ et al. (1993) Scales for assessment of diagnosis and severity of mental disorders. Acta Psychiatr. Scand. 372(87). Brandon TH, Irvin JE, Hendricks PS et al. (2002) The increasing power of placebos in trials of antidepressants. JAMA 288, 44. Cooper B (2003) Evidence-based mental health policy: a critical appraisal. Br. J. Psychiatry 183, 10. Croudace T, Evans J, Harrison G et al. (2003) Impact of the ICD-10 Primary Health Care (PHC) diagnostic and management guidelines for mental disorders on detection and outcome in primary care: cluster randomized controlled trial. Br. J. Psychiatry 182, 20. Daley LE, Bourke GJ, McGilvray J (1991) Interpretation and Uses of Medical Statistics. Blackwell Scientific, Oxford. Edwards E, Kornacki MJ, Silversin J (2002) Unhappy doctors: what are the causes and what can be done? BMJ 324, 83. Everitt BS, Dunn G (1992) Applied Multivariate Data Analysis. Edward Arnold, Oxford. Freeman C, Tyrer P (1992) Research Methods in Psychiatry: a Beginner’s Guide, 2nd edn. Gaskell, London. Gilbody SM, Whitty P (2002) Improving the delivery and organization of mental health services: beyond the conventional randomized controlled trial. Br. J. Psychiatry 180, 1. Gilbody SM, House AO, Sheldon TA (2002) Outcomes research in mental health: a systematic review. Br. J. Psychiatry 181, 170. Higgit A, Fonagy P (2002) Reading about clinical effectiveness. Br. J. Psychiatry 181, 170.

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Hrobjartssom A, Gotzsche PC (2001) Is the placebo powerless? An analysis of clinical trails comparing placebo with no treatment. New Engl. J. Med. 344, 159. Kotzin S (2002) MEDLINE and PubMed will be able to synthesise clinical data. BMJ 324, 79. Lancet (1993) Facts, figures and fallacies [series on statistics]. Lancet 342, 15. Leucht S, Wahlbeck K, Hamann J, Kissling W (2003) New generation antipsychotics versus low-potency conventional antipsychotics: a systematic review and meta-analysis. Lancet 361, 1581. Leuchter AF, Cook IA, Witte EA et al. (2002) Changes in brain function of depressed subjects during treatment with placebo. Am. J. Psychiatry 159, 12. Liddle PF (1987) The symptoms of chronic schizophrenia: a reexamination of the positive– negative dichotomy. Br. J. Psychiatry 151, 14. Rose D (2003) Collaborative research between users and professionals: peaks and pitfalls. Psychiatr. Bull. 27, 40. Sackett DL, Straus SE, Richardson WS et al. (2000) Evidence Based Medicine: How to Practice and Teach EBM. Churchill Livingston, New York. Safer DJ (2002) Design and reporting modifications in industry-sponsored comparative psychopharmacology trials. J. Nerv. Ment. Dis. 190, 58. Snaith P (1993) What do depression rating scales measure? Br. J. Psychiatry 163, 29. Stolk P, Berg MJ, Hemels ME, Einarson TR (2003) Meta-analysis of placebo rates in major depressive disorder trails. Ann. Pharmacother. 37, 189. Swales J (2000) The troublesome search for evidence: three cultures in need of integration. J. R. Soc. Med. 93, 40. Tansella M (2002) The scientific evaluation of mental health treatments: an historical perspective. Evidence Based Mental Health 5, 4. Thompson C (1989) The Instruments of Psychiatric Research. John Wiley, Chichester. Trivedi P, Wykes T (2002) From passive subjects to equal partners: qualitative review of user involvement in research. Br. J. Psychiatry 181, 46. Tryer P, King M, Fluxman J (2003) Treatment of common mental disorders in general practice: are current guidelines useless? Br. J. Psychiatry 183, 7. Williams DD, Garner J (2002) The case against ‘the evidence’: a different perspective on evidencebased medicine. Br. J. Psychiatry 180, 8.

Descriptive psychopathology

2

Descriptive psychopathology attempts to portray in words, as subtly and accurately as possible, the nature of experiences, perceptions and behaviour. It defines, differentiates and inter-relates such experiences. It owes a great deal to the philosophical discipline called ‘phenomenology’ – a method (developed by Husserl) of scrupulously inspecting one’s own conscious processes, without assuming anything about external causes or consequences of those ‘phenomena’ and without altering the phenomena by observational methods. This school of thought has influenced psychiatry through the philosopher/ psychiatrist Karl Jaspers. The development of sympathy and intuitive understanding allows for the objective observation of phenomena in others, by relating them to phenomena in ourselves. Descriptive psychopathology may be seen, with epidemiology, as a scientific basis for the practice of psychiatry. It should not be confused with ‘dynamic psychopathology’ – the attempt to explain the phenomena of mental disorder in terms of psychodynamic theories of aetiology.

DISORDERS OF APPEARANCE AND BEHAVIOUR Appearance (state of health, posture, cleanliness, clothing, self-care) is an important indication of other mental functions. Mood may be expressed in the form of:

• • •

Appearance (facial expression, posture) Manner (response to others) Motility (degree and form of movements).

MOTOR DISORDERS (OF GENERAL BEHAVIOUR) The degree and quality of activity are important. There may be increased restless motor activity in agitation or in hypomania, but the quality will differ.

14

DESCRIPTIVE PSYCHOPATHOLOGY

The form of abnormal movements may be classified (after Hamilton, 1974) as follows. DISORDERS OF ADAPTIVE MOVEMENTS

• • •

Expressive behaviour – e.g. tearfulness, unhappy facial expression, paucity of movements or downcast appearance in depression; laughing, expansive gesturing and overactivity in hypomania. Obstruction – seen in catatonia and consisting of irregular hindrance and blocking of movements. Mannerisms – abnormal, repetitive goal-directed movements (e.g. bizarre methods of walking or eating) commonly seen in chronic schizophrenia.

NON-ADAPTIVE MOVEMENTS Spontaneous movements – habitual, not goal-directed Tics are sudden involuntary twitchings of groups of muscles, particularly facial (seen in extreme form in Gilles de la Tourette syndrome). • Static tremor of hands, head or upper trunk indicates anxiety, hyperthyroidism, hysteria or ‘essential’ tremor, lithium toxicity, parkinsonism. • Spasmodic torticollis involves spasm of neck muscles with twisting of head, which may become permanent. • Chorea is abrupt, random jerky movements resembling fragments of goal-directed behaviour. • Athetosis is slow, semi-rotary writhing movements. • Orofacial dyskinesia is restless movements of tongue, mouth and facial muscles (seen in the elderly and following chronic neuroleptic ingestion). • Stereotypies are regular, repetitive non-goal-directed movements; e.g. repetitive foot tapping, body rocking. Stereotyped utterances can occur. Stereotypies are seen in chronic schizophrenia, mental handicap and infantile autism.

•

Induced movements Automatic obedience – the subject does whatever is asked of him or her. Echopraxia – the subject imitates the movements of the interviewer. Echolalia – words or phrases are imitated. Perseveration – the senseless repetition of a previously requested movement; i.e. the repetition of a response after withdrawal of the stimulus. Special variants of this are palilalia (the perseverated word is repeated with increasing frequency) and logoclonia (perseveration of the last syllable of the last word). These are seen in organic disorders and occasionally in catatonia. • Forced grasping – the offered hand is repeatedly grasped and shaken, despite requests not to do so. Seen in frontal lobe lesions. • Mitmachen – the body can be put into any posture, despite instructions to resist. • Mitgehen – an extreme form of mitmachen in which very slight pressure leads to movement in any direction. • Negativism – apparently motiveless resistance to suggestion or attempts at movement.

• • • •

DISORDERS OF PERCEPTION

15

Disorders of posture • Postural mannerisms – strange and abnormal postures adopted habitually. • Perseveration of posture – may be seen in schizophrenia and lesions of the midbrain. If the subject’s body is placed in an awkward posture and left, the posture is held for a period before slowly relaxing, despite asking the patient to relax. If a plastic resistance is felt to initial movement, this is termed ‘waxy flexibility’ (or flexibilitas cerea).

DISORDERS OF PERCEPTION SENSORY DISTORTIONS Sensory distortions are changes in the quality, intensity or spatial form of a perception. Examples are:

• • •

Hyperacusis – in mania, hyperthyroidism. Hypoacusis – in some acute organic states. Xanthopsia, micropsia – produced by psychedelics and temporal lobe lesions.

SENSORY DECEPTIONS Hallucinations Hallucinations are perceptions which arise in the absence of any external stimulus (Esquirol, 1833). They are actual sense deceptions, not distortions of real perceptions. Hallucinations are perceived as being located in the external world. They are perceived as having the same qualities as normal perceptions – i.e. vivid, solid. Hallucinations are not subject to conscious manipulation, in the same sense that normal perceptions cannot be produced or dismissed at will. Illusions Illusions are distortions of perceptions of real objects; e.g. flowery wallpaper is perceived as swarming snakes. Illusions are perceived as having the same qualities as normal perceptions, but often are more fleeting than hallucinations. Pseudohallucinations Pseudohallucinations are not perceived by the actual sense organs, but experienced as emanating from within the mind. They are a form of imagery. Although vivid they lack the substantiality of normal perceptions. Pseudohallucinations are located in subjective rather than objective space. They are not subject to conscious control or manipulations. Other mental images • Eidetic images – previous perceptions are reproduced as a mental image of vivid intensity and uncanny detail. May be regarded as a form of pseudohallucination. • Pareidolia – vivid mental images occurring without conscious effort when perceiving an ill-defined stimulus; e.g. glowing fire.

16


DISORDERS OF THOUGHT DISORDERED CONTENT DELUSIONS A delusion is a fixed false idea held in the face of evidence to the contrary, and out of keeping with the patient’s social milieu.

• • • • •

Held unshakeably. Not modified by experience or reason. Content often bizarre. Not dependent on disintegration of general intellectual functioning or reasoning abilities. Often infused with a sense of great personal significance.

Types • Autochthonous or primary delusions have no discernible connection with any previous interactions or experiences. They arise fully formed as sudden intuitions, like sudden ‘brainwaves’. They are often preceded by a period of ‘delusional mood’ (or ‘delusional atmosphere’) in which the subject is aware of something strange happening; he/she then suddenly realizes the personal significance of this feeling with a complete delusional understanding. This period of delusional perception is seen as having two stages: first, the real perception of some object or event and, second, the delusional misinterpretation of that event. • Secondary delusions emerge understandably from other psychic experiences or current preoccupations; e.g. prevailing affect, fears, personal stress, habitual attitudes of mind. • Overvalued ideas are intense preoccupations with marked associated emotional investment. The patient holds tenaciously to the idea, demonstrably false, with virtual certainty but not unshakeable conviction. OBSESSIONS AND COMPULSIVE PHENOMENA

• •

‘Obsession’ refers to impulses and thoughts. ‘Compulsion’ is confined to motor acts.

Obsessional phenomena describes persistent intrusion into consciousness of unwanted thoughts, feelings or impulses, despite the individual’s recognition of their senseless nature and resistance to them. Although rejected by the individual, phenomena are owned as being ‘his’ or ‘hers’ (cf. passivity phenomena experienced as being something imposed from outside). Thoughts are often of a repugnant or bizarre nature, e.g. violent, sexual and blasphemous themes. These thoughts are resisted initially, at the cost of mounting anxiety. Resistance may lessen after time. PASSIVITY PHENOMENA Passivity phenomena are a variety of phenomena which have in common the apparent disintegration of boundaries between the self and the surrounding world. The individual

DISORDERS OF THOUGHT

17

experiences outside control of, or interference with, his/her thinking, feeling, perception or behaviour.

• • •

Thought insertion and withdrawal – the experience of thoughts being put into or taken out of the mind by some external agency or force. Thought broadcast – the experience that others can read or hear the individual’s thoughts as they are ‘broadcast’ from him or her. ‘Made actions’ – either simple motor actions or more complex patterns of behaviour are experienced as being caused by an outside agency.

DISORDERED FORM OF THINKING ACCELERATED TEMPO This produces increased rate of delivery of speech (‘pressure of speech’) and ‘flight of ideas’. There is loss of coherent goal-directed thinking with increasingly obscure associations between ideas. Vague connections may be prompted by rhyme, sounds of words (‘clang associations’) and associations only acceptable in other contexts. Punning is a common feature. It is characteristic of hypomania, mania and may occur in delirium, and in rare organic states, e.g. hypothalamic lesions. DECREASED TEMPO – PSYCHIC RETARDATION Subjectively experienced as ‘muzziness in thinking’ or difficulty in concentration, leading to difficulty in decision-making and pseudo-dementia. It is characteristic of retarded depressive states; said to occur rarely in manic stupor. SCHIZOPHRENIC THOUGHT DISORDER Bleuler considered disturbance of association of ideas to be a fundamental feature of schizophrenia. In contrast to the thought disorder of hypomania, the logical associations between ideas are not only loosened, but often incomprehensible to the listener. See also Table 2.1.

• • • •

Omission – a sudden discontinuation of a chain of thought. Derailment – a disruption of the continuity of speech by the insertion of novel and inappropriate material to the chain of thought. Fusion – a merging and ‘interweaving’ of separate ideas. Drivelling – refers to the muddling of elements within an idea to the extent that the meaning is totally obscured to a listener. Table 2.1 Some descriptive terms Clinician

Descriptive terms

Bleuler (1951) Cameron (1944) Goldstein (1944) Schneider (1959)

Loosening of associations, condensation Overinclusive thinking Concrete thinking Derailment, drivelling, desultory thinking, fusion, omission, substitutions

18

•


Desultory thinking – ideas are expressed correctly in terms of syntax and grammatical construction, but juxtaposed inappropriately. The ideas would be comprehensible if expressed in another context or in isolation.

Other features of schizophrenic thought disorder Thought blocking – a sudden cessation of speech mid-sentence with an accompanying sense of subjective distress. A patients may complain that his/her mind has ‘gone blank’ or that his/her thoughts have been interfered with. • Clang associations – Verbal stereotypy – repetition of a word or phrase which has no immediate relevance to the context. – Condensations – common themes from two or more separate ideas are combined to form an incomprehensible concept.

•

DISORDERS OF EMOTION

• •

Mood – the emotional ‘tone’ prevailing at any given time. A ‘mood state’ will last over a longer period. Affect – synonymous with ‘emotion’ and also meaning a short-lived feeling state. Related to cognitive attitudes and understandings, and to physiological sensations. When examining for disorders of emotion, look for:

1 The quality of the emotion: anxiety, sadness, cheerfulness, suspiciousness, irritability, apathy 2 The appropriateness of the emotion to what is being said and to behaviour 3 The constancy of the emotion at interview and what factors appear to influence it. ABNORMAL EMOTIONAL PREDISPOSITION Abnormal emotional predisposition is found in disorders of personality and signifies a consistent tendency to particular stereotyped emotional expressions. Thus a person may be:

• • • •

Dysthymic – always tending to be sad and miserable. Hyperthymic – always tending to be overcheerful, unrealistically optimistic. Cyclothymic – tending to marked swings of mood from cheerful to unhappy. Affectless – emotionally cold and indifferent.

ABNORMAL EMOTIONAL REACTIONS

• •

Anxiety is a fear with no adequate cause. Fear and anxiety may be normal experiences, but are regarded as pathological if they are excessive or prolonged, or interfere markedly with normal life. Anxiety is usually accompanied by somatic and autonomic changes. Depression is a feeling of misery, inner emptiness, hopelessness and helplessness, accompanied by morbid preoccupations. Such emotions may be normal in the bereaved, but are regarded as pathological if excessive, prolonged, and accompanied

DISORDERS OF SELF-AWARENESS

• •

19

by disturbance of appetite, sleep, concentration, etc., or by depressive delusions. Depression is often associated with (or may present as) somatic complaints, hypochondriasis or a feeling of bodily insecurity. Euphoria and ecstasy are excessive and unrealistic cheerfulness and a feeling of extreme well-being. Apathy is the loss of all feeling. No emotional response can be elicited.

ABNORMAL EXPRESSION OF EMOTION

• • • •

• • •

Denial or dissociation of affect – as seen in hysteria (la belle indifférence) or occasionally in situations of extreme danger. Emotional indifference – as may be seen in ‘psychopathic’ disorder. Expected emotional response is not shown to others, or to his/her own antisocial behaviour. Perplexity – anxious and puzzled bewilderment. Seen in early schizophrenia and confusional states. Emotional incongruity – the abnormal presence or absence of emotions; e.g. fatuous euphoria in a situation which would normally evoke a depressed mood. The criterion of ‘understandability’ is therefore employed; i.e. the mood is not understandable to the ‘normal’ person. Emotional incongruity is characteristic of acute schizophrenic disorder. Emotional blunting – insensitivity to the emotions of others and a dulling of the normal emotional responses. It is characteristic of chronic schizophrenia. Emotional lability – rapid fluctuations of emotion. The emotions may be appropriate in a less intense form, but the rapid change is not. Emotional lability is seen in organic disorders, brain stem lesions, mania, and some personality disorders. Emotional incontinence – an extreme form of emotional lability, with complete loss of control over the emotions. It is seen in organic disorders, especially pseudobulbar palsy.

DISORDERS OF SELF-AWARENESS Self-experience has four aspects, according to Jaspers (1959):

• • • •

Awareness of the existence of activity of the self Awareness of the unity of the self at any one time Awareness of the continuity of self-identity through time Awareness of the self as distinct from the outside world.

The final three aspects may be abnormal in schizophrenia. AWARENESS OF THE EXISTENCE OF ACTIVITY OF THE SELF All psychic life involves the experience of a unique and fundamental activity of the self. All emotions, behaviour, ideas, etc., are experienced as ‘being mine’. This experience is absent in depersonalization, in which the sense of awareness of existence as a person is altered or lost. This is often accompanied by derealization, the loss of the sense of reality of surroundings. These experiences may be seen in dissociative hysteria, temporal lobe epilepsy, extreme fatigue or anxiety and psychotic illness of all sorts.

20


The alteration of awareness of one’s activities (moods, thoughts, acts) as belonging to the self is seen in passivity experiences. In these the mental phenomena are often seen as being under the passive influence of some outside force or person. This is the elementary, primary experience of being actually and directly influenced. This is characteristic of schizophrenia.

DISORDERS OF INTELLECTUAL FUNCTIONS CONSCIOUSNESS Consciousness is the state of awareness of the self and its environment. Reduced levels of consciousness are seen in:

• • • •

Clouding of consciousness – disorientation in time, place, person, disturbances of perception and attention and subsequent amnesia. Drowsiness – further reduction in level of consciousness, with unconsciousness if unstimulated, but can be stimulated to a wakeful state. Stupor – further loss of responsiveness, which can be only aroused by considerable stimulation. Awareness of environment is often maintained in depressive or catatonic stupor, but not in organic stupor (cf. neurological and psychiatric definitions). Coma – profound reduction of conscious level with very little or no response to stimulation.

ATTENTION AND CONCENTRATION The intensity and extent of attention may be abnormal, as may the ability to sustain attention (i.e. to concentrate). Attention may be intensified in a restricted area in those with preoccupations (depressive, hypochondriacal, etc.). Attention may be reduced or absent in certain restricted areas in those with hysterical denial. Attention may be easily distracted in hypomania or organic psychoses. In the latter, the ability to concentrate may be very variable. Tests of attention 1 Reverse order of months of year. 2 Subtraction of serial 7s from 100. 3 A series of digits repeated forwards and backwards. Record time and accuracy for these tests.

MEMORY Memory involves the registration of data, the retention in the mind and recall at will – both immediately and at a later time. Thus anything interfering with registration (e.g. alcohol, organic psychosis, head injury), retention (e.g. Korsakoff ’s psychosis) or recall (organic or hysterical amnesia) will lead to defect of memory.

INSIGHT

21

Tests of memory 1 Recall of past personal life events which can be corroborated. 2 Recall of recent personal life events. Note any specific periods of amnesia (e.g. retrograde or anterograde amnesia) or any particular topics which are forgotten (e.g. hysterical amnesia). 3 Short-term memory can be tested using recall of a simple name and address after 5 minutes, repeating a sentence (e.g. Babcock sentence) and digit span. 4 General knowledge tests (e.g. names of royal family, prime minister, recent events in the newspapers, dates of first and second world wars). Note any confabulation to fill in the memory gaps with false information.

LANGUAGE FUNCTIONS (PARTICULARLY CENTERED IN THE TEMPORAL LOBE) Language functioning is tested both by listening to spontaneous conversation and by direct testing. Observe any errors in the form of:

• • • •

•

Dysarthria – disorder of articulation of speech. Neologizing – new words which do not exist. Paraphasia – words which are slightly incorrect. Dysphasias: – Receptive – disorder of the comprehension of words due to dysfunction of Wernicke’s area in the temporal lobe. – Expressive – disorder of expressing thoughts in the correct form of words, due to dysfunction of Broca’s area in the posterior frontal lobe. – Intermediate, particularly nominal dysphasia – inability to name objects correctly. This should always be tested for in assessment of intellectual function. Test by using a series of objects. Perseveration – inappropriate repetition of a previous name, word, theme or act.

VISUOSPATIAL FUNCTIONS (PARTICULARLY CENTRED IN THE PARIETAL LOBE) Visuospatial functioning is tested by observation and by direct testing. Test the ability to copy an asymmetrical object, to draw a clock face, to construct a star from matchsticks (constructional dyspraxia). Test right–left orientation and ability to name fingers (finger agnosia). Observe any difficulty in dressing and in finding his/her way about (dressing apraxia, topographical disorientation).

INSIGHT Insight according to Lewis (1934) is a ‘correct attitude to morbid change in oneself ’. The concept is multidimensional, incorporates both current and retrospective components, and is usually not an ‘all-or-none’ phenomenon (Amador and David, 2004).

22


According to Amador et al. (1993), insight includes:

• • • •

Recognition of illness (signs, symptoms, etc.) Attribution of illness (attributes of illness phenomena to a mental disorder) Awareness of treatment – benefit–compliance Awareness of social consequences of illness – e.g. disability, involuntary commital to hospital, response/concern of relatives.

Partial insight (i.e. retrospective insight) may not be the same as pseudo-insight. Medication compliance and awareness of illness are separate but overlapping constructs which contribute to insight (Amador and David, 2004). Issues: Is loss of insight consequent upon cognitive deficit, perhaps with a specific pattern of localization (e.g. parietal), or is persistent symptomatology only partially related to these factors?

REFERENCES AND FURTHER READING Amador XF, David AS (2004) Insight and Psychosis, 2nd edn. Oxford University Press, London. Amador XF, Strauss DH, Yale SA, Flaum MM et al. (1993) Assessment of insight in psychosis. Am. J. Psychiatry 150, 873. American Psychiatric Association (2000) Diagnostic and Statistical Manual of Mental Disorders, 4th edn: DSM-IV-TR. American Psychiatric Association, Washington, DC. Boyce WT, Essex MJ, Woodward HR et al. (2002) The confluence of mental, physical, social, and academic difficulties in middle childhood. I: Exploring the ‘head waters’ of early life morbidities. J. Am. Acad. Child Adolesc. Psychiatry 41, 580. Chessick RD (2002) Psychoanalytic peregrinations. IV: What is phenomenology? J. Am. Acad. Psychoanal. 30, 673. Fabrega H (2001) Culture and history in psychiatric diagnosis and practice. Psychiatr. Clin. North Am. 24, 391. Flashman LA (2002) Disorder of awareness in neuropsychiatric syndromes: an update. Curr. Psychiatry Rep. 4, 246. Flashman LA, McAllister TW (2002) Lack of awareness and its impact in traumatic brain injury. NeuroRehabilitation 17, 285. Hamilton M (ed.) (1974) Fish’s Clinical Psychopathology. Wright, Bristol. Harrison PJ (1991) Are mental states a useful concept? Neurophilosophical influences on phenomenology and psychopathology. J. Nerv. Ment. Dis. 179, 309. Jaspers K (1959) General Psychopathology, 7th edn, trans. Hoenig J and Hamilton M. Manchester University Press, Manchester. Leff JP, Isaacs AD (eds) (1981) Psychiatric Examination in Clinical Practice, 2nd edn. Blackwell Scientific, Oxford. Lewis A (1934) The psychopathology of insight. Br. J. Med. Psychol. 14, 332. Manschreck TC (1992) Delusional disorders. Psych. Ann. 22(5). Markova IS, Berios GE (1992) The meaning of insight in clinical psychiatry. Br. J. Psychiatry 160, 850. Maser JD, Patterson T (2002) Spectrum and nosology: implications for DSM-V. Psychiatr. Clin. North Am. 25, 855. McDougall GM, Reade B (1993) Teaching biopsychosocial integration and formulation. Can. J. Psychiatry 38(5), 359. McGuire MD, Marks I, Neese RM et al. (1992) Evolutionary biology: a basic science for psychiatry? Acta Psychiatr. Scand. 86, 89.


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Miller LJ, O’Connor E, DiPasquale T (1993) Patients’ attitudes toward hallucinations. Am. J. Psychiatry 150(4), 584. Mortimer AM (1992) Phenomenology: its place in schizophrenia research. Br. J. Psychiatry 161, 293. Schneider K (1959) Clinical Psychopathology, trans. Hamilton M. Grune & Stratton, New York. Sims A (ed.) (1988) Symptoms of the Mind: an Introduction to Descriptive Psychopathology. Ballière Tindall, London. Spitzer M (1992) The phenomenology of delusions: the need for a detailed description of symptoms. Psych. Ann. 22(5), 252. World Health Organization (1992) The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. WHO, Geneva.

Schizophrenia

3

CONCEPTS Modern concepts of schizophrenia are in part a distillation of historical concepts. No distinct aetiology or pathophysiology is presumed. There have been several early clinical descriptions: demence précoce (Morel, 1856); dementia paranoides (Kahlbaum, 1860); katatonia (Kahlbaum, 1868); hebephrenia (Hecker, 1870).

EARLY CLINICAL CONCEPTS

• • •

•

Greisinger (1870): ‘unitary psychosis’ – schizophrenia as part of a single psychotic disorder. Kraepelin (1893): dementia praecox – chronic disorder distinct from ‘manic depressive insanity’; onset in adolescence; progressive deterioration in mental function (84% of his patients); four subtypes (hebephrenic, catatonic, paranoid, simplex); ‘single morbid process’, presumed organic. Bleuler (1911): the schizophrenias – collection of psychoses with fundamental symptoms (‘four As’) representing the splitting (‘schizo’) of psychic functions. (Hallucinations, etc., are secondary phenomena of lesser importance.) – Ambivalence (coexisting conflicting ideas) – Loosening of associations – Affective incongruity and blunting – Autism (withdrawal). Jaspers (1913): schizophrenia characterized by non-understandability of mental functions (‘praecox feeling’).

EARLY SOCIOLOGICAL CONCEPTS Schizophrenia is: not an illness but a myth; a role forced upon the individual; a product of society; a sane reaction to an insane world.

DEVELOPMENT OF OPERATIONAL CRITERIA

25

OTHER CONCEPTS/CLASSIFICATIONS

• • • •

Langfeldt (1939): process schizophrenia (insidious onset, chronic course) versus schizophreniform (acute onset, affective symptoms, good outcome). Leonhard (1957): systemic schizophrenia (catatonia, hebephrenia, paraphrenia) versus non-systemic (affect-laden paraphrenia, schizophasia and periodic catatonia). Strömgen (1968): brief reactive psychosis (‘psychogenic psychosis’). Schneider (1959): strict phenomenological approach, devoid of aetioloical theory.

SYMPTOM RANKING First-rank symptoms (FRS), in the absence of organic illness, signify schizophrenia:

• • • • • • • •

Hearing thoughts spoken aloud. ‘Third person’ hallucinations. Hallucinations in the form of a commentary. Somatic passivity. Thought withdrawal or insertion. Thought broadcasting. Feelings or actions experienced as under the control of an external force. Delusional perception (see Chapter 2). Second-rank symptoms (other hallucinations, etc.) have less diagnostic significance. Schneider’s FRS have been very influential, but have limitations:

1 Specificity – occur in other ‘functional psychoses’ – about 20 per cent in psychotic depression and 40 per cent in acute mania. 2 Sensitivity – about 20 per cent of chronic schizophrenics never showed FRS. 3 Prognosis – FRS have no predictive/prognostic value.

DEVELOPMENT OF OPERATIONAL CRITERIA Influential Bleulerian and sociological views led to a diffuse (over-diagnosable) and unreliable concept of schizophrenia (especially in the USA) compared with phenomenological (Kraepelinian, Schneiderian) concepts in Europe. Regional differences were exposed in a USA/UK project (1972) and International Plot Study of Schizophrenia (IPSS). Pressure to standardize the diagnosis led to development of operational, atheoretical, diagnostic criteria:

• • •

Research diagnostic criteria (RDC) – illness duration of at least 2 weeks, Schneiderian plus other criteria emphasized. Feighner’s criteria – 6 months’ duration, more restrictive, favour poor prognosis. Catego – computerized diagnostic algorithms generated from Present State Examination. Updated now to Catego 5 generated from SCAN-PSE-10.

26

•

•

SCHIZOPHRENIA

DSM criteria (Diagnostic and Statistical Manual of Mental Disorders, American Psychiatric Association) – successive sets of diagnostic criteria (DSM-III, 1980; DSM-III-Revised, 1987; DSM-IV, 1994; DSM-IV-TR, 2000) essentially favouring a more ‘Kraepelinian’ concept of schizophrenia. DSM-V is under development and is likely to reflect more trait/dimensional approaches as well as neurobiological distinctions. Multiaxial system: – Axis I – major clinical syndrome. – Axis II – developmental or personality disorder. – Axis III – psychosocial stressors (1–7 scale). – Axis IV – highest level of functioning in past year (GAF: 10–100 scale).

CURRENT DIAGNOSTIC CRITERIA

•

•

ICD-10 (International Classification of Diseases, 10th edn; WHO, 1992; see Table 3.1). This groups together schizophrenia, schizotypal states and delusional disorder. It has greater congruence with the DSM system (see below), but differs because there is more reliance on FRS. Only one month’s illness duration is necessary. The category of post-schizophrenic depression is included. DSM-IV (APA, 1994; see Table 3.2). This was developed from DSM-III-Revised. There is greater emphasis on negative symptoms. Delusional disorder is not classified separately. There is no mention of prodromal symptoms. Schizoaffective disorder is not classified under Mood. Table 3.3 compares ICD-10 and DSM-IV.

Table 3.1 ICD-10 criteria for schizophrenia A minimum of 1 very clear symptom (and usually ⭓2 if less clear-cut) from groups (a)–(d) below, or symptoms from ⭓2 of the groups (e)–(h), which have been present for most of the time during a period of 1 month or more: (a) thought echo, insertion, withdrawal, broadcasting (b) delusions of control, influence, passivity; delusional perception (c) hallucinatory voices of running commentary, third-person discussion, or other types of voices coming from some part of the body (d) persistent delusions of other kinds that are culturally inappropriate and completely impossible (e) persistent hallucinations in any modality: daily for weeks/months, or accompanied by half-formed nonaffective delusions, or with persistent overvalued ideas (f) breaks in thought fluency, i.e. incoherence, irrelevant speech, neologisms (g) catatonic behaviour: excitement, stupor, mutism, posturing, waxy flexibility, negativism (h) negative symptoms: apathy, paucity of speech, blunted emotions, social withdrawal; not due to depression or neuroleptic medication (i) a significant and consistent change in the overall quality of some aspects of personal behaviour (loss of interest, social withdrawal, aimlessness) Subtypes: paranoid, hebephrenic, catatonic, undifferentiated, post-schizophrenic depression, residual, simple schizophrenia.

DEVELOPMENT OF OPERATIONAL CRITERIA

27

CURRENT CONTROVERSIES ON THE NATURE OF SCHIZOPHRENIA Clinical heterogeneity is not disputed, but underlying aetiological mechanism(s) are still unclear (Hirsch and Weinberger, 2003). VIEW 1 Schizophrenia is a single aetiopathological process leading to diverse manifestations (e.g. neurosyphilis). VIEW 2 There are multiple disease entities of different aetiopathological processes leading to schizophrenia (e.g. mental retardation, epilepsy).

Table 3.2 DSM-IV criteria for schizophrenia A. Characteristic symptoms: ⭓2 of the following, present for a significant time period during 1 month (or less if successfully treated): (1) delusions (2) hallucinations (3) disorganized speech (e.g. frequent derailment or incoherence) (4) grossly disorganized or catatonic behaviour (5) negative symptoms (e.g. affective flattening, alogia, avolition)

B.

C.

D.

E.

[NB: Only one ‘A’ symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a running commentary on the person’s behaviour or thoughts, or two or more voices conversing.] Social/occupational dysfunction: For a significant time-period since the illness onset, ⭓1 major area of functioning such as work, interpersonal relations or self-care is markedly below the level achieved prior to the onset (or of onset in childhood/adolescence – failure to achieve expected level of interpersonal, academic, or occupational achievement). Duration: Continuous signs of illness for ⭓6 months; period must include at least one month of symptoms that meet criterion ‘A; (i.e. active-phase symptoms), and may include periods of prodromal or residual symptoms. During prodromal or residual periods, illness may manifest by only negative symptoms or ⭓2 symptoms listed in criterion ‘A’ present in attenuated form (e.g. odd beliefs, unusual perceptual experiences). Schizoaffective and mood disorder exclusion: Schizoaffective disorder and mood disorder with psychotic features have been ruled out since: (1) no major depressive or manic episodes occurred concurrently with active-phase symptoms; or (2) if mood episodes occurred during active-phase symptoms, their total duration was brief relative to the duration of active and residual periods. Substance/general medical condition exclusion: Not due to the direct effects of a substance (e.g. drugs of abuse, medication) or a general medical condition.

Subtypes: • Paranoid – prominent delusions and/or auditory hallucinations. • Catatonic – dominated by stupor, negativism, posturing. • Disorganized – prominent disorganization of speech and behaviour, inappropriate/flat affect. • Undifferentiated – prominent delusions, hallucinations, disorganization; but not meeting criteria of other types. • Residual – meets ‘A’ criteria but criteria for other subtypes no longer met; yet some continuing disturbance (i.e. negative symptoms). Schizophreniform disorder: Meets ‘A’, ‘D’ and ‘E’ criteria but episode greater than 1 month, less than 6 months.

28

SCHIZOPHRENIA

Table 3.3 ICD-10 and DSM-IV classifications of schizophrenia and schizophrenia-like disorders ICD-10

DSM-IV

Schizophrenia – paranoid – hebephrenia – catatonic – undifferentiated – residual Post-schizophrenic depression Simple schizophrenia Other schizophrenia Unspecified schizophrenia Schizoaffective disorder Schizotypal disorder Persistent delusional disorder Acute and transient psychotic disorder Induced psychotic disorder

Schizophrenia – paranoid – disorganized – catatonic – undifferentiated – residual

Other non-organic psychotic disorder caused by a medical condition Unspecified non-organic psychosis

Schizoaffective disorder Delusional disorder Brief psychotic disorder Schizophreniform disorder Shared psychotic disorder Psychotic disorder Psychotic disorder Substance-induced psychosis Psychotic disorder not otherwise specified

VIEW 3 There are specific symptom clusters within schizophrenia reflecting different disease processes that combine differently in patients. Type I/type II syndromes (Crow, 1980) Type I – acute, positive symptoms, good response to neuroleptics, good prognosis, brain structurally normal, presumed dysfunction in dopamine system. • Type II – chronic, negative symptoms, poor treatment response and prognosis, abnormal cerebral structures (ventriculomegaly, cortical atrophy).

•

Positive and negative symptoms (Andreasen et al., 1990) • Positive symptoms – hallucinations, delusions, formal thought disorder, bizarre behaviour. • Negative symptoms – affective blunting, alogia (impoverished thinking and speech), avolition/apathy, anhedonia/asociality, disturbance of attention. The positive/negative dichotomy is less influential now. There is large symptom overlap in patients, and inconsistency of neuroimaging and biochemical research. Three patterns of symptoms are now advocated. Positive, negative, disorganization syndromes Positive syndrome – reality distortion syndrome: delusions, hallucinations. Negative syndrome – psychomotor poverty syndrome: negative symptoms. Disorganization syndrome – disorganization: positive formal thought disorder, inappropriate affect, poverty of content of speech.

• • •

EPIDEMIOLOGY

29

Cognitive impairment (Sharma and Antonova, 2003) Kraepelin originally considered cognitive deficits as a major aspect of schizophrenia. This is again considered a core facet, especially since subtle deficits (e.g. poor scholastic performance, memory loss) may antedate psychotic symptoms. Cognitive impairment is also a stronger predictor (than other symptoms) of poor function and vocational performance. Deficit syndrome (Carpenter et al., 1988) Primary, enduring negative symptoms (restricted affect; diminished emotional range; poverty of speech; diminished sense of purpose and social drive) reflect a distinct neural substrate. There is emphasis on distinguishing primary from secondary negative symptoms (secondary to positive symptoms, depressed mood, parkinsonism).

NEURODEVELOPMENTAL VERSUS NEURODEGENERATIVE HYPOTHESES

•

•

Neurodevelopment (Lewis and Levitt, 2002; Keshavan and Murray, 2004) – static lesion from CNS disruption in utero; typical symptoms emerge later. Evidence includes: – Post-mortem and neuroimaging findings. – Excess of obstetric complications, minor physical anomalies, abnormal dermatoglyphics. – Season of birth phenomenon. – Epidemiological association with prenatal exposure to influenza infection. Neurodegenerative – progressive degeneration (Kraepelin). Evidence includes: – Deteriorative course of illness. – Gliosis seen in earlier post-mortem (PM) studies, but not found in recent PM studies.

CONTINUUM OF PSYCHOSIS (GREISINGER, 1870; CROW, 1990) This view holds that there is a single psychosis, with schizophrenia most severe, affective disorders least severe, schizoaffective disorders occupying an intermediate position.

EPIDEMIOLOGY See Jones and Buckley (2003). INCIDENCE

• • • •

15–20 per 100 000 per year. 6–8 fold increased incidence among Britains of Afro-Caribbean family descent (Harrison et al., 1988). Lifetime risk: 0.9 per cent. Median age at onset: males ⫽ 28 years, females ⫽ 32 years.

30

• • • • •

SCHIZOPHRENIA

Other gender differences: males – more obstetric complications, poorer premorbid adjustment, poorer prognosis, less genetic predisposition(?), more structural brain abnormalities. Increased incidence of winter births (esp. if low genetic risk). Increased obstetric complications, left-handedness, abnormal determatoglyphics. There is much interest in a reported association of possible exposure during 2nd trimester to 1957 A2 influenza. Substance abuse co-morbidity is now a significant problem (see Chapter 10).

PREVALENCE

• • •

0.5–1 per cent; higher in Sweden, Croatia, Southern India; lower among US Hutterites. Increased prevalence among lower social classes – the breeder hypothesis (poor social conditions inducing schizophrenia) versus the social drift hypothesis (patients drift down the social scale while paternal occupations show normal class distribution). Increased prevalence in urban versus rural settings, especially for males.

MORTALITY Between 4 and 10 per cent die by suicide (see Chapter 11). There are also increased cardiovascular and respiratory deaths, and deaths by homicide.

AETIOLOGICAL FACTORS GENETICS Family studies See Table 3.4. There is a 0.5 per cent morbid risk in relatives of normal subjects. Twin studies Twin studies address the nature/nurture issue. Monozygotic:dizygotic (MZ:DZ) rate ⫽ 48%:4%, suggesting a strong genetic component (especially for paranoid subtype). However, MZ twins discordant for schizophrenia show more brain abnormalities than the normal co-twin (Suddath et al., 1990).

Table 3.4 Family studies Relationship to schizophrenic

Morbid risk (%)

Parent Sibling Child of schizophrenic Child of two schizophrenics

5 10 14 46

AETIOLOGICAL FACTORS

31

Adoptive studies Adoptive studies test for genetic versus environmental influences by examining rates of schizophrenia in adopted-away offspring of schizophrenic and of normal parents. Results: 10 per cent and 13 per cent, versus 0 per cent from normal parents. Schizophrenia spectrum ‘Good genetics requires good phenotypes’ (Kendler and Diehl, 1993) – unclear whether genetic liability is restricted (to schizophrenia only) or broad (many disorders)? Studies (Kendler and Diehl, 1993) suggest a moderate inheritance risk which includes schizophrenia-like personality disorders and schizophrenia-like non-affective psychoses. See Table 3.5. Molecular genetics This is a major focus of research (Waterwort et al., 2002). How many genes are involved? Where are they? How common are they? What is their functional impact:

• •

Effect on cellular processes (functional genomics)? Effect on protein development and expression (proteomics)?

Genome-wide scans provide evidence (but confusing and inconsistent) of susceptibility genes on chromosome 5, 6, 8, 10, 13, 15, 22; research is complicated by differing thresholds Lod score values for linkage analysis, diagnostic variability, phenocopy selection. Recent focus has been on candidate genes; e.g. chromosome 15 abnormal alleles at the locus of the alpha-7 nicotinic acetylcholine receptor subunit gene, and abnormal alleles on chromosome 6 region related to dysbindin (a developmental protein) gene. Polymorphisms of COMT (catechol O-methyltransferase) gene are associated with poorer prefrontal cortex functioning in schizophrenia (Weinberger et al., 2001). There is intense interest in examining genes regulating neurodevelopment (e.g. SNAP 23 – synaptosomal-associated protein 23, neuroregulin) to determine whether these are differentially expressed (under/over-expressed, different alleles) in schizophrenia. The genetics of treatment response (pharmacogenetics) is now also a major focus (Malhotra, 2001). Vulnerability markers Evoked potential (P 300) abnormalities in ‘unaffected’ first-degree relatives. Smooth-pursuit eyetracking abnormalities in 34 per cent of parents of schizophrenics (Holzman et al., 1974) and in schizotypal patients (Siever et al., 1993).

• •

Table 3.5 Schizophrenia spectrum Prevalence rate

1st-degree relative of schizophrenics 1st-degree relatives of healthy controls

Morbid risk (%)

Schizotypal/paranoid personality disorder

Schizophreniform schizophrenia-like psychoses

Affective disorder

8 2

3.7 1.5

25 23

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SCHIZOPHRENIA

High-risk studies Repeated, longitudinal evaluations (cognitive, neurological, psychiatric) of children of schizophrenic parents suggest early, subtle manifestations of schizophrenic genotype (CNS soft signs, attentional deficits, social deficits – ‘pandysmaturation’; Fish et al., 1992). The general pattern of CNS maldevelopment permits evaluation of relative genetic and environmental contributions to illness (Cannon et al., 1993). Prodromal studies There is intense interest in early detection of psychosis in the prodrome stage (McGorry et al. 2003; McGlashan, 2003). Educational programmes may help bring patients into treatment earlier – shorten the duration of untreated psychosis (DUP) which may be ‘biologically toxic’. Early use of antipsychotics may delay onset of psychosis (McGorry et al., 2002). These approaches are contentious and of ethical concern (McGlashan, 2001).

NEUROCHEMISTRY Dopamine hypothesis This view postulates dopamine (DA) overactivity in mesolimbic pathways. It is a very influential theory, largely based on:

• • • • • •

Amphetamine-induced schizophrenia-like psychosis – amphetamine increases DA release. Antipsychotics block DA (especially D2) receptors to an extent which correlates with clinical potency. Cis-fluphenthixol (DA blocker) is clinically effective but transfluphenthixol (no DA blockade) ineffective. Post-mortem studies (although contaminated by neuroleptic treatment) show increased DA and DA receptors in caudate and nucleus accumbens. Direct evidence (PET studies of neuroleptic-native patients) is conflicting and controversial: increased DA receptors (Johns Hopkins group – Wong et al., 1986) versus no increase (Karolinska Institute group – Farde et al., 1987). Relationship between plasma homovanillic acid, psychopathology and response to neuroleptics (Kahn and Davidson, 1993).

Recent theories include: deficit in corticofugal/corticothalamic DA inhibitory output (Carlsson, 1995); DA receptor supersensitivity occurs with neuroleptic treatment (Grace, 1992); interaction of DA with other neurotransmitters. Serotonin (5-HT) LSD (5-HT agonist) induces psychosis; m-chlorophenyl-piperazine (MCPP; a 5-HT agonist) worsens psychosis. • Ritanserin (5-HT2/5-HT1c antagonist) improves psychosis; clozapine (5-HT2 antagonist) is an effective treatment for psychosis.

•

There is a suggested mechanism of 5-HT modulatory effect on DA system.


33

Noradrenaline • There is evidence for over- and underactivity; clozapine induces potent noradrenergic blockage. Other neurotransmitters, neuropeptides/phospholipids GABA – reduced GABA receptors in hippocampus on PM studies. Glutamate – excess glutamate receptors in frontal cortex in PM studies; hypothesis of decreased glutamatergic inhibition of subcortical and mesiotemporal DA neurones. • Possible abnormalities of cholecystokinin (CCK), neurotensin. • Abnormalities of essential fatty acid metabolism (brain membrane components). • Application of molecular genetics and proteonomic techniques likely to yield more complex changes at subcellular level.

• •

NEUROPATHOLOGY Schizophrenia is not ‘the graveyard of neuropathologists’. • There is a 6 per cent decrease in brain weight and 4 per cent reduction in anterior– posterior length. • There are inconsistent findings in cortex, corpus callosum, basal ganglia, thalamus. • Temporal lobe(s) are implicated (left ⬎ right) – reversed planum temporale asymmetry; decreased area of hippocampus, amygdala, parahippocampal gyrus; reduced cell number and abnormal cellular arrangement (pre-alpha cell migratory failure during 2nd trimester) in hippocampus and entorhinal cortex.

NEUROIMAGING

• • • •

Early CT studies showed non-specific ventricular enlargement, cortical sulcal prominence. PET and MRI studies show that frontal and temporal lobes are major sites for abnormalities (see Chapter 15). Current evidence favors generalized cortical tissue loss and functional disconnectivity in schizophrenia. There may be progressive tissue loss in patients with more active illness (Mathalon et al., 2001) which may represent complex disease–host interaction (Weinberger and McClure, 2002). Structural brain abnormalities are subtle but reproducible (Shenton et al., 2001). Family members ‘at risk’ also show similar but more subtle brain changes (Lawrie et al., 2002; Seidman et al., 2002).

PSYCHOPHYSIOLOGY AND IMMUNOLOGY

•

Evoked potential (P 300) – failure of sensorimotor gating (impaired prepulse inhibition; Braff, 1993); related to earlier theories of defective filter (Broadbent) and overarousal (Venables).

34

• • • •

SCHIZOPHRENIA

Abnormal smooth-pursuit eye movements – may infer dysfunction in frontal eye fields region (Leve et al., 1993). Immunological interest stems partly from epidemiology: geographical variations in prevalence, increased urban prevalence, season of birth phenomenon, association with prenatal exposure to influenza – direct viral CNS toxicity? immunological response? epiphenomenon (e.g. temperature)? Inconclusive immunological findings – increased B lymphocytes, decreased T lymphocytes, increased CSF antibodies to some viruses. There is a negative association with rheumatoid arthritis.

LIFE EVENTS Vulnerability–stress models of schizophrenia propose a strong relationship between inherent vulnerability and life stressors to induce/exacerbate symptoms of schizophrenia. This is a heuristic model, yet there is only moderate support for the influence of stress/life events (LEs) (more evident in other disorders, especially depression) and many methodological difficulties, including retrospective falsification, defining period of observation for LEs, measurement of LEs.

FAMILY DYNAMICS Early theories included a schizophrenogenic mother, double-blind communication, skew and schism of marital roles, abnormal family communication. All are disregarded now. Recent emphasis has been on relatives’‘expressed emotion’ and relapse, but a meta-analysis of twin studies confirmed a small but significant effect of shared environment over and above that of the genetic contribution. Also, there is evidence from high-risk studies (Tienari et al., 2004) for a possible aetiological role of family relational style (‘constricted’/lacking boundaries/critical) via gene–environment interactions.

MANAGEMENT NEUROLEPTICS/ANTIPSYCHOTIC MEDICATIONS (see Chapter 21) There has been a gradual shift from older (conventional, ‘typical’) antipsychotics to newer (atypical, second-generation) antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole, sertindole, zotepine. In a US multicentre trial of treatment-refractory patients (Kane et al., 1988), 30 per cent were treated with clozapine, compared with 4 per cent with chlorpromazine. By 12 months, 60–70 per cent showed improvement. Other atypical antipsychotics are first-line and maintenance treatment choices. Evidence for the superiority of atypicals (over conventionals) is under debate for positive symptoms, but is stronger for negative symptoms. Cognitive benefits are subtle but major (Sharma and Antonova, 2003). There are possibly broader effects beyond psychosis, including a possible antisuicidal effect of

MANAGEMENT

35

clozapine (Meltzer et al., 2003) and a possible antiaggressive effect (Buckley et al., 2003). However, medication and treatment compliance is a major challenge (Lacro et al., 2002). ELECTROCONVULSIVE THERAPY (ECT) (see Chapter 22) Electroconvulsive therapy may be helpful in catatonic states, occasionally in secondary depression. PSYCHOSOCIAL TREATMENTS (see Chapter 24) Psychosocial treatments aim to maximize abilities and minimize disabilities. Components include:

• • • • • • •

Cognitive retraining Crisis management Education Vocational rehabilitation Family therapy Group therapy Social skills training.

Psychoeducational and family intervention strategies are used. High expressed emotion of relatives (HEE: critical comments, hostility, emotional over-involvement; rated from Camberwell family interview) is predictive of relapse (Vaughn and Leff, 1976; see Table 3.6). Intervention strategies aim to reduce HEE and relapses (see Table 3.7). Consumer movement now encourages ‘recovery’ approaches involving consumer support groups, and peer-support treatment programmes (Thompson et al., 2001). PSYCHOTHERAPY Psychotherapy is supportive, practical problem-oriented, and encourages compliance. Cognitive–behavioral therapy (CBT) is now advocated for persistent delusions Table 3.6 Relapse rates in 9 months after discharge Relapse rate (%) Patient on neuroleptics, low expressed emotion (EE) family Patient on neuroleptics, high EE family, less than 35 hours’ contact weekly No neuroleptics, high EE family, more than 35 hours’ contact

12 42 92

Table 3.7 Intervention strategies

Family intervention Routine treatment

Relapse 0–9 months (%)

Relapse 0–24 months (%)

10 48

33 71

36

SCHIZOPHRENIA

and hallucination. CBT can be adapted to address compliance issues – ‘compliance therapy’.

PROGNOSIS

• • •

Good prognosis – 1/3. Intermediate prognosis – 1/3. Poor prognosis – 1/3.

The illness course may plateau after the first 5 years (Carpenter and Strauss, 1991). WHO-coordinated IPSS, DOSMeD and ISoS studies (initial report, 1973; Jablensky et al., 1992; Harrison et al., 2001) indicate a more benign course in developing countries. PREDICTORS OF POOR OUTCOME

• • • • • • • • •

Male gender. History of obstetric complications. Abnormal premorbid personality. Low IQ. Single status. Early age at onset. Insidious onset. Substance abuse. Family history of schizophrenia.

Enduring negative symptoms early in the course predict a poor outcome. The duration of active psychosis without/prior to neuroleptic treatment predicts a poor response to neuroleptics and poor outcome.

SCHIZOAFFECTIVE DISORDER Kasanin (1933) described patients with illness of both affective and schizophrenic symptoms, with sudden onset after a stressor, and good premorbid adjustment. Subsequent definitions and application of different diagnostic criteria led to confusion and poor reliability of schizoaffective (SA) disorder – ␬ ⫽ 0.19 for concordance among seven diagnostic criteria (Brockington and Leff, 1979). See Table 3.8. Table 3.8 DSM-IV criteria for schizoaffective disorder A. Uninterrupted period of illness during which, at some instances, either a major depressive or manic episode is concurrent with symptoms satisfying criterion ‘A’ for schizophrenia. B. Delusions or hallucinations present for 2 weeks during the same period of illness in the absence of prominent mood symptoms. C. Mood symptoms present for significant extent of total duration of active and residual phases of the illness. D. Exclusion of substance/general medical condition. Subtypes: bipolar, depressive.

DELUSIONAL DISORDER

37

SA is unlikely to be either:

• •

Co-occurrence of schizophrenia and affective disorder in a patient. A separate disease entity.

SA is more likely to be either:

• • •

A subtype of schizophrenia. A subtype of affective disorder. A heterogeneous disorder, intermediate between schizophrenia and affective disorder (i.e. continuum model).

Available data from family and twin studies suggest a continuum. A schizodepressive subtype is more related to schizophrenia; a schizomanic subtype is more related to affective disorder. MANAGEMENT OF SCHIZOAFFECTIVE DISORDER Treatment is individualized according to the pre-eminence of either schizophrenic or affective symptoms.

• • •

Lithium or valproic acid – most beneficial for mainly affective SA patients; schizophrenic symptoms, less response. Neuroleptics – used in combination with lithium or antidepressant; more effective than neuroleptic monotherapy. ECT – useful in patients with mainly affective symptoms, perplexity, or a family history of SA.

PROGNOSIS OF SCHIZOAFFECTIVE DISORDER The prognosis is intermediate between schizophrenia and affective disorder. Schizomanics have a more episodic course and better outcome; schizophrenic symptoms are associated with poor outcome. Early onset is associated with schizophrenic symptoms and poor outcome (see Table 3.9).

DELUSIONAL DISORDER Delusional disorder is a contentious nosological entity. Is it a distinct mental disorder (‘paranoia’), or a milder form of schizophrenia (‘late paraphrenia’ ‘senile schizophrenia’), or part of a spectrum of disorders (‘paranoid spectrum’: Munro, 1992)? Table 3.9 Schizoaffective disorder (SA) and schizophrenia

Cologne follow-up study Marneros et al. (1989)

Very poor outcome Very good outcome

SA (%)

Schizophrenia (%)

6 51

52 12

38

SCHIZOPHRENIA

Table 3.10 DSM-IV criteria for delusional disorder A. B. C. D. E.

⭓1 month duration of non-bizarre delusions. Never had any criteria ‘A’ for schizophrenia. Functioning not markedly impaired and behaviour not obviously odd/bizarre (apart from impact of delusion). Mood episodes, if ever present, brief in duration relative to total duration of illness. Exclusion of substance/general medical condition.

Subtypes: • Persecutory. • Jealous (corresponds to description of ‘morbid jealously’ – Shepperd, 1961). • Erotomanic (corresponds to description of ‘de Clerambaut’s Syndrome, see Chapter 15). • Somatic (corresponds to description of ‘monosymptomatic hypochondrical psychosis – Munro, 1992). • Grandiose. • Mixed and unspecified.

Table 3.11 Clinical differential diagnosis of delusional disorders Disorder

Delusions

Hallucinations

Other clinical attributes

Paranoia

Present but not prominant Prominent

Personality well preserved

Paraphrenia

Present, well encapsulated Multiple

Paranoid schizophrenia

Multiple

Prominent

Personality disorder

Absent

Absent


Absent

Absent

Organic delusional syndrome

Present, single or multiple

Often present

Illness suggestive of paranoid schizophrenia, but with preservation of rapport and affect Thought-disorder, blunted affect, suspiciousness; social isolation Anger, suspiciousness, but no psychotic features Obsessions may appear bizarre (‘overvalued ideas’), not delusional Other organic features usually evident

Adapted from Munro (1992).

Genetic and outcome studies support the present classification under the rubric of schizophrenia/related psychotic disorders. See Tables 3.10 and 3.11. MANAGEMENT OF DELUSIONAL DISORDER It is notoriously difficult to treat. There is a chronic course, with limited insight and poor compliance with medication. Atypical antipsychotics have been shown to be effective, although poor compliance is the major impediment to good outcome.

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Sernyak MJ, Leslie DL, Alarcon RD et al. (2002) Association of diabetes mellitus with use of atypical neuroleptics in the treatment of schizophrenia. Am. J. Psychiatry 159, 561. Sharma T, Antonova L (2003) Cognitive function in schizophrenia: deficits, functional consequences, and future treatment. Psychiatr. Clin. North Am. 26, 25. Shenton ME, Dickey CC, Frumin M, McCarley RW (2001) A review of MRI findings in schizophrenia. Schizophr. Res. 49, 1. Siever LJ, Kalus OF, Keefe RSE (1993) The boundaries of schizophrenia. In: Powchic P, Schulz SC (eds), The Psychiatric Clinics of North America. WB Saunders, Philadelphia. Siris SG (2001) Suicide and schizophrenia [review]. J. Psychopharmacol. 15, 127. Smith TE, Hull JW, Huppert JD, Silverstein SM (2002) Recovery from psychosis in schizophrenia and schizoaffective disorder: symptoms and neurocognitive rate-limiters for the development of social behavior skills. Schizophr. Res. 55, 229. Suddath RL, Christison GW, Torrey EF et al. (1990) Anatomical abnormalities in the brains of monozygotic twins discordant for schizophrenia. New Engl. J. Med. 322, 789. Tait L, Birchwood M, Trower P (2003) Predicting engagement with services for psychosis: insight, symptoms and recovery style. Br. J. Psychiatry 182, 123. Thompson PM, Vidal C, Giedd JN et al. (2001) Mapping adolescent brain change reveals dynamic wave of accelerated gray matter loss in very early-onset schizophrenia. Proc. Natl. Acad. Sci. USA 98: 11650. Tienari P, Wynne LC, Sorri A et al. (2004) Genotype–environmental interaction in schizophrenia–spectrum disorder: long-term follow-up of Finnish adoptees. Br. J. Psychiatry 184, 216. Turnington D, Kingdon D, Turner T (2002) Effectiveness of a brief cognitive–behavioral therapy intervention in the treatment of schizophrenia. Br. J. Psychiatry 180, 523. Vaughn C, Leff JP (1976) The influence of family and social factors on the course of schizophrenic illness. Br. J. Psychiatry 129, 125. Walsh E, Buchanan A, Fahy T (2002) Violence and schizophrenia: examining the evidence. Br. J. Psychiatry 180, 490. Walsh E, Moran P, Scott C et al. (2003) Prevalence of violent victimisation in severe mental illness. Br. J. Psychiatry 183, 233. Waterwort DM, Bassett AS, Brzustowicz LM (2002) Recent advances in the genetics of schizophrenia. Cell. Mol. Life Sci. 59, 331. Weinberger DR, Egan MF, Bertolino A et al. (2001) Prefrontal neurons and the genetics of schizophrenia. Biol. Psychiatry 50, 825. Weinberger DR, McClure RK (2002) Neurotoxicity, neuroplasticity, and magnetic resonance imaging morphometry: what is happening in the schizophrenic brain? Arch. Gen. Psychiatry 59, 553. Wong DF, Wagner HN, Tune LE et al. (1986) Positron emission tomography reveals elevated D2 dopamine receptors in drug-naive shizophrenics. Science 234, 1558. World Health Organization (1992) The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. WHO, Geneva. Wykes T, Brammer M, Mellers J et al. (2002) Effects on the brain of a psychological treatment. Cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia. Br. J. Psychiatry 181, 144. Zygmunt A, Olfson M, Boyer CA et al. (2002) Interventions to improve medication adherence in schizophrenia. Am. J. Psychiatry 159, 1653.

Affective disorders

4

CLASSIFICATIONS Classification is unsatisfactory and continues to be contentious. There is ongoing debate as to whether the forms of affective disorder described below represent separate disorders or a continuum of severity. See Table 4.1. Primary versus secondary Is mood disturbance independent, or a manifestation of either another psychiatric disorder or physical illness? There is little clinical difference, and neurobiological parameters (e.g. dexamethasone suppression test) do not discriminate. Unipolar versus bipolar (Leonard, 1962; Angst, 1966; Perris, 1966) • Unipolar – ⭓3 complete episodes of depression, never manic. • Bipolar – ⭓1 episode of depression and of mania, or multiple episodes of mania: – I – major depressive and manic episodes, or manic episodes alone – II – major depressive episodes, but manic or hypomanic episodes only attributable to treatment (electroconvulsive therapy, antidepressants). Bipolar patients are more likely to have earlier and more acute onset, and tend to have a different pattern of familial inheritance. ENDOGENOUS (‘MELANCHOLIA’)/PSYCHOTIC VERSUS NEUROTIC/REACTIVE DEPRESSION It is contentious as to whether these terms specify distinct subgroups of aetiological and clinical significance or whether they describe a continuum of severity. Nomenclature is confusing: ‘psychotic’ is used by the British to describe major depression (‘endogenous’) with or without psychosis, while US authors refer to ‘psychotic’ solely in a phenomenological context. Melancholia refers to severe depression with anhedonia, diurnal variation in mood, lack of reactivity, psychomotor retardation or agitation, early morning wakening, and anorexia/marked weight loss. Neurotic and reactive depression were originally thought to be more clearly associated with precipitating ‘life events’, although this distinction is less clear now. Attempts

44

AFFECTIVE DISORDERS

Table 4.1 ICD-10 and DSM-IV classification of affective disorders ICD-10

DSM-IV

Depressive episode Mild (without/with somatic symptoms) Moderate Severe (without/with psychotic symptoms)

Depressive disorders Major depressive episodes Mild Moderate Severe

Recurrent depressive disorder Mild, moderate, severe In remission Other/unspecified

– without psychotic features – with psychotic features [Mood congruent or mood incongruent] In partial remission In remission In full remission Single Recurrent

Bipolar affective disorder Current episode hypomania Current episode manic (without/with psychotic symptoms) Other/unspecified episodes

Bipolar disorder Hypomanic episode Manic episode Mild Moderate Severe – without psychotic features – with psychotic features [Mood congruent or mood incongruent] In partial remission In full remission

Current episode depression – mild – moderate – severe (without/within psychotic symptoms) Current episode mixed Currently in remission Other/unspecified

Bipolar I disorder – single manic episode – most recent episode – hypomanic/mixed/depressed/unspecified Bipolar II disorder

Manic episode Hypomania Mania (without/with psychotic features) Other/unspecified episodes Persistent mood disorders Cyclothymic disorder Dysthymia NOS Other/unspecified Other/unspecified mood disorders

Cyclothymic disorder Dysthymic disorder Depressive disorder Mood disorder due to medical condition or substance abuse

to discriminate subgroups further have examined melancholic versus non-melancholic, psychotic versus non-psychotic, or characteristics on the basis of cluster analysis of symptoms. Overall, research supports the continuum viewpoint. Cyclothymia There is recognition in ICD-10 and DSM IV of Kraepelin’s original concept of patients with less severe mood disturbance and persistent instability of mood with chronic course. It is common in relatives of patients with major affective disorder. Some patients in middle age eventually develop major affective disorder superimposed on cyclothymia.

CLINICAL FEATURES

45

Dysthymia This is equated in ICD-10 and DSM-IV to chronic, low-grade ‘neurotic’ depression which is rarely severe enough to fulfill the criteria for recurrent depressive disorder (mild or moderate). It is frequently complicated by superimposed major depressive episodes – ‘double depression’. Boundaries between dysthymia, chronic unremitting major depression and depressive personality traits are controversial.

CLINICAL FEATURES MAJOR DEPRESSIVE ILLNESS (‘PSYCHOTIC’/RETARDED/‘ENDOGENOUS’) Mood • Persistent depression of mood. • Qualitatively different from normal unhappiness. • Loss of reactivity to circumstances (‘autonomous’). • Diurnal rhythm. • Pervasive. Speech and cognition Decreased tempo and reduction in quantity of speech. Guilt, self-blame, worthlessness and hypochondriasis. Impaired concentration or slowed thinking, indecisiveness, not associated with incoherence or loosening of associations. • Suicidal, morbid and paranoid ideation.

• • •

Somatic/biological/behavioural features Poor appetite, weight loss or, less commonly, increased appetite or significant weight gain. • Insomnia or hypersomnia – characteristic early morning wakening but also onset of insomnia. • Psychomotor retardation, agitation – loss of energy and fatigue, decreased libido and loss of interest in pleasure and work activities.

•

‘HYPOMANIC’ AND ‘MANIC’ STATES Mood • Persistent elevation of mood. • Irritability a common feature. • May be intermingled with transient depression of mood (‘manic’/‘hypomanic’ may be used to indicate degree of severity, or presence or absence of delusions and hallucinations). Speech and cognition Pressure of speech, increased tempo of thinking, impaired concentration and ‘flight of ideas’. • Distractibility, attention easily drawn to irrelevances. • Inflated self-image (grandiose, expansive).

•

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AFFECTIVE DISORDERS

Somatic/biological/behavioural features • Increased drive and activity: physical, social, work, libido. • Excessive activity in risk-taking pursuits, indiscretion socially. • Insomnia often earliest sign, but no fatigue (EEG shows reduction in delta sleep) • Appetite good; weight loss is due to overactivity.

EPIDEMIOLOGY Statistics vary widely, depending on diagnostic criteria and ‘caseness’ issues. Depressive symptoms are very common (13–20 per cent point prevalence). Results of an epidemiologic catchment area study were:

• • •

1 month prevalence of 2.2 per cent for major depression. Lifetime prevalence of 5.8 per cent for major depression. Lifetime prevalence of 0.012 per cent for bipolar disorder.

Females are more affected than males. Lifetime prevalence for males is 2.3–4.4 per cent and for females, 4.9–8.7 per cent. Lifetime incidence for males is 10 per cent and for females, 20 per cent. The lifetime prevalence for bipolar type I is 0.8 per cent. For type II it is 0.5 per cent. There are no consistent gender differences in rates of bipolar disorder. Other observations • There is concern over increased depression and bipolar illness in young people. • Onset: – Bipolar disorder most often in mid-20s. – Unipolar disorder in late 20s. – Women have peak onset in 30s, males in 40s. • There is a higher prevalence of depression in lower social group females (Brown and Harris, 1978). • Prevalence is higher in urban areas and among the divorced. • Ethnic differences in the USA appear more related to social class differences. Depression may be becoming more common. From 1910 to 1950 the risk of depression rose in each generation with associated earlier age at onset – the ‘birth cohort effect’. Unipolar depression was the biggest cause of lifetime disability in the WHO Global Burden of Disease study.

AETIOLOGICAL FACTORS GENETICS Family studies High rates of mood disorders have been found in first-degree relatives of bipolar patients – about 20 per cent. The rate of mood disorder in first-degree relatives of unipolar patients is about 10 per cent.


47

Table 4.2 Percentages of parents affected

Bipolar adoptees Bipolar non-adoptees Normal controls

Biological

Adoptive

28 26 5

12 – 9

Unipolar forms tend to ‘breed true’, but bipolar forms are associated with elevated risk of both unipolar and bipolar disorder in relatives. Twin studies • Unipolar – MZ:DZ ⫽ 54%:24%. • Bipolar – MZ:DZ ⫽ 79%:19%. Adoptive studies Mendlewicz and Rainer (1977) studied relatives of adult bipolar probands who had been adopted early in life and compared them with those of normal adoptees, biological parents of patients with poliomyelitis and bipolar non-adoptees (see Table 4.2). Molecular genetics This is a major area of research. For bipolar disorder, genome-wide search reveals evidence of susceptibility genes on chromosomes 4, 12, 13, 18, 21 and 22 (Berrettini, 2001; Liang et al., 2002; Sklar, 2002; Shaw et al., 2003). Chromosomes 13 and 22 are also associated with schizophrenia (see Chapter 3). For unipolar depression, studies suggest that genetic factors may account for 40–70 per cent of the risk. Genome-wide search reveals susceptibility genes on chromosomes 1, 2, 5, 8, 10, 11, 15, 18, 19 (Zubenko et al., 2003).

NEUROCHEMISTRY NEUROTRANSMITTER ABNORMALITIES Serotonin Evidence includes:

•

•

Decreased: – Plasma tryptophan – CSF 5-hydroxyindoleacetic acid (5-HIAA) (especially in suicides) – Platelet 5-HT uptake – 3H-imipramine binding in platelet, in frontal cortex, and in hippocampus – Prolactin response to neuroendocrine challenge tests (intravenous tryptophan, oral fenfluramine) – responses are then normalized with antidepressant therapy. Increased: – 5-HT2 receptor binding in platelets, in cortex of suicides.

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AFFECTIVE DISORDERS

Noradrenaline Evidence includes:

• • •

Decreased: – Growth hormone response to neuroendocrine challenge tests (amphetamine, clonidine, desipramine) – Platelet CAMP turnover with stimulation by clonidine. Increased: – Platelet ␣2-adrenergic-receptor binding – Beta-adrenergic receptors in suicides. Normal: – CSF, plasma, urinary measures of noradrenaline and MHPG.

Acetylcholine There is little evidence of abnormality, apart from the cholinergic basis for sleep disturbances in affective disorder (see Chapter 14), findings which are consistent with postsynaptic muscarinic supersensitivity. Dopamine There have been mixed results in studies of neuroendocrine responses to either apomorphine or amphetamine. NEUROENDOCRINE ABNORMALITIES

• • •

There is blunted growth hormone in response to insulin challenge, and blunted thyroid-stimulating hormone in response to TRH. Hypercortisolaemia and loss of normal circadian rhythm of cortisol. Failure of cortisol suppression in a dexamethasone suppression test (DST) is seen in 50–60 per cent of depressed patients. Initial optimism that this would be a ‘trait’ marker rather than a ‘state’ marker has not held up, and DST non-suppression is seen also in alcoholism, anorexia nervosa, schizophrenia, etc.

Neurochemical and neuroendocrine studies are difficult to assimilate and to detect a consistent pattern for various reasons:

• • • •

There is uncertainty about the origin of metabolites; i.e. does plasma MHPG reflect central noradrenaline metabolism? Effects of diet and menstrual status need to be accounted for. Some of these (e.g. appetite) are behavioural features of depression. There are varying methodologies, assay techniques, etc. There are variable criteria for affective illness and patient selection between studies (e.g. unipolar vs. bipolar). Collectively, the results suggest the overall possibility of:

• •

Subsensitivity of noradrenaline postsynaptic receptors Presynaptic 5-HT dysfunction.

It is most likely that there is an interaction between two or more neurotransmitter systems, perhaps modulated by neuropeptides.


49

NEUROPEPTIDES The exact role of neuropeptides on mood is unknown. Elevated corticotropin releasing factor (CRF) is associated with depression, and CRF neural pathways interact extensively with serotonergic and noradrenergic systems. Administration of CRF in animal studies produces depressive behavior. Research into the effect of CRF receptor antagonists on depression is ongoing. Antagonists to human substance P (neurokinin 1) receptors were originally developed as a treatment for pain but did not meet with success. However, their efficacy for improving depressive symptoms has been demonstrated in a placebo-controlled trial (Kramer et al., 1998) and further research is under way (Stout et al., 2001). PSYCHOIMMUNOLOGY

• • •

There are decreased numbers of natural killer cells, and T-cell replication. There is decreased interleukin-2. There is increased monocyte activity.

Immune deficits are thought to be related to the end-products of sympathetic nervous system and hypothalamic–pituitary–adrenal axis activation (i.e. glucocorticoids and catecholamines), which modulate the immune system. Animal models support the involvement of catecholamine and glucocorticoid lymphocyte receptors in the immune alterations related to depression (Silberman et al., 2004).

NEUROIMAGING/NEUROPATHOLOGY (see Chapter 15) MRI studies suggest a reduction of hippocampus and caudate nucleus size in depression. PET studies indicate reduced metabolic activity and perfusion in cingulate gyrus, dorsolateral prefrontal cortex and left angular cortex (pronounced in depressive ‘pseudodementia’ patients). In stroke victims, dysphoria is associated with lesions in the anterior left hemisphere, whereas euphoria is associated with right hemispheric strokes.

ORGANIC CAUSES See Table 4.3.

Table 4.3 Examples of high prevalence of depression in medical illness Patient population

Patients with depression

Cancer outpatients Cancer inpatients CVA MI Parkinson’s disease

33% 42% 47% 45% 39%

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AFFECTIVE DISORDERS

Endocrine disorders • Hypothyroidism • Hyperparathyroidism

• •

Cushing’s syndrome Addison’s disease

• •

Infective causes Post-influenza Brucellosis

• •

Infectious mononucleosis Hepatitis

• •

Metabolic causes Iron-deficient anaemia B12/folate-deficient anaemia

• •

Hypercalcaemia Hypomagnesia

Neurological causes Post CVA Multiple sclerosis Parkinson’s disease

• •

Intracranial tumours Epilepsy

• • •

Depression, particularly epilepsy – associated with non-dominant (right-sided) temporal lesions, although later refuted in several studies. Drugs Reserpine Alpha-methyldopa L-dopa

• • •

• • •

Steroids Barbiturates Prolonged use of amphetamines

The oral contraceptive pill is no longer considered to be ‘depressogenic’.

PSYCHOLOGICAL THEORIES Psychodynamics • Loss of love object. • Regression to primitive emotional level where lost object is ‘incorporated into self ’ and bitterly attacked by superego. • Depressive position characterized by guilt, helplessness, and fear of the loss of love. Early childhood experiences Bowlby emphasized early maternal deprivation, but research has been complicated by poor methodology. The observed relationship between prolonged absence of a parent during early life and subsequent depression (Brown et al., 1986) seems more related to the absence of care rather than the specific figure (maternal vs. paternal) or type of separation (death, divorce).


51

Cognitive/behavioural theories • Wolpe – depression is conditioned by repeated losses in the past. • Seligman – ‘learned helplessness’ is a consequence of repeated exposure to uncontrollable traumas. • Beck – there is a ‘negative cognitive trait’ of self-defeating thoughts. Premorbid personality Early research suggested that depressed patients were premorbidly more introverted, shy and obsessional, while manic patients had vivacious, cyclothymic personalities. However, depression compounds ‘retrospective’ assessment, and in more recent research premorbid characteristics show only a minor association.

SOCIOLOGICAL THEORIES Brown and Harris (1978) described high rates of depression among inner-city London lower social group females. This suggested vulnerability factors which predispose to depression only in the presence of provoking agents. Vulnerability factors • Excess of threatening life events or major difficulties prior to onset of depression. • Unemployed status. • Unsupportive relationship with spouse or partner. • Three or more children under age of 15 living at home. • Loss of mother before age 11. Subsequent studies (Brown et al., 1986) only partly replicated Brown and Harris’ hypothesis, and further suggest that low self-esteem is a major vulnerability factor.

LIFE EVENT STUDIES Methodological problems include: colouring of retrospective information by depression (‘search for meaning’); inadequate controls; separating dependent life events (may be secondary to depression, e.g. marriage break-up) from independent life events (e.g. job loss due to business liquidation); difficulty in corroborating history. Nevertheless, there seems to be an excess of life events preceding depression as well as mania.

INTEGRATIVE MODELS OF DEPRESSION A review of animal studies supports an integrative model of depression based on a stress paradigm (Newport et al., 2002): 1 Disrupted parenting which produces stress. 2 Stress results in hypersecretion of CRH. 3 CRH elevation causes hyper-responsivity in the hypothalamic–pituitary–adrenal axis.

52

AFFECTIVE DISORDERS

COURSE AND PROGNOSIS These are dependent on concepts and definitions of affective disorder used in studies and clinical policies. The original Kraepelinian view of good outcome of ‘manic–depressive insanity’ (relative to the chronicity of schizophrenia) is now questioned. Short-term prognosis Approximately 67 per cent of patients respond to treatment within 8 weeks. Even when treated, the risk of recurrence of major depression is substantial:

• • •

50 per cent after one episode 70 per cent after two episodes 90 per cent after three episodes.

Thirty per cent of patients will become chronically depressed. Long-term prognosis Inter-episode intervals of depression and mania tend to lengthen over time, although this pattern is reversed in elderly people, where affective episodes also last longer and are more likely to leave residual symptoms. In a 25-year follow-up (Angst and Preisig, 1995), 13 per cent of patients failed to recover and had continued symptoms and disability, resembling dysthymia rather than major depression; severity of initial psychopathology was predictive of outcome. Thirteen per cent died of suicide. In an 18-year follow-up (Lee and Murray, 1988), 25 per cent had poor outcome (death, continued disability); only 11 per cent recovered and showed no further psychiatric morbidity. Severity of the initial psychopathology was predictive. Predictors of poor outcome Early onset. Severity of symptoms at index admission. Co-morbid personality disorder. Co-morbid dysthymia – ‘double depression’.

• • • •

TREATMENT PSYCHOTHERAPY (see Chapter 23) COGNITIVE BEHAVIOURAL THERAPY (CBT) This is systematic treatment aimed at challenging ‘logical errors’, ‘automatic thoughts’ and ‘generalizations’. Research supports its effectiveness in the treatment of depression. It needs to be of at least 16-weeks duration, and appears to be as effective as pharmacotherapy in reducing later relapse. The use of CBT as a maintenance treatment needs further research. There is no consensus that combined CBT plus medication is better than either modality singly.

TREATMENT

53

INTERPERSONAL PSYCHOTHERAPY (IPT) This is exploration of the origins of depression in terms of interpersonal losses, role disputes and transitions, social isolation, and/or deficits in social skills. It is effective in the acute treatment of depression, particularly for vocational and social sequelae of illness. The efficacy as maintenance therapy is still under investigation.

PHYSICAL APPROACHES PHARMACOLOGY (see Chapter 21) Numerous antidepressant medications are available. Claims for the superiority of an individual antidepressant are unsubstantiated, and this is also true overall, even for comparison of newer antidepressants (SSRIs, etc.). The newer antidepressants – SSRIs and SNRIs – are safer in overdose, and have more tolerable side-effects than older antidepressants (TCAs and MAOIs). MAOIs are best used for ‘atypical depression’ and are not generally used as a first-line drug in major depression. Recent research indicates that patients with recurrent depression should receive longterm maintenance treatment at the dose that produced the initial response (Kupfer et al., 1992). COMBINATION THERAPIES Combination therapies are reserved primarily for treatment-resistant depression (see later). The addition of low-dose lithium to an antidepressant regimen may augment the effect. Atypical antipsychotics given in combination with SSRIs have shown clinical efficacy. Lithium • Treatment of mania (3–4 days for therapeutic effect) – 75 per cent response rate. • Prophylaxis for bipolar disorder usually commenced when there are two or more affective disturbances within 2 years. • 50 per cent of patients relapse within 3 years, with poor compliance with medication being the key factor. Valproate Valproate is another first-line agent in mania. Patients with mixed affective disorder may respond better than those with ‘pure’ mania (McElroy et al., 1992). Carbamazepine The overall response rate in mania is 65 per cent; i.e. less than with lithium. It is generally used as a second-line drug, for treatment resistance or lithium intolerance. There is no evidence yet to support its use in unipolar disorder. Atypical antipsychotics Atypical antipsychotics are effective for the management of acute mania.

54

AFFECTIVE DISORDERS

ELECTROCONVULSIVE THERAPY See Chapter 22. Sleep deprivation Total sleep deprivation is reported to induce rapid clinical improvement in about 30 per cent of patients. REM deprivation (causing ‘REM pressure’) results in improvement in 30–60 per cent. The mechanism is unclear – it may restore circadian rhythm through an improved sensitivity of neurotransmitter/melatonin.

MANAGEMENT OF TREATMENT-RESISTANT DEPRESSION 1 Review the diagnosis, physical investigations and social/family factors. Pay particular attention to interpersonal and family dynamics that may inhibit resolution of symptoms. Continue with periodic review/update of diagnosis, management, etc. 2 Enhance present physical treatments: – Maximize dose of antidepressant. – Switch to a different class of antidepressant if failure follows an adequate trial. 3 Add in: – Atypical antipsychotic – Lithium. 4 Physical treatment measures (see Chapter 22): – Electroconvulsive therapy – Vagal nerve stimulation (VNS) – Transcutaneous magnetic stimulation (TMS).

OTHER SYNDROMES MIXED AFFECTIVE STATES During transition from mania to depression and vice versa, Kraepelin held that mood, cognition and behaviour may vary independently, producing ‘mixed’ states. There are six combinations: 1 2 3 4 5

Manic stupor (elation, increased thought tempo, motor retardation). Excited (agitated) depression (decreased thought, depressed mood, overactivity). Anxious mania (increased thought tempo, overactivity, anxious mood). Unproductive mania (decreased thought tempo, overactivity, elation). Depression with flight of ideas (depressed mood, motor retardation, increased thought tempo). 6 Inhibited mania (decreased thought tempo, motor retardation, elation). States were usually transitional, but sometimes persistent. Some studies suggest up to 30 per cent of bipolar patients present with mixed symptoms in their first episode.

OTHER SYNDROMES

55

BEREAVEMENT REACTIONS Uncomplicated bereavement or typical grief 1 ‘Stunned’ phase – emotions blunted – lasts few hours to 2 weeks. 2 Mourning phase – intense yearning and distress – autonomic features – unhappiness, futility, anorexia, restlessness, irritability, preoccupation with deceased – transient hallucinatory episodes and guilt-denial. 3 Acceptance and readjustment – several weeks after onset of mourning. The duration of typical grief varies with culture – on average 6–12 months. Atypical grief • Chronic grief – typical depressive illness may emerge with morbid preoccupation with worthlessness, prolonged functional impairment, marked psychomotor retardation. Other features include: excessive guilt, denial, identification, antisocial behaviour. • Inhibited grief or delayed grief. • Non-specific and mixed reactions – psychosis, neurosis, etc. ATYPICAL OR ‘MASKED’ DEPRESSION This is illness presenting as either (1) physical conditions or (2) non-affective psychiatric disorders:

• •

Chronic pain, hypochondriasis, somatoform disorders, conversion disorders – usually show absence of significant organic pathology, poor response to medical treatment and some depressive features. Pseudodementia, anxiety states, behavioural change (e.g. shoplifting in middleaged women).

SEASONAL AFFECTIVE DISORDER (SAD) There is a history of major affective disorder with at least three previous winter depressive episodes. There is onset and remission of each depressive episode; these occur within specific 60-day periods of each other. Seasonal mood disturbances outweigh (by more than 3:1) any non-seasonal mood disturbance (if present). There is an absence of a clear-cut seasonally changing psychosocial variable. ‘Atypical’ depressive features can be anxiety, irritability, increased fatigue, increased sleep, appetite, weight gain (‘carbohydrate craving’). Mild ‘hypomania’ is often experienced in summer. The true prevalence is unknown. Four per cent of a population in Washington (USA) had winter SAD (Kasper et al., 1989). More females than males are affected, although this may be a selection bias. Pathophysiology Pathophysiology is unknown. The dysregulation of melatonin postulate is:

• • •

Melatonin deficit. ‘Phase shift’ in normal circadian output of melatonin. Dopamine-mediated abnormality in melatonin secretion.

56

AFFECTIVE DISORDERS

Treatment Ultraviolet light therapy (bright, but not dim) suppresses blood melatonin – unclear whether morning therapy is best time of day. RAPID CYCLING MANIA There have been four or more episodes of depression/mania/hypomania in the previous 12 months. Episodes are damarcated by a switch to an episode of opposite polarity or by a period of remission. Usually (⬎80 per cent) patients are lithium-treatment failures. Carbamazepine or sodium valproate are the usual agents of choice.

REFERENCES AND FURTHER READING Abas M, Hotopf M, Prince M (2002) Depression and mortality in a high-risk population: 11-year follow-up of the Medical Research Council Elderly Hypertension Trial. Br. J. Psychiatry 181, 123. American Psychiatric Association (2002) Work Group on Bipolar Disorder: Practice Guideline for the Treatment of Patients with Bipolar Disorder Revised. Am J Psychiatry 159, 1. Andrews G, Szabo M, Burns J (2002) Preventing Major Depression in Young People. Br. J. Psychiatry 181, 460. Angst J, Preisig M (1995) Course of a clinical cohort of unipolar, bipolar and schizoaffective patients. Results of a prospective study from 1959 to 1985. Schweiz. Arch. Neurol. Psychiatr. 146, 5–16. Arnold LM (2003) Gender differences in bipolar disorder. Psychiatr. Clin. North Am. 36, 595. Austin MP, Mitchell P, Goodwin GM (2001) Cognitive deficits in depression: possible implications for functional neuropathology. Br. J. Psychiatry 178, 200. Bearden CE, Hoffman KM, Cannon TD (2001) The neuropsychology and neuroanatomy of bipolar affective disorder: a critical review. Bipolar Disorders 3, 106. Berrittini W (2001) Molecular genetic studies of bipolar disorder. Bipolar Disorders 3, 276. Breslau N, Kilbev MM, Andreski P (1993) Nicotine dependence and major depression. New evidence from a prospective investigation. Arch. Gen. Psychiatry 50, 31. Brown GW, Harris T (1978) Social Origins of Depression. Tavistock, London. Brown GW, Andrews B, Harris T et al. (1986) Social support, self esteem and depression. Psycholog. Med. 16, 813. Casacalenda N, Perry JC, Looper K (2002) Remission in major depressive disorder: a comparison of pharmacotherapy, psychotherapy, and control conditions. Am. J. Psychiatry 159, 1354. Coryell W, Solomon D, Turvey C et al. (2003) The long-term course of rapid-cycling bipolar disorder. Arch. Gen. Psychiatry 60, 914. Eagles JM, Howie FL et al. (2002) Use of health care services in seasonal affective disorder. Br. J. Psychiatry 180, 449. Ferrier IN, Thompson JM (2002) Cognitive impairment in bipolar affective disorder: implications for the bipolar diathesis. Br. J. Psychiatry 180, 293. Harmer C, Hill SA, Taylor MJ et al. (2003) Towards a neuropsychological theory of antidepressant drug action: potentiation of norepinephrine activity increases positive emotional bias. Am. J. Psychiatry 160, 990. Harrison PJ (2002) The neuropathology of primary mood disorder. Brain 125, 1428. Heim C, Nemeroff CB (2001) The role of childhood trauma in the neurobiology of mood and anxiety disorders: pre-clinical and clinical studies. Biol. Psychiatry 49, 1023.


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Hill J, Pickles A, Burnside E et al. (2002) Child sexual abuse, poor parental care and adult depression: evidence for the different mechanisms. Br. J. Psychiatry 179, 104. Hokfelt T, Bartfai T, Bloom F (2003) Neuropeptides: opportunities for drug discovery. Lancet Neurology 2, 463. Hume W (2001) Exercise was more effective in the long term than sertraline or exercise plus sertraline for major depression in older adults. Evidence-Based Ment. Health 4, 105. Irwin M (2002) Psychoneuroimmunology of depression: clinical implications. Brain Behav Immun. 16, 1. Jaffee SR, Moffitt TE, Caspi A et al. (2002) Differences in early childhood risk factors for juvenileonset and adult depression. Arch. Gen. Psychiatry 59, 215. Jane-Llopis E, Hosman C, Jenkins R, Anderson P (2003) Predictors of efficacy in depression prevention programmes: meta-analysis. Br. J. Psychiatry 183, 384. Kasper S, Wehr TA, Bartko JJ et al. (1989) Epidemiological findings of seasonal changes in mood and behaviour. Arch. Gen. Psychiatry 46, 823. Kendler KS, Kessler RC, Neale MC et al. (1993) The prediction of major depression in women: toward an integrated etiological model. Am. J. Psychiatry 150, 1139. Kendler KS, Gardner CO, Prescott CA (2002) Toward a comprehensive developmental model for major depression in women. Am. J. Psychiatry 159, 1133. Klerman GL (1988) The current age of youthful melancholia. Br. J. Psychiatry 152, 4. Knapp M (2003) Hidden costs of mental illness. Br. J. Psychiatry 183, 477. Koike AK, Unutzer J, Wells KB (2002) Improving the care for depression in patients with comorbid medical illness. Am. J. Psychiatry 159, 1738. Kramer MS, Cutler N, Feighner J (1998) Distinct mechanism for antidepressant activity by blockade of central substance P receptors. Science 281, 1640. Kupfer DJ (1992) Maintenance treatment in recurrent depression: current and future directions. Br. J. Psychiatry 161, 309. Kupfer DJ, Frank E, Perel JM et al. (1992) Five-year outcome for maintenance therapies in recurrent depression. Arch. Gen. Psychiatry 49, 769. Lecrubier Y, Clerc G et al. (2002) Efficacy of St John’s Wort Extract WS 5570 in major depression: a double-blind, placebo-controlled trial. Am. J. Psychiatry 159, 1361. Lee AS, Murray RM (1988) The long-term outcome of Maudsley depressives. Br. J. Psychiatry 153, 741. Levinson DF, Zubenko GS, Crowe RR et al. (2003) Genetics of recurrent early-onset depression (GenRED): design and preliminary clinical characteristics of a repository sample for genetic linkage studies. Am. J. Med. Genet. 119B, 118. Liang SG, Sadovnick AD, Remick RA et al. (2002) A linkage disequilibrium study of bipolar disorder and microsatellite markers on 22q13. Psychiatr. Genet. 12, 231. Liotti M, Mayberg HS, McGinnis S, Brannan SL et al. (2002) Unmasking disease-specific cerebral blood flow abnormalities: mood challenge in patients with remitted unipolar depression. Am. J. Psychiatry 159, 1830. Marangell LB, Rush AJ, George MS et al. (2002) Vagus nerve stimulation (VNS) for major depressive episodes: one year outcomes. Biol. Psychiatry 51, 280. Marks IM (2002) The maturing of therapy: some brief psychotherapies help anxiety/depressive disorders but mechanisms of action are unclear. Br. J. Psychiatry 180, 200. Martin JLR, Barbanoj MJ, Schlaepfer TE et al. (2003) Repetitive transcranial magnetic stimulation for the treatment of depression: systematic review and meta-analysis. Br. J. Psychiatry 182, 480. Matthews K, Eljamel MS (2003) Vagus nerve stimulation and refractory depression: please can you switch me on doctor? Br. J. Psychiatry 183, 181. McElroy SL, Keck PE, Pope HG (1992) Valproate in the treatment of bipolar disorder: literature review and clinical guidelines. J. Clin. Psychopharmacol. 12(Suppl.), s42. McLoughlin DM (2003) Repetitive transcranial magnetic stimulation is of unknown effectiveness in people with depression [review]. Evidence-Based Ment. Health 6, 118.

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Mendlewicz J, Rainer JD (1977) Adoption study supporting genetic transmission in manicdepression. Nature 268, 327. Mortensen PB, Pedersen CB, Melbye M et al. (2003) Individual and familial risk factors for bipolar affective disorders in Denmark. Arch. Gen. Psychiatry 60, 1209. Mulder RT (2002) Personality pathology and treatment outcome in major depression [review]. Am. J. Psychiatry 159, 359. Nemeroff CB, Owens MJ (2002) Treatment of mood disorders. Nature Neuroscience 5 (Suppl.), 1068. Newport DJ, Stowe ZN, Nemeroff CB (2002) Parental depression: animal models of an adverse life event. Am. J. Psychiatry 159, 1265. Parker G, Roy K, Mitchell P et al. (2002) Atypical depression: a reappraisal. Am. J. Psychiatry 159, 1470. Perugi G, Akiskal HL (2002) The soft bipolar spectrum redefined: focus on the cyclothymic, anxious-sensitive, impulse-dyscontrol, and binge-eating connection in bipolar II and related conditions. Psychiatr. Clin. North Am. 25, 713. Raison CL, Miller AH (2003) When not enough is too much: the role of insufficient glucocorticoid signaling in the pathophysiology of stress-related disorders. Am. J. Psychiatry 160, 1554. Remick RA (2002) Diagnosis and management of depression in primary care: a clinical update and review. CMAJ 167, 1253. Rice F, Harold G, Thapar A (2002) The genetic aetiology of childhood depression [review]. J. Child Psychol. Psychiatry 43, 65. Schatzberg AF (2002) Major depression: causes or effects? Am. J. Psychiatry 159, 1077. Schlaepfer TE (2003) Efficacy of repetitive transcranial magnetic stimulation (rTMS) in the treatment of affective disorders. Neuropsychopharmacology 28, 201. Scott J, Palmer S, Paykel E et al. (2002) Use of cognitive therapy for relapse prevention in chronic depression. cost-effectiveness study. Br. J. Psychiatry 182, 221. Shaw SH, Mroczkowski-Parker Z, Shekhtman T et al. (2003) Linkage of a bipolar disorder susceptibility locus to human chromosome 13q32 in a new pedigree series. Mol. Psychiatry 8, 558. Shelton RC, Tollefson GD, Tohen M et al. (2001) A novel augmentation strategy for treating resistant major depression. Am J. Psychiatry 158, 131. Silberman DM, Ayelli-Edgar V, Zorrilla-Zubilete M et al. (2004) Impaired T-cell dependent humoral response and its relationship with T lymphocyte sensitivity to stress hormones in a chronic mild stress model of depression. Brain Behav. Immun. 18, 81. Sklar P (2002) Linkage analysis in psychiatric disorders: the emerging picture. Annu. Rev. Hum. Genet. 3, 371. Stimpson N, Agrawal N, Lewis G (2002) Randomized controlled trials investigating pharmacological and psychological interventions for treatment-refractory depression: a systematic review. Br. J. Psychiatry 181, 284. Stout SC, Owens MJ, Nemeroff CB (2001) Neurokinin-1 receptor antagonists as potential antidepressants. Ann. Rev. Pharmacol. Toxicol. 41, 877. Strakowski SM, DelBello MP, Zimmerman ME, Getz GE et al. (2002) Ventricular and periventricular structural volumes in first-versus multiple-episode bipolar disorder. Am. J. Psychiatry 159, 1841. Taylor L, Faraone SV, Tsuang MT (2002) Family, twin, and adoption studies of bipolar disease. Curr. Psychiatry Rep. 4, 130. Thase ME (2002) What role do atypical antipsychotic drugs have in treatment-resistant depression? J. Clin. Psychiatry 63, 95. Thomas CM, Morris SM (2003) Cost of depression among adults in England in 2000. Br. J. Psychiatry 183, 514. UK ECT Review Group (2003) Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet 361, 799.


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Ustun TB, Kessler TC (2002) Global burden of depressive disorders: the issue of duration. Br. J. Psychiatry 181, 181. Volkmar FR (2002) Changing perspectives on mood disorders in children. Am. J. Psychiatry 159, 893. Whitfield G, Williams C (2003) The evidence base for cognitive–behavioural therapy in depression: delivery in busy clinical settings. Adv. Psychiatr. Treat. 9, 21. Zubenko GS, Maher B, Hughes HG et al. (2003) Genome-wide survey for genetic loci that influences the development of depressive disorders in families with recurrent, early-onset, major depression. Am. J. Med. Genet. 123B, 1.

Neurotic disorders

5

ANXIETY DISORDERS See Table 5.1. Anxiety disorders include various combinations of mental and physical manifestations of anxiety not attributed to real danger and occurring either in attacks (panic disorder) or as a persisting state (generalized anxiety disorder). Other neurotic features may be present (obsessional or hysterical symptoms) but do not dominate the clinical picture.

Table 5.1 ICD-10 and DSM-IV classifications of anxiety-related disorders ICD-10

DSM-IV

Phobic anxiety disorders Agoraphobia – with panic disorder – without panic disorder Social phobias Specific (isolated) phobias Other phobias

Phobic anxiety disorders Agoraphobia

Other anxiety disorders Panic disorder

Generalized anxiety disorder Mixed anxiety and depressive disorder Other anxiety disorders

Social anxiety disorder Specific phobia

Panic disorder – with agoraphobia – without agoraphobia Generalized anxiety disorder Anxiety disorder due to physical illness or substance abuse



Reaction to severe stress and adjustment Acute stress reaction Post-traumatic stress disorder Adjustment disorders

Reaction to severe stress and adjustment Acute stress disorder Post-traumatic stress disorder

ANXIETY DISORDERS

61

‘Anxiety’ suggests (Lewis):

• • • •

An emotional state with the subjectively experienced quality of fear. An unpleasant emotion which may be accompanied by a feeling of impending death. A feeling directed towards the future, perceiving a threat of some kind. A subjective bodily discomfort and manifest bodily disturbance.

There may be no recognizable threat – or one which, by reasonable standards, is out of proportion to the emotion it seemingly provokes.

PANIC DISORDER Recurrent attacks of panic (anxiety) occur unpredictably and unexpectedly, though certain situations (e.g. being away from one’s secure surroundings – panic disorder with agoraphobia) may become associated with them. Clinical symptoms • There is sudden onset of intense apprehension, anxiety, fear, often with feeling of impending doom or even death. Feelings of unreality may occur. • Somatic effects can include dyspnoea, palpitations, chest pain, choking or smothering sensations, paraesthesias, flushes, sweating, faintness, etc. • There may develop ‘anticipatory fear’ of loss of control, so the individual becomes afraid of being left alone in public places. Anticipatory fear may itself precipitate an attack.

GENERALIZED ANXIETY DISORDER There is a generalized persistent anxiety without the specific symptoms that characterize phobic anxiety disorder or panic disorder. Clinical symptoms • There is subjective apprehension, fear, worries (see above). • Motor tension. • Autonomic hyperactivity. • Vigilance and scanning – the person complains of feeling ‘on edge’, has difficulty sleeping, has interrupted sleep or fatigue on waking.

EPIDEMIOLOGY OF ANXIETY DISORDERS An anxiety disorder often begins in early adult life, but may occur for the first time in middle age. Women are more affected than men. There is a 4–7 per cent prevalence in the normal population. It accounts for 27 per cent of psychiatric consultations in general practice, and 8 per cent of psychiatric outpatients.

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NEUROTIC DISORDERS

PREDISPOSING FACTORS FOR ANXIETY DISORDERS GENETICS

• • •

There is a problem of small samples and diagnosis. MZ:DZ ⫽ 65%:13% (Slater and Shields). There is some evidence of genetic influence on neurotic ‘traits’ measured by personality tests and reflected in autonomic reactivity (e.g. GSR habituation).

EARLY CHILDHOOD

• • • •

Separation experiences. Childhood trauma. Undue emphasis on achievement. Demands for excessive conformity.

OTHER

• •

Current situational stress, uncertainty, conflict. Biological factors (see p. 66)

COURSE AND COMPLICATIONS OF ANXIETY DISORDERS There is a variable course and prognosis – the more chronic and established the condition, the worse the prognosis. Males are (?) more likely to improve than females. Premorbid stability has an important influence. Agoraphobia may develop, or secondary depression. Alcohol abuse and abuse of anxiolytics are not uncommon.

TREATMENT OF ANXIETY DISORDERS Reassurance, counselling and social intervention should be aimed at current situational stresses. PSYCHOTHERAPY

• • •

Cognitive–behavioural: more effective in panic disorder. Identify and ‘label’ morbid anticipatory thoughts and replace with realistic cognitions. Insight-orientated: explore covert conflicts. ‘Anxiety management’ training: – Distraction techniques. – Cognitive control. – Breathing/relaxation exercises – reduce chronic hyperventilation. – Education – somatic effects of anxiety and overbreathing.

DRUG THERAPY

•

Serotonin reuptake inhibitors are a first-line treatment. They are more effective than benzodiazepines in reducing anxiety, anger, and hostility in the long term.

PHOBIC DISORDERS

• • • • •

63

Benzodiazepines provide symptomatic relief in the short term. Azapirones are equal in efficacy to benzodiazepines in reducing anxiety, but are more effective at reducing anger and hostility. Beta-blockers are not useful in panic disorder, otherwise they reduce anxietyrelated symptoms in adequate dosage. MAOIs have anxiolytic properties. There is some evidence for usefulness in panic disorders. Novel antianxiety agents – Venlafaxine blocks the reuptake of serotonin as well as noradrenaline (norepinephrine) and provides long-term relief from anxiety.

PSYCHOSURGERY Surgery is reserved only for cases of chronic, intractable, incapacitating anxiety that is unresponsive to other measures.

PHOBIC DISORDERS In phobic disorders (Marks):

• • • •

Fear is out of proportion to the demands of the situation. It cannot be explained or reasoned away. It is beyond voluntary control. The fear leads to an avoidance of the feared situation.

CLINICAL SYNDROMES RELATED TO EXTERNAL STIMULI AGORAPHOBIA Agoraphobia is strictly a fear of open spaces, but the term is often used for fear of shopping, crowds, etc. Agoraphobia accounts for 60 per cent of phobic patients seen by psychiatrists; 66 per cent are female. Most develop symptoms between the ages 15 and 35. Other non-phobic symptoms are common, including generalized anxiety, panic attacks, depression and depersonalization. Predisposing and associated factors • Passive, anxious and dependent premorbid personality. • Stable family. • Similar to general population in terms of education, social class. • Often precipitated by major life event. • History of childhood fears and enuresis. • Higher incidence of sexual problems in female group compared with control population. Course and prognosis There is a fluctuating course, once established. It may persist for many years.

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SOCIAL PHOBIA Social phobia accounts for 8 per cent of phobic patients seen by psychiatrists; 60 per cent are women. It usually develops after puberty and peaks in late years. It is a persistent, irrational fear of, and compelling desire to avoid, situations in which the individual may be exposed to the scrutiny of others. There is also fear that the individual may behave in a manner (e.g. blushing, shaking, vomiting) that will be humiliating or embarrassing. Social phobia is probably not a homogeneous clinical entity but may represent the prominent symptomatic manifestation of a wide variety of psychological disorders. ANIMAL PHOBIAS AND OTHER SPECIFIC PHOBIAS These account for 17 per cent of phobic patients seen by psychiatrists. Women suffer more than men from animal phobias, otherwise the sex incidence is equal. Onset is in childhood for animal phobias. There is a persistent, irrational fear of, and compelling desire to avoid, an object or a situation – other than being alone in public places away from home (agoraphobia) or embarrassment in certain social settings (social phobia). There is relative absence of other psychiatric symptoms. It tends to pursue a continuous course. ILLNESS PHOBIA Illness phobia accounts for 15 per cent of phobic patients consulting psychiatrists. It occurs equally in both sexes. Illness phobia is a persistent, intense fear of illness, focused on specific disorders such as cancer, heart disease or veneral illness, or an intense fear of death and dying. There are chronic ruminations but no apparent attempts at resistance. A previous illness in a relative or individual may act as the precipitant. The patient may have other mental illness (e.g. depression), and illness phobia fades as this is treated.

TREATMENT OF PHOBIC DISORDERS All treatment rests on careful assessment with respect to:

• • • • • •

The degree to which the manifest anxiety is a reflection of basic personality traits, or may be considered to be a state arising in the setting of relatively normal personality structure. The presence or absence of stress supposed to be related to the course of the condition. The presence of any dangerous coping strategies (e.g. alcohol abuse). The attitudes of others, especially family, towards the patient’s illness. Is the disorder being covertly encouraged? The presence or absence of secondary gain factors. The presence or absence of other clinical syndromes (e.g. depression).

PHOBIC DISORDERS

65

BEHAVIOUR THERAPY Systematic desensitization There is gradual exposure to the phobic stimulus with increasing intensity until the patient habituates and the avoidance response is extinguished. This is combined with relaxation training, then practice in fantasy before situational exposure. Good response is associated with:

• • • • •

Phobias that are specific. Good relaxation response. Patient motivation. Encouragement and support from the therapist. Positive involvement of relatives.

Poor response is associated with:

• • • •

The presence of free-floating anxiety. Poor motivation. The presence of secondary gain. Severe obsessions.

Flooding (implosion) This can be in fantasy or in real life. There is supervised maximum exposure to the feared stimulus until anxiety reduction/exhaustion. This is effective (especially exposure in vivo) for phobias where free-floating anxiety is prominent. Modelling The patient observes the therapist (the model) engaging in non-avoidance behaviour with the feared stimulus. There is some evidence that a combination of flooding, associated modelling and moderate doses of diazepam given 4 hours before sessions is particularly effective in treating agoraphobia. DRUG THERAPY

• • • •

SSRIs are the drug treatment of choice and are well tolerated with no abuse potential. Benzodiazepines are effective but only for short-term management of fear-associated anxiety until other measures are successful. Beta-blockers are effective for short-term management of performance fears. MAOIs and TCAs are less effective and have a greater side-effect burden.

PSYCHOTHERAPY Behavior therapy is effective using either systematic desensitization or flooding. Cognitive–behavioural therapy is effective at modifying dysfunctional thoughts involving fear.

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NEUROTIC DISORDERS

BIOLOGICAL ASPECTS OF ANXIETY The following abnormal autonomic responses to stimuli in anxious patients may indicate underlying dysfunction of the autonomic nervous system, reflecting increased sympathetic tone or parasympathetic abnormalities. Cardiac function • Higher basal rate. • Less deceleration after stress. • More beat-to-beat fluctuation. • Increased awareness of heart function. Electrodermal response Increased skin conductance. Decreased habituation. More spontaneous fluctuation.

• • •

Peripheral blood flow More vasodilation. Decreased renal and splanchnic flow.

• •

Neurotransmitter abnormalities Findings conflict, probably owing to differences in diagnostic groups studied.

• • • •

Circulating adrenaline – increased. Circulating noradrenaline – ? increased. Platelet MAO – increased. Central noradrenaline and 5-HT – increased activity.

Responses to sodium lactate infusion Sodium lactate provokes panic attacks in susceptible patients, compared with controls. Imipramine is effective in blocking lactate-induced panic. Panic is provoked because of:

• • • •

Abnormal metabolism. Production of alkalosis. Reduction of ionized calcium. Interaction with hyperactive ␤-adrenergic receptors.

Mitral valve prolapse (MVP) Studies (see Pariser et al., 1979) have suggested a 40–50 per cent incidence of MVP in patients with panic disorder or agoraphobia. Incidence in the general population is 6–20 per cent. Evidence does not suggest that MVP causes panic attacks (e.g. patients with panic disorder and MVP respond to imipramine as patients solely with panic disorder, but MVP persists).

POST-TRAUMATIC STRESS DISORDER

67

Both MVP and panic may form part of a general syndrome of primary autonomic dysfunction. or MVP may act as an autonomic precipitant interacting with a predisposition (genetic) to panic disorder. Hyperventilation syndrome Physiological effects of reduced PCO2:

• • • • •

Vasoconstriction of cerebral arteries. Reduced availability of O2 in oxyhaemoglobin. Increased irritability of autonomic sensory and motor nervous system. Bronchoconstriction and tachycardia. Exaggerated sinus rhythm.

Symptoms produced:

• • • • •

Light-headedness or faintness. Breathlessness and palpitations. Sweating, fatigue and stiffness. Dry mouth with aerophagy and globus. Chronic malaise.

Some researchers think that hyperventilation causes panic attacks, others that it is merely a consequence (see diagram below).

Anticipatory cognitions

Panic attacks

Hyperventilation

Symptoms

POST-TRAUMATIC STRESS DISORDER (PTSD) Familiar terms are ‘combat neurosis’, ‘shell-shock syndrome’ and ‘traumatic neurosis’ in the UK – stemming from experiences in war, but PTSD is also now seen as a response to natural disasters (e.g. Hillsborough deaths Pugh and Trimble, 1993; Australian bush fire-fighters McFarlane et al., 1990; Coconut Grove fire), to rape, to traffic accidents, to trauma, etc.

68

NEUROTIC DISORDERS

Rates of PTSD are related to specific types of traumatic events (Kessler et al., 1995):

• • • •

rape – 65 per cent combat – 38.8 per cent natural disaster – 3.7 per cent criminal assault – 1.8 per cent.

The lifetime prevalence in the community is 1–9 per cent. Chronic PTSD is seen in 1.3 per cent of males and in 4.7 per cent of females (Breslau et al., 1995). There are high rates of co-morbidity (Kessler et al., 1995):

• • • • • •

alcohol abuse/dependency – 52 per cent depression – 48 per cent substance dependency – 34 per cent social phobia – 28 per cent generalized anxiety disorder – 17 per cent panic disorder – 7 per cent.

CLINICAL FEATURES OF PTSD 1 There has been exposure to a traumatic event, lying outside normal human experience and which would clearly cause suffering in almost everyone. The person’s response involves intense fear, helplessness. 2 There is persistent re-experiencing – recurrent nightmares, flashbacks, reliving of episode, psychological distress and/or physiological reactivity on exposure to cues which resemble/symbolize the trauma. 3 There is persistent avoidance of stimuli related to the trauma. 4 Symptoms of hyperarousal are present – hypervigilance, startle reflexes, sleep disturbance, decreased habituation to auditory stimuli. 5 There is psychosocial impairment: ICD-10 criteria emphasize onset within 6 months of the traumatic event.

AETIOLOGY OF PTSD There has been much debate about the extent of individual determinants of PTSD. Not everyone experiencing major trauma develops PTSD, and the neurobiological basis is not clear.

• • • • • •

PTSD may be due to a complex neurobiological response mechanism that engenders maximal and sustained response to stress. There is evidence of increased hypothalamic–pituitary–adrenal axis reactivity. Lower basal cortisol levels and more glucocorticoid receptors are seen in individuals with PTSD. Elevated catecholamine levels may account for some PTSD symptoms. Smaller hippocampal volumes are seen in those with PTSD. A previous traumatic event and/or prior history of psychiatric illness are predisposing factors for PTSD.

OBSESSIONAL/COMPULSIVE STATES

69

MANAGEMENT OF PTSD

• • • • • • • • • •

Rule out a physical illness or cause. Rule out alternative psychiatric illness and/or detect and treat secondary disorder – depression, substance abuse, suicidal behaviour. Suicidal behaviour in Vietnam survivors related to ‘combat guilt’ (Hendin and Haas, 1991). Consider cognitive–behavioural therapy, with graded exposure to imagery. Some evidence points to the efficacy of therapy involving saccadic eye movements. Psychoeducation – explanation regarding stress. Interpersonal psychotherapy. Psychodynamic psychotherapy. Relaxation training. Group therapy. Drugs: – SSRIs are a first-line treatment. – Atypical antidepressants – nefazodone, venlafaxine. – Mood stabilizers useful. – Atypical antipsychotics. – Antiadrenergics. – Imipramine, amitryptiline shown to be effective. – MAOIs sometimes used but side-effect tolerability poor. – Benzodiazepines not generally recommended because of liability of abuse and chronicity of PTSD.

PROGNOSIS FOR PTSD Prognosis is good if:

• • • •

Healthy premorbid function. Brief trauma of lesser severity. No personal or family history of psychiatric illness. Good social support.

The condition becomes chronic in a minority, and the course is fluctuating. Emphasis today is towards early intervention and prevention – ‘debriefing’ to avert the development of chronic PTSD. In a preliminary trial, a ‘morning after pill’ of propranolol immediately in the emergency department after a traumatic event was encouraging. There is increasing PTSD research and research on ‘resilience’ (what characteristics make people able to cope with adversity), particularly global terrorism.

OBSESSIONAL/COMPULSIVE STATES Obsessions are recurrent, persistent ideas, thoughts, images or impulses that the patient regards as alien and absurd, while recognizing them as products of his/her own mind. Attempts are made to ignore and suppress them.

70

NEUROTIC DISORDERS

Table 5.2 Phenomenology of obsessional–compulsive states Obsessional doubting – 42%. Fears of contamination – 45%. Bodily fears – 36%. Insistence on symmetry – 31%.

Aggressive thoughts – 28%. Checking compulsions – 63%. Washing – 50%. Counting – 36%.

From Rasmussen and Tsuang (1986).

Compulsions are voluntary motor actions which are reluctantly performed despite being regarded as alien or absurd. The act is performed with a subjective sense of compulsion coupled with a desire to resist it (at least initially). When the individual does attempt to resist, there is a mounting sense of tension which can only be relieved by yielding. The phenomenology of obsessional–compulsive states is shown in Table 5.2. Symptoms may complicate:

• • • • •

Depressive illness (found in 30 per cent) – low rate of suicide in depressed patients with obsessive–compulsive disorder (OCD). Schizophrenic disorder. Early dementia and other organic brain syndromes. Anorexia nervosa. Generalized anxiety state.

Fears of harming a baby may occur as part of puerperal illness.

EPIDEMIOLOGY OF OCD The sex distribution is equal. The most common age at onset is early adulthood:

• • • •

65 per cent of patients onset ⬍25 years. 15 per cent after age 35 years. Mean age at onset ⫽ 20 years. Mean age of presenting to psychiatric services ⫽ 27.5 years (Rasmussen and Tsuang, 1986).

Prevalence 0.5 per cent of general population, but recorded lifetime rates of 2–3 per cent in ECA study (overestimated). • 1 per cent of psychiatric outpatient and inpatient population. • 4 per cent of the ‘neurotic’ group.

•

AETIOLOGY OF OCD GENETICS Up to 20 per cent of first-degree relatives have subclinical OCD symptoms. There have been few twin studies: MZ ⫽ 50–80 per cent; DZ ⫽ 25 per cent. The condition is strongly linked to Tourette’s disorder.

OBSESSIONAL/COMPULSIVE STATES

71

NON-GENETIC FACTORS Neurochemistry and neuroanatomy Glutamatergic-serotonin modulation in the caudate nucleus is thought to be involved. The primary pathology may be in the caudate nucleus. The frontal lobe also is implicated. PET studies show glucose hypermetabolism in fronto-orbital gyrus and caudate nuclei (Baxter et al., 1992); these abnormalities are normalized with effective pharmacotherapy (Swedo et al., 1992, Rosenberg et al., 2000). PANDAs Paediatric autoimmune neuropsychiatric disorders are associated with streptococcal infection. They are characterized by the abrupt onset of OCD or tics and are thought to be the result of an autoimmune response to group A ␤-haemolytic streptococcal infection. Premorbid personality The meticulous (‘anankastic’) type personality is associated in 15–35 per cent. Concern is with orderliness, cleanliness, checking, rigidity. Psychoanalytic theory Freud’s views were expounded in his lecture ‘Notes upon a Case of Obsessional Neurosis’ (the Rat Man):

• • •

Defensive regression to pregenital anal-erotic stage of development. Defensive mechanism against aggressive and cruel impulses. Key defences: reaction formation, undoing, isolation (see p. 298).

Psychological theory One view is that OCD is a defect of the arousal system (Beech). Major defensive reactions are precipitated by minor alterations to incoming stimuli, perceived as dangerous and threatening. The defensive response is thus seen as preventive or placatory activity aimed at controlling unpleasant internal states. Learning theory cannot account fully for obsessional phenomena, which are not a motor response to an anxious thought, but simply the repetitive intrusion into consciousness of an anxious thought or impulse alone.

TREATMENT OF OCD Psychotherapy Cognitive–behavioural therapy has been shown to decrease symptomology (Benazon et al., 2002). Ruminations are more difficult to treat. ‘Thought stopping’ may be helpful. Loop-type techniques also are helpful. Drugs and surgery SSRIs are effective in relieving symptoms and also cause normalizing changes in neurochemistry in the caudate nucleus, as seen by proton magnetic resonance spectroscopy (Rosenberg et al., 2000).

72

NEUROTIC DISORDERS

Fluoxetine, sertraline, citalopram, clomipramine, paroxetine and fluvoxamine have all been used, but there is no clear superiority of any one agent. Combining serotonergic drug treatment with CBT exposure and response prevention is the mainstay of treatment. Case reports of atypical antipsychotic utilization exist and further research is needed. Psychosurgery (anterior cingulotomy, subcaudate tractotomy, limbic leucotomy, capsulotomy) is indicated only in severe cases of chronic, incapacitating illness when other methods have failed (Sachdev et al., 1992).

COURSE AND PROGNOSIS OF OCD With treatment, the majority of individuals diagnosed with OCD experience a chronic, fluctuating course. About half of those with OCD will experience partial remission; and of those, half will experience relapse. Only 12 per cent achieve full remission. Monitor treatment with Yale–Brown Obsessive Compulsive Scale (YBOCS). Poor prognostic factors are:

• • • •

Co-morbid psychiatric disorder. Earlier onset, longer duration of illness. Poor insight into the illness. More severe, bizarre symptoms – symmetry, ordering, hoarding obsessions.

REFERENCES AND FURTHER READING Ackerman DL, Greenland S (2002) Multivariate meta-analysis of controlled drug studies for obsessive–compulsive disorder. J. Clin. Psychopharmacol. 22, 309. Allgulander C, Hirschfeld RM, Nutt DJ (2002) Long-term treatment strategies in anxiety disorders. Psychopharmacol. Bull. 36 (Suppl. 2), 79. American Psychiatric Association (1998) Practice guideline for the treatment of patients with panic disorder. Am. J. Psychiatry 155 (Suppl. May), 1. Andersch S, Hetta J (2002) A naturalistic fifteen-year follow-up study of panic disorder patients. Eur. Psychiatry 17 (Suppl. 1), 166. Andrews G, Slade T (2002) Agoraphobia without a history of panic disorder may be part of the panic disorder syndrome. J. Nerv. Ment. Dis. 190, 624. Arnold PD, Richter MA (2001) Is obsessive–compulsive disorder an autoimmune disease? CMAJ 165, 1353. Baldwin D, Evans D, Hirschfeld RSK (2002) Can we distinguish anxiety from depression? Psychopharmacol. Bull. 36, 158. Ballenger J (2001) Overview of different pharmacotherapies for attaining remission in generalized anxiety disorder. J. Clin. Psychiatry 62 (Suppl.), 11. Ballenger J, Davidson J, Lecrubier Y et al. (2000) Consensus statement on posttraumatic stress disorder from the International Consensus Group on Depression and Anxiety. J. Clin. Psychiatry 61, 60. Barzega G, Maina G, Venturello S, Bogetto F (2001) Gender-related distribution of personality disorders in a sample of patients with panic disorder. Eur. Psychiatry 16, 173. Baxter LR, Schwartz JM, Bergman KS et al. (1992) Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive–compulsive disorder. Arch. Gen. Psychiatry 49, 681.


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Benazon NR, Ager J, Rosenberg DR (2002) Cognitive behavior therapy in treatment-naive children and adolescents with obsessive–compulsive disorder: an open trail. Behav. Res. Ther. 40, 529. Benazon NR, Moore GJ, Rosenberg DR (2003) Neurochemical analyses in pediatric obsessive– compulsive disorder in patients treated with cognitive–behavioral therapy. J. Am. Child Adolesc. Psychiatry 42, 1279. Borkovec TD, Newman MG, Castonguay LG (2003) Cognitive–behavioral therapy for generalized anxiety disorder with integrations from interpersonal and experiential therapies. CNS Spectr. 8, 382. Brawman-Mintzer O (2002) Pharmacologic treatment of generalized anxiety disorder. Psychiatr. Clin. North Am. 24, 119. Breslau N (2002a) Post-traumatic stress disorder. New Engl. J. Med. 346, 1495. Breslau N (2002b) Gender differences in trauma and posttraumatic stress disorder. J. Gend. Specif. Med. 5, 34. Breslau N, Davis GC, Andreski P (1995) Risk factors for PTSD-related traumatic events: a prospective analysis. Am. J. Psychiatry 152, 529 Breslau N, Chilcoat H, Kessler R, Davis G (1999) Previous exposure to trauma and PTSD effects of subsequent trauma: results from the Detroit Area Survey of Trauma.. Am. J. Psychiatry 156, 902. Brunello N, Davidson J, Deahl M et al. (2001) Posttraumatic stress disorder: diagnosis and epidemiology, comorbidity and social consequences, biology and treatment. Neuropsychobiology 43, 150. Carlbring P, Gustafsson H, Ekselius L, Andersson G (2002) 12-month prevalence of panic disorder with or without agoraphobia in the Swedish general population. Soc. Psychiatry Psychiatr. Epidemiol. 37, 207. Craske MG, Roy-Byrne P, Stein MB et al. (2002) Treating panic disorder in primary care: a collaborative care intervention. Gen. Hosp. Psychiatry 24, 148. Davidson JRT (2002) Surviving disaster: what comes after the trauma? Br. J. Psychiatry 181, 366. Dougherty DD, Baer L et al. (2002) Prospective long-term follow-up of 44 patients who received cingulotomy for treatment-refractory obsessive–compulsive disorder. Am. J. Psychiatry 159, 269. Dugas MJ, Ladouceur R, Leger E et al. (2003) Group cognitive–behavioral therapy for generalized anxiety disorder: treatment outcome and long-term follow-up. J. Consult. Clin. Psychol. 71, 821. Falsetti SA, Davis J (2001) The nonpharmacologic treatment of generalized anxiety disorder. Psychiatr. Clin. North Am. 24, 99. Fava GA, Rafanelli C, Grandi S et al. (2001) Long-term outcome of panic disorder with agoraphobia treated by exposure. Psychol. Med. 31, 891. Foa EB, Davidson JRT (eds) (1999) The Expert Consensus Guideline Series. Treatment of Posttraumatic Stress Disorder. J. Clin. Psychiatry 60 (Suppl. 16), 3–76. Friedman MJ (2002) Future pharmacotherapy for post-traumatic stress disorder: prevention and treatment. Psychiatr. Clin. North Am. 25, 427. Gershuny B, Baer L, Jenike M et al. (2002) Comorbid PTSD; impact on treatment outcome for OCD. Am. J. Psychiatry 159, 852. Gillette GM, Skinner RD, Rasco LM et al. (1997) Combat veterans with posttraumatic stress disorder exhibit decreased habituation of the P1 midlatency auditory evoked potential. Life Sci. 61, 1431. Golier J, Yehuda R (2002) Neuropsychological processes in post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 295. Golier J, Yehuda R, Bierer LM et al. (2003) The relationship of borderline personality disorder to posttraumatic stress disorder and traumatic events. Am. J. Psycyhiatry 160, 2018. Golier J (2002) Neuropsychological processes in post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 295. Gorman JM (2003) Treating generalized anxiety disorder. J. Clin. Psychiatry 64 (Suppl. 2), 24. Grossman R, Buchsbaum MS, Yehuda R (2002) Neuroimaging studies in post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 317.

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Grossman R, Yehuda R, New A et al. (2003) Dexamethasone suppression test findings in subjects with personality disorders: associations with posttraumatic stress disorder and major depression. Am. J. Psychiatry 160, 1291. Hanna GL, Veenstra-VanderWeele J, Coz NJ et al. (2002) Genome-wide linkage analysis of families with obsessive–compulsive disorder ascertained through pediatric probands. Am. J. Med. Genet. 114, 541. Hansen ES, Hasselbalch S, Law I et al. (2002) The caudate nucleus in obsessive–compulsive disorder. Reduced metabolism following treatment with paroxetine: a PET study. Int. J. Neuropsychopharmacol. 5, 1. Hemmings S, Kinnear C, Niehaus D et al. (2003) Investigating the role of dopaminergic and serotonergic candidate genes in OCD. Eur. Neuropsychopharmacol. 13, 93. Hendin H, Haas AP (1991) Suicide and guilt as manifestations of PTSD in Vietnam combat veterans. Am. J. Psychiatry 148, 586. Hollander E, Kaplan A, Allen A, Cartwright C (2000) Pharmacotherapy for obsessive–compulsive disorder. Psychiatr. Clin. North Am. 23, 643. Hull AM (2002) Neuroimaging finding in post-traumatic stress disorder: a systematic review. Br. J. Psychiatry 181, 102. Kessler RC (2000) Posttraumatic stress disorder: the burden to the individual and to society. J. Clin. Psychiatry 61 (Suppl. 5), 4. Kessler RC, Sonnega A, Bromet E et al. (1995) Posttraumatic stress disorder in the National Comorbidity Survey. Arch. Gen. Psychiatry 52, 1048. Kessler RC, Keller MB, Wittchen HU (2001) The epidemiology of generalized anxiety disorder. Psychiatr. Clin. North Am. 24(1), 19. Kessler RC, Andrade L, Bijl R et al. (2002) The effects of co-morbidity on the onset and persistence of generalized anxiety disorder in the ICPE surveys. International Consortium in Psychiatric Epidemiology. Psychol. Med. 32, 1213. Lepine J (2002) The epidemiology of anxiety disorder: prevalence and societal costs. J. Clin. Psychiatry 63 (Suppl.), 4. Liebowitz MR, Turner SM, Piacentini J et al. (2002) Fluoxetine in children and adolescents with OCD: a placebo-controlled trail. J. Am. Acad. Child Adolesc. Psychiatry 41, 1431. Lipstiz JD, Marshall RD (2001) Alternative psychotherapy approaches for social anxiety disorder. Psychiatr. Clin. North Am. 24, 817. Marshall RD, Garakani A (2002) Psychobiology of the acute stress response and its relationship to the psychobiology of post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 385. Mataix Cols D, Rauch SL, Baer L et al. (2002) Symptom stability in adult obsessive–compulsive disorder: data from a naturalistic two-year follow-up study. Am. J. Psychiatry 159, 263. Matthews K, Eljamel MS (2003) Status of neurosurgery for mental disorder in Scotland: selective literature review and overview of current clinical activity. Br. J. Psychiatry 182, 404. McDonough M, Kennedy N (2002) Pharmacological management of obsessive-compulsive disorder: a review for clinicians. Harvard Rev. Psychiatry 10, 127. McFarlane A (1990) An Australian disaster: the 1983 bushfires. Int. J. Mental Health 19(2), 36. McFarlane AC, Yehuda R, Clark CR (2002) Biologic models of traumatic memories and posttraumatic stress disorder. Psychiatr. Clin. North Am. 25, 253. Mellman TA, David D, Bustamante V et al. (2001) Predictors of post-traumatic stress disorder following severe injury. Depress. Anxiety 14, 226. Millet B, Chabane N, Delorme R et al. (2003) Association between the dopamine receptor D4 gene and OCD. Am. J. Med. Genet. 116, 55. Moreau C, Zisook S (2002) Rationale for a posttraumatic stress spectrum disorder. Psychiatr. Clin. North Am. 25, 775. Mundo E, Richter MA, Zai G et al. (2002) 5HT1Dbeta receptor gene implicated in the pathogenesis of obsessive–compulsive disorder: further evidence from a family-based association study. Mol. Psychiatry 7, 805.


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Murray J, Ehlers A, Mayou RA (2002) Dissociation and post-traumatic stress disorder two prospective studies of road traffic accident survivors. Br. J. Psychiatry 180, 363. Nutt D (2000) The psychobiology of posttraumatic stress disorder. J. Clin. Psychiatry 61, 24. Nutt D, Ballenger J, Sheehan D, Wittchen H (2002) Generalized anxiety disorder: comorbidity, comparative biology and treatment. Int. J. Neuropsychopharmacol. 5, 315. Otto MW, Tuby KS, Gould RA, McLean RY, Pollack MH (2001) An effect-size analysis of the relative efficacy and tolerability of serotonin selective reuptake inhibitors for panic disorder. Am. J. Psychiatry 158, 1989. Overbeek T, Schruers K, Vermetten E, Greiez E (2002) Comorbidity of OCD and depression prevalence, symptom severity, and treatment effect. J. Clin. Psychiatry 63, 1106. Pariser SF, Jones BA, Pinta ER et al. (1979) Panic attacks: diagnostic evaluations of 17 patients. Am. J. Psychiatry 136(1), 105. Pereira A (2002) Combat trauma and the diagnosis of post-traumatic stress disorder in female and male veterans. Mil. Med. 167, 23. Perugi G, Toni C, Frare F (2002) Obsessive–compulsive bipolar comorbidity: a systematic exploration of clinical features and treatment outcome. J. Clin. Psychiatry 63, 1129. Phillips KA (2002) The obsessive–compulsive spectrums. Psychiatr. Clin. North Am. 25, 791. Pigott TA (2003) Anxiety disorders in women. Psychiatr. Clin. North Am. 26, 621. Pitman RK, Sander KM, Zusman RM et al. (2002) Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol. Psychiatry 51, 189. Pugh C, Trimble MR (1993) Psychiatric injury after Hillsborough. Br. J. Psychiatry 163, 425. Rabios D, Batten SV, Keane TM (2002) Implications of biological findings for psychological treatments of post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 443. Rosario-Campos M, Leckman J, Mercadante M (2001) Adults with early-onset OCD. Am. J. Psychiatry 158, 1899. Rosenberg DR, MacMaster FP, Keshavan MS et al. (2000) Decrease in caudate glutamatergic concentrations in pediatric obsessive–compulsive disorder patients taking paroxetine. J. Am. Acad. Child Adolesc. Psychiatry 39, 1096. Sachdev P, Hay P, Cumming S (1992) Psychosurgical treatment of obsessive–compulsive disorder. Arch. Gen. Psychiatry 49, 582. Saxena S, Brody AL, Ho ML et al. (2002) Differential cerebral metabolic changes with paroxetine treatment of obsessive–compulsive disorder vs major depression. Arch. Gen. Psychiatry 59, 250. Serpell L, Livingstone A, Neiderman M et al. (2002) Obsessive–compulsive disorder, obsessive– compulsive personality disorder, or neither? Clin. Psychol. Rev. 22, 647. Shear MK (2002) Building a model of posttraumatic stress disroder. Am. J. Psychiatry 159, 1931. Shear MK, Houck P, Greeno C, Masters S (2001) Emotion-focused psychotherapy for patients with panic disorder. Am. J. Psychiatry 158, 1993. Sheikh JI, Leskin GA, Klein DF (2002) Gender differences in panic disorder: findings from the National Comorbidity Survey. Am. J. Psychiatry 159, 55. Solvason HB, Ernst H, Roth W (2003) Predictors of response in anxiety disorders. Psychiatr. Clin. North Am. 26, 411. Sorenson SB (2002) Preventing traumatic stress: public health approaches. J. Truama Stress 15, 3. Stein MB, Jang KL, Taylor S (2002) Genetic and environmental influences on trauma exposure and posttraumatic stress disorder symptoms: a twin study. Am. J. Psychiatry 159, 1675. Stimpson NJ, Thomas HV, Weightman AL et al. (2003) Psychiatric disorder in veterans of the Persian Gulf War of 1991: a systematic review. Br. J. Psychiatry 182, 391. Swedo SE, Leonard HL, Kruesi MJ et al. (1992) Cerebrospinal fluid neurochemistry in children and adolescents with obsessive–compulsive disorder. Arch. Gen. Psychiatry 49, 29. Swedo SE, Pietrini P, Leonard HL et al. (1992) Cerebral glucose metabolism in childhood-onset obsessive–compulsive disorder: revisualization during pharmacotheraphy. Arch. Gen. Psychiatry 49, 690. Thomas CS (2002) Psychological consequences of traumatic injury. Br. J. Psychiatry 180, 392.

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True WR, Rice J, Eisen SA et al. (1993) A twin study of genetic and environmental contributions to liability for post-traumatic stress symptoms. Arch. Gen. Psychiatry 50, 257. Tuke R, Polat A, Ozdemir O et al. (2002) Comorbid conditions in obsessive–compulsive disorder. Compr. Psychiatry 43, 204. Ursano RJ (2002) Post-traumatic stress disorder. New Engl. J. Med. 346, 130. Yehuda R (2002a) Current status of cortisol findings in post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 341. Yehuda R (2002b) Recent advances in the study of biological alterations in post-traumatic stress disorder (PTSD). Psychiatr. Clin. North Am. 25, 76. Yehuda T (2002c) Post-traumatic stress disorder. New Engl. J. Med. 346, 108.

Personality: development and disorders

6

Personality can be defined as the distinctive, enduring patterns of behaviour (including thought, perception and emotions) that characterize each individual’s interaction with the social and personal situations of his or her life.

PERSONALITY DEVELOPMENT THEORIES FREUD

• • •

The oral stage relates to narcissism, dependence, envy, jealousy. The anal stage relates to obsessionality, orderliness, obstinacy, frugality; also rage and sadomasochism. The phallic stage relates to competitiveness and ambition.

Character is that pattern of adaptation to instinctual and environmental forces which is habitual for the individual. It results from a combination of: innate biological predisposition, id forces, early ego defences, environmental influences and early identification and imitation. Character traits owe their existence to successful repression, leading to persistence. Neurotic symptoms result from a failure of repression. ADLER Lifestyle is the individual’s active adaptation to the social milieu. The individual is motivated by a striving for superiority as a defence against the helplessness of inferiority. HORNEY Horney emphasizes the important effect of culture. There are three character types depending on the predominant mode of relating to others: compliant/self-effacing, aggressive/expansive, detached/resigned. SULLIVAN The individual has two major goals (and states): satisfactions (of biological needs) and security (in relationships with others). Anxiety is the response to adult disapproval and personality development is the process of learning to deal with this anxiety.

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ERIKSON Personality development takes place through (potentially) eight ‘stages’. These are a series of alternative attitudes which develop into a ‘sense of the attribute’. ‘Epigenesis’ refers to the process of development of the ego through these stages. 1 Basic trust versus mistrust (oral/sensory) – awareness of consistency and continuity, leading to ego identity. 2 Autonomy versus shame and doubt (muscular/anal) – self-control vs. loss of self-esteem. 3 Initiative versus guilt (locomotor/genital) – planning tasks, but failure leads to guilt. 4 Industry versus inferiority (latency) – recognition is won by doing things, the danger is inferiority. 5 Identity versus role confusion (puberty) – may lead to the ‘identity crisis’, between inner sense of continuity and outer vulnerability in one’s meaning for others. 6 Intimacy versus isolation (young adulthood) – the capacity to commit oneself to others. 7 Generativity versus stagnation (adulthood) – productivity/creativity or self-absorption. 8 Integrity versus despair (maturity) – in the awareness of the closeness of death. MEYER Pathological personality reactions are regressions to former, previously protective phylogenetic reactions which are now maladaptive. Symptoms are the individual’s attempt to cure himself or herself. Personality disorder results from disorganization of habits. PIAGET Piaget investigated the development of cognition in children. Human intelligence is an extension of biological adaptation, has a logical substructure and develops in four stages (another ‘epigenetic’ theory). 1 Sensorimotor (0–2 years) – learns object permanence, differentiates self from objects, aware of effects of self on objects. 2 Preoperational (2–7 years) – uses symbols, language develops, egocentric. 3 Concrete operational (7–12 years) – capable of logical thought, develops concept of conservation, classifies, relates. 4 Formal operational (12⫹) – capable of abstract thought, hypothesis, concerned with ideologies.

PERSONALITY DISORDERS DEFINITIONS DSM-IV and ICD-10 presume a major category of personality disorders (PDs), with features (see Table 6.1):

• •

Deeply ingrained, maladaptive patterns of behaviour. Recognizable in adolescence or earlier.

PERSONALITY DISORDERS

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Table 6.1 ICD-10 and DSM-IV classification of personality disorders ICD-10

DSM-IV Cluster A

Paranoid Schizoid

Paranoid Schizoid Schizotypal Cluster B

Antisocial Emotionally unstable Impulsive type Borderline type histrionic other specific (includes narcissistic)

Dissocial Borderline Histrionic Narcissistic

Cluster C Anxious (avoidant) Dependent Anankastic Pers. disorder unspecified

Avoidant Dependent Obsessive–compulsive Pers. disorder mixed Pers. disorder NOS

Notes: Enduring change not attributable to gross brain damage or disease. Affective (cyclothmic) pers. disorder, which was under this category in ICD-9, now categorized under Mood Disorders. Paranoid – pervasive mistrust, cold affect and hypersensitive. Schizoid – social withdrawal, social discomfort, bland constricted affect, aloof and insensitive. Schizotypal – eccentric, magical thinking, isolated, ideas of reference, illusions, tangential communications. More common in relatives of patients with schizophrenia. Dissocial – see Chapter 18. Borderline – self detrimental impulsivity, unstable, intense relationships, intense affect, identity confusion, shifts of mood, chronic anhedonia. Frequently co-morbid substance abuse, eating disturbance, hypersexuality, self-mutilation. Prone to brief psychotic episodes (micropsychoses). Histrionic – colourful, dramatic, superficial, unable to maintain deep relationships, self centred and dependent. Narcissistic – self important, attention demanding, unable to empathize and exploitative. Avoidant – shy, hypersensitive to rejection, socially withdrawn and low self-esteem. Dependent – lacking in self confidence, requires others to assume responsibility and subordinates own needs to those of others. Obsessive–compulsive – perfectionistic, orderly, devoted to work and emotionally constricted.

• • •

Continuing throughout most of adult life. The patient or others have to suffer. An adverse effect on the individual or society.

Particularly notable points are that great care must be taken in the diagnosis of personality disorder during an episode of another psychiatric disorder (e.g. affective disorder). Also, distinctions on the one hand from ‘normality’ and on the other from chronic neurotic and psychotic disorders are not clear. Distinguish between behaviour and personality. Some regard ‘personality disorder’ as fundamentally a social diagnosis – the assignment of a sick role to those whom society finds troublesome. This is a pejorative diagnosis, a diagnosis of despair (Lewis and Appleby, 1988). There is a large overlap between PDs: 54 per cent of patients with DSM-III-PD met criteria for another PD (Pfohl et al., 1986).

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EPIDEMIOLOGY PD rates are variable, and unreliable, being very dependent on sampling, assessment and definition:

• • • • •

General population – 10 per cent. Epidemiological Catchment Area (ECA) study – 6 per cent. A prison population – 20–80 per cent. Psychiatry outpatient attenders – 10–40 per cent. Primary care attenders – 7 per cent (one-third of those with ‘conspicuous’ psychiatric morbidity will have PD).

CLASSIFICATION AND MEASUREMENT DIMENSIONAL APPROACHES The trait approach (Cloninger, 1987) considers personality as a constellation of traits – a set of dimensions along each of which any individual will vary. Differences between normal and abnormal are viewed as quantitative. The dimensional approach is also applied along psychiatric ‘continua’; e.g. schizophrenic spectrum disorders, borderline spectrum. Approaches may show overlap on psychobiological measures. Typical assessments These include (see Chapter 1):

• • •

Catell Sixteen Personality Factor Test (16PF). Minnesota Multiphasic Personality Inventory (MMPI). Eysenck Personality Inventory (EPI).

CATEGORICAL (TYPOLOGICAL) APPROACH Personality types are recognizable as consistent groupings of characteristics. This approach is less theoretically sound, but intuitive, convenient, and widely used in clinical practice. Early examples include:

• • • •

Hippocrates – choleric, phlegmatic, sanguine, melancholic. Kretschmer (1921) – endomorph (social, relaxed), ectomorph (restrained, aloof), mesomorph (muscular, active). Schneider (1923) – 10 types of ‘psychopathic personality’. Henderson (1939) – ‘aggressive’, ‘creative’, ‘inadequate’ subtypes of psychopaths.

AETIOLOGICAL THEORIES Theories are diverse. Many researchers tend to favour a specific theory, although the biopsychosocial model may be a more appropriate and integrative approach.

PERSONALITY DISORDERS

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PSYCHODYNAMIC THEORY Defensive, non-adaptive personality patterns develop as a result of a disruptive early environment. Under the personality dysfunctioning lies defective and infantile ego functions (see Chapter 23); e.g. poor impulse control, defective object relations, intolerance of affect, unstable identification and super-ego lacunae. Borderline PD uses primitive defence mechanisms (splitting, projective identification) which may result from pathological early object relations and difficulties at the separation/individuation stage of development. Reality testing is distorted by intense internal needs and conflicts, leading to habitual distortion of thought, judgement and perception obvious to others but not the individual. Poor self-image is combined with infantile feelings of entitlement. Aggressive impulses are poorly integrated, resulting in persistently disturbed relationships with others. Such mechanisms develop as responses to early childhood relationships, and particular personality traits relate to particular disturbances of upbringing. Psychodynamic development may be halted at a particular stage owing to environmental stress, or the individual may regress to that stage under further stress later in life. BEHAVIOURAL PSYCHOLOGY (SKINNER) ‘The self is a repertoire of behaviour appropriate to a given set of contingencies.’ Behaviour is shaped and maintained by its consequences. Personality is governed by environmental forces. GENETICS Diagnostic imprecision causes difficulties. Central markers include serotonin dysregulation in sociopathy, borderline PD and impulse disorders, sleep and dysregulation and eye-tracking abnormalities (see Chapter 3). Peripheral markers include platelet MAO, DST suppression.

• • • • • • •

Polymorphisms in the COMT gene are associated with anger-related traits (Rujescu et al., 2003). An association has been shown between a functional promoter polymorphism in the dopamine D2 receptor gene and detached personality trait, as seen in schizoid or avoidant behavior (Jonsson et al., 2003). Criminality, social introversion, pattern of crime (sexual, violent criminal career) have all been shown to have higher MZ concordance. Danish adoption studies: – Biological father criminal – 21 per cent criminality in adoptees. – Neither father criminal – 10 per cent criminality in adoptees. – Both fathers criminal – 36 per cent criminality in adoptees. XYY individuals show evidence of increased criminality independent of low IQ and socioeconomic status. XY individuals show greater aggression and greater reported/detected criminality than XX. There is a prominent influence in schizotypal (see Chapter 3), antisocial PD (see Chapter 18).

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• •


Female criminals have higher genetic loading than males. Relatives of females with Briquet’s syndrome/somatization disorder have high rates of antisocial PD.

SOCIOCULTURAL FACTORS Social learning theory emphasizes personality traits of children derived from the shaping influence of parents (direct reinforcement or modelling). Most likely this is a complex interaction; e.g. match of temperament with parental expectations, subcultural expectation. TEMPERAMENT The New York Longitudinal Study followed 133 subjects from infancy to adulthood. Behaviour is said to consist of:

• • •

Abilities (the ‘what’). Motivations (the ‘why’). Temperament (the ‘how’).

Nine categories of temperament are defined (e.g. biological rhythmicity, activity level, mood, withdrawal, adaptability). Three temperamental constitutions are found:

• • •

The easy child (40 per cent) – regular, positive, adaptable. The difficult child (10 per cent) – irregular, negative, not adaptable. The slow-to-warm-up child (15 per cent) – mildly negative, slow to adapt.

Temperament is partly governed by genetics, not by sex or parental attitudes (except parental conflict, which related to early adult adjustment). Continuity of temperament over time from infancy was very evident given stability of the environment. The difficult child was most vulnerable to development of behaviour disorders. Optimal development depends on consonance between individual and environment – ‘goodness of fit’. DEVIANT CHILDREN GROWN UP Children referred to a child guidance clinic were followed up at 30 years. Conductdisordered children were particularly likely to become sociopathic adults, with more criminality, marital discord and occupational failure. Psychiatric disorders were also more common. Severity and variety of conduct disorder were predictive. NEGATIVE CHILDHOOD EXPERIENCES Childhood sexual abuse (CSA), physical abuse and early separation or loss are associated with PD. However, these are non-specific risk factors; e.g. CSA is not a specific risk factor for borderline PD. Decreased ‘social integration’, by failing to provide containment for impulsivity, may be related to PDs characterized by poor impulse control.


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ASSESSMENT AND TREATMENT Multidimensional • Rule out any organic cause, such as focal or diffuse brain disorder, toxic or metabolic disorder, seizure disorder. • Rule out other or evaluate for co-morbid psychiatric disorder. Ensure that the problem is persistent since adolescence, not episodic. • Hospitalization is probably best avoided (brief if required for crisis such as co-morbidity, suicidality/deliberate self-harm). The person may function better in a partial hospitalization setting. Pharmacotherapy SSRI therapy decreases impulsivity in borderline personality and is useful for co-morbid depression. Mood stabilizers are effective in managing mood lability, anger and aggression. Atypical antipsychotics are preferred for cognitive–perceptual disturbances. Psychotherapy There is some evidence for the role of dialectical behaviour therapy in deliberate self-harm (DSH). CAT therapy carries some weak evidence. Group therapy may be more useful than individual for some PDs (not for paranoid disorders).

PROGNOSIS A 10- to 25-year follow-up of borderline PDs showed a range of outcomes:

• •

Suicide – 3–9 per cent (co-morbidity, depression) ‘Clinical recovery’/maturation out of behavioural difficulties – 50–60 per cent.

REFERENCES AND FURTHER READING Abraham RE (1993) The development profile: the psychodynamic diagnosis of personality. J. Pers. Dis. 7(2), 105. American Psychiatric Association (2001). Practice guidelines for the treatment of patients with borderline personality disorder. Am. J. Psychiatry 158 (Suppl. 10), 1. Bateman AW, Fonagy P (1999) Effectiveness of partial hospital hospitalisation in the treatment of borderline personality disorder: a randomized controlled trail. Am. J. Psychiatry 156, 1563. Blair RJR (2003) Neurobiological basis of psychopathy. Br. J. Psychiatry 182, 5. Canadian Journal of Psychiatry (1993) Borderline personality disorder. Can. J. Psychiatry 38(1) (Suppl.). Casey P (2000) The epidemiology of personality disorders. In: Tyrer P (ed.), Personality Disorders: Diagnosis, Management and Course, 2nd edn, pp. 71–79. Butterworth–Heinemann, Oxford. Cloninger CR (1987) A systematic method for clinical description and classification of personality variants. Arch. Gen. Psychiatry 44, 573.

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Coid JW (2003) Epidemiology, public health and the problem of personality disorder. Br. J. Psychiatry 182 (Suppl. 44), s3. Costa PT, Widiger TA (eds) (2002) Personality Disorders and the Five-factor Model of Personality, 2nd edn. American Psychological Association, Washington, DC. Crandell LE, Patrick MP, Hobson RP (2003) ‘Still-face’ interactions between mothers with borderline personality disorder and their 2-month-old infants. Br. J. Psychiatry 183, 239. Davidson SE (2002) Principles of managing patients with personality disorder. Adv. Psychiatr. Treat. 8, 1. Duggan C, Milton J, Egan V et al. (2003) Theories of general personality and mental disorder. Br. J. Psychiatry 182 (Suppl. 44), s19. Frankenburg FR, Zanarini MC (2002) Divalproex sodium treatment of women with borderline personality disorder and bipolar II disorder: a double-blind placebo-controlled pilot study. J. Clin. Psychiatry 63, 442. Fullerton J, Cubin M, Wang TH et al. (2003) Linkage analysis of extremely discordant and concordant sibling pairs identifies quantitative-trait loci that influence variation in the human personality trait neuroticism. Am. J. Hum. Genet. 72, 879. Jonsson EG, Cichon S, Gustavsson JP et al. (2003) Association between a promoter dopamine D2 receptor gene variant and the personality trait detachment. Biol. Psychiatry 53, 577. Kendell RE (2002) The distinction between personality disorder and mental illness. Br. J. Psychiatry 180, 110. Koenigsberg HW, Harvey PD, Mitropoulou V et al. (2002) Characterizing affective instability in borderline personality disorder. Am. J. Psychiatry 159, 784. Lewis G, Appleby L (1988) Personality disorder: the patients psychiatrists dislike. Br. J. Psychiatry 153, 44. Linehan MM, Dimeff LA, Reynolds SK et al. (2002) Dialectical behavior therapy versus comprehensive validation therapy plus 12-step for the treatment of opioid dependent women meeting criteria for borderline personality disorder. Drug Alcohol Depend. 67, 13. Miller MC (2001) Personality disorders. Med. Clin. North Am. 85, 819. Nagin DS, Tremblay RE (2001) Parental and early childhood predictors of persistent physical aggression in boys from kindergarten to high school. Arch. Gen. Psychiatry 58, 389. Nickell AD, Waudby CJ, Trull TJ (2002) Attachment parental bonding and borderline personality disorder features in young adults. J. Pers. Disord. 16, 148. Paris J (1993) Personality disorders: a biopsychosocial model. J. Pers. Disord. 7(3), 255. Paris J (2002) Clinical practice guidelines for borderline personality disorder. J. Pers. Disord. 16, 107. Paris J, Zweig-Frank H (2001) A 27-year follow-up of patients with borderline personality disorder. Compr. Psychiatry 42, 482. Pfohl B, Coryell W, Zimmerman M et al. (1986) DSM-III personality disorder: diagnostic overlap and internal consistency of individual DSM-III criteria. Comp. Psychiatry 27, 21. Rendu A, Moran P et al. (2002) Economic impact of personality disorders in UK primary care attenders. Br. J. Psychiatry 181, 62. Rinne T, van den Brink W, Wouters L, van Dyck R (2002) SSRI treatment of borderline personality disorder: a randomized, placebo-controlled trail for female patients with borderline personality disorder. Am. J. Psychiatry 159, 2948. Rujescu D, Giegling I, Gietl A et al. (2003) A functional single nucleotide polymorphism (V158M) in the COMT gene is associated with aggressive personality traits. Biol. Psychiatry 54, 34. Samuels J, Eaton WW et al. (2002) Prevalence and correlates of personality disorders in a community sample. Br. J. Psychiatry 180, 523. Sanislow CA, Grilo CM, Morey LC et al. (2002) Confirmatory factor analysis of DSM-IV criteria for borderline personality disorder: findings from the collaborative longitudinal personality disorder study. Am. J. Psychiatry 159, 284.


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Schmahl CG, McGlashan TH, Bremmer JD (2002) Neurobiological correlates of borderline personality disorder. Psychopharmacol. Bull. 36, 69. Skodol AE, Gunderson JG, McGlashan TH et al. (2002a) Functional impairment in patients with schizotypal, borderline, avoidant, or obsessive–compulsive personality disorder. Am. J. Psychiatry 159, 276. Skodol AE, Gunderson JG, Pfohl B et al. (2002b) The borderline diagnosis. I: Psychopathology, comorbidity, and personality structure. Biol. Psychiatry 51, 936. Skodol AE, Siever LJ, Livesley WJ et al. (2002c) The borderline diagnosis. II: Biology, genetics, and clinical course. Biol. Psychiatry 51, 951. Stone MH (1993) Long-term outcome in personality disorder. Br. J. Psychiatry 162, 299. Torgersen S, Kringlen E, Cramer V (2001c) The prevalence of personality disorders in a community sample. Arch. Gen. Psychiatry 58, 596. Trull TJ (2001) Structural relations between borderline personality disorder features and putative etiological correlates. J. Abnorm. Psychol. 110, 471. Tyrer P (1988) Personality Disorders: Diagnosis, Management and Course. Wright, London. Tyrer P (2002) Practice guideline for the treatment of borderline personality disorder: a bridge too far. J. Pers. Disord. 16, 13. Tyrer P, Duggan C, Coid J (2003) Ramifications of personality disorder in clinical practice. Br. J. Psychiatry 182, s1. Verheul R, Van Den Bosch LMC et al. (2003) Dialectical behaviour therapy for women with borderline personality disorder: 12-month randomised clinical trial in the Netherlands. Br. J. Psychiatry 182, 135. White CN, Gunderson JG, Zanarini MC, Hudson JI (2003) Family studies of borderline personality disorder: a review. Harvard Rev. Psychiatry 11, 8. Zanarini MC (2003) The longitudinal course of borderline psychopathology: 6-year prospective follow-up of the phenomenology of borderline personality disorder. Am. J. Psychiatry 160, 274. Zimmerman M (1994) Diagnosis of personality disorders: a review of issues and research methods. Arch. Gen. Psychiatry 51, 225.

Eating disorders

7

OBESITY Obesity has been defined as a body mass index (BMI) above 30. In England, 17 per cent of males and 21 per cent of females are obese. It is the most common nutritional disorder in the UK. There has been an alarming increase in the number of children who are obese. Obesity is most common in lower social class, middle-aged females. Obesity is associated with an increased risk of cardiovascular disorders (MI, CVA, hypertension), diabetes, cancer (breast, ovarian, colon), osteoarthritis, sleep apnoea and accidents.

AETIOLOGY OF OBESITY Basically, obesity results from food intake in excess of energy requirements.

• • • • •

Emotional factors – Boredom, loneliness or stress may contribute to excessive food intake. Environmental factors – There may be a more sedentary lifestyle due to technological advances. There is greater availability and consumption of energy-dense foods. Learned behaviour – Food is given by parents at times of stress, and guilt evinced if the food is not taken. Organic – Organic causes are rare for extreme obesity: hypothyroidism, hypopituitarism, hypoglycaemic attacks, hypothalamic damage (? ventromedial nucleus). Molecular/genetic: – Genetics are thought to account for 25–70 per cent of variations in bodyweight. – Adoption studies support a genetic contribution to weight. – Early-onset obesity is related to mutation in genes for leptin, leptin receptor, prohormone convertase 1 and proopiomelanocortin (POMC). – Abnormal hormonal regulation of neural circuits that control food intake and energy expenditure appear to be involved in obesity.

ANOREXIA NERVOSA (AN)

87

MANAGEMENT OF OBESITY Diet A calorie-controlled diet to decrease energy balance by 500–600 kcal/day will result in weight loss of about 0.5–1.0 kg/week. Numerous types of diets exist, but there is a high relapse rate associated with dieting alone. Psychotherapy Group psychotherapy may be particularly helpful. Marital therapy may be necessary to alter family patterns. Ultimately, management may require inpatient supervision in a therapeutic milieu. Behaviour therapy Self-monitoring is the key to behaviour therapy. Regulation of environmental cues for eating, alteration of eating behaviour and self-reinforcement in weight loss (also group reinforcement, e.g. ‘Weight Watchers’) has proven effective. Cognitive factors are important: guilt and feelings of failure are common, so attempt to reduce these. Drug therapy Orlistat (inhibits fat absorption by inhibiting lipase) and sibutramine (enhances satiety via noradrenergic/serotonin reuptake inhibition) show effectiveness in promoting weight loss. Surgical therapy Surgery is generally limited to those with morbid obesity (BMI ⬎ 40). Gastric bypass, gastric banding, and vertical banded gastroplasty are effective in providing sustained long-term weight loss.

ANOREXIA NERVOSA (AN) EPIDEMIOLOGY OF AN

• •

• • • •

Anorexia nervosa is the third most common chronic illness in teenage females (Lucas et al., 1991). Annual incidence: – 14.6/100 000 for females. – 1.8/100 000 for males. – Unclear whether incidence is increasing – some increase suggested for 15- to 24-year age-group. Prevalence – 0.5–3.7 per cent in adolescent/early adult females. There are higher rates in certain groups; e.g. ballet dancers, gymnasts. AN is over-represented in higher social classes (I & II). 90 per cent of females have onset within 5 years of menarche. Seasonal pattern of onset (maximum May)?

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EATING DISORDERS

Table 7.1 Predisposing factors for AN

Individual Familial Cultural

Predisposing factors

Precipitating factors

Perpetuating factors

Leads to dissatisfaction with body weight and shape

Dieting to feelings of self-worth and control

Starvation symptoms and reactions from others

Adapted from Garner (1993).

Adverse life effects are more evident in ‘late onset’ (⬎25 years) AN. Eighty-four per cent of AN patients have a lifetime diagnosis of another psychiatric disorder (Halmi et al., 1991), with major depression in 68 per cent of patients.

AETIOLOGY OF AN The aetiology is multifactorial (see Table 7.1). Psychological factors There are inconsistent data on personality disorder – high rates of avoidant personality have been described. A specific association with childhood sexual abuse is overestimated.

• • •

Body image disturbance is a core feature – body shape misperception or disparagement. Morbid fear of fatness, pursuit of thinness, weight phobia – body thinness is viewed as a cognitive construct equated with self-worth and control. Twenty-five per cent of AN patients are overweight before onset. Psychodynamics – regression to the ‘prepubertal’ state; fear of becoming a sexualized adult; fixation at the oral (pregenital) stage.

Familial factors There are high rates of psychiatric illness – particularly depression, alcoholism, psychosexual disturbances and obsessive–compulsive disorder (OCD) in mothers (Halmi et al., 1991). Earlier descriptions emphasize the family as the site of pathology: a dominant, intrusive mother; a passive, ineffectual father; an enmeshed, overprotective, rigid family structure with conflict avoidance. It is unclear whether these characteristics are cause or effect. Twin studies affirm genetic and non-genetic environmental contributions. Cultural factors • The western ‘thinness-conscious’ culture. • Role conflict – changing expectations for and by women. • Food as a form of communication. Biological factors Familial aggregation – association with (unipolar) depression may suggest genetic predisposition.

•

ANOREXIA NERVOSA (AN)

89

Table 7.2 Medical complications and laboratory abnormalities in AN Neurological Cardiovascular Metabolic Endocrine Haematological Gastrointestinal

Renal Musculoskeletal Other

• •

‘Pseudoatrophy’ on brain-imaging, EEG abnormalities and seizures; peripheral neuritis; anatomic dysfunction Bradycardia; hypotension; decreased heart size; QT prolongation; arrhythmias; oedema Dehydration hypoglycaemia, hypercholesterolaemia; ↑ plasma amylase, ↑ liver function tests; ↓ plasma proteins (oedema) ↓ K+, ↓ Mg2+, ↓ CA2+, ↓ phosphate ↑ GH, cortisol (positive dexamethasone suppression test) ↓ gonadotropin, oestrogens, testosterone ↓ T3 (sick euthyroid syndrome) Normochronic, monocytic or iron-deficient anaemia, leucopenia, relative lymphocytosis, hypocellular marrow Swollen salivary glands; dental caries, erosion of enamel (vomiting), delayed gastric emptying; acute gastric dilations (bulimic episodes, vigorous refeeding, constipation; acute pancreatitis Partial diabetes insipidus; pre/acute/chronic renal failure Osteoporosis, stress fractures; stunted growth; muscle cramps Hypothermia, bacterial infections (TB, staph), lanugo (hair on trunk); normal secondary sexual hair pattern unaffected; low birthweight, ↑ miscarriage and congenital malformation, perinatal mortality if patients conceive before complete restoration of weight

Twin studies – MZ:DZ ⫽ 54%:9%. Neurochemical abnormalities have been postulated: – Deficiency in serotonin may contribute to blunted satiety responses. – 5-HT abnormalities persist even after weight restoration (Kaye et al., 1991). – Cholecystokinin (CCK) may also cause dysregulation of satiety. – Abnormalities in hypothalamic–pituitary–gonadal axis (see Table 7.2) also are implicated. – Blunted prolactin (5-HT mediated). – Response to D-fenfluramine challenge (Monteleone et al., 2000).

However, neurochemical hypotheses are difficult to establish, since many of the abnormalities may reflect secondary effects of starvation.

CLINICAL FEATURES AND DIFFERENTIAL DIAGNOSIS OF AN These are described in current diagnostic criteria (see Table 7.3). Differential diagnosis • Psychiatric – depression, schizophrenia, OCD, psychotic disorder. • Medical – hypopituitarism, thyrotoxicosis, diabetes mellitus, neoplasia, reticulosis, malabsorption.

MANAGEMENT OF AN General principles • Use a multifaceted approach (APA, 2000; Royal College of Psychiatrists, 2000): – Detect and treat medical complications. – Encourage a ‘normal’ balanced diet to regain ‘normal’ weight. – Educate about diet and exercise.

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EATING DISORDERS

Table 7.3 IDC-10 and DSM-IV diagnostic criteria for anorexia nervosa ICD-10

DSM-IV

1. Bodyweight ⭐15% of expected Quetelet’s body-mass index ⭐17.5 (weight (kg)/[height (m)]2) 2. Self-induced weight loss Avoidance of ‘fattening foods’ ⭓1 of: – self-induced vomiting – self-induced purging – overexercising – misuse of diuretics/stimulants 3. Body image distortion Dread of fatness a persistent ‘overvalued’ idea 4. Abnormalities of hypothalamic–pituitary–gonadal axis Amenorrhoea; ↓ libido, decreased potency in males ↑ GH, cortisol; ↓ T3

A. Refusal to maintain bodyweight ⭓ minimal normal weight for age and height B. Intense fear of fatness C. Body-image disturbance D. Amenorrhoea in post-menarchal females Subtypes: restricting, binge eating/purging

5. If onset is prepubertal, this sequence of pubertal events is delayed

Behavioural approaches • Encourage a regular diet (3000 kcal daily) to attain 1.5 kg weekly weight gain; smaller intake if severe weight loss (tube or IV feeding rarely necessary); restoration to at/near ideal bodyweight as target – i.e. body mass index of 20–25. • Nurse supervision during and after meals helps to avoid surreptitious vomiting, disposal of food and/or over-exercising. Psychological approaches Cognitive–behavioural therapy (CBT), psychoanalytic psychotherapy and family therapy are effective in producing weight gain (Dare et al., 2001). Education: dietary, exercise; body function/sexual and psychological maturation; life skills support. Pharmacological approaches There is a limited role. Atypical antipsychotics have been shown to result in weight gain. Antidepressants and anxiolytics can be given as clinically indicated. SSRIs may be beneficial.

PROGNOSIS FOR AN The prognosis is generally poor. There are high drop-out rates from treatment, and no consistent evidence that treatment clearly alters outcome. One 20-year follow-up (Zipfel et al., 2000) showed:

• • •

50.6 per cent recovered. 10.4 per cent still had DSM-IV criteria. 15.6 per cent died.

There is a high mortality from complications of AN, including suicide. Even ‘recovered’ anoretics show psychopathology.

BULIMIA NERVOSA (BN) OR ‘DIETARY CHAOS SYNDROME’

91

Factors indicating poor prognosis • Older age at onset. • Premorbid obesity. • Illness duration ⬎6 years. • Personality disturbance. • Bulimic behaviour. • Male gender.

BULIMIA NERVOSA (BN) OR ‘DIETARY CHAOS SYNDROME’ Note that a further category has been proposed in DSM-IV – ‘binge-eating disorder’:

• •

Recurrent distressing episodes of uncontrolled overeating. Not satisfying the diagnostic criteria for BN.

It is unclear whether this group differs in pathophysiology, treatment outcome, etc.

EPIDEMIOLOGY OF BN

• • • • •

80 per cent of US students have reported binge eating. Bulimia nervosa affects 4 per cent of female adolescents. Peak onset is later than for AN – late adolescence or early 20s. A history of longstanding dietary difficulties is common. BN is more common than AN. About 30 per cent of BN cases have a prior history of AN.

AETIOLOGY OF BN This is multifactorial; factors are similar to those in AN (see above). Psychological factors • There are high rates of depression/dysphoria, alcohol abuse, personality disturbance (borderline, labile). • There is poor self-esteem and sense of personal control. Familial factors There are high rates of psychiatric disturbance, particularly depression. Cultural factors As for AN (see above). Biological factors Twin studies – MZ:DZ ⫽ 22%:9%. Serotonin dysfunction is more extensively studied in BN: – Deficits in CSF 5-HIAA persist after treatment. – Blunted GH response to D-fenfluramine challenge.

• •

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EATING DISORDERS

Table 7.4 ICD-10 and DSM-IV criteria for bulimia nervosa ICD-10

DSM-IV

1. Persistent preoccupation with eating; craving for food; episodes of overeating 2. Attempts to counteract the ‘fattening’ effect of food by ⭓1 of: – self-induced vomiting – alternate periods of starvation – purgative abuse – diuretic/stimulant misuse

A. recurrent episodes of binge eating B. recurrent inappropriate compensatory behaviour to prevent weight gain C. A and B occur for ⭓ twice weekly for 3 months

3. ‘Morbid dread of fatness’

• •

Dopamine abnormalities also found – ↓ CSF HVA. CCK also is implicated in dysregulation of appetite in BN.

CLINICAL FEATURES OF BN See Table 7.4.

• • • •

Patient has a defined weight threshold. In contrast to AN, weight may be normal (typical bulimia nervosa – F50.3, ICD-10). Body-shape disturbances are somewhat less prominent in BN. There are similar medical and psychiatric complications to AN. Medical complications are generally less frequent or severe.

MANAGEMENT OF BN As with AN, the approach is multifaceted. Most are treated as outpatients. The criteria for hospitalization are similar to AN (see above). Psychological approaches • Psychoeducation, nutritional counselling, relaxation training are all used. • CBT: – Intensive, weekly over 5 months. – Many components include self-monitoring (diary-keeping). • Self-reporting – establish cognitive and behavioural strategies to alter low frustration tolerance, poor impulse control, negative self-concept, poor recognition and identifications of emotions. • CBT is more effective than interpersonal therapy (Agras et al., 2000). • CBT is most effective for attitudes to weight and shape. • CBT is more effective in the short term than antidepressants. A combination of CBT and antidepressants may be best. • Group psychotherapy can be used. Family therapy also is helpful, where clinically indicated. Self-help and support groups are beneficial.


93

Pharmacological approaches SSRI antidepressants are effective independent of mood status, at dosages similar to treatment of depression. Naltrexone and ondansetron may reduce binging and purging.

PROGNOSIS FOR BN Overall the outlook is better than for AN, but there are high rates of relapse and psychosocial impairment. One prospective 5-year study of 102 BN females (Fairburn et al., 2000) showed:

• •

Continuously ill – half to two-thirds. Subsequent relapse after initial ‘recovery’ – 33 per cent.

REFERENCES AND FURTHER READING Agras S, Walsh T, Fairburn C et al. (2000) A multicenter comparison of cognitive–behavioral and interpersonal psychotherapy for bulimia nervosa. Arch. Gen. Psychiatry 57, 459. American Psychiatry Association (2000) Practice Guideline for the Treatment of Patients with Eating Disorders, 2nd edn. APA, Washington, DC. Ben-Tovin D, Walker K, Gilchrist P et al. (2001) Outcome in patients with eating disorders: a 5-year study. Lancet 357, 1254. Boschi V, Siervo M, D’Orsi P et al. (2003) Body composition, eating behavior, food-body concerns and eating disorders in adolescent girls. Ann. Nutr. Metab. 47, 284. Bray GA (2002) Etiology and natural history of obesity. Clin. Fam. Pract. 4, 249. Brownell KD, Wadden TA (1992) Etiology and treatment of obesity: understanding a serious, prevalent and refractory disorder. J. Consult. Clin. Psychol. 60, 505. Chowdhury U, Lask B (2001) Clinical implications of brain imaging in eating disorders. Psychiatr. Clin. North Am. 24, 227. Crisp A (2002) Treatment of anorexia nervosa: is ‘where’ or ‘how’ the main issue. Eur. Eat. Disord. Rev. 10, 223. Dare C, Eisler I, Russell G et al. (2001) Psychological therapies for adults with anorexia nervosa: randomised controlled trail of out-patient treatments. Br. J. Psychiatry 178, 216. Diamanti A, Bracci F, Gambaraa M et al. (2003) Gastric electric activity assessed by electrogastrography and gastric emptying scintigraphy in adolescents with eating disorders. J. Peditatr. Gastroenterol. Nutr. 37, 35. Fairburn CG, Jones R, Peveller R (1991) Three psychological treatments for bulimia nervosa. Arch. Gen. Psychiatry 48, 463. Fairburn CG, Cooper Z, Norman P, O’Connor M (2000) The natural course of bulimia nervosa and binge eating disorder in young women. Arch. Gen. Psychiatry 57, 659. Flegal KM, Carroll MD, Ogden CL, Johnson CL (2002) Prevalence and trends in obesity among US adults, 1999–2000. JAMA 288, 1723. Halmi KA, Eckert E, Marchi P et al. (1991) Comorbidity of psychiatric diagnosis in anorexia nervosa. Arch. Gen. Psychiatry 48, 712. Halmi KA, Sunday SR, Strober M et al. (2000) Perfectionism in anorexia nervosa: variation by clinical subtype, obsessionality, and pathological eating behaviour. Am. J. Psychiatry 157, 1799. Hsu LKG (1990) Eating Disorders. Guilford Press, New York. Hsu LKG, Rand W, Sullivan S et al. (2001) Cognitive therapy, nutritional therapy and their combination in the treatment of bulimia nervosa. Psychol. Med. 31, 871.

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Johnson JG, Cohen P, Kotler L et al. (2002) Psychiatric disorders associated with risk for the development of eating disorders during adolescence and early adulthood. J. Consult. Clin. Psychol. 70, 119. Kaye WH, Gwirstman HE, George DT et al. (1991) Altered serotonin activity in anorexia nervosa after long term weight restoration. Arch. Gen. Psychiatry 48, 556. Kaye WH, Lilenfeld LR, Berrettini WH et al. (2000) A search for susceptibility loci for anorexia nervosa: methods and sample description. Biol. Psychiatry 47, 749. Keel P, Mitchell J, Miller K et al. (1999) Long term outcome of bulimia nervosa. Arch. Gen. Psychiatry 56, 63. Klump KL, Kaye WH, Strober M (2001a) The evolving genetic foundations of eating disorders. Psychiatr. Clin. North Am. 24, 215. Klump KL, Miller KB, Keel PK et al. (2001b) Genetic and environmental influences on anorexia nervosa syndromes in a population-based twin sample. Psychol. Med. 31, 737. Klump K, Wonderlich S, Lehoux P et al. (2002) Does environment matter? A review of nonshared environment and eating disorders. Int. J. Eat. Disord. 31, 118. Labib M (2003) The investigation and management of obesity. J. Clin. Pathol. 56, 17. Lucas AR, Beard CM, O’Fallon WM et al. (1991) 50-year trends in the incidence of anorexia nervosa in Rochester, Minnesota: a population-based study. Am. J. Psychiatry 148, 917. McGuire MT, Jeffery RW, French SA (2002) The psychologic correlates of obesity. Clin. Fam. Pract. 4, 319. Mitchell JE, Peterson CB, Myers T, Wonderlich S (2001) Combining pharmacotherapy and psychotherapy in the treatment of patients with eating disorders. Psychiatr. Clin. North Am. 24, 315. Monteleone P, Brambilla F, Bortolotti F, Maj M (2000) Serotonergic dysfunction across the eating disorders: relationship to eating behaviour, purging behaviour, nutritional status and general psychopathology. Psychol. Med. 30, 1099. Nielsen S (2001) Epidemiology and mortality of eating disorders. Psychiatry Clin. North Am. 24, 214. Norman RJ, Davies MJ, Lord J, Moran LJ (2002) The role of lifestyle modification in polycystic ovary syndrome. Trends Endocrinol. Metab. 13, 251. Padwal R, Li SK, Lau DCW (2003) Long-term pharmacotherapy of overweight and obesity: a systematic review and meta-analysis of randomized controlled trials. Int. J. Obesity 27, 1437. Palmer RL, Birchall H et al. (2002) Self-help for bulimic disorders: a randomised controlled trial comparing minimal guidance with face-to-face or telephone guidance. Br. J. Psychiatry 181, 230. Paul T, Kirsten S et al. (2002) Self-injurious behavior in women with eating disorders. Am. J. Psychiatry 159, 408. Polivy J, Herman C (2002) Causes of eating disorders. Annu. Rev. Psychol. 53, 187. Powers PS, Santana CA (2002) Eating disorders: a guide for the primary care physician. Prim. Care 29, 81. Pratt B, Woolfenden S (2002) Interventions for preventing eating disorders in children and adolescents. Cochrane Database Syst. Rev. 2, CD002891. Rome ES, Ammerman S, Rosen DS et al. (2003) Children and adolescents with eating disorders: the state of the art. Pediatrics 111, e98. Rosenblum J, Forman S (2002) Evidence-based treatment of eating disorders. Cur. Opin. Pediatrics 14, 379. Rosenblum J, Forman S (2003) Management of anorexia nervosa with exercise and selective serotonergic reuptake inhibitors. Cur. Opin. Pediatrics 15, 346. Royal College of Psychiatrists (2000) Eating Disorders in the UK: Policy for Service Development and Training. RCP, London. Rudolf M, Sahota P, Barth J et al. (2001) Increasing prevalence of obesity in primary school children: a cohort study. BMJ 322, 1094. Shea MT, Stout R et al. (2002) Short-term diagnositc stability of schizotypal, borderline, avoidant, and obsessive–compulsive personality disorders. Am. J. Psychiatry 159, 2036. Sigman GS (2003) Eating disorders in children and adolescents. Pediatr. Clin. North Am. 50, 1139.


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Steinhausen H (2002) The outcome of anorexia nervosa in the 20th century. Am. J. Psychiatry 159, 1261. Walsh BT, Agras WS, Devlin MJ et al. (2000) Fluoxetine for bulimia nervosa following poor response to psychotherapy. Am. J. Psychiatry 157, 1332. Westen D, Harnden-Fischer J (2001) Personality profiles in eating disorders: rethinking the distinction between axis I and axis II. Am. J. Psychiatry 158, 547. World Health Organization (1998) Obesity: Preventing and Managing the Global Epidemic. WHO, Geneva. Yanovski SZ (2003) Binge eating disorder and obesity in 2003: could treating and eating disorder have a positive effect on the obesity epidemic? Int. J. Eat. Disord. 34, s117. Zabinski MG, Wilfley DE, Pung MA et al. (2001) An interactive internet-based intervention for women at risk of eating disorders: a pilot study. Int. J. Eat. Disorder. 30, 129. Zipfel S, Lowe B, Reas DL et al. (2000) Long-term prognosis in anorexia nervosa: lessons from a 21 year follow-up study. Lancet 355, 721.

Human sexuality

8

NORMAL BEHAVIOUR EPIDEMIOLOGY Kinsey et al. (1948, 1953) • 93 per cent of men and 28 per cent of women masturbated by age 20. • Males show peak of sexual activity in late adolescence. • Women show peak of sexual activity in their 30s. • 75 per cent of males achieve orgasm within 2 minutes of penetration. • Recent US studies show 45–90 per cent of adolescent males and 25–40 per cent of adolescent females masturbate. Johnson et al. (2001) UK survey 1999–2001.

• • •

29.8 per cent of males, 21.1 per cent of females reported having two or more heterosexual partners within previous year of study (51.9 per cent of males, 38.7 per cent females in 16–24 age-group). 5.4 per cent males had a history of having had a homosexual partner (10.5 per cent males in London). 2.0 per cent males, 0.6 per cent females reported ever injecting illicit drugs.

Centers for Disease Control and Prevention (2002) US high school survey 1991–2001.

• • • •

42.9 per cent of females, 48.5 per cent of males had experience with sexual intercourse. In general, teens are less sexually active and more likely to use condoms since 1991. A 16 per cent decrease in sexual experiences among high school students. A 24 per cent decrease in multiple sex partners.

SEXUAL DYSFUNCTIONS

97

PHYSIOLOGY Masters and Johnson (1966) and Kaplan (1978) Phases of response cycle:

• • • • •

Desire – affected by personal, social, cultural, hypothalamic and hormonal factors. Arousal – excitement, mediated by parasympathetic nervous system. Genital vasoconstriction leads to erection in male or swelling and lubrication in female. Plateau – maintenance of arousal state. Orgasm – emission, in male only. Ejaculation or, in female, ejaculatory equivalent. Both mediated by sympathetic nervous system. Resolution – with a longer refractory period in the male (can be 24 hours if over 60 years) and very short refractory period in the female (allowing for multiple orgasms).

NEUROPHYSIOLOGY

• • •

Exact mechanism of orgasm unknown. Dopaminergic effects result in increased sexual activity. Antidopaminergic drugs cause decreased sexuality and impotence. Noradrenergic effects (␣2 receptors) reduce sexual activity.

RELATIONSHIP BEHAVIOUR Consider:

• • • •

Communication – within the relationship. Commitment – to the relationship. Conflict – within the relationship. Context – of the sexual encounter (culture, personal, surroundings).

SEXUAL DYSFUNCTIONS See Table 8.1. DEFINITIONS Male • Erectiled dysfunction (‘impotence’) – inability to sustain an erection adequate for penetration. Commonest disorder presenting in males at clinic. • Ejaculatory impotence – inability to ejaculate despite adequate erection. Uncommon. • Premature ejaculation – ejaculation before, during or immediately after penetration. Usually in young men. Common. Female Anorgasmia (‘frigidity’) – orgasm achieved rarely or never. Vaginismus – involuntary contraction of vaginal introitus in response to attempts at penetration.

• •

98

HUMAN SEXUALITY

Table 8.1 ICD-10 and DSM-IV classification of sexual disorders ICD-10

DSM-IV

Sexual dysfunction Lack of sexual desire Sexual aversion/lack of enjoyment

Sexual desire disorders Hypoactive sexual desire Sexual aversion Sexual arousal disorders Female sexual arousal disorder Male erectile disorder Orgasm disorders Female orgasmic disorder Male orgasmic disorder Premature ejaculation Sexual pain disorder Vaginismus Dyspareunia

Failure of genital response

Orgasmic dysfunction Premature ejaculation Non-organic vaginismus Non-organic dyspareunia Excessive sexual desire

Disorders of sexual preference Exhibitionism Fetishism Fetishistic transvestism Paedophilia Sadomasochism Other disorders of sexual preference

Gender identity disorders Transsexualism Dual-role transvestism Gender identity disorder of childhood Other gender identity disorders

Sexual dysfunction due to general medical condition Substance-induced sexual dysfunction Paraphilias Exhibitionism Fetishism Transvestic fetishism Paedophilia Sexual sadism Sexual masochism Voyeurism Paraphilia NOS (necrophilia, zoophilia, etc.) Sexual disorders NOS Gender identity disorders Gender identity disorder Gender identity disorder NOS

Psychological and behavioural disorders associated with sexual development and orientation

Either sex • Low sex drive. • Dyspareunia – pain on intercourse. CLASSIFICATIONS Can be classified as:

• •

Primary or secondary; i.e. no history of normal function or onset later in life after a period of normal functioning. Symptomatic or functional; i.e. due to organic or psychological cause. Can be further classified as:

• • •

Acute or insidious onset. Total or partial. Global or situational. – or according to stage affected (see Table 8.2).

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99

Table 8.2 Classification of dysfunction according to stage affected Stage

Male

Initiation Arousal

Avoidance, low drive Premature ejaculation Erectile impotence Lack of urge to penetrate Ejaculatory impotence

Penetration Orgasm

Female

Lubricative failure Vaginismus Anorgasmia

ASSESSMENT AIMS OF ASSESSMENT 1 To define the dysfunction. 2 To assess whether it is organic, functional or both. Often a mild dysfunction due to organic causes (e.g. diabetes mellitus) can lead to ‘performance anxiety’, and thus to a much worse ‘functional’ disorder. 3 To determine the immediate causes. 4 To assess the couple’s resources and motivation. 5 To decide on the correct management and likely prognosis. Always see the sexual partner; see both partners together also if possible. The problem • Exact nature of problem, precise examples sought. • Frequency and timing of dysfunction. • Total or partial? If partial, seek situational circumstances. • Any sign of normal function, e.g. morning erections in male. • Mode of onset: acute or insidious, primary or secondary? • Duration of problem. • Course of problem: constant or fluctuating? Current influences Environmental conditions: sexual stress, relationship with partner, other stresses, timing and setting of sexual encounters. • Personal variables: sexual knowledge and experience, emotional reaction (guilt, anxiety), cognitive avoidance, contraceptive habits, fear of conception. • Organic condition: important in only about 10 per cent presenting to a psychiatrist. Age is often an important factor. • Consequences of problem: avoidance of intercourse, partner’s reaction.

•

Resources Personal resources: motivation, honesty, flexibility, ability to verbalize, history of sex drive. • Sexual relationship: commitment, willingness to be involved in treatment, conflict. In 30 per cent, both partners have dysfunctions. • Professional resources: time and personnel available to treat the disorder.

•

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PROGRAMME OF ASSESSMENT History • Take a full history of the complaint: look for precise diagnosis, indication of aetiology and prognostic signs. • Family background and personal history: parental relationships, attitude to sex. • Sexual and marital history: degree of sexual knowledge, past sexual experiences, relationship with sexual partner, contraceptive methods, children, attitudes to pregnancy. • Drug and alcohol abuse. Examination Assess mental state: depression, anxiety. Physical examination, including genitalia.

• •

Investigations Physical investigations may be indicated, particularly with impotence and if there is total absence of any sign of erection in a man with previously normal sexual history. Include urinalysis for sugar, liver function tests, testosterone level. The nocturnal penile tumescence strain gauge is a useful diagnostic tool. Intersexual disorders:

• • • • • •

Virilizing adrenal hyperplexia (adrenogenital syndrome) – commonest female intersex disorder, autosomal recessive, XX genotype, excess of androgens from in utero. Turner’s syndrome (X genotype) – see Chapter 20. Usually assigned as females because of female-looking genitalia. Klinefelter’s syndrome (XXY genotype) – males with low androgen production, rudimentary sex organs. Testicular feminization syndrome (Y genotype) – X-linked recessive, endorgan insensitivity to androgens; assigned as females because of female-looking genitalia. Enzymatic disorders (5␣-reductase deficiency; 17 hydroxysteroid deficiency) – low testosterone results in ambiguous genitalia and female habitus; assigned as females. Hermaphroditism – true hermaphrodite (46XX or 46XY) is rare, possesses both testes and ovaries; pseudohermaphroditism usually results from endocrine or enzymatic defect in person with normal chromosomes; gender assignment according to morphology or genitalia.

AETIOLOGY Previous experiences • Restrictive upbringing leading to intrapsychic conflict. • Traumatic early sexual encounters. • Abnormal family relationships.

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Current circumstances • Sexual stresses (e.g. concerning contraception or pregnancy). • Non-sexual stresses (e.g. lack of privacy, recent childbirth). • Relationship difficulties (e.g. partner rejection, sexual sabotage). • Ignorance or guilt resulting in failure to engage in effective sexual behaviour. • Psychiatric disorder (e.g. depression, schizophrenia with sexual delusions). • ‘Performance anxiety’ – fear of failure arising from demand for performance by partner or excessive need to please partner. • ‘Spectatoring’ – observing own behaviour and not allowing automatic responses or recognizing erotic sensations. Organic factors An organic cause of impotence is suggested by:

• • • •

Penis never fully turgid/generalized dysfunction (i.e. not situational). No associated significant life event. Previous uninterrupted period of normal sexual function. Sexual interest being maintained.

Age Erectile dysfunction increases dramatically with age: 0.1 per cent under 20 years; 7 per cent 40–50 years; 75 per cent over 70 years. General illness Endocrine – diabetes mellitus, thyroid disorder, HPA axis disorder. Cardiovascular – atheromatous, Leriche’s syndrome, heart failure. Hepatic – cirrhosis. Renal/urological – Peyronie’s disease, hydrocele, varicocele, renal failure. Others – respiratory failure, intersex disorders, congenital (severe) hypospadias.

• • • • •

Local disorders Look for urethritis, balanitis, penile or vaginal trauma, chordee, castration, radical surgery (prostatectomy, colostomy, etc.). Drugs • Decreased libido – antipsychotics, antiandrogens, antidepressants (most varieties but SSRIs least likely); alcohol increases libido acutely but libido reduces with chronic misuse. • Impaired erection – antipsychotics, antidepressants, beta-blockers. • Priapism – may occur with antipsychotics. • Impaired ejaculation – antipsychotics, antidepressants. • Hyperprolactinenia – secondary to antipsychotic therapy causes amenorrhoea in females; sometimes also breast engorgement/galactorrhea.

TREATMENT OF SEXUAL DYSFUNCTION Attend to any organic cause, if possible, but only 10 per cent of cases of impotence presenting to psychiatrists (and a much lower proportion of other dysfunctions) have

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an organic cause, and this is often not reversible. Psychological factors almost always play an important part, and these can be treated. Behaviour therapy This is the treatment of choice. ‘Masters and Johnson’ techniques are used. It is shortduration, symptom-focused therapy, seeing the couple together after initial individual interviews. The aim is to reduce performance anxiety, reduce spectatoring and reduce the pressure of sexual demands on the self and from the partner. Autonomic responses (erection, orgasm, etc.) are not concentrated on. Instead, increased pleasure and confidence and reduction of anxiety are aimed at, with the presumption that normal sexual activity will follow. Therapy may be performed intensely every day for 2 weeks, but under the NHS weekly therapy sessions for 6–10 weeks are more common and almost as successful. Sequence of therapy 1 Supply and discuss sexual information (anatomy, physiology, partner discord, erroneous beliefs). 2 Direct attempts to modify attitudes by explanation, by sanctioning behaviour, etc. 3 Establish effective communications, assumption of joint responsibility. 4 Explain ‘giving to get’ (i.e. mutual exchange of rewards). 5 Define and discuss precise goals of therapy. 6 Clear sexual assignments are given, explained and discussed (‘homework’). Couple set aside a time each day for these and report back. 7 Homework starts with ‘non-demand pleasuring’ (or ‘sensate focus technique’). Prohibit coition for the first week or more. Couple take turns in caressing each other, avoiding genital areas initially. This is discovery of what is pleasurable, mutual enhancement of non-orgasmic sexual pleasure, without being concerned about erections, orgasms or performance. This is therefore a form of desensitization. 8 Discuss resistances, guilt and anxieties when reporting back in therapy sessions. Couple progress from caressing non-sexual areas (back, legs, etc.) to caressing sexual areas (breasts, vulva, penis), but not aiming at orgasm or penetration. 9 Progress is made to specific techniques as appropriate: – Erectile impotence – gradual introduction of penis with female superior or side by side. Then male relaxes and enjoys it. Instruction given to focus on erotic sensations and stop rationalizing (‘get out of your head and into your body’). May proceed to extravaginal orgasm before finally achieving intravaginal orgasm. – Ejaculatory impotence – vigorous penile stimulation with lotion or cream, gradually bringing penis nearer to vagina and continuing stimulation as inserted. – Premature ejaculation – Seman’s technique. Female squeezes base of penis or glans as orgasm approaches (initially extravaginally, then intravaginally), thus preventing ejaculation, and then proceeds to arousal again. May be repeated several times before ejaculation is allowed. – Vaginismus – relaxation training, gradual approach to intercourse as for erectile impotence. Vaginal dilators may be used initially. – Anorgasmia– masturbation, use of vibrators, gradual progress to coitus with clitoral stimulation.

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Drug and physical therapies Modern treatments include:

• • • • • •

Oral phosphodiesterase type 5 inhibitors: sildenafil, vardenafil, tadalafil – caution with heart disease. Intracavernosal penile injections (effect lasts 1–2 hours) of prostaglandin E1. Penile prosthetic implants. External vacuum devices. Penile surgery – microrevascularization, penile vein ligation. Hormone replacement – testosterone.

Psychotherapy It is rarely useful to enter into prolonged analytic therapy unless sexual dysfunction is part of an extensive neurotic or personality problem. Broader marital therapy sessions may be indicated.

PROGNOSIS FOR SEXUAL DYSFUNCTION Good prognosis is indicated by:

• • • • • • •

Previously normal sexual function. Acute onset. Short duration of dysfunction. High motivation. Involved, motivated partner. Absence of other psychological problems. Marked improvement in first few therapy sessions. Cure rates with behavioural therapy (Masters and Johnson):

• • • •

Primary impotence – 50 per cent. Secondary impotence – 70–80 per cent. Premature ejaculation – 100 per cent. Female dysfunction – 80 per cent.

These figures are from uncontrolled series and may be over-optimistic.

PARAPHILIAS EXHIBITIONISM Exhibitionism is deliberate exposure of genitalia by an adult male in the presence of an unwilling female and not as a prelude to sexual intercourse. ‘Indecent exposure’ is the criminal offence. Victims are usually strangers, especially pubertal girls. Exposure is often regarded by the victim as a nuisance rather than a danger. Reaction of the family is often worse than the victim’s own reaction and may lead to greater disturbance in the victim. No personality difference is found between those exposed to and those not.

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CLASSIFICATION (ROOTH, 1971)

• •

Type 1 – 80 per cent of cases. Inhibited young men, emotionally immature, struggle against the impulse, usually expose flaccid penis, feel guilty afterwards. Good prognosis. Type 2 – 20 per cent of cases. Sociopathic personality, expose erect penis, often masturbate while exposing, little guilt, may take sadistic pleasure. Worse prognosis.

EPIDEMIOLOGY

• • • • • •

Commonest single sexual offence. 3000 convictions per year in England and Wales. Peak age of onset is 15–25 years. Incidence in persons under 25 years has doubled since 1945. 75 per cent are under 40 years. 5 per cent are subnormal or psychotic.


• • • • • •

Personality factors – immature, passive, obsessional if type 1. Enjoyment of risk taking. Dissociative behaviour in response to stress or depression. Witness response (fear or disgust) may reinforce behaviour. Often poor sexual performance – with impotence or premature ejaculation and increased masturbation. Possibly close ambivalent relationships with mother and poor distant relationship with father.

MANAGEMENT The first court appearance is often sufficient deterrent. Psychiatric management is suggested if there has been more than one offence:

• • •

Aversive behavioural techniques (e.g. covert sensitization). Group therapy with other exhibitionists may be helpful. Injections with antiandrogen compounds – long-acting agonists of luteinizing hormone-releasing hormone – may help control sexual impulses.

PROGNOSIS Good: 80 per cent only offend once. Poor prognostic indicators (type 2) Exposure to children aged under 10. Previous convictions for other offences. Attempt to contact victim physically. Late onset associated with psychosis or brain damage.

• • • •

Good prognostic indicators (type 1) Stable personality. Regular work record.

• •

PARAPHILIAS

• •

105

Heterosexual relationship. Sympathetic wife.

PAEDOPHILIA Paedophilia is defined as erotic attraction to prepubescent children. There are no accurate data available on prevalence. Fifty per cent are relatives or friends of the target child. Seventy per cent of children participate actively. Characteristically there are three groups of offenders:

• • •

Immature adolescents. Middle-aged men with marital difficulties. Elderly, socially isolated men.

INCEST Characteristically there are three types of incestuous father:

• • •

Endogamic – confining all his sexual and social activities to his family. Often yearning for a sexually inaccessible person. Paedophilic – and hence attracted to daughters. Promiscuous – ignores sexual taboos, part of general hedonism.

TRANSVESTISM Transvestism is a disturbance of general role behaviour – i.e. cross-dressing. It is not a disorder of core gender identity. Transvestism is not itself an offence, though the person may be charged with ‘behaviour likely to cause a breach of the peace’ or with theft of women’s underwear. EPIDEMIOLOGY There are possibly 30 000 transvestites in the UK. Fifty per cent are married. Thirtyfive per cent of men are homosexual (most of women are homosexual). Fifteen per cent are permanent cross-dressers. Transvestism is most common in social classes II and III. CLINICAL FEATURES

• • • •

Usually evident before age 10. May develop increasingly prominent female interests. May use female clothing for fetishistic masturbation. Older transvestites often belong to clubs and act socially as females.

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TRANSSEXUALISM Transsexualism is disturbance of the core gender identity, usually a biological male who is convinced that he is female. It is not itself an offence, but the person may be charged with ‘breach of the peace’. CLINICAL FEATURES

• • •

Many have been fetishistic transvestites before becoming fully transsexual and homosexual in orientation. Usually convinced of ‘wrong sex’ before age 8. Often has poor work record, difficulty in forming relationships, low sex drive.

MANAGEMENT Transsexualism tends to be intractable, but the person may fluctuate in the desire for sex-change surgery. Surgery should be postponed until the person has lived as the opposite-sex person for 2 years. Pre- and post-surgical counselling is necessary. Success is related to premorbid personality, acceptance of surgical limitations, effectiveness and motivation to maintain opposite-sex lifestyle. Hormone therapy is mainly of cosmetic benefit.

HOMOSEXUALITY Gender identity appears to be established by age 3 years, in most in response to social factors – sex assignment and rearing. Gender constancy is acquired later and may also reflect social factors. Homosexuality is not regarded as a psychiatric disorder. However, conflict arising from homosexuality may precipitate psychiatric ill-health:

• • •

Interpersonal problems in relationship(s) – as with a heterosexual relationship. Sexual dysfunction – behavioural approaches as in heterosexual therapy may be used. Psychiatric ill-health – depression, anxiety, etc. Counselling, psychotherapy and pharmacotherapy may be used as appropriate.

REFERENCES AND FURTHER READING Abel GG, Osborn C (1992) The paraphilias: the extent and nature of sexually deviant and criminal behavior. Clin. Forensic Psych. 15, 675. Adson PR (1992) Paraphilias and related disorders. Psych. Ann. 22(6). Andersson KE (2003) Erectile physiological and pathophysiological pathways involved in erectile dysfunction. J. Urol. 170, s6. Bailey JM, Pillard RC, Neale NC, Agyei Y (1993) Heritable factors influence sexual orientation in women. Arch. Gen. Psychiatry 50, 217. Bancroft JHJ (1974) Sexual dysfunction in men. Medicine (Series 1) 30, 1790.


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Baron M (1993) Genetic linkage and male homosexual orientation. BMJ 304, 12. Berrios DC, Hearst N, Perkins LL (1992) HIV antibody testing in young, urban adults. Arch. Intern. Med. 152, 397. Blanker MH, Bosch JL, Groeneveld FP et al. (2001) Erectile and ejaculatory dysfunction in a community-based sample of men 50 to 70 years old: prevalence, concern, and relation to sexual activity. Urology 57, 763. Blythe MJ, Rosenthal SL (2000) Female adolescent sexuality: promoting health sexual development. Obstet. Gynec. Clin. North Am. 27, 125. Brannon GE (2002) Paraphilias. Emedicine. www.emedicine.com/topic3127.htm. Bridges LJ, Moore KA (2002) Religious involvement and children’s well-being: what research tells us (and what it doesn’t). Child Trends: Research Brief, Washington, DC. Briken P, Hill A, Berner W (2003) Pharmacotherapy of paraphilias with long-acting agonists of luteinizing hormone-releasing hormone: a systematic review. J. Clin. Psychiatry 64, 890. Brock GB, McMahon CG, Chen KK et al. (2002) Efficacy and safety of tadalafil for the treatment of erectile dysfunction: results of integrated analyses. J. Urol. 168, 1332. Byne W, Parsons B (1993) Human sexual orientation: the biologic theories reappraised. Arch. Gen. Psychiatry 50, 228. Centers for Disease Control and Prevention (2002) Trends in Sexual Risk Behaviors Among High School Students, United States, 1991–2001. MMWR, 51, 856. Cochran SD, Mays V (2000) Lifetime prevalence of suicide symptoms and affective disorders among men reporting same-sex sexual partners: results from NIHANES III. Am. J. Pub. Health 90, 578. Duncan P, Dixon RR, Carlson J (2003) Childhood and adolescent sexuality. Pediatr. Clin. North Am. 50, 765. Feldmann, J, Middleman ABM (2002) Adolescent sexuality and sexual behaviour. Cur. Opin. Obstetrics Gyn. 14, 489. Ferguson KJ, Stapleton JT, Helms CM (1991) Physicians’ effectiveness in assessing risk for human immunodeficiency virus infection. Arch. Intern. Med. 151, 561. Frank E, Anderson C, Rubinstein D (1978) Frequency of sexual dysfunction in ‘normal’ couples. New Engl. J. Med. 299, 111. Goldstein I, Lue TF, Padma-Nathan H et al. (1998) Oral sildenafil in the treatment of erectile dysfunction. New Engl. J. Med. 338, 1397. Green J, Miller D (1985) Male homosexuality and sexual problems. Br. J. Hosp. Med. 33, 353. Gregoire A (1992) New treatments for erectile impotence. Br. J. Psychiatry 160, 315. Hawton K (1985) Drug treatments in psychiatry: sexual dysfunction. Br. J. Hosp. Med. 34, 207. Hawton K, Catalan J, Martin P et al. (1986) Long-term outcome of sex therapy. Behav. Res. Ther. 24, 665. Johnson AM, Mercer CH, Erens B et al. (2001) Sexual behaviour in Britain: partnerships, practices and HIV risk behaviors. Lancet 358, 1835. Jorm AF, Korten AE, Rodgers B et al. (2002) Sexual orientation and mental health: results from a community survey of young and middle-aged adults. Br. J. Psychiatry 180, 423. Kaplan HS (1978) The New Sex Therapy. Peregrine, London. Kay DSG (1992) Masturbation and mental health: uses and abuses. Sexual Marital Ther. 7, 97. King M, McKeown E, Warner J (2003) Mental health and quality of life of gay men and lesbians in England and Wales: a controlled, cross-sectional study. Br. J. Psychiatry 183, 552. Kinsey AC, Pomeroy WB, Martin CE (1948) Sexual Behaviour in the Human Male. WB Saunders, Philadelphia. Kinsey AC, Pomeroy WB, Martin CE et al. (1953) Sexual Behaviour in the Human Female. WB Saunders, Philadelphia. Laws DR, O’Donohue W (1997) Sexual Deviance: Theory, Assessment and Treatment. Guilford Press, New York.

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Le Vay S (1991) A difference in hypothalamic structure between heterosexual and homosexual men. Science 253, 1034. Lonczak HS, Abbott RD, Hawkins JD et al. (2002) Effects of the Seattle Social Development Project on sexual behavior, pregnancy, birth, and sexually transmitted disease outcome by age 21 years. Arch. Pediatr. Adolesc. Med. 156, 438. MacDonald NE, Wells GA, Fisher WA et al. (1990) High-risk STD/HIV behavior among college students. JAMA 263, 3155. Masters WH, Johnson VE (1966) Human Sexual Response. Little, Brown, Boston. Masters WH, Johnson VE (1970) Human Sexual Inadequacy. Little, Brown, Boston. McColl P (1994) Homosexuality and mental health services. BMJ 308, 550. Mullen PE, Martin JL, Anderson JC, Romans SE, Herbison GP (1994) The effect of child sexual abuse on social interpersonal and sexual function in adult life. Br. J. Psychiatry 165, 35. Myer TL, Cheng TL (2002) Unveiling the secrecy behind masturbation. Pediatr. Rev. 23, 148. Neinstein LS (1996) Adolescent sexuality. In: Neinstein LS (ed.), Adolescent Health Care: a Practical Guide, pp. 628–9. Williams & Wilkins, Baltimore. Nusbaum MR (2003) Chronic illness and sexual functioning. Am. Fam. Physician 67, 347. Philpot CD (2003) Paraphilia and aging. Clin. Geriatr. Med. 19, 629. Rooth FG (1971) Indecent exposure and exhibitionism. Br. J. Hosp. Med. 5, 521. Rosen RC (2001) Psychogenic erectile dysfunction: classification and management. Urol. Clin. North Am. 28, 269. Seftel AD (2003) Erectile dysfunction in the elderly: epidemiology, etiology and approaches to treatment. J. Urology 169, 1999. Seidman SN, Rieder RO (1994) A review of sexual behavior in the United States. Am. J. Psychiatry 151, 330. Snaith RP (1991) Transsexualism [editorial]. Lancet 338, 603. Wise TN (1985) Fetishism – etiology and treatment: a review from multiple perspectives. Comp. Psychiatry 26, 249.

Alcohol dependence

9

ICD-10 AND DSM-IV ICD-10 and DSM-IV emphasize a spectrum of psychological and physical effects:

• • • • • • • • • • • •

Alcohol abuse. Alcohol dependence (see Chapter 10 for definition). Alcohol intoxication. Alcohol withdrawal. Alcohol delirium. Alcohol persisting dementia. Alcohol persisting amnestic disorder. Alcohol psychotic disorder – with delusions or with hallucinations. Alcohol mood disorder. Alcohol anxiety disorder. Alcohol sexual dysfunction. Alcohol sleep disorder.

EPIDEMIOLOGY OF DEPENDENCE National Institute on Alcohol Abuse and Alcoholism (NIAAA) (2000) guidelines for safe use of alcohol:

• • • •

Men – two drinks per day. Women – one drink per day. Men and women older than 65 years – ⭐1 drink per day. Standard drink (USA) ⫽ 12 g of alcohol: – one 12 oz bottle of beer (4.5 per cent strength); – one 5 oz glass of wine (12.9 per cent); – 1.5 oz of 80-proof distilled spirits.

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Table 9.1 SAMHSA 2002 National Survey in USA Use of alcohol in age groups

Previous month (%)

Previous year (%)

12–17 years 18–25 years 26–34 years 35 ⫹ years

17.6 60.5 61.4 52.1

34.6 77.9 77.9 66.1

Table 9.2 Per capita consumption of alcohol (litres of pure alcohol) by country Country

1997

1998

1999

2000

Romania Rep. Ireland France Germany UK Russia USA Japan

11.4 9.7 10.9 10.8 8.2 7.5 6.6 6.4

13.3 9.7 10.8 10.6 8.0 8.1 6.6 6.5

12.2 11.0 10.7 10.6 8.4 8.7 6.7 6.6

12.3 10.8 10.5 10.5 8.4 8.1 6.7 6.5

Adapted from NTC Publications (2002). World Drink Trends. NTC Publications Ltd, Henley-on-Thames, UK.

General surveys See Table 9.1 for results of a national survey in the USA, and Table 9.2 for per capita consumption in various countries. The National Center for Social Research (2002) survey among secondary school pupils in England showed that 4 per cent of 11- to 15-year-olds used alcohol in the previous week. Hospital/practice surveys Thirty per cent of patients in general health care have alcohol-related disabilities. Hospital admission rates

• • •

25 per cent of emergency hospital admissions in England and Wales are attributable to excessive alcohol consumption. Alcoholism accounts for 10 per cent of all psychiatric admissions in the UK. 7.9 per cent of the US population needed treatment for an alcohol problem in 2002.

Prevalence among specific groups

• • • • •

There has been a disproportionate rise in females – 6 per cent have alcohol-related disabilities. There has been a rise in adolescent drinking – 4 per cent of US high school students abuse alcohol daily. 35 per cent of homeless have alcohol disorders. In the elderly, alcohol abuse is surreptitious and effects more marked. 4–6 per cent of the medical profession abuse alcohol.

EPIDEMIOLOGY OF DEPENDENCE

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Table 9.3 Odds ratios for co-morbid diagnoses Co-morbid diagnosis

Odds ratio

Antisocial personality Drug dependence Mania Schizophrenia Panic disorder Major depression

21.0 11.2 6.2 4.0 2.4 1.7

Adapted from Helzer and Pryzbeck (1991).

Co-morbidity Forty-seven per cent of alcoholics meet criteria for another psychiatric disorder (see Table 9.3). Curran et al. (2003) measured co-morbid substance use disorders in emergency room patients who had a primary psychiatric diagnosis and found the following rates:

• • • •

Schizophrenia – 16.1 per cent. Bipolar – 15.6 per cent. Depression – 17.3 per cent. Anxiety – 5.7 per cent.

Age and sex The age of onset of alcoholism is in the late teens or 20s for males. The course is often insidious. Recognition of alcohol dependence is often not until the 30s. Onset is later in females. They are more likely to drink alone, delay seeking treatment, have higher rates of co-morbid depression, stronger genetic predisposition to alcoholism and more physical complications – especially cirrhosis.

• • • •

Overall sex ratio – male:female ⫽ 4:1. Higher rates are in urban areas. Marital status – often divorced or separated. Social class – lowest prevalence in ‘middle’ social groups.

High-risk occupational groups Those who manufacture or sell alcohol. Commercial travellers, frequent overseas travellers. Entertainers, doctors, journalists.

• • •

Permissive factors include job mobility, with absence of restraining structures of home/regular workplace; absence of supervision at work; ready availability of alcohol. Ethnic factors Dependence is high in North American, Afro-Caribbean and Irish; low in Jewish and in Chinese – may relate to different isoenzymes of acetaldehyde dehydrogenase.

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AETIOLOGY OF DEPENDENCE GENETICS Family studies • There is a sevenfold increase in risk of alcoholism among first-degree relatives of alcoholics versus controls. • Twin studies – MZ:DZ ⫽ 70%:43% for males (Pickens et al., 1991), 47%:32% for females (Kendler et al., 1992). Adoption studies Danish, Swedish and US (Iowa) studies indicate:

• • • •

Sons of alcoholics are four times more likely to be alcoholic than sons of nonalcoholic, whether raised by alcoholic biological parents or by non-alcoholic adoptive parents. Sons of alcoholics raised by non-alcoholic adoptive parents are no more susceptible to another non-alcoholic adult psychiatric disorder. There is a higher rate of childhood conduct disorder in male offspring of alcoholics. Alcoholism and antisocial personality are genetically independent disorders for both males and females.

Cloninger (1987) proposed, on the basis of Swedish data, type I/II subgrouping of alcoholism:

• •

Type I – predominantly female, later onset than type II, not associated with antisocial behaviour, higher psychological dependency, more guilt, more related to environmental factors than genetic, abusers show high traits of dependency and harm avoidance. Type II – predominantly males, onset usually before 25 years, high genetic component, parental alcoholism, parental antisocial behaviour, more alcohol-related aggression, more legal problems, less likely to achieve abstinence, more impulsive/ antisocial personality traits.

Chromosomes Variations in allele compositions for alcohol dehydrogenase and aldehyde dehydrogenase may contribute to risk patterns for alcoholism among oriental populations. Vulnerability markers Abnormalities in P3 event-related potential are associated with genetic risk for substance use disorders (Iacono et al., 2002). MOLECULAR GENETICS A number of alcohol-responsive genes have been found (Pandey et al., 2003). Neuropeptide Y (NPY) is of particular interest; decreased expression of NPY has been proposed as a substrate for the predisposition to alcohol-seeking behaviors and alcoholism (Ilveskoski et al., 2001). Mayfield et al. (2002) propose that alcohol alters genes expression involved in cAMP signalling pathways that modulate alcohol sensitivity as well as withdrawal anxiety.

CLINICAL FEATURES

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BIOCHEMICAL FACTORS Alcohol has complex interactions with multiple systems (Ciraulo et al., 2003).

• • • • •

Dopamine (DA) – Acute alcohol consumption stimulates DA release in nucleus accumbens. Chronic alcohol use results in down-regulation of D2 receptors. Serotonin (5-HT) – Alcohol interferes with serotonin function. Greater reduction of serotonin function is associated with impulsivity, aggression, suicidality and psychiatric disorders. Growth homone (GH) – Chronic alcoholism is associated with reduced GH response to stimulus challenge, and is reflective of severe dependence. Opioids – Endogenous opioid system mediates reinforcing effects of alcohol and may be altered in those with high risk for alcoholism. Other receptor/neuropeptides.

PSYCHOLOGICAL FACTORS Meszaros et al. (1999) used a ‘tridimensional personality questionnaire’ to measure the three personality dimensions: novelty seeking (NS), harm avoidance (HA) and reward dependence (Cloninger et al., 1987) in detoxified alcoholics and found that NS is a strong predictor for relapse in detoxified males, and that HA predicts ‘early’ relapse (4 weeks) in females. Operant conditioning: relief of withdrawal symptoms promotes further abuse. SOCIOCULTURAL FACTORS

• • • •

Cultural values, role of alcohol in social activities. Per capita consumption and cultural patterns of alcohol usage correlate with prevalence of alcohol-related disabilities. Peer-group pressures. Occupation-related factors.

CLINICAL FEATURES The alcohol dependency syndrome (Edwards and Gross, 1976): 1 Stereotyped pattern of drinking – The ordinary drinker drinks in accordance with variety of cues. The dependent drinker drinks to avoid symptoms of withdrawal; ‘personal drinking repertoire’ is increasingly narrowed. 2 Prominence of drink-seeking behaviour – The dependent drinker gives priority to maintaining alcohol intake. Unpleasant consequences (social, financial, physical) fail to deter. 3 Increased tolerance to alcohol – There is metabolic tolerance (increased liver clearance makes relatively trivial contribution). Presumably, changes occur at synaptic junctions. In later stages of dependence, tolerance may be suddenly lost (not known why). 4 Repeated withdrawal symptoms – Initially there are mild symptoms at any time of day as alcohol levels fall. To incur symptoms, the individual generally has to consume 200–300 g of alcohol a day for several years. 5 Relief or avoidance of withdrawal symptoms by further drinking.

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6 Subjective awareness of compulsion to drink – The desire for a further drink is seen as irrational, resisted, but the further drink is taken (analogous to classic description of compulsive disorder). 7 Reinstatement after abstinence – Many patients find abstinence surprisingly easy to maintain in, say, a ward setting where drinking cues are removed. Relapse into the earlier stage of dependence (reinstatement) is rapid (within 72 hours of drinking) for those severely dependent and varies (weeks, months) for lesser degrees.

COMPLICATIONS OF ALCOHOL DEPENDENCE: ‘ALCOHOL-RELATED DISABILITIES’ CNS EFFECTS WITHDRAWAL SYMPTOMS The spectrum of symptoms is wide: tremor, nausea (or retching), sweating (drenching in early morning), mood disturbance (fearful, depressive), hyperacusis, tinnitus, itching, muscle cramps, sleep disturbance, perceptual distortions and hallucinations, convulsions and fully developed syndrome of delirium tremens.

• • • • • •

Acute tremulousness – 34 per cent. Transient hallucinosis – 11 per cent. Auditory hallucinosis – 2 per cent. Convulsions – ⬍12 per cent. Wernicke–Korsakoff syndrome – ⬍3 per cent. Full-blown delirium tremens – 5 per cent.

Delirium tremens is typically seen 3–5 days after selective or absolute withdrawal, although prodromal features occur earlier. Trauma or infection present from outset in up to 50 per cent of cases and biochemical evidence of liver damage in up to 90 per cent. There may be vivid hallucinations, delusions, profound confusion and inattention, with agitation and restlessness, sleeplessness, autonomic overactivity and fearful affect. Primary disorder of the reticular activating system is suggested by inattention, overarousal, insomnia and overactivity. There is a 10–20 per cent mortality rate related to autonomic instability. Alcoholic hallucinosis, in a restricted sense, applies to rare conditions in which auditory hallucination occurs alone in clear consciousness. Voices are frequently offensive and critical. This may be followed by secondary delusional interpretation. It usually clears in a few days, where there is no evidence for association with schizophrenia. WERNICKE–KORSAKOFF SYNDROME Wernicke’s encephalopathy (also see Chapter 13) This is caused by thiamine deficiency. There are acute degenerative changes in thalamus, hypothalamus, mamillary bodies. Signs are:

• •

Confusion/clouding of consciousness. Ocular palsies and nystagmus.

COMPLICATIONS OF ALCOHOL DEPENDENCE

• •

115

Staggering gait. Peripheral neuropathy.

Treatment with thiamine is usually effective in promptly resolving ataxia and ocular symptoms, but cognitive symptoms are slower to resolve. Korsakoff syndrome There are degenerative changes in upper brain stem, thalamus, hypothalamus and mamillary bodies. Signs are:

• • • •

Inability to form new memories and retrograde amnesia extending to days/years. Confabulation – apparent recollection of imaginary events and experiences. Relative preservation of other intellectual functions and clear consciousness. Peripheral neuropathy.

Wernicke’s encephalopathy and Korsakoff ’s psychosis may be viewed as successive stages of the same disease process; i.e. Korsakoff ’s psychosis is the residual state of which Wernicke’s encephalopathy is the acute organic reaction (see diagram below).

Wernicke syndrome

Response to treatment (thiamine) 84% cases Resolution of symptoms

6% 20% Thiamine treatment Korsakoff’s syndrome 80% Established Korsakoff’s ⫾ alcohol dementia

Prevention/treatment of Wernicke’s encephalopathy with thiamine may prevent Korsakoff ’s psychosis. Only 20 per cent of patients with Korsakoff ’s psychosis show any improvement when treated with thiamine. ALCOHOLIC DEMENTIA There is debate as to whether this is actually a manifestation of evolving Korsakoff ’s. There are mild to moderate cognitive deficits, including impaired memory and judgement, social and personal neglect, and paranoia. Dementia rarely occurs before age 40 years. Females may be more at risk. It is usually accompanied by other CNS and liver evidence of alcohol damage. It is associated with CT/MRI evidence of ‘atrophy’, especially in the frontal lobes. In a small number of patients without full dementia who maintain abstinence, radiological ‘atrophy’ reverses with time (see Chapter 15).

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ALCOHOL DEPENDENCE

OTHER CNS EFFECTS

• • • • • • •

Seizures. Peripheral neuropathy. Myopathy – acute or subacute with more proximal muscle weakness. Women are more susceptible than men. Optic atrophy – loss of visual acuity, central ⫹ colour vision, leading to blindness associated with methanol poisoning, thiamine and B12 deficiency. Cerebellar degeneration. Marchiafava–Bignami disease – primary degeneration of the middle lamina of the corpus callosum; cognitive and behavioural changes manifest by dementia, disinhibition and aggressiveness. Recurrent seizures and altered consciousness are late events. Central pontine myelinolysis – sudden-onset pseudobular palsy; quadriplegia, fatal condition.

PSYCHIATRIC EFFECTS

• • • •

Co-morbidity (see above). Suicide and deliberate self-harm (see Chapter 11). Homicide. Other forensic disorders.

OTHER PHYSICAL EFFECTS Respiratory • Orofacial/laryngeal carcinoma. • COPD/lung cancer related to 80 per cent smoking rate in alcoholics. • Klebsiella pneumonia in alcoholics. • Reactivation of primary TB focus in alcoholics. Cardiovascular • Cardiomyopathy. • Hypertension – alcohol-associated may not respond well to antihypertensives. • Sinus tachycardia with intoxication and withdrawal. Gastrointestinal Gastritis. Barrett’s oesophagitis. Oesophageal varices. Mallory–Weiss oesophageal rupture. Peptic/gastric ulceration – in 20 per cent of alcoholics. Bleeding may be exacerbated by vitamin K deficiency secondary to cirrhosis. • Carcinoma of stomach. • Possible association with large bowel/rectal carcinoma. • Pancreatitis. • Diabetes mellitus.

• • • • •

COMPLICATIONS OF ALCOHOL DEPENDENCE

117

Liver damage Liver damage is related to lifetime intake, enhanced by nutritional deficiences. Fatty infiltration is the earliest feature – decreased fatty acid oxidation.

• •

Alcoholic hepatitis – Acute episode resembles viral hepatitis: 10–30 per cent die, a proportion go on to cirrhosis. Occurs usually after 10 years’ abuse. Cirrhosis – Up to20 per cent of chronic alcoholics suffer. Eighty per cent of all cases of cirrhosis are related to alcohol abuse. Women are more susceptible. Vulnerability may be due in part to histocompatibility antigen HLA-B8, found in approximately 25 per cent of the population. Alternatively, HLA-A28 may have a protective effect. Note that hepatotoxicity may occur at ‘therapeutic’ doses of acetaminophen.

Haematological • Macrocytosis – folate deficiency and direct toxic effect of alcohol. • Anaemia: – Iron deficiency – absorption, blood loss. – B12 – nutritional deficiency. – Malabsorption. – Liver stores. • Thrombocytopenia – splenic sequestration due to enlarged spleen secondary to liver disease; suppression of platelet formation due to toxic effect of alcohol. Neoplasm May be orofacial, GI, respiratory, liver. Fetal alcohol syndrome (FAS), or fetal alcohol spectrum disorder (FASD) In FAS there are facial anomalies: microcephaly, short palpebral fissures, flat philtrum, thin upper lip, small mid-face, low-set ears; mental retardation/low IQ, neurobehavioral problems (ADHD in up to 50 per cent), low birthweight, skeletal defects, congenital heart disease, congenital renal disease.

• • •

Incidence of 1.9 per 1000 live births in the USA. Alcohol in pregnancy is associated with increased stillbirth, increased neonatal mortality. Effects of alcohol are thought to be dose-related.

Endocrine There may be sexual problems and feminization in males – erectile impotence due to impaired metabolism of estrogen by liver and suppression of testosterone production. Menstrual irregularities occur in females.

SOCIAL EFFECTS OF ALCOHOL DEPENDENCE Disabilities may precede the psychological and physical by several years. Family/marital difficulties include:

•

Physical/sexual abuse of partner, ‘reactive’ psychiatric disorder (usually depression) in partner.

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ALCOHOL DEPENDENCE

Table 9.4 Useful laboratory tests Test

Sensitivity

Specificity

GGT MC AST Alkaline phosphatase

80⫹ V50⫹ 40⫹ 60

80⫹ 90⫹ 80 50

AST/ALT ⬎ 2 is often seen in alcoholism.

• • •

Increased divorce. Increased abuse of children. Increased risk of later alcoholism in children, developing other psychiatric disorders, later marrying an alcoholic.

EFFECTS IN SOCIETY The cost of alcohol-related disabilities is estimated to be between 2 and 6 per cent of gross domestic product, with almost two-thirds accounted for by morbidity/premature mortality, and the remainder being for medical care, alcohol-related violent crime and car accidents, and fetal alcohol syndrome.

• • •

Employment – 21⁄2 times as many days off work, decreased productivity, more accidents at work. Accidents – 80 per cent of fatal car accidents involve alcohol; 40 per cent of casualty trauma involves alcohol. Crime – In the USA, 40 per cent of prison inmates are under the influence of alcohol when crime committed; alcohol is consumed prior to almost half of all murders.

RECOGNITION AND DETECTION OF ALCOHOL DEPENDENCE

• • • •

A high index of suspicion is warranted. There is a 75 per cent chance if the patient smells of drink during consultation. There is a 20–30 per cent rate of alcohol abuse/misuse in general hospital patients, and a high rate in casualty/emergency service users, vagrants. CAGE and MAST questionnaires will improve detection in outpatient clinics and in primary care. Laboratory tests are helpful (see Table 9.4).

MANAGEMENT OF ALCOHOL DEPENDENCE GENERAL GUIDELINES Make an initial comprehensive, multidimensional assessment of alcohol-related disabilities. Involve the spouse/significant relationship.

MANAGEMENT OF ALCOHOL DEPENDENCE

119

A goal-orientated treatment plan is required. Recent research suggests a better outcome is achieved if treatment is tailored or ‘matched’ to patients’ attributes rather than standardized. There is some evidence that earlier-onset alcoholics with a family history of alcoholism respond better to pharmacotherapy, specifically naltrexone (Monterosso et al., 2001), while the less severely affected respond better to a cognitive–behavioural approach (Litt et al., 1992). Alcoholism with co-morbidity • Patients need careful evaluation with collateral history. • Relationship of co-morbidity (primary, secondary, co-related) needs to be determined. • Where the mechanism of depression is unclear, antidepressant medication should be delayed until 2 weeks of abstinence. • Inpatient treatment advocated for: – Significant current or past psychiatric co-morbidity. – Significant physical co-morbidity/complications of alcoholism. – History of seizures, prominent DTs. – Risk of suicide, homicide. Characteristics of the patient are more predictive of response and outcome than either setting or programme characteristics. DETOXIFICATION

• • • • • •

Give attention to hydration and electrolyte balance; multivitamin, folic acid, and thiamine given. Intramuscular/vascular thiamine should be given prior to any glucose load to avoid depletion of thiamine stores and subsequent precipitation/ exacerbation of Wernicke–Korsakoff syndrome. Give attention to general medical conditions and the risk of respiratory depression/ infection. Co-morbid physical illness/sepsis are associated with high mortality in acute Wernicke–Korsakoff syndrome. Benzodiazepines are the mainstay of withdrawal treatment, in tapering dose or as-needed dose per CIWA scale (Sullivan et al., 1989); they are the treatment of choice for withdrawal seizures/DT. Lorazepam or oxazepam (no metabolites/renal clearance) are favoured in patients with liver dysfunction or the elderly. Give antipsychotics as needed for alcoholic hallucinosis. An ␣2-adrenergic blocker (clonidine) is useful to lessen noradrengergic symptoms. Anticonvulsants carbamazepine and divalproex have shown efficacy for detoxification but are not in widespread use.

PHARMACOLOGICAL MAINTENANCE TREATMENTS

• • •

Disulfiram – an aversive agent, inhibits aldehyde dehydrogenase. Problems with compliance limits its efficacy. Naltrexone – an opioid blocker, reduces relapse rates (Pettinati et al., 2000). Acamprosate – restores NMDA receptor tone in the glutamate system and is shown to increase abstinence rates. In combination with naltrexone it further enhances relapse prevention (Kiefer et al., 2003).

120

•

ALCOHOL DEPENDENCE

Serotonergic drugs – no consistency in studies as to relapse prevention. They are used to treat co-morbid depression.

PSYCHOSOCIAL REHABILITATION Principles of treatment ‘No cure’ – achieving abstinence ⫽ remission. All efforts are aimed at motivating the patient towards abstinence. Education is essential about addiction, compulsive behaviours, medical complications. Emotional insight is stressed. Involvement of family/significant relationships is critical to treatment. Induction into AA’s Twelve-Step Facilitation (TSF) Therapy is especially helpful for alcoholics who drink heavily in social situations. • Group/individual therapy aims at self-understanding and realization of the effect of addiction on the patients’ life. • Continued participation in support/follow-up programme, AA, etc., should be encouraged.

• • • • • •

Modalities Individual therapy: – Cognitive–behavioral therapy (CBT) (see Chapter 23) is shown to have durable effects. – Motivational enhancement therapy (MET) motivates individuals to utilize their own resources to effect change in their behaviour. It is most effective in alcoholics with high levels of anger. – Coping skills training. • Group therapy. • Couples therapy. • Family therapy.

•

PROGNOSIS FOR ALCOHOL DEPENDENCE Patient attributes rather than treatment factors are a better predictor of outcome. There is a poor prognosis with:

• • • • • •

Established brain damage. Co-morbid psychiatric illness, especially antisocial personality disorder. Criminal history. Low IQ. Poor support. Low motivation.

Follow-up Sixty per cent with ‘good’ outcome at 20.8 months; 40 per cent in remission and 19 per cent with no more than three relapses and continuous sobriety 6 months prior to survey (Castle Craig Hospital Extended Care Unit Follow-up Study, 1999). • Self-reports for follow-up study are about 90 per cent reliable (Secades-Villa and Fernandez-Hermida, 2003).

•


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REFERENCES AND FURTHER READING Anderson P, Cremona A, Paton A et al. (1993) The risk of alcohol. Addiction 8, 1493. Babor TF, Hofmann M, DelBoca JK et al. (1992) Types of alcoholics. I: Evidence for an empirically derived typology based on indicators of vulnerability and severity. Arch. Gen. Psychiatry 49, 599. Bolnick JM, Rayburn WF (2003) Substance use disorders in women: special considerations during pregnancy. Obstet. Gynecol. Clin. North Am. 30, 545. Brook DW, Brook JS, Zhang C et al. (2002) Drug use and the risk of major depressive disorder, alcohol dependence, and substance use disorders. Arch. Gen. Psychiatry 59, 1039. Brun A, Andersson J (2001) Frontal dysfunction and frontal cortical synapse loss in alcoholism: the main cause of alcohol dementia? Dement. Geriatr. Cogn. Disord. 12, 289. Castle Craig Hospital (1999) Castle Craig Hospital Extended Care Unit Follow-up Study 1999. www.castlecraig.co.uk/treatment/ecu_followup_1999p.htm (accessed 1 January 2004). Chasnoff IJ (1991) Drugs, alcohol, pregnancy, and the neonate: pay now or later. JAMA 266, 1567. Chick J (1993) Benno Pollack Lecture, (1992) Alcohol dependence: an illness with a treatment? Addiction 8, 1481. Ciraulo DA, Piechniczek-Buczek J, En I (2003) Outcome predictors in substance use disorders. Psychiatr. Clin. North Am. 26, 381. Cloninger CR (1987) Neurogenic adaptive mechanisms in alcoholism. Science 23, 410. Collins GB (1993) Contemporary issues in the treatment of alcohol dependence. Psychiatr. Clin. North Am. 16, 33. Condren RM, O’Connor J, Browne R (2001) Prevalence and patterns of substance misuse in schizophrenia: a catchment area case–control study. Psychiatr. Bull. 25, 17. Curran GM (2003) Emergency department use of persons with comorbid psychiatric and substance abuse disorders. Ann. Emerg. Med. 41, 659. Edwards G, Gross MM (1976) Alcohol dependence: provisional description of a clinical syndrome. BMJ 1, 1058. Enoch MA, Goldman D (2002) Problem drinking and alcoholism: diagnosis and treatment. Am. Fam. Physician 65, 441. Faculty of Public Health Medicine (1991) Alcohol and the Public Health. Macmillan, London. Fleming MF, Mundt MP, French MT et al. (2002) Brief physician advice for problem drinkers: long-term efficacy and benefit–cost analysis. Alcohol Clin. Exp. Res. 26, 36. Gelernter J, Goldman D, Risch N (1993) The Al allele at the D2 dopamine receptor gene and alcoholism. JAMA 269, 1673. Greenfield S, Manwani SG, Nargiso JE (2003) Epidemiology of substance use disorders in women. Obstet. Gynecol. Clin. North Am. 30, 413. Hearne R, Connolly A, Sheehan J (2002) Alcohol abuse: prevalence and detection in a general hospital. J. Royal Soc. Med. 95, 84. Heath DB (2001) Culture and substance abuse. Psychiatr. Clin. North Am. 24, 479. Heilig M, Thorsell A (2002) Brain neuropeptide Y (NPY) in stress and alcohol dependence. Rev. Neurosci. 13, 85. Helzer JE, Pryzbeck TR (1991) The co-occurrence of alcoholism with other psychiatric disorders in the general population and its impact on treatment. J. Stud. Alcohol 49, 219. Hopfer CJ, Crowley TJ, Hewitt JK (2003) Review of twin and adoption studies of adolescent substance use. J. Am. Acad. Child Adolesc. Psychiatry 42, 710. Iacono WG, Carlson SR, Malone SM, McGue M (2002) P3 event-related potential amplitude and the risk for disinhibiroty disorders in adolescent boys. Arch. Gen. Psychiatry 59, 750. Ilveskoski E, Kajander OA, Lehtimäki T et al. (2001) Association of neuropeptide Y polymorphism with the occurrence of type 1 and type 2 alcoholism. Alcohol Clin. Exp. Res. 10, 1420.

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Jackson KM, Sher KJ, Wood PK, Bucholz KK (2003) Alcohol and tobacco use disorders in a general population: short-term and long-term associations from the St Louis Epidemiological Catchment Area Study. Drug Alcohol Depend. 71, 239. Johnson BA, Roache JD, Ait-Daoud N et al. (2002) Ondansetron reduces the creving of biologically predisposed alcoholics. Psychopharmacology 160, 408. Kendler KS, Heath AC, Neale MC et al. (1992) A population-based twin study of alcoholism in women. JAMA 268, 1877. Kiefer F, Jahn H, Tarnaske T (2003) Comparing and combing naltrexone and acamprosate in relapse prevention of alcoholism: a double-blind, placebo-controlled study. Arch. Gen. Psychiatry 60, 92. Koren G, Nulman I, Chudley AE, Loocke C (2003) Fetal alcohol spectrum disorder. CMAJ 169, 1181. Lingford-Hughes A, Nutt D (2002) Neurobiology of addiction and implications for treatment. Br. J. Psychiatry 182, 97. Litt MD, Babor TF, DelBoca FK et al. (1992) Types of alcoholics. II: Application of an empirically derived typology to treatment matching. Arch. Gen. Psychiatry 49, 609. Madden JS (1993) Depression: alcohol and depression. Br. J. Hosp. Med. 50(5), 265. Markianos M, Lykouras L, Moussas G et al. (2001) Changes in dopamine receptor responsivity during alcohol detoxification may predict relapse. Drug Alcohol Depend. 64, 363. Martin SE (2001) The links between alcohol, crime and the criminal justice system: explanations, evidence and interventions. Am. J. Addict. 10, 136. Mayfield RD, Lewohl JM, Dodd PR et al. (2002) Patterns of gene expression are altered in the frontal and motor cortices of human alcoholics. J. Neurochem. 81, 802. McGovern MP, Carroll KM (2003) Evidence-based practices for substance use disorders. Psychiatr. Clin. North Am. 26, 991. Meszaros K, Lenzinger E, Hornik K et al. (1999) The tridimensional personality questionnaire as a predictor of relapse in detoxified alcohol dependents. The European Fluvoxamine in Alcoholism Study Group. Alcohol. Clin. Exp. Res. 23, 483. Monterosso JR, Flannery BA, Pettinati HM et al. (2001) Predicting treatment response in naltrexone: the influence of craving and family history. Am. J. Addict. 10, 258. National Institute on Alcohol Abuse and Alcoholism (2000) NIH publication no. 00-1583. National Survey on Drug Use and Health, Substance Abuse and Mental Health Services Administration (SAMHSA) (2002). www.samhsa.gov/oas/nhsda/2k2nsduh/Results/2k2Results.htm. Overman GP, Teter CJ, Guthrie SK (2003) Acamprosate for the adjunctive treatment of alcohol dependence. Ann. Pharmacother. 37, 1090. Pandey SC, Carr LG, Heilig M et al. (2003) Neuropeptide y and alcoholism: genetic, molecular, and pharmacological evidence. Alcohol. Clin. Exp. Res. 27, 149. Pettinati HM, Volpicelli JR, Pierce JD et al. (2000) Improving naltrexone response: an intervention for medical practicioners to enhance medication compliance in alcohol dependent patients. J. Addict. Dis. 19, 71. Pickens RW, Svikis DS, McGue M et al. (1991) Heterogeneity in the inheritance of alcoholism: a study of male and female twins. Arch. Gen. Psychiatry 48, 19. Rice DP, Kelman S, Miller LS (1991) Estimates of economic costs of alcohol and drug abuse and mental illness, 1985 and 1988. Public Health Rep. 106, 280. Sattar SP, Petty F, Burke WJ (2003) Diagnosis and treatment of alcohol dependence in older alcoholics. Clin. Geriatr. Med. 19, 743. Secades-Villa R, Fernandez-Hermida JR (2003) The validity of self-reports in a follow-up study with drug addicts. Addict. Behav. 28, 1175. Shivani R, Goldsmith RJ, Anthenelli RM (2002) Alcoholism and psychiatric disorders: diagnostic challenges. Alcohol Res. Health 26, 90. Sullivan JT, Sykora K, Schneiderman J et al. (1989) Assessment of alchol withdrawal: the revised clinical institute withdrawal assessment for alcohol scale (CIWA-Ar). Br. J. Addict. 84, 1353.

Drug dependence and gambling

10

ICD-10 AND DSM-IV SUBSTANCE DEPENDENCE Substance misuse which results in clinically significant impairment or stress, as evident by ⭓3 of the following during a 12-month period: 1 Tolerance – markedly increased amounts of substance required to achieve intoxication or desired effect, or markedly diminished effect with continued use of the same amount of the substance. 2 Withdrawal – Characteristic. Withdrawal syndrome for the substance, or the same (or similar) substance is used to relieve or avoid withdrawal. 3 Substance is often taken in larger amounts or over a longer period than was intended. 4 Persistent desire or unsuccessful efforts to reduce or control substance use. 5 Excessive time in activities necessary to obtain the substance, use the substance, or recover from effects. 6 Loss or reduction in important social, occupational, or recreational activities. 7 Continued substance use despite knowledge of a persistent or recurrent physical/ psychological problem which is caused/exacerbated by the substance.

• •

With physiological dependence – evidence of tolerance or withdrawal. Without physiological dependence – no evidence of tolerance or withdrawal.

SUBSTANCE ABUSE (SA) A. Pattern of substance misuse leading to clinically significant impairment or distress, as manifested by ⭓1 of the following occurring during a 12-month period: 1 Recurrent substance use resulting in a failure to fulfill major role obligations at work, school or home. 2 Recurrent substance use in situations in which it is physically hazardous. 3 Recurrent substance-related legal problems.

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4 Persistent substance use despite recurrent social or interpersonal problems having origin in or caused or exacerbated by the effects of the substance. B. Never met criteria for dependence for this class of substance.

EPIDEMIOLOGY OF SUBSTANCE ABUSE Lifetime illicit drug use in the USA (SAMHSA Household Survey on Drug Abuse, 2002):

• • • • • • • •

Marijuana/hashish – 40.4 per cent. Cocaine – 14.4 per cent. Crack – 3.6 per cent. LSD – 10.4 per cent. Inhalants – 9.7 per cent. Methamphetamine – 5.3 per cent. Ecstasy – 4.3 per cent. Non-medical use of prescribed medications – 19.8 per cent.

Of the US population 8.3 per cent actively used illicit drugs in 2002; 3.3 per cent needed treatment in 2002 for a drug problem, of which 0.6 per cent actually received help. Co-morbidity 45 per cent of patients with alcohol abuse/dependence have at least one other psychiatric disorder. • 72 per cent of patients with drug abuse/dependence have at least one other psychiatric disorder. • Co-occurrence of substance and psychiatric disorders portends negatively for successful treatment of either. • Over half of schizophrenic patients in the USA have substance use disorder.

•

Possible associations: 1 Vulnerability hypothesis – SA may precipitate schizophrenia in predisposed individuals. It is unlikely as a primary cause. 2 Self-medication hypothesis: – SA counteracts negative symptoms, depressed mood. – SA counteracts side-effects of treatment. Age, sex and class Eighty per cent begin SA before age 18, with peak abuse period in 20s–30s (20–24 for females, 20–30 for males). Risk lessens after age 40. Volatile SA (inhalants, etc.) are mostly used by young adolescents. • Overall – male:female ratio ⫽ 4:1. • All classes are affected, but lower groups are over-represented, especially in the USA.

•

AETIOLOGICAL THEORIES OF SUBSTANCE ABUSE

125

Pattern of abuse • Episodic abuse generally seen with less addictive drugs, continuous course with highly addictive drugs. • Cannabis is the first drug of abuse in 70 per cent of opiate addicts. • Polysubstance abuse is common: 90 per cent of opiate abusers also abuse benzodiazepines (especially diazepam or temazepam, oral and IV). • Other drug use is more ‘contained’: – Volatile SA is often experimental; only 20 per cent become chronic abusers and polysubstance abusers. – Ecstasy (NMDA) is used mainly for recreational purposes – dance parties or ‘raves’. • Only one-third of opiate users are in contact with treatment agencies at any time. • Average duration of use before seeking treatment is 9 years. • Average duration of intravenous use before seeking treatment is 4 years.

AETIOLOGICAL THEORIES OF SUBSTANCE ABUSE Theories are diverse and conjectural. A multifactorial perspective is required. GENETICS Twin studies in adolescents suggest a modest influence of genetics in conveying liability for non-alcohol substance use disorders (Hopfer et al., 2003). PHARMACOLOGICAL AND PHYSIOLOGICAL THEORIES (also see Chapter 9) Abnormalities are observed in many neurotransmitter systems:

• • •

Opiate receptor. Dopamine. Serotonin. There is intensive research on the neuropharmacology of craving:

• •

May relate to the ability to increase dopamine (DA) activity in nucleus accumbens. Reinforcing effects may occur from stimulation of corticofugal DA pathways.

PSYCHOLOGICAL THEORIES (see Table 10.1)

•

• •

Behavioural: – Modelling. – Primary direct reinforcement (psychic effect of SA promotes continued abuse). – Secondary reinforcement (interaction of environmental cues and pharmacologic effects of drug). Analytic – regression/fixation at oral stage of development (see Chapter 23). Sociocultural: – 50 per cent of heroin addicts are from single parent/divorced families. – There are high rates of parental alcoholism. – Peer group activation (e.g. ecstasy abuse).

Table 10.1 Psychopharmacology and clinical characteristics of commonly abused drugs Drugs

Pharmacology

Route of administration

Psychic effects

Physical effects

Withdrawal effects

Dependence Treatment

Opioids: heroin morphine meperidine methadone pentazocine

Bind to opioid receptors; naltrexone, naloxone – competitive antagonists Tolerance develops with usage; also cross-tolerance within opioid group Withdrawal commences 4–6 hours after last dose, peaks 28–48 hours, lasts 7–10 days

Oral, IV, IM, subcutaneously

Euphoria, relaxation, drowsiness, personality change, hypoactivity, ↓ appetite, ↓ libido

Miosis, bradycardia, itching, nausea, constipation

Craving, agitation, restlessness, tachycardia, dilated pupils, perspiration, yawning, diarrhoea, abdominal cramps, ‘goose flesh’

Yes

Overdose: cardiorespiratory support, naloxone Detoxification: methadone buprenorphine, clonidine

Cocaine

Blocks re-uptake of serotonin and catecholamines, especially dopamine – inhibits transporter uptake site; various dopamine agonists/ autoreceptors studied for ↓ craving

Chewing, sniffing, smoking, IV

Euphoria, excitement, confusion, paranoid psychosis, formication (‘cocaine bugs’)

Mydriasis, tremor, tachycardia, perforated nasal septum, fever, seizures, cardiorespiratory arrest, CVA

‘Crash’: craving, depression, insomnia, psychomotor agitation

Yes

↓ Craving: amantadine, propranolol for severe craving

Crack-cocaine

–

Smoking

Extreme agitation, psychosis

–

–

Yes

–

Amphetamines

Sympathomimetics, detected by urinalysis toxicology if ⭐48 hours after last dose

Oral, IV

Euphoria, excitement, hyperalertness, irritability/aggression, paranoia, psychosis, hallucinosis

Mydriasis, tachycardia, Dysphoria, anergia hyperreflexia Overdose: cardiac arrhythmia, hyperpyrexia

Yes

Overdose: sedation, antiarrhythmic, acidify urine Detoxification: self-resolution; neuroleptic only if psychosis prolonged

Hallucinogens lysergic acid diethylamide (LSD) mescaline psilocybin (‘magic mushrooms’)

Sympathomimetic; 5-HT agonist; onset of effects in 1 hour, last 8–12 hours; flashback may occur spontaneously even 1 year after stopping LSD

Oral

Depersonalization, derealization, hyperperceptualization, false sense of ability, anxiety, ideas of reference, impaired judgement, flashbacks, psychotic or mood disturbance

Red eyes, mydriasis, ataxia, tachycardia

None

No

Phenylcyclidine (PCP)

Receptor sites located in calcium ion channel of NMDA subtype of glutamate

Oral, IV, sniffing, smoking

Hallucinations, paranoid schizophreniform psychosis, depressed consciousness aggression

Nystagmus, ↑ blood pressure

Craving, depression, anergia

Yes

Cannabis marijuana ‘hashish’

Active compound is tetrahydocannabinol; G-protein receptor for cannabinoids recently discovered; onset of effect is minutes to 1 hour; effect lasts 6–12 hours

Smoking

Euphoria, relaxation, heightened perceptual awareness, Cannabis psychosis – disputed entity

Conjunctival infection, dry mouth, tachycardia, respiratory tract irritation

–

Yes

Barbiturates

CNS depressants

Oral, IM, IV

Anxiolytic/respiratory CNS, depression with higher doses

Cellular signs, respiratory depression in overdose

Restlessness, insomnia, Yes anorexia, nausea, seizures, delirium

Withdrawal with benzodiazepine and anti-convulsant cover

Benzodiazepines

CNS depressants; bind to benzodiazepines-GABA receptor complex; also see Chapter 21

Oral, IV

Anxiolytic; impaired concentration, judgement; memory disturbance

Ataxia, nausea, respiratory depression

Agitation, insomnia, tremor, restlessness

Gradual withdrawal

Yes

Abstinence, rehabilitation

Desipramine for craving; haloperidol for agitation/ psychosis, avoid chlorpromazine Overdose: with hypertension ataxia, adrenergic crisis Abstinence

(Continued)

Table 10.1 Continued Drugs

Pharmacology

Route of administration

Psychic effects

Physical effects

Withdrawal effects

Dependence Treatment

Belladonna, alkaloids homatropine atropine scopolamine hyoscyamine

–

–

Euphoria Overdose: confusion, visual hallucinations

Mydriasis, dry mouth, light sensitivity, pyrexia

–

Yes

Overdose: physostigmine 2 mg IV

Ecstasy (MDMA-3,4 methylenedioxymethamphetamine)

Neurotoxic effect on serotonin nerve terminals (stimulates SHT release and blocks SHT re-uptake), especially in frontal cortex and hippocampus

Oral

Euphoria, heightened perceptual awareness, paranoid psychoses, anxiety reactions have been reported

Appetite loss, – tachycardia, jaw tension, Bruxism, perspiration fulminant hyperthermia, disseminated intravascular coagulopathy

?

Supportive measures, especially fluid replacement

Gamma hydroxybutyric acid (GHB)

A naturally occurring fatty acid found in all body tissues that regulates GABA/dopamine/5-HT/ ACh At high dose acts as a CNS depressant/ anaesthetic

Oral

Euphoria, disinhibition, drowsiness, confusion

Repiratory depression, bradycardia, hypothermia, decreased cardiac output, coma

Yes

Benzodiazepines, phenobarbital, antipsychotics

Inhalation – ‘bagging’

Initial euphoria, disinhibition, later apathy, impaired judgement

Irritation of eyes, – throat, perioral rash, odour on breath, CNS depression, ataxia, nystagmus, polyneuropathy, arrhythmias, hepatorenal damage, aplastic anaemia

Yes, but rare

Abstinence

Volatile CNS depressants substance abuse (VSA): toluene acetone benzene trichloroethylene halogenated hydrocarbons

Similar to alcohol withdrawal: sweating, anxiety, autonomic hyperactivity, delirium

MANAGEMENT OF SUBSTANCE ABUSE

•

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Access and availability: – There is convincing evidence in support of environmental influences. – Ease of availability of ‘crack’ cocaine (inexpensive also) led to increased misuse in high-risk groups: medical personnel, prostitutes.

MANAGEMENT OF SUBSTANCE ABUSE PHARMACOLOGICAL TREATMENTS

•

• • •

• • •

Methadone – long-acting synthetic opiate used in opiate addiction for maintenance or detox. – Maintenance therapy at doses of 20–70 mg, with regular urine monitoring for abuse of other drugs. – Moderate/high dosage of methadone required to maintain abstinence. – There is a variable drop-out from maintenance programmes. Persistence is associated with better outcome, less physical morbidity, slower progression of HIV infection. Levomethadyl acetate (LAAM) – long-acting synthetic opiate agonist used in opiate addiction. – Potential for life-threatening arrhythmias due to QT prolongation limits its use to opiate addicts who fail other treatments. Naltrexone – opiate antagonist used in detoxification and maintenance. – Generally less acceptable to abuser than methadone. Compliance limits its usefulness. Buprenorphine – mixed opioid agonist–antagonist. – As effective as methadone in opiate detoxification and maintenance. – Also available combined with naloxone. – Does not require special licensing to prescribe in the USA as with methadone/ LAAM. Clonidine – used in opiate withdrawal for autonomic suppression but does not help withdrawal symptoms of insomnia or muscular aches. Benzodiazepines – used as an adjunct to opioid withdrawal for anxiety/ insomnia. Other agents not yet in routine clinical use/under investigation. Numerous agents are currently being investigated for treating cocaine and marijuana use disorders but their use is not supported by convincing evidence.

PSYCHOSOCIAL TREATMENTS Aim to tackle underlying psychological/social/environmental factors perpetuating SA. Increase awareness, and develop alternative coping mechanisms. Foster cognitive– behavioural strategies to manage craving and eliminate reinforcing behaviours. Biopsychosocial treatments combined with pharmacological therapy improve treatment outcomes (Albanese and Shaffer, 2003).

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PROGNOSIS FOR SUBSTANCE ABUSE There is a high initial relapse after treatment. Follow-up shows high psychiatric morbidity, continued use, high mortality (suicide, accidents, physical complications of SA, AIDS). Therapeutic communities are associated with better outcomes than methadone treatment alone in opiate dependence. Factors associated with poor outcome • Early age of initial abuse. • Long history of abuse. • IV abuse. • Early drop-out from maintenance programmes. • Antisocial personality disorder.

PREVENTION OF ABUSE AND DISEASE

• • • • •

Limit substance availability bycustoms surveillance, severe penalties for supplying/ using illicit drugs, specialized drug-crime police squads. Educate medical personnel. Educate the public. Access the wider drug-abusing population rather than focusing on short-term treatment of some patients. This raises service and public health policy issues. Outreach programmes are essential.

SA AND HIV (ALSO SEE CHAPTER 13) Twenty-five per cent of adults and adolescents in the USA with AIDS used injected drugs (CDC, 2000). The horizontal spread via needle-sharing and sexual practices is more severe in minority populations. Needle-exchange programmes result in lower annual rates of HIV seroprevalence (Pollack, 2001).

PATHOLOGICAL GAMBLING This is categorized in ICD-10 as Habit and Impulse Disorder, and in DSM-IV as an Impulse Control Disorder NOS.

• • • • •

There are frequent, repeated episodes of gambling that dominate the individual’s life to the detriment of social, occupational, material and family commitments. The person may experience ‘craving’, a ‘rush’, ‘blackouts’, withdrawal syndrome. Males are affected more than females (4 per cent of Gamblers Anonymous members are females). Females tend to present earlier. Addiction usually begins in childhood/early adolescence. Predisposing factors include family history of addiction disorders, parental rejection or criticism resulting in chronic low self-esteem.


•

131

Progression from social gambler to pathological gambler may be precipitated/ exacerbated by death of a parent/relative, birth of a child, physical illness or personal threat to life, job demotion or promotion, or substance abuse.

PHASES OF ADDICTION There are four phases: winning, losing, desperation, giving up. Stress-related physical illness, depression, deliberate self-harm and criminal behaviour are common sequelae of the final two phases. Two-thirds of Gamblers Anonymous members have committed some illegal activity to support their gambling. MANAGEMENT OF PATHOLOGICAL GAMBLING Abstinence is the goal of treatment. Often there are multiple additions and other co-morbid psychiatric disorders need to be treated. Individual, group and family therapy along similar principles to those for other addiction disorders are used. Pharmacological treatment has only a limited role except in co-morbid conditions.

REFERENCES AND FURTHER READING Albanese MJ, Shaffer HJ (2003) Treatment considerations in patients with addictions. Prim. Psychiatry 10, 55. Cairney S, Maruff P, Burns C, Currie B (2002) The neurobehavioural consequences of petrol (gasoline) sniffing. Neurosci. Biobehav. Rev. 26, 81. Carroll KM, Ball SA, Nich C et al. (2001) Targeting behavioral therapies to enhance naltrexone treatment of opioid dependence. Arch. Gen. Psychiatry 58, 755. Carruthers S (2003) The ins and outs of injecting. J. Subst. Use 8, 11. Centers for Disease Control and Prevention. HIV/AIDS surveillance report 2000. 12, 14. Chander G, McCaul ME (2003) Co-occurring psychiatric disorders in women with addictions. Obstet. Gynecol. Clin. North Am. 30, 469. Ciraulo DA, Piechniczek J, Iscan EN (2003) Outcome predictors in substance use disorder. Psychiatr. Clin. North Am. 2, 381. Cohn JA (2002) HIV-1 infection in injection drug users. Infect. Dis. Clin. North Am. 16, 745. D’Aunno T, Pollack HA (2002) Changes in methadone treatment practices: results from a national panel study, 1988–2000. JAMA 288, 850. Dettmer K, Saunders B, Strang J (2001) Take home naloxone and the prevention of deaths from opiate overdose: two pilot schemes. BMJ 322, 895. Dyer JE, Roth B, Hyma BA (2001) Gamma-hydroxybutyrate withdrawal syndrome. Ann. Emerg. Med. 37, 147. Ernst M, Grant SJ et al. (2002) Decision making in adolescents with behavior disorders and adults with substance abuse. Am. J. Psychiatry 160, 10. Farre M, Mas A, Torres M et al. (2002) Retention rate and illicit opioid use during methadone maintenance interventions: a meta-analysis. Drug Alcohol Depend. 65, 283. Ferentzy P, Skinner W (2003) Gamblers Anonymous: a critical review of the literature. The Electronic Journal of Gambling Issues: eGambling [on-line serial], 9. Available: www.camh.net/ egambling/issue9/research/index.html.

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Fiellin DA, O’Connor PG (2002) Office-based treatment of opioid-dependent patients. New Engl. J. Med. 347, 817. Freese TE, Miotto K, Reback CJ (2002) The effects and consequences of selected club drugs. J. Subst. Abuse Treat. 23, 151. Fudala PJ, Bridge TP, Herbert S et al. (2003) Office-based treatment of opiate addiction with a sublingual-tablet formulation of buprenorphine and naloxone. New Engl. J. Med. 349, 949. Goldstein RZ, Volkow ND (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am. J. Psychiatry 159, 1642. Gonzalez G, Oliveto A, Kosten TR (2002) Treatment of heroin (diamorphine) addiction: current approaches and future prospects. Drugs 63, 1331. Gossop M, Stewart D, Browne N, Marsden J (2002) Factors associated with abstinence, lapse or relapse to heroin use after residential treatment: protective effect of coping responses. Addiction 97, 1259. Green AI, Canuso CM, Brenner MJ, Wojcik JD (2003) Detection and management of comorbidity in patients with schizophrenia. Psychiatr. Clin. North Am. 26, 115. Halpern JH, Pope HG (2001) Hallucinogens on the internet: a vast new source of underground drug information. Am. J. Psychiatry 158, 481. Hopfer CJ, Crowley TJ, Hewitt JK et al. (2003) Review of twin and adoption studies of adolescent substance use. J. Am. Acad. Child Adolesc. Psychiatry 42, 710. Hser YI, Hoffman V, Grella CE, Anglin D (2001) A 33-year follow-up of narcotics addicts. Arch. Gen. Psychiatry 58, 503. Huestis MA, Choo RE (2002) Drug abuse’s smallest victims: in-utero drug exposure. Forensic Sci. Int. 128, 20. Johnston LD, O’Malley PM, Bachman JG (2003) Monitoring the Future: National Results on Adolescent Drug Use – Overview of Key Findings: 2002. National Institute on Drug Abuse, Bethesda, MD. Kalivas PW (2002) Predisposition to addiction: pharmacokinetics, pharmacodynamics, and brain circuitry. Am. J. Psychiatry 160, 1. Kandel DB (2002) Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis. Cambridge University Press, New York. Koesters SC, Rogers PD, Rajasingham CR (2002) MDMA (‘ecstasy’) and other ‘club drugs’: the new epidemic. Pediatr. Clin. North Am. 49, 415. Kosten TR, George TP (2002) The neurobiology of opioid dependence: implications for treatment. Sci. Pract. Perspect. 1, 13. Kurtzman TL, Otsuka KN, Wahl RA (2001) Inhalant abuse by adolescents. J. Adolesc. Health 28, 170. Lingford-Hughes A, Nutt D (2003) Neurobiology of addiction and implications for treatment. Br. J. Psychiatry 182, 97. Luty J (2003) What works in drug addiction? Adv. Psychiatr. Treat. 9, 280. McGovern MP, Carroll KM (2003) Evidence-based practice for substance use disorders. Psychiatr. Clin. North Am. 26, 991. McLellan AT (2002) Have we evaluated addiction treatment correctly? Implications from a chronic care perspective. Addiction 97, 249. Moeller MF, Kraemer T (2002) Drugs of abuse: monitoring in blood for control of driving under the influence of drugs. Ther. Drug Monit. 24, 210. Murray JM, Law MG, Gao Z et al. (2003) The impact of behavioral changes on the prevalence of human immunodeficiency virus and hepatitis C among injecting drug users. Int. J. Epedemiol. 32, 715. National Institute on Drug Abuse (2002) Epidemiologic trends in drug abuse. Proceedings of the Community Epidemiology Work Group, December 2001, Vol. II. National Institute on Drug Abuse, Bethesda, MD.


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National Research Council Committee on Data and Research on Illicit Drugs (2002) For debate: executive summary of the National Research Council’s report: informing America’s policy on illegal drugs: what we don’t know keeps hurting us. Addiction 97, 647. Pennings EJM, Leccese AP, de Wolff FA (2002) Effects of concurrent use of alcohol and cocaine. Addiction 97, 773. Pollack HA (2001) Cost-effectiveness of harm reduction in preventing hepatitis C among injection drug users. Med. Decis. Making 21, 357. Ricaurte GA, Yan J, Hatzidimitriou G et al. (2002) Severe dopaminergic neurotoxicity in primates after a common recreational dose regimen of MDMA (‘ecstasy’). Science 297, 2260. Rounsaville BJ, Petry NM, Carroll KM (2003) Single versus multiple drug focus in substance abuse clinical trails research. Drug Alcohol Depend. 70, 17. Silberg J, Rutter M, D’Onofrio B, Eaves L (2003) Genetic and environment risk factors in adolescent substance use. J. Child Psychol. Psychiatry 44, 664. Sinha R, Easton C, Renee-Aubin L, Carroll KM (2003) Engaging young probation-referred marijuana-abusing individuals in treatment: a pilot trial. Am. J. Addict. 12, 314. Substance Abuse and Mental Health Services Administration (2002) Results from the 2001 National Household Survey on Drug Abuse. Vol. I: Summary of National Findings. Office of Applied Studies, Rockville, MD. Toneatto T, Skinner W (2000) Relationship between gender and substance use among treatmentseeking gamblers. The Electronic Journal of Gambling Issues: eGambling [on-line serial], 1. Available: www.camh.net/egambling/issue1/research/index.html. Van Ree JM, Gerritis MAFM, Vanderschuren LJMJ (1999) Opioids, reward and addicts: an encounter of biology, psychology, and medicine. Pharmacol. Rev. 51, 341. Volkow ND, Chang L, Wang G-J et al. (2001) Higher cortical and lower subcortical metabolism in detoxified methamphetamine abusers. Am. J. Psychiatry 158, 383.

Suicide and non-fatal deliberate self-harm

11

SUICIDE DEFINITIONS

• • • • •

Kessel – suicide and ‘deliberate self-poisoning/injury’. ‘Deliberate self-injury’ substituted for ‘attempted suicide’ because many patients ‘performed their acts in the belief that they were comparatively safe’. Kreitman – suicide and parasuicide: ‘Parasuicide’ refers to ‘a behavioural analogue of suicide but without considering a psychological orientation towards death being in any way essential to the condition’. Morgan – non-fatal deliberate self-harm (DSH): ‘A deliberate non-fatal act, whether physical, drug overdose or poisoning, done in the knowledge that it was potentially harmful, and in the case of drug overdosage, that the amount taken was excessive.’ Beck – suicide: ‘A wilful self-inflicted life-threatening act which has resulted in death.’ Durkheim: proposed three forms of suicide: – Egoistic. – Anomic. – Altruistic.

EPIDEMIOLOGY OF SUICIDE

•

• •

Figures from the Centers for Disease Control and Prevention (2001): – Suicide is the eleventh leading cause of death in the USA and the third major cause of death in the 15–34 year age-group. – Males complete suicide at a rate four times that of females. – Whites commit suicide at twice the rate of blacks. In the UK, suicide is the second leading cause of death in the 15–34 year age-group. Methods of suicide: firearms 55.1 per cent, suffocation 20.2 per cent, poisoning 17.0 per cent, fall 2.1 per cent, cut/pierce 1.5 per cent, drowning 1.1 per cent.

PSYCHIATRIC ILLNESS AND SUICIDE

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Table 11.1 Suicide rates per 100 000 population

England and Wales Ireland America Hungary Mexico

• •

1960

1999

11.2 3.0 10.6 25.0 1.9

15.1 22.7 21.1 60.1 (2001) 6.4 (1995)

Worldwide, almost one million suicides and over ten million suicide attempts occur annually. See Table 11.1. Highest rates are in the spring, lowest in December.

FACTORS ASSOCIATED WITH INCREASE IN SUICIDE RATES

• • • • •

Psychiatric illness. Unemployment. Social isolation. Poverty. Gun ownership.

VICTIM CHARACTERISTICS

• • • • • • •

A psychiatric diagnosis is evident in over 90 per cent of victims; 60 per cent suffer from a mood disorder. Alcohol and other substance use, schizophrenia, bipolar disorder and personality disorder are commonly seen in suicide victims. Males exceed females for all age-groups. Rates are highest in the divorced or widowed. Married have lowest rates. Urban dwellers exceed rural. Socioeconomic class – higher in lowest and highest groups, lower in middle groups. Religion – strong religious affiliation is a protective factor. Occupation – higher-risk groups are doctors, lawyers, police officers, hotel and bar trade owners. Unemployment – there is a strong statistical association, especially for males.

PSYCHIATRIC ILLNESS AND SUICIDE EPIDEMIOLOGY AND ASSOCIATIONS FIGURES FOR SUICIDE ATTEMPTS See Hawton et al. (2003a):

• • •

Affective disorder – 73.9 per cent. Alcoholism – 24.3 per cent. Drugs – 3.6 per cent.

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• • •

SUICIDE AND NON-FATAL DELIBERATE SELF-HARM

Neurotic/stress-related/somatoform disorder – 26.1 per cent. Schizophrenia – 4.5 per cent. Personality disorder (diagnosed 12–20 months later) – 45.9 per cent.

DEPRESSION Fifteen per cent of patients hospitalized for mood disorder will kill themselves. Greater risk of suicide is seen with psychotic depression. Risk factors include:

• • • • •

General – male, older living alone. Specific – history of previous suicide attempt. Agitation, insomnia. Impaired memory, self-neglect. Hopelessness.

ALCOHOLISM Fifteen per cent of alcoholics kill themselves. Risk factors are (Preuss et al., 2003):

• • • •

Separated or divorced. Drug dependence. Substance-induced psychiatric disorder. More severe course of alcoholism. Of note, gender did not predict future suicide attempts in alcoholics.

SCHIZOPHRENIA (RAYMONT, 2001) Suicide is the principal cause of premature death in schizophrenics. Between 9 and 13 per cent of schizophrenics commit suicide; 20–40 per cent attempt suicide. Their characteristics are:

• • • •

Male, young, unemployed, socially isolated. Early in illness, immediately after discharge from first admission. High or low premorbid functioning. Numerous relapses, poor global functioning, hopelessness. Fifty per cent had contact with mental health services within 7 days of suicide.

PERSONALITY DISORDER Co-morbidity with other psychiatric disorders; risk highest in antisocial and borderline personalities. PHYSICAL ILLNESS CNS disorders carry a high risk; AIDS, multiple sclerosis, epilepsy (especially TLE), head injury, peptic ulcer disease, cancer. The risk of suicide is reported to be higher in people with low cholesterol, particularly for males. The relationship is poorly understood.

PSYCHIATRIC ILLNESS AND SUICIDE

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SPECIAL POPULATIONS Adolescents • Rare before age 14 years; rate increasing in adolescents. • Risk factors include psychiatric illnesses, substance use (especially alcohol), male gender, disrupted family relations, availability of lethal means, involvement in legal system, lack of religious involvement. Elderly The rate is increasing in the elderly. Up to 74 per cent of elderly suicide victims visited a primary care provider within 1 month of death. • Comprising only 13 per cent of the US population, those 65 years and older accounted for 18 per cent of deaths by suicide in 2000. • In 2000, death by suicide for white males over 84 years was 59 per 100 000, greater than five times the national rate. • 80–90 per cent of elderly suicides have depressive illness. – Often the first episode of depression. – Deliberate self-harm in elderly more closely associated with completed suicide. – Denial of suicide more common. – Physical illness is more associated, especially if debilitating physical illness.

• •

General hospital inpatients Suicide rates are generally low, but still three to four times higher than among the general population. • At-risk groups are: patients admitted post DSH, patients with debilitating illness, patients being investigated for physical complaints which are part of a depressive disorder, women with postpartum psychiatric complications.

•

Prison inmates Rates are three to four times higher than in the general population. Remand prisoners are at particular risk; also prisoners convicted of murder/ violent/sexual crimes. • One-half of suicides occur in the first 3 months of imprisonment; one-half have have seen the doctor in the week prior to suicide. • 90 per cent occur by hanging. • One-third have a previous psychiatric history, almost one-half a history of DSH.

• •

BIOLOGICAL FACTORS IN SUICIDE NEUROCHEMISTRY Research shows a general lack of serotonergic activity in the prefrontal cortex of suicide victims, which would confer less behavioral inhibition and make them more likely to act on suicidal thoughts.

• •

Lower CSF 5-HIAA levels are associated with more lethal suicide attempts. Decreased CSF 5-HIAA is the most consistent finding in patients with DSH.

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• •


Post-mortem studies show a decreased number of 5-HT receptors in the prefrontal cortex, hypothalamus, occipital cortex and brain stem. Suicide victims have abnormalities of the hypothalamic–pituitary–adrenal axis and of noradrenergic systems.

GENETICS

• •

Twin studies – MZ:DZ ⫽ 11.3%:1.8% (Roy et al., 1991). Suicidal behaviour clusters in families. Familial clustering probably represents an inherited genetic variation in the serotonin-related genes, which are the object of ongoing research.

MANAGEMENT AND PREVENTION OF SUICIDE 1 Detect high-risk groups: – Despite epidemiological and clinical associations that denote risk, prediction of suicide is extremely difficult. – Limit access to lethal means of suicide. 2 Active treatment of any mental illness: – Psychopharmacology – use medications appropriate to diagnosis. Lithium and clozapine are associated with reduced suicidal behaviour. – Psychotherapy – dialectical behavior therapy reduces parasuicidal acts.

NON-FATAL DELIBERATE SELF-HARM EPIDEMIOLOGY AND ASSOCIATIONS OF DSH It is difficult to assess the true extent. Hospital-based information is likely to underestimate.

• • • •

DSH is reported in 4 per cent of the general population. 14 per cent of college students report DSH. It is highly associated with personality disorder, especially borderline. A decline in the late 1970s has continued, especially among females.

RISK FACTORS

• • • • • • •

Childhood trauma. Teenage to early adulthood. Female. Eating disorder. Marital status: divorced ⬎ single ⬎ widowed; least for married. Urban/rural: urban ⬎ rural; high rates in ‘inner city’ areas associated with overcrowding, lack of facilities, less social cohesion. Social class: inverse relationship; strong association with unemployment both for males (relative risk 12.1) and for females (13.6).

NON-FATAL DELIBERATE SELF-HARM

•

• • •

139

Psychiatric illness: – Most attempters have symptoms of psychological distress, but definite psychiatric illness found in under one-third. – Most common diagnoses are ‘reactive’ depression, alcoholism, panic disorder (high rates from ECA study now disputed), personality disorder (borderline, sociopathic). Most commit DSH as an impulsive act. 65 per cent followed some major life event. 50 per cent followed a serious argument with partner/friend.

REPETITION OF DSH AND EVENTUAL SUICIDE One per cent involved in DSH commit suicide in the first year, 3–5 per cent within 5–10 years. The greatest risk is in the first 6 months. The risk remains high for 5 years, but markedly decreases then if there has been no DSH during this period. In general, the closer to demographic and clinical characteristics of completed suicide the greater the risk with DSH. However, prediction for individual patients is very difficult:

• •

10 per cent of DSH attempters ultimately commit suicide. 50 per cent of suicides had a history of DSH.

Predictors of repetition Number of previous episodes of DSH. Features of personality disorder. History of violence. Alcoholism. Unmarried, lowest social class. Females equivalent to males.

• • • • • •

Factors of DSH indicating suicidal intent • Isolation. • Timing. • Precautions to avoid intervention. • Suicidal note. • Anticipatory acts. • ‘Subjective’ appraisal of state of mind. • ‘Dangerousness’ of attempt.

MANAGEMENT OF DSH Preceding the episode: • 36 per cent had attended their GP within 1 week of DSH. • 82 per cent had contact with some agency within 1 month of DSH. • Efforts are needed to increase detection, to avoid prescription of agents to be used for DSH, and effective recognition and treatment of psychiatric illness. After the episode: ‘First-ever’ episodes respond best to therapy. There is a high default rate from clinic attenders.

• •

140


Treatments • Psychotherapy; dialectical behavior therapy, family therapy. • Social support. • Treat mood disorder, thought disorder, substance use disorder. • Pharmacology – lithium reduces suicide risk; well–managed depression will reduce risk. • ECT may reduce suicidality in a manic or several depressed state. For those with repeated DSH, the above interventions have been of limited effectiveness.

REPEATED SELF-MUTILATION EPIDEMIOLOGY

• • •

Types: – Repeated minor lacerations (usually of the wrist) – the largest group. – Psychotic patients. – Seriously suicidal. Incidence: – 3–4 per cent in the general psychiatric population within 1 month. – 15 per cent of the subnormal population within 1 month. Age and sex – younger; women more than men in hospital populations.

SYMPTOMS

• • •

Mounting tension, sense of emptiness/loss. Depressive feeling described less commonly. Emotional relief on self-injury.

CORRELATES

•

• •

The ‘typical’ wrist-cutter is described as young, female, aged 16–24. – May have nursing or other medical connections. – Low self-esteem, expressing dislike of own body. – May have associated anorexia/bulimia nervosa. – Around 50 per cent have used alcohol or drugs to excess. – Some research has shown increased incidence of menstrual irregularity. – Poor verbalizer. Childhood – increased incidence of broken homes and hospitalization before age 5. Precipitants – recent loss, rejection or impasse in relationships.

MANAGEMENT Management is difficult. A carefully coordinated team response is needed to mutilating behaviour (minimize ‘gain’). Therapy explores areas of self-image/esteem. Tension reduction might be achieved by relaxation techniques.


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Inskip HM, Harris EC, Barraclough B (1999) Lifetime risk of suicide for affective disorder, alcoholism and schizophrenia. Br. J. Psychiatry 172, 35. Jenkins GR, Hale R, Papanastassiou M et al. (2002) Suicide rate 22 years after parasuicide: cohort study. BMJ 325, 1155. Kelly BD, McLoughlin DM (2002) Euthanasia, assisted suicide and psychiatry: a Pandora’s box. Br. J. Psychiatry 181, 278. Kessler RC, Borges G, Walters EE (1999) Prevalence of and risk factors for lifetime suicide attempts in the national comorbidity study. Arch. Gen. Psychiatry 56, 617. Klonsky ED, Oltmanns TF, Turkheimer E (2003) Deliberate self-harm in a nonclinical population: prevalence and psychological correlates. Am. J. Psychiatry 160, 1501. Koller GP, Preuss UW, Bottlender M et al. (2003) Impulsivity and aggression as predictors of suicide attempts in alcoholics. Eur. Arch. Psychiaty Clin. Neruoscience 252, 155. Luoma JB, Martin CE, Pearson JL (2002) Contact with mental health and primary care providers before suicide: a review of the evidence. Am. J. Psychiatry 159, 909. Mann JJ (2002) A current perspective of suicide and attempted suicide. Ann. Intern. Med. 136, 302. Mann JJ (2003) Neurobiology of suicidal behavior. Nat. Rev. Neurosci. 4, 819. Mann JJ, Malone KM, Psych MR et al. (1996) Attempted suicide characteristics and cerebrospinal fluid amine metabolites in depressed inpatients. Neuropsychopharmacology 15, 576. Mann JJ, McBride PA, Brown MP et al. (2000) A serotonin transporter gene promoter polymorphism (5-HTTLPR) and prefrontal cortical binding in major depression and suicide. Arch. Gen. Psychiatry 57, 729. Marttunen MJ, Hillevi MA, Henriksson MM, Lonngvist JK (1991) Mental disorder in adolescent suicide. Arch. Gen. Psychiatry 48, 834. McGlure GMG (2001) Suicide in children and adolescents in England and Wales 1970–1998. Br. J. Psychiatry 178, 469. Munroe J, O’Sullivan D, Andrews C et al. (1999) Active monitoring of 12 760 clozapine recipients in the UK and Ireland: beyond pharmacovigilance. Br. J. Psychiatry 175, 576. National Institute of Mental Health (2003) Older Adults: Depression and Suicide Facts. www.nimh.nih.gov/publicat/elderlydepsuicide.cfm (accessed 22 December 2003). Oquendo MA, Kamali M, Ellis SP et al. (2002) Adequacy of antidepressant treatment after discharge and the occurrence of suicidal acts in major depression: a prospective study. Am. J. Psychiatry 159, 1746. Owens D, Horrocks J, House A (2002) Fatal and non-fatal repetition of self-harm. a systematic review. Br. J. Psychiatry 181, 193. Preuss UW, Schucket MA, Smith TL et al. (2003) Predictors and correlates of suicide attempts over 5 years in 1237 alcohol-dependent men and women. Am. J. Psychiatry 160, 56. Purselle DC, Nemeroff CB (2003) Serotonin trasporter: a potential substrate in the biology of suicide. Neuropsychopharmacology 28, 613. Raymont V (2001) Suicide in schizophrenia: how can research influence training and clinical practice? Psychiatr. Bull. 25, 46. Reed J (2002) Delivering psychiatric care to prisoners: problems and solutions. Advan. Psychiatr. Treat. 8, 117. Reed J (2003) Mental health care in prisons. Br. J. Psychiatry 182, 287. Roy A, Segal NI, Centerwall BS, Robinette CD (1991) Suicide in twins. Arch. Gen. Psychiatry 48, 29. Rucci P, Frank E, Kostelnik B, Gagiolini A et al. (2002) Suicide attempts in patients with bipolar i disorder during acute and maintenance phases of intensive treatment with pharmacotherapy and adjunctive psychotherapy. Am. J. Psychiatry 159, 1160. Souery D, Oswald P, Linkowski P, Mendlewicz J (2003) Molecular genetics in the analysis of suicide. Ann. Med. 35, 191.


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Spivak B, Shabash E, Sheitman B et al. (2003) The effects of clozapine versus haloperidole on measures of impulsive aggression and suicidality in chronic schizophrenia patients: an open, nonrandomized, 6-month study. J. Clin. Psychiatry 64, 755. Tomassini C, Juel K, Holm NV et al. (2003) Risk of suicide in twins: 51 year follow up study. BMJ 327, 373. Turvey CL, Conwell Y, Jones MP et al. (2002) Risk factors for late-life suicide: a prospective, community-based study. Am. J. Geriatr. Psychiatry 10, 398. UK Government (1992) The Health of the Nation: A Strategy for Health in England. HMSO, London. Vythilingam M, Chen J, Bremner JD et al. (2003) Psychotic depression and mortality. Am. J. Psychiatry 160, 574. Walker BF (2003) Risk of suicide remains high fifteen years after deliberate self-harm. Evidence Based Ment. Health 6, 106. Wilkinson S, Taylor G, Templeton L et al. (2002) Admissions to hospital for deliberate self-harm in England 1995–2000: an analysis of hospital episode statistics. J. Public Health Med. 24, 179. World Health Organization (2001) The World Health Report 2001. Mental Health: New Understanding, New Hope. www.who.int/whr2001/2001/main/en/chapter2/002g.htm (accessed 22 December 2003). Wright JH, Beck AT (1994) Cognitive therapy. In: Hales RE, Yudofsky SC, Talbott JA (eds), Textbook of Psychiatry, 2nd edn. American Psychiatric Press, Washington, DC.

Uncommon psychiatric syndromes

12

DELUSIONAL MISIDENTIFICATION CAPGRAS’ SYNDROME (‘DELUSION OF DOUBLES’) CLINICAL FEATURES This is the belief that a person known to the patient has been replaced by an exact double. Usually the person implicated is a close relative, particularly spouse. This is not part of organic confusion, but repeated misidentification of a specific person or people. AETIOLOGY It is usually part of a paranoid disorder, particularly schizophrenic, but may be affective or as a primary delusional disorder. It could be the result of an ambivalent attitude to the person implicated. It may occur in the presence of organic brain disease, particularly frontal lobe dysfunction. MANAGEMENT Treat the underlying disorder; support the relative.

OTHER CONDITIONS

• • • • •

Fregoli’s syndrome – ‘ordinary’ people in the patient’s environment are ‘persecutors in disguise’; less common than Capgras’. Syndrome of intermetamorphosis: person A becomes person B, B becomes C, C becomes A, etc. Syndrome of subjective doubles – rare, but when it occurs it usually co-exists with Capgras’. The patient believes that doubles of him/herself exist. Lycanthropy – the belief that the patient has been transformed into an animal. Reduplicative paramnesia – the belief that two identical places exist. It is clearly associated with diffuse brain injury.

SUBTYPES OF DELUSION DISORDER

•

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Autoscopy – hallucination of oneself in a ‘near-death experience’. Is this a psychiatric disorder, a metaphysical experience or a neurophysiological dysfunction?

SUBTYPES OF DELUSION DISORDER When unassociated with any other secondary psychiatric or organic disorder, the primary condition is considered a subtype of delusional disorders (see Chapter 3).

DE CLÉRAMBAULT’S SYNDROME CLINICAL FEATURES This is the delusional belief that another person (the object), often of unattainably higher social status, loves the patient (the subject) intensely. The subject is usually female. There may be sudden onset of delusion. ‘Pure’ erotomania is an isolated phenomenon. ‘Secondary’ erotomania is much more common and occurs in the setting of paranoid, manic or other disorder. The subject may be importunate and disrupt the object’s life and, after rejection, the love may turn to hatred. AETIOLOGY If the ‘pure’ form, it may be projection of denied, narcissistic self-love. MANAGEMENT Treat the underlying disorder if secondary. It can be very resistant to physical treatments and psychotherapy if in the ‘pure’ form.

OTHELLO SYNDROME (‘MORBID JEALOUSY’) CLINICAL FEATURES This is the delusion of infidelity on the part of the sexual partner. Normal phenomena are interpreted to fit in with this conviction. The patient may examine underwear, sexual organs, etc., in an attempt to find proof. There is a desire to extract a confession, which may lead to severe aggression and murder. AETIOLOGY It may be associated with alcoholism (in a jealous, insecure personality), organic psychosis, schizophrenia (particularly paranoia) or with paranoid, obsessional personality. It might be a projection of the patient’s own desires for infidelity or of repressed homosexuality, or the result of other feelings of inadequacy. MANAGEMENT Treat the underlying condition. Antipsychotic medications may help. Geographical separation from the partner is often advisable.

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MONOSYMPTOMATIC HYPOCHONDRIACAL PSYCHOSIS (MUNRO, 1980) CLINICAL FEATURES Hypochondriacal delusions may take various forms; e.g. skin infestation by insects (Ekbom’s syndrome), internal parasitosis, delusion of lumps under the skin (leading to excoriation), conviction of personal ugliness or emission of foul smell, delusional body image disturbance, delusional pain. Some are coenaesthopathic states with exaggeration or distortion of subjective experience and sensation. The patient is convinced of the physical cause and gathers ‘evidence’ for this. Multiple opinions are sought and bizarre treatments are suggested by the patient. Increasing anger and paranoia may be expressed. The delusional system may remain ‘encapsulated’ for years, without general thought disorder or personality deterioration.

HYSTERIA – ALLIED SYNDROMES COUVADE SYNDROME CLINICAL FEATURES The husband (usually) develops extreme anxiety and various physical symptoms, as of pregnancy, when his wife is pregnant. He may have morning sickness, abdominal pains, constipation, food cravings, etc. It tends to present in the third or ninth month of the wife’s pregnancy. The name ‘couvade’ refers to the ancient ritual of the husband retiring to bed and simulating labour pains during the wife’s labour. AETIOLOGY This may be a manifestation of understandable anxiety in an anxious father-to-be. It could be expression of frustrated creativity, jealousy of attention paid to wife or over-identification with wife. MANAGEMENT Simple reassurance is usually adequate.

GANSER’S SYNDROME (‘SYNDROME OF APPROXIMATE ANSWERS’) This is classified in ICD-10 under ‘other dissociative disorders’; classified as dissociative disorder NOS in DSM-IV. CLINICAL FEATURES The patient gives approximate answers (absurdly wrong but almost correct, such as ‘a horse has five legs’), which are inconsistent. There may also be hysterical conversion symptoms (e.g. ataxia), dissociative amnesia (altered level of consciousness) and

HYSTERIA – ALLIED SYNDROMES

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occasionally pseudohallucinations. Onset is often sudden and related to stressful (or criminal) circumstances. AETIOLOGY There is an hysterical twilight state. Occasionally, it is post-epileptic or associated with depression. It may be similar to the ‘buffoonery state’ of acute or catatonic schizophrenia. MANAGEMENT The person usually recovers when the stressor is removed.

MULTIPLE PERSONALITY DISORDER (MERSKEY, 1992) This rare condition is now termed dissociative identity disorder. The patient has two or more distinct personalities. with dramatic changes from one personality to another. There is amnesia for existence and events during the other personality. There is a history of childhood sexual abuse in more than 70% of patients. Epilepsy was noted in 25 per cent in one study. There is a wide range of psychopathology (Ross et al., 1990). DIFFERENTIAL DIAGNOSIS Malingering; dissociative fugue; dissociative amnesia; schizophrenia. MANAGEMENT AND PROGNOSIS

• • • •

Thorough assessment, often forensic. Hypnotherapy and individual psychotherapy are used. Reintegration is the goal of therapy. Medication is of limited value.

Prognosis is poor and related to the number, type and chronicity of personalities. Earlier onset confers poor prognosis.

MÜNCHAUSEN SYNDROME This is classified under ‘other disorder of adult personality and behaviour’ in ICD-10. In DSM-IV it is factitious disorder. Symptoms are generated intentionally under voluntary will, motivated to assume the sick role, with absence of external incentives (economic gain, avoiding criminal prosecution, etc.). DSM-IV emphasizes whether there are predominantly psychological or physical symptoms, or both. CLINICAL FEATURES The patient gives plausible, often dramatic, history and symptoms of acute physical illness in the absence of that illness. He/she may inflict self-injury or simulate symptoms

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in a bizarre way (e.g. insert needles into chest, swallow blood, etc.). A common complaint is of abdominal symptoms. There is a history of multiple hospital admissions and multiple operations. Lying is pathological with a lack of personal rapport. Variants of the syndrome present with psychiatric symptoms or false bereavements. It may present with factitious illness in a child or dependent (Münchausen by proxy). AETIOLOGY There is hysterial behaviour in severely disordered personality. The person is masochistic, attention-seeking, and may seek analgesic drugs. MANAGEMENT Sufferers frequently abscond from psychiatric treatment. Occasionally there is a degree of treatable depression. There is a need to limit behaviour – keep a hospital registry of such patients.

FOLIE À DEUX (LASÉQUE AND FAIRET, 1877) Induced or shared psychosis – ICD-10, DSM-IV. CLINICAL FEATURES Usually one member of a couple is psychotic and the other comes to share the delusional beliefs. It may occur in families or groups (folie à plusieurs). Persecutory or hypochondriacal delusions may become shared by the submissive member of an overinvolved pair. There may not be evidence of this dominance and submission, however, and it may be difficult to decide which members are primarily psychotic. It most frequently occurs in a mother and daughter relationship. AETIOLOGY Often there is over-identification with the psychotic person in a submissive, overdependent personality. The person may have low IQ. MANAGEMENT Treat the psychotic member, if identifiable. Supportive and family therapy is often indicated. Psychosis will need treatment if is co-morbid and independent; i.e. folie simultanée.

DEPRESSION – ALLIED SYNDROME COTARD’S SYNDROME (‘NIHILISTIC DELUSIONS’) CLINICAL FEATURES There are delusions of negation, to a varying degree. The patient may believe that his/her body or self has disappeared and he/she no longer exists, even that the whole universe no longer exists. This occurs more commonly in women. Often it is associated


149

with anxiety and irritability. It may be associated with mutism, delusions of selfblame, hallucinations (e.g. of rotting smells), refusal to eat. AETIOLOGY It is frequently a depressive symptom, but may have a basis in organic brain disease (acute or chronic). Depersonalization is frequently the underlying phenomenon. Treat as per underlying condition.

REFERENCES AND FURTHER READING Asher R (1951) The Mü nchausen syndrome Lancet i, 339. Dorahy MJ, Lewis CA (2002) Dissociative identity disorder in Northern Ireland: a survey of attitudes and experience among clinical psychologists and psychiatrists. J. Nerv. Ment. Dis. 190, 707. Elmore JL (2000) Dissociative spectrum disorders in the primary care setting. Prim. Care Companion J. Clin. Psychiatry 2, 37. Eminson M, Postlethwaite RJ (2000) Münchausen Syndrome by Proxy Abuse: a Practical Approach. Butterworth–Heineman, Oxford. Enoch MD, Trethowan WH (1979) Uncommon Psychiatric Syndromes, 2nd edn. Wright, Bristol. Higland KB, Flume PA (2002) A ‘story’ of a woman with cystic fibrosis. Chest 121, 1704. Huntjens RJ, Postma A, Peters ML et al. (2003) Interidentity amnesia for neutral, episodic information in dissociative identity disorder. J. Abnorm. Psychol. 112, 290. Manschreck TC (1992) Delusional disorders. Psych. Ann. 22(5), 241–51. Mehta NJ, Khan IA (2002) Cardiac Mü nchausen syndrome. Chest 122, 1649. Mersky H (1992) The manufacture of personalities: the production of multiple personality disorder. Br. J. Psychiatry 160, 327. Munro A (1980) Monosymptomatic hypochondriacal psychosis. Br. J. Hosp. Med. 24, 34. O’Shea B (1984) Mü nchausen’s syndrome. Br. J. Hosp. Med. 31, 269. Ross CA, Miller SD, Reager P et al. (1990) Structured interview data on 102 cases of multiple personality disorder from four centers. Am. J. Psychiatry 147, 596. Shepherd M (1961) Morbid jealousy, some clinical and social aspects of a psychiatric syndrome. J. Ment. Sci. 107, 687. Spier SA (1992) Capgras’ syndrome and the delusions of misidentification. Psychiatr. Ann. 22, 279. Trethowan WH (1979) Uncommon psychiatric disorder. Br. J. Hosp. Med. 22, 490. Zylstra RG, Miller KE, Stephens WE (2000) Mü nchausen syndrome by proxy: a clinical vignette. Prim Care Companion J. Clin. Psychiatry 2, 42.

Organic psychiatry

13

DIFFERENTIAL DIAGNOSIS Stage 1: Organic or functional? • Functional causes: – Depressive pseudodementia. – Hysterical pseudodementia (including Ganser’s syndrome). – Schizophrenic disturbance. – Simulation (malingering). Stage 2: Acute or chronic? Features of acute organic disorder (delirium): – Acute onset. – Impaired consciousness. – Perceptual abnormalities. – Fluctuating course. • Features of chronic organic disorder (dementia): – Insidious onset. – Clear consciousness. – Global impairment of cerebral functions. – Steady, progressive course.

•

Stage 3: Focal or diffuse lesion? Stage 4: Precise aetiology.

DEMENTIA Dementia is a global, progressive deterioration of all mental functions (memory, language, recognition, intellect, and personality) occurring in clear consciousness.

LOCALIZATION OF CEREBRAL FUNCTION

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DIFFERENTIAL DIAGNOSIS OF DEMENTIA Clinical • Amnesic syndrome. • Dysphasic syndromes. • Parietal lobe syndrome. • Frontal lobe syndrome. • Subcortical dementias. • Pseudodementia. Aetiological Primary/degenerative • Alzheimer’s, Pick’s, Huntington’s, Creutzfeld–Jakob, frontal lobar, Lewy-body, Parkinson’s, multiple sclerosis, Wilson’s disease. Secondary Vascular – multi-infarct dementia, subarachnoid, subdural haematoma. Infective – abscess, encephalitis, neurosyphilis, AIDS, prion diseases, encephalopathies. • Traumatic – head injury, punch-drunk syndrome, haematoma. • Neoplastic – primary/secondary degree neoplasia, paraneo-plastic syndrome (especially CA bronchi). • Inflammatory – encephalopathies, SLE, cranial arteritis. • Metabolic – hepatic, renal, cardiac failure, anaemia, hypoglycaemia, vitamin deficiencies, metal toxicity. • Endocrine – hypothyroidism, hypo/hyper-parathyroid, Addison’s disease. • Hydrocephalus – normal-pressure or obstructive.

• •

LOCALIZATION OF CEREBRAL FUNCTION DYSFUNCTION OF FRONTAL LOBES Prefrontal and orbital cortex Personality changes include ‘pseudopsychopathic’ – disinhibition, facetious humour, euphoria (said to be related to orbitofrontal area). ‘Pseudodepressive’ changes include apathy, loss of initiative, slowing of thought and motor activity (said to be related to dorsolateral area). There can also be inattention, distractability, perseveration of actions (as seen in cardsorting tasks), difficulty in programming and planning behaviour (seen in Porteus Maze tasks) and urinary incontinence. Motor and premotor cortex Features are contralateral spastic paresis, reduced fine motor control, gegenhalten, grasp reflex, reduced verbal fluency, impaired spelling, motor Jacksonian and adversive attacks. Damage to Broca’s area (dominant premotor cortex) produces expressive dysphasia.

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DYSFUNCTION OF PARIETAL LOBES

• • • •

• •

Cortical sensory loss. Astereognosis. Sensory Jacksonian fits. Disorders of body schema: – Sensory inattention. – Constructional apraxia. – Dressing apraxia. – Topographical agnosia. – Hemisomatognosia, autotopagnosia. Anosognosia (denial of the disorders). If posterior dominant parietal lobe – Gerstmann’s syndrome: – Right–left disorientation. – Finger agnosia. – Dyscalculia. – Dysgraphia.

DYSFUNCTION OF TEMPORAL LOBES Auditory functions • Impaired auditory sensation – verbal (dominant), musical (non-dominant), auditory agnosia. • Sensory dysphasia (Wernicke’s area – dominant). Visual functions Contralateral, upper quadrant, homonymous hemianopia (optic radiation). Prosopagnosia (inability to recognize faces).

• •

Memory • Bilateral lesions – global amnesia with normal immediate recall (includes Korsakoff ’s psychosis). • Unilateral lesions – dominant: impaired verbal memory; non-dominant: impaired non-verbal (spatial) memory. Personality/psychosis Related to temporal lobe epilepsy. Dominant – ? schizophreniform. ? Emotional lability, aggressive behaviour. Reduced sexual activity usually. Klü ver–Bucy syndrome – extensive bitemporal lesions.

• • • • •

NEUROPSYCHIATRIC ASSESSMENT

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DYSFUNCTION OF OCCIPITAL LOBES There are visual impairments: cortical blindness (bilateral), contralateral homonymous hemianopia (unilateral), scotomata (focal), loss of visual perception, visual object agnosia, alexia without agraphia.

DYSFUNCTION OF DIENCEPHALON AND BRAINSTEM (‘THE BASAL SYNDROME’)

• • • •

Korsakoff-type amnesia. Hypersomnia. Emotional lability. Hypothalamus: – Polydipsia and polyuria. – Appetite disturbance. – Elevation of temperature.

OCCLUSION OF SPECIFIC ARTERIES Anterior cerebral • Contralateral lower-limb paresis and sensory deficits. • Clouding of consciousness. Middle cerebral Clouding of consciousness. Contralateral hemiplegia, hemianaesthesia and hemianopia. Motor and sensory aphasia if dominant.

• • •

Posterior cerebral As for middle cerebral. Contralateral hemianalgesia and spontaneous pain (thalamus).

• •

Posterior inferior cerebellar artery Ipsilateral – facial analgesia, Horner’s syndrome, ataxia, weakness of vocal cords and tongue. • Dissociated or contralateral analgesia.

•

Basilar artery Headache, vertigo, coma, flaccid quadriplegia or monoplegia, total anaesthesia, hyperpyrexia, ipsilateral cranial nerve palsies and cerebellar signs.

NEUROPSYCHIATRIC ASSESSMENT Assess Attention, memory, language, visuospatial functions, calculation, abstract thinking, handedness, facial asymmetry, abnormal movements, primitive reflexes (e.g. palmomental/grasp/snout reflexes), ‘soft signs’.

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‘Soft signs’: These include non-normative performance on a motor or sensory test identical or akin to a test item of the traditional neurological examination, but not associated with any localizable neurological disorder. They are related to cognitive dysfunction, learning difficulties and psychiatric disturbance, but are also frequently found in children without these problems. Include – synkinetic (mirror) movements, poor coordination, impaired constructional ability, speech impediments, hyperactive reflexes, impaired special senses. They are not always reliably detected. Best discriminators of dementia (especially from depression) Clinical • Tests of orientation. • Recalling an address after 5 minutes. • Sentence repetition (Babcock). • Tests of general information. • No evidence of depressed mood. The quality of answers is of prime importance. Look for: – Perseveration. – Confabulation. – Dysphasia – especially nominal dysphasia. History No history of depression.

•

Investigations Psychometry – verbal performance discrepancy. Sulcal widening on CT scan (and ventricular dilatation to a lesser extent). EEG abnormalities.

• • •

Depression/pseudodementia (also see Chapter 17) 8 per cent diagnosed as dementing later found to be depressed. 2.5 per cent diagnosed as depressed later found to be dementing.

• •

DELIRIUM Between 10 per cent and 30 per cent of all medical/surgical inpatients have had delirium. There is a higher prevalence in the elderly or seriously ill. Risk factors include increasing age, underlying dementia or physical illness. ICD-10 criteria for delirium 1 Impairment for consciousness and attention. 2 Global disturbance of cognition (perceptual-impaired disturbances, orientation, memory, comprehension). 3 Psychomotor disturbances (hypo- or hyper-activity). 4 Disturbance of sleep–wake cycle. 5 Emotional disturbances (anxiety, fear, depression, apathy, perplexity).

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Aetiology There are multifactorial aetiological mechanisms, but relative similarity of individual clinical pictures. Aetiology is undetermined in 5–20 per cent of the elderly delirious. Dementia coveys increased risk. Most common causes are CVA, UTI, diabetes, ischaemic heart disease, metabolic abnormalities, major organ failure, drug toxicity (prescribed or alcohol or illicit). There is significant mortality – up to 76 per cent of elderly, hospitalized delirious patients die during hospitalization. Management • Adequate investigation – history from staff, relatives. • Baseline laboratory tests, EEG, CT/MRI. • Treat underlying cause, if known. • Treat any (other) reversible component; e.g. infection, anaemia, dehydration. • Nurse in well-lit room, avoid under/overstimulation from environment. • Agitation – use lowest effective dosage of atypical antipsychotics.

THE DEMENTIAS Common dementias include (per cent of total cases):

• • • • •

Alzheimer’s disease – 50–70 per cent. Vascular dementia – 5–15 per cent. Alzheimer’s ⫹ vascular dementia – 10–15 per cent. Lewy-body dementia – 5–15 per cent. Other – ⬍10 per cent.

ALZHEIMER’S DISEASE (AD) This historically refers to presenile dementia before 65 years, but now also includes dementia after age 65. EPIDEMIOLOGY About 3 per cent of the population aged over 65 years have AD, 50 per cent over 85 years. Age is the most important risk factor for AD, but AD is not just a form of accelerated aging! There is a higher prevalence in females (2:1), even when controlled for greater longevity in females and increased CVA in males. AETIOLOGY See the diagram on page 156. Genetics • Trisomy 21 – There is an association between AD and Down syndrome. All develop the typical histopathological lesions of AD (amyloid plaques, neurofibrillary tangles before age 40 years).

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Unknown, probably multifactorial Proposed model (Blass, 1993): Environmental factors

Aging

Genetic abnormalities

Cytoskeletal abnormalities (neurofibrillary tangle, etc.)

Mitochondrial abnormalities

Amyloidosis

Impaired cellular homeostasis in response to stress

Loss of synaptic connections

Inflammatory reaction

Clinical syndrome

• • •

Chromosome 21 – Mutations are found in the gene encoding for ‘amyloid precursor protein’ (APP), seen in familial AD. Chromosome 14 – Early-onset AD. Chromosome 19 – Sporadic, late-onset AD.

Risk factors • Head trauma (some similarity in neuropathology findings in punch-drunk syndrome). • Low educational level. Neuropathology The ‘amyloid hypothesis’ Either increased amyloid ␤-peptide synthesis or decreased amyloid clearance in the brain results in aggregation of these peptides to form amyloid plaques (AP). APs are seen particularly in the outer three layers of cortex, but all layers are affected – hippocampus, parietal regions usually first affected. The deposition of these neuritic plaques precedes AD. The extent of APs correlates with severity of clinical illness, and are hypothesized to be the pathogenesis of AD. Apolipoprotein E (APOE) APOE is a cell membrane protein that transports cholesterol into the cell. Homozygotes for APOE 4 on chomosome 19 have a higher risk of AD than heterozygotes. APOE 4 is thought to increase the risk for AD by either increasing the sythesis of AP, or decreasing the clearance of amyloid ␤-peptides. Neurofibrillary tangles (NFTs) NFTs are intracellular hyperphosphorylated ␶ proteins that accumulate and form paired helical filaments. The extent of NFTs serves as a marker of severity of illness. Other abnormalities: • Glial proliferation. • Granulovascular degeneration – especially in hippocampus. • Hirano inclusion bodies.

THE DEMENTIAS

•

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Selective neuronal cell loss – early in hippocampal regions, nucleus basalis of Meynert; visuosensory and sensorimotor areas relatively spared until later. The loss of synapses correlates best with degree of cognitive impairment.

Neurochemistry Cholinergic loss Evidence includes:

• • • •

Reduced cholinergic neurotransmission in the cortex and hippocampus. Reduced cholinergic cells in nucleus basalis of Meynert, medial septum and diagonal band. Cholinergic deficit correlated with cognitive dysfunction. Correlations between cortical cholinergic reduction, basalis nucleus reduction and cortical plaque density.

Noradrenergic loss There is cell loss in locus coeruleus, especially in early-onset AD; correlates with depression in AD. Serotonergic loss There is loss in cortical 5-HT2 receptors, especially in frontal and temporal lobes. Cell loss and NFT accumulation also in nucleus raphe dorsalis. Other neurotransmitters/neuropeptides: • Decreased somatostatin. • Decreased GABA. • Decreased dopamine. OTHER ABNORMALITIES

• • •

Oxidative damage caused by accumulation of free radicals is implicated in AD – ? related to abnormal phosphorylation of ‘tau’. There is deficiency of mitochondrial ␣-ketoglutarate dehydrogenase complex or pyruvate dehydrogenate complex. Mitochondrial enzymatic systems – ? may explain decreased glucose utilization in AD brain.

Immunology Immunohistochemistry shows:

• • • •

Localized inflammatory reaction in AD. Complement in SPs. Neuroglial reaction to amyloid. Increased acute-phase reactants.

However, these are probably not primary events because there is little evidence for an autoimmune or infectious process. Classification of AD See Table 13.1. Features of Klü ver–Bucy syndrome (hyperorality, hypersexuality, placidity, increased touching) are seen in type I AD, reflecting bitemporal damage. CLINICAL FEATURES There is generally an insidious onset. Memory failure is usually the presenting feature, often accompanied by lability of mood, anxiety, depression or apathy, with impaired attention.

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Table 13.1 Type I and type II Alzheimer’s

Pathology Neurochemistry Clinical features

Type I

Type II

Later onset – SDAT ⫹ ⫹ Females ⬎ males

Early onset ⫹ ⫹ ⫹ (esp. frontal, temporal) ⫹⫹⫹ More rapid, fulminant More aphasia, myoclonus, increased genetic loading

Adapted from Roth (1986).

There may be abnormal, disinhibited behaviour, often an exaggeration of former personality traits. Agitation is a feature, especially at night. ‘Sundowning’ is confusion and wandering at night. There are generally three phases:

• • •

First phase – memory (2 years) predominantly affected. Second phase – general cognitive decline, development of expressive/receptive dysphoria, logoclonia, seizures, delusions, hallucinations. Third, terminal phase – profound dementia, neurological signs ↑↑, primitive reflexes ↑, double incontinence.

MANAGEMENT See Chapter 17. There should be a thorough initial assessment. Clarify the diagnosis, rule out any medical cause, treat all/any reversible component (e.g. hypoxia, mild heart failure, anaemia). Education Intensive family and psychosocial support is necessary. Psychotherapy Reality orientation, reminescence therapy are useful. Drug pharmacotherapy Acetylcholinesterase inhibitors target cognitive symptoms – memory and attention – and may delay but not alter disease progression. Commonly used drugs include donepezil, galantamine and rivastigmine. No clear evidence at present for superior efficacy between these drugs, but there may be advanages in dosing and tolerability. Drugs stabilize functioning in the first year and make subsequent decline more gradual. Uncertainty as to how early to start treatment and how long to continue. • NMDA receptor antagonists (e.g. memantine) slow the rate of cognitive and functional decline. • Experimental treatments include NSAIDs, oestrogen, statins, heavy metal chelators (may enhance amyloid clearance); amyloid vaccine is also under investigation. • Vitamin E and selegiline may delay but not alter disease progression. • Antipsychotics may be used to target behavioral symptoms and psychosis. • Antidepressants can be given for depressive symptoms.

•

Future treatments Research is under way involving vaccination with antibodies to amyloid ␤-peptide.

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PROGNOSIS Severity of cognitive impairment is a crude index of survival time. Deterioration to death is within 2–5 years of hospital admission.

MILD COGNITIVE IMPAIRMENT (MCI) The cognitive ability of the elderly naturally declines with age. The term MCI refers to a state between normal age-related cognitive decline and dementia. MCI is marked by objective evidence of memory deficits but with intact general cognitive and activity functioning. A significant proportion of individuals diagnosed with MCI will progress to Alzheimer’s disease – up to 36 per cent per year. More research is needed to ascertain whether MCI represents an early stage of AD. The rate of death for those diagnosed with MCI is about 1.7 times that of those without the diagnosis.

VASCULAR DEMENTIA (VaD) This is the most common form of dementia after Alzheimer’s disease. EPIDEMIOLOGY VaD represents 5–15 per cent of dementias. As with AD, prevalence increases with age. AETIOLOGY VaD is caused by either ischemic injury from embolic and or atherothrombotic vessel occlusions. An autosomal dominant gene on chromosome 19 conveys small vessel disease which results in VaD in 50 per cent of carriers. CLINICAL FEATURES There is acute onset with patchy, stepwise deterioration. There is fluctuating cognitive impairment with episodes of nocturnal confusion. Depression and ‘emotional incontinence’ may be prominent. Personality is often preserved until late, and insight is often intact. Focal neurological deficits are common, and hypertension is present in most cases. Frequently, there is evidence of arteriosclerosis elsewhere. The Hatchinski index (using the above clinical features) may give a diagnostically indicative score. Binswanger’s chronic progressive subcortical encephalopathy with white matter degeneration may be caused by arteriosclerosis. TREATMENT AND PROGNOSIS Treatment is similar to that for AD, but additional importance is placed on controlling the risk factors for coronary artery disease and stroke. There is a slightly longer time course than with AD. Death occurs in 4–5 years; 50 per cent of deaths result from ischaemic heart disease.

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ORGANIC PSYCHIATRY

PICK’S DISEASE EPIDEMIOLOGY The peak age of onset is 40–60 years, and it is most common in men. It accounts for about 5 per cent of dementias. AETIOLOGY A minority of cases are due to an autosomal dominant gene with variable penetrance. Pathology • Frontal and temporal lobes are particularly affected. • ‘Knife-blade’ atrophy is seen due to neuronal loss. • Pick’s cells are present. These are swollen cells with silver-staining inclusion bodies (‘balloon cells’). • Fibrous gliosis is present. • SPs or NFTs are absent. CLINICAL FEATURES Personality deterioration occurs early, with a ‘frontal lobe’ syndrome of disinhibition. Perseveration and dysphasia are characteristic. There is a less generalized cognitive decline than in AD. Hyperalgesia is experienced late in illness in some patients. PROGNOSIS There is a slower time-course than in Alzheimer’s disease, being 2–10 years to death. The average is 5 years from diagnosis.

HUNTINGTON’S CHOREA EPIDEMIOLOGY The prevalence is 2–10 cases per 100 000 population. The age at onset is usually 25–50 years. AETIOLOGY

• • • •

There is a single autosomal dominant gene on chromosome 4 with almost 100 per cent penetrance. The gene is located on proximal arm of chromosome 4 (Gusella et al., 1993). There is selective loss of GABA neurones, particularly in basal ganglia. GABA and glutamic acid decarboxylase have been shown to be reduced, resulting in dopamine hypersensitivity. Glutamate excitotoxicity a possible mechanism?

Pathology There is atrophy of caudate and putamen in particular, but also of cortex (especially frontal).

THE DEMENTIAS

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CLINICAL FEATURES

• • • • • • • • • •

May present with chorea or with mental changes. Often they develop independently. Psychiatric illness may precede chorea. Personality change is often realized retrospectively. Characteristically the person becomes irritable, distractable, apathetic and depressed. Psychotic disorders, particularly a paranoid psychosis, may develop. Insidious onset of global dementia may develop. Chorea, initially of face and upper limbs, may develop. There may also be intention tremor, ataxic gait, dysarthria and rigidity. In children, rigidity, tremor and fits are more common and there is more rapid deterioration. There is a high rate of suicide among (unaffected) relatives. CT/MRI – show dilated ventricles, caudate atrophy. PET/SPECT – show frontal and basal ganglia hypometabolism. EEG – ‘flat’.

PROGNOSIS In adults, death occurs within 13–16 years; within 8 years in children.

CREUTZFELDT–JAKOB DISEASE (CJD) EPIDEMIOLOGY CJD is rare and occurs equally in males and females. Onset is usually within the range 50 to 70 years of age for the sporadic form; the average is 30 years with the variant form (vCJD) – thought to be an animal crossover from eating beef from cows infected with bovine spongiform encephalopathy. Sporadic CJD accounts for 80–85 per cent of cases; inherited form, 5 per cent; iatrogenic form, 5 per cent; other forms, 5–10 per cent. AETIOLOGY It is a prion disorder – neurodegenerative infective protein pathogens which are encoded on human chromosome 20. It also appears as an inherited autosomal dominant form. Disease may be transmitted iatrogenically from infected CNS stereotactic needles, or corneal transplant. Pathology There is spongiform, neuronal degeneration with astrocytic glial proliferation. CLINICAL FEATURES

• • • •

Personality change, apathy, depression, anxiety, fatigue, withdrawal, slowness, memory loss, organic psychosis. Seizures, myoclonic jerks, cortical blindness. CT/MRI – cortical atrophy, worse frontally. Abnormal EEG in 90 per cent – periodic triphasic complexes seen in CJD but not vCJD.

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PROGNOSIS CJD is rapidly progressive over 6 months to 2 years.

FRONTAL LOBE DEMENTIA This is a ‘spongiform’ disease predominantly affecting frontal lobe, producing characteristic frontal lobe syndrome. The EEG is normal. There is a family history in 50 per cent of cases.

LEWY-BODY DEMENTIA This is a recently described dementia which may be the second most common. It is characterized by confusional states, fluctuating cognitive impairment, psychotic symptoms (hallucinations, delusions, depression), mild/variable short-term memory loss, some mild extrapyramidal features or extreme sensitivity to EPS effects with neuroleptic treatment. The pathological hallmark is the Lewy-body (LB) – intracellular inclusion bodies of ubiquitin, ␶ protein, and other proteins. LBs are classically seen in Parkinson’s disease, especially in substantia nigra. They are also seen cortically and subcortically in LB dementia, especially in hippocampus.

HYDROCEPHALUS Types 1 Non-obstructive and communicating – secondary to brain atrophy 2 Obstructive and non-communicating – secondary to obstruction of CSF flow within the ventricular system. 3 Obstructive and communicating (‘normal pressure hydrocephalus’) – secondary to obstruction of CSF flow in the subarachnoid space or failure of normal absorption. Fifty per cent of cases may be due to subarachnoid haemorrhage, meningitis, head injury. CLINICAL FEATURES

• • • •

Memory impairment. Slowness and apathy. Unsteady gait. Incontinence.

MANAGEMENT AND PROGNOSIS Ventriculo-atrial shunt to lower the intraventricular pressure may help. The prognosis is best in idiopathic disease, especially when the duration of illness is short.

VITAMIN DEFICIENCIES

163

SUBCORTICAL DEMENTIA Initially described in progressive supranuclear palsy (Steele–Richardson–Olszewski syndrome), this is now recognized in other dementing processes (e.g. Parkinson’s disease, Huntington’s chorea). CLINICAL FEATURES

• • • •

Forgetfulness. Slowing of thought processes – delayed answers (‘bradyphrenia’). Personality change – apathy, irritability, depression. Decreased ability to manipulate acquired knowledge.

MANAGEMENT AND PROGNOSIS

• •

No specific treatment. Very gradual deterioration.

PUNCH-DRUNK SYNDROME This is usually the result of repeated mild head injuries (e.g. in boxers). There is cerebral atrophy with brain stem and hippocampal–limbic damage. CLINICAL FEATURES

• • • •

Cerebellar lesions – ataxia, festinant gait. Pyramidal lesions – spasticity. Extrapyramidal lesions – tremor. Intellectual and personality deterioration.

VITAMIN DEFICIENCIES NICOTINIC ACID DEFICIENCY (PELLAGRA)

• • •

‘Dermatitis, dementia and diarrhoea.’ May be florid confusion with hallucinations. May appear ‘hysterical’.

THIAMINE (B1) DEFICIENCY Wernicke’s encephalopathy • Acute onset of: – Ophthalmoplegia and nystagmus. – Clouding of consciousness. – Ataxia. – Peripheral neuropathy. In 84 per cent of cases this results in Korsakoff ’s psychosis.

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AETIOLOGY

•

•

Korsakoff ’s psychosis: – Thiamine deficiency. – Head injury. – Carbon monoxide (CO) poisoning. – Tumour. – Anaesthetic accident. Thiamine deficiency: – Alcoholism. – Starvation. – Hyperemesis.

Pathology Parenchymal loss. Proliferation of blood vessels. Petechial haemorrhages.

• • •

Table 13.2 Psychiatric aspects of endocrine disorders Condition

Clinical features

Cushing’s syndrome

Psychiatric features in 50 per cent Depression Acute anxiety Paranoid features Euphoria – particularly when on steroids Restlessness and agitation May present as ‘agitated depression’ or ‘anxiety neurosis’ Rarely delirium Very rarely functional psychosis Fatigue Apathy Psychomotor retardation, rarely organic psychosis ‘Myxoedematous madness’ (Asher, 1949) Slowing of cognitive functions Psychiatric features are frequently present Depression Apathy Mild cognitive impairment Impotence Paroxysms of anxiety, tachycardia, sweating, headache, hypotension Depression Apathy Irritability Cognitive impairment Rarely delirium and coma Fatigue Depression Occasionally cognitive impairment Delirium Cognitive impairment Agitation and depression Epilepsy

Hyperthyroidism

Hypothyroidism

Addison’s disease

Phaeochromocytoma Hypopituitarism

Hyperparathyroidism

Hypoparathyroidism

DRUGS AND TOXINS

•

Affecting walls of third ventricle, mamillary bodies, thalamus (medial–dorsal nucleus).

CLINICAL FEATURES

• • •

Very poor retention of recent memories, sometimes with confabulation. Retrograde amnesia. Apathy or euphoria.

VITAMIN B12 DEFICIENCY Clinical features are:

• • • •

165

Depression and apathy. Dementia. Subacute combined degeneration of the cord. Pernicious anaemia.

ENDOCRINE DISORDERS (PSYCHIATRIC ASPECTS) See Table 13.2.

DRUGS AND TOXINS Table 13.3 Drugs causing toxic confusion Anticholinergics Isoniazid Cycloserine Mecamylamine Bromides Almost all psychotropics in the elderly

Table 13.4 Toxins Alcohol – see Chapter 9 Metals: Lead – Gastrointestinal disturbance – Peripheral motor neuropathy – Acute and chronic organic psychosis Mercury – Coarse tremor – Erythism (nervous, timid, irritable) Manganese – Headaches – Emotional lability – Impotence – Parkinsonism – Delirium

Amphetamines Hallucinogens Corticosteroids Barbiturates Digoxin

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INFECTIONS NEUROSYPHILIS SHOWING CSF CHANGES

• •

•

•

• •

Many are asymptomatic. There is up to 10 per cent occurrence rate in untreated cases of syphilis. Increasing incidence is seen in individuals with HIV infection. Meningovascular: – Usually 1–5 years after primary infection. – Inflammation and exudate from leptomeninges. – Arteritis. – Headache, malaise. – Lethargy, irritability. – Delirium and/or dementia. – Cranial nerve disturbance – optic nerve, 8th nerve. Tabes dorsalis: – Usually 8–12 years after primary infection. – Atrophy of dorsal roots and posterior columns. – Lightning pains. – Degenerative joint disease. – Ataxia due to proprioceptive loss. – Paraesthesias of limbs. – Argyll–Robertson pupils. – 20 per cent of general paresis cases have tabes. General paresis (GPI): – Usually 5–25 years after primary infection. – Spirochaetes found in the brain. – Thickened dura, atrophied brain. – Inflammatory changes – perivascular lymphocytes and plasma cells. – Degenerative changes with cortical thinning. – Neurological proliferation with ‘rod cells’. – Insidious onset, though 50 per cent present abruptly. Personality changes – irritable, emotionally labile, frontal lobe changes, impaired insight. Cognitive changes – poor concentration, dementia.

CLASSIC PICTURES

• • • •

Simple dementing – 20–40 per cent. Depressive – 25 per cent. Grandiose – 10 per cent. Also seen: – Manic elation. – Paranoid schizophreniform. – Neuraesthenia.

Treatment Penicillin is the only proven effective treatment.

INFECTIONS

167

HERPES SIMPLEX ENCEPHALITIS Onset is rapid. There are severe inflammatory changes which may be necrotizing and haemorrhagic. Infection especially affects medial temporal and orbital regions. The viral aetiology of this disorder may also imply latent infection in other psychiatric disorders. CLINICAL FEATURES

• • •

Pyrexia. Focal signs (temporal lobe). Delirium, often with marked hallucinations.

PROGNOSIS In 15 per cent there are severe sequelae – dementia, focal deficits, amnesic syndrome. Seventy per cent of cases are fatal.

OTHER INFECTIONS/PSYCHIATRIC SEQUELAE

• • • • •

Typhus. Trypanosomiasis (sleeping sickness). Cerebral malaria (Plasmodium falciparum, malignant tertiary malaria). Encephalitis lethargy – delirium followed by fatigue, parkinsonism, personality change. Acute disseminated encephalomyelitis.

NEUROPSYCHIATRY OF ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) AETIOLOGY This is multifactorial

• • • • •

Cytopathic effects of virus on CNS (e.g. AIDS dementia). Secondary to CNS infection. Secondary to systemic illness/metabolic derangement. Secondary/exacerbation of pre-existing mental co-morbid illness (e.g. substance abuse, depression). Secondary to psychosocial stressors (stigma, withdrawal of social support, financial insecurity).

AIDS dementia complex (ADC) This is the most common neuropsychiatric complication of human immunodeficiency virus (HIV) infection and can occur before AIDS develops. It is associated with initially poor concentration, mental and motor slowing, apathy – subcortical dementia features; later, profound dementia, frontal release signs. In the early stages it is difficult to detect cognitive impairment on neuropsychological testing.

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ORGANIC PSYCHIATRY

MRI shows subcortical involvement, widespread changes in cortical grey and white matter and possibly vacuolation in the spinal cord. Post-mortem studies have shown:

• • •

An encephalitic process. HIV-infected multinucleated giant cells and endothelial cells. Decreased neuronal density.

Psychosis This may be paranoid, schizophrenia-like, affective-like, organic psychosis (CNS involvement, opportunistic infection, CNS lymphoma, zidovudine or other medication-related). Affective disorder There were reports of major depression and of mania which appeared secondary to HIV infection; this responded to zidovudine treatment. Many symptoms of depression overlap with clinical features of AIDS itself. Depression also is a grief reaction. Suicide is 66 times more common than in the general population (Marzuk et al., 1988). Adjustment disorders The most prominent adjustment disorders are anxiety and depression. Worries concern illness progression, impact on family and friends, social status, and work. MANAGEMENT

•

•

• •

Full evaluation: – Immunology (CD4 count is best marker in illness progression). – Neuropsychological tests. – Neuroimaging. – CSF, biochemistry. – Full psychiatric and psychosocial evaluation. Psychosocial: – Education. – Supportive psychotherapy. – Counselling. – Information for patient and family about illness before cognitive deficits appear. – Mobilize family and financial support. Medical: – Treat infection, metabolic derangements, dehydration, drug toxicity. Pharmacological: – ‘Highly active anti-retroviral therapy’ (HAART) has improved survival following diagnosis of ADC. – Zidovudine (AZT) partially ameliorates cognitive deficits. – Antidepressants – use lower doses, agents with less anticholinergic toxicity. – Neuroleptics – atypical antipsychotics for hallucinations/delusions. – Psychostimulants – methylphenidate is worthy of consideration with psychomotor retardation. – Lithium – used in some HIV-mania cases, also helpful in leucopenia secondary to AZT. – ECT – if no response to mood stabilizers or antidepressants.

METABOLIC DISORDERS (PSYCHIATRIC ASPECTS)

169

METABOLIC DISORDERS (PSYCHIATRIC ASPECTS) HEPATIC FAILURE This may present with psychiatric disturbance. Exacerbations and remissions are typical. Non-specific EEG changes are often an early sign; triphasic waves are seen later. CLINICAL FEATURES

• • • • •

Delirium, confusion, irrational and uninhibited behaviour. Hypersomnia, coma. Labile mood. Memory impairment. Neurological abnormalities.

URAEMIA There may be a progressive but fluctuating course. CLINICAL FEATURES

• • • • • •

Memory impairment. Malaise, fatigue, drowsiness. Depression. Occasionally functional psychosis. Acute delirium in 30 per cent. Seizures in 30 per cent.

ELECTROLYTE DISTURBANCE

• • • •

Sodium depletion – weakness, giddiness, lassitude, nausea, muscle cramps. Potassium depletion – depression, malaise, sleep disturbance. Hyper- and hypo-calcaemia. Hypomagnesaemia.

ACUTE INTERMITTENT PORPHYRIA There is dominant autosomal inheritance with variable penetrance. Metabolic error of haem breakdown leads to porphobilinogen in the urine. It may be a response to barbiturates, alcohol, methyldopa or oral contraceptives. CLINICAL FEATURES

• • •

Abdominal – colicky pain, vomiting, constipation. Neurological – peripheral neuropathy, bulbar palsies, epilepsy. Psychiatric: – Delirium in 50 per cent, depression and emotional lability. – Psychosis, especially paranoid. – ‘Hysteria’ – may be diagnosed.

170

• • • • • • •

ORGANIC PSYCHIATRY

Skin changes, renal involvements, arthritis. Cerebral SLE in 60 per cent. Transient, fluctuating mental disturbance. Acute organic reaction is commonest; chronic organic reaction is sometimes seen. Depressive psychosis is less often seen. Schizophreniform psychosis is rare. Neurotic reactions are frequent.

MULTIPLE SCLEROSIS Psychiatric illness may antedate neurological symptoms. • Depression – reactive, drug-related (steroids)? intrinsic? • Schizophreniform psychosis. • Mania/euphoria – related to cognitive impairment. • Dementia.

SEQUELAE OF HEAD INJURY Injury may be focal (haemorrhage, infarct, contusion) or diffuse (diffuse axonal injury; DAI): 1 Primary (at time of impact). 2 Secondary (oedema, hypoxia, increased intracranial pressure). Prognosis is worsened by:

• • •

Long post-traumatic amnesia (see below). Penetrating injury. Intracranial bleeding.

Impaired consciousness Long duration of impaired consciousness suggests a poor prognosis. If longer than 1 month:

• •

40 per cent die without regaining consciousness. 20 per cent return to work.

Retrograde amnesia Retrograde amnesia covers the period between injury and the last clear memory from before the injury. Initially, the period is lengthy but it shrinks over time. The final duration is often less than 1 minute. This is not a good prognostic indicator. Post-traumatic amnesia (PTA) (anterograde amnesia) Anterograde amnesia covers the period between injury and recovery of normal, continuous memory after the injury. There may be ‘islands’ of memory before this full recovery. PTA is a good prognostic indicator. Duration is related to:

• • •

Neurological sequelae. Psychiatric sequelae. Time off work.

SEQUELAE OF HEAD INJURY

171

A duration of less than 12 hours suggests probable full recovery; more than 48 hours – probably some residual damage.

PSYCHIATRIC SEQUELAE OF HEAD INJURY AETIOLOGICAL FACTORS

• • • • • • • • •

Amount of brain damage – correlates closely with sequelae. Location of brain damage – especially left temporal lobe. Development of epilepsy – 5 per cent of closed injuries; 30 per cent of penetrating injuries. Premorbid personality. Family history of psychiatric disorder. Past history of psychiatric disorder. Emotional factors and the ‘meaning’ of the injury to the patient. Insecure convalescent environment. Compensation and litigation factors.

CLASSIFICATION Neuroses (‘post-concussional syndrome’) Neuroses are the commonest psychiatric sequelae (11–22 per cent of severe injuries) and are often underestimated.

• • • • • • •

Mild depression. Fatigue – frequently self-limiting but may not disappear for 1 year. Anxiety, phobias, hypochondriasis. Irritability and sensitivity to noise. Somatic complaints – headache, dizziness, impotence. Hysterical symptoms. Loss of sexual interest.

Personality changes These are common (6–18 per cent of severe injuries).

• •

Injuries with brain damage: – As part of dementia. – Due to frontal lobe damage. – As reduced control over aggression. Injuries without brain damage: – Usually an exaggeration of previous traits.

Psychoses These occur in 5–8 per cent of severe injuries.

•

Affective: – Usually depressive psychosis. – Associated with right hemisphere and frontal damage.

172

• •

ORGANIC PSYCHIATRY

Schizophreniform: – Especially paranoid, may be with morbid jealousy. – Rarely show ‘process’ schizophrenia. Associated with temporal lobe damage.

Cognitive impairment This occurs in 3 per cent of severe injuries. It is more likely with:

• • • • •

Long post-traumatic amnesia. Left parietal or left temporal lobe damage. Penetrating injury. Haemorrhage or infection. Increasing age. Recovery may progress over 10 or more years.

MEDICO-LEGAL ASPECTS OF HEAD INJURY The ‘compensation issue’ is more likely to contribute to disability when:

• • • •

The patient feels someone else is at fault. It is an industrial injury. Financial compensation is possible. The patient has low social status and/or is male.

Attitudes towards ‘compensation neurosis’ have recently altered. Symptoms may persist independently of compensation issues and disability is often underestimated. Compensation will depend on: 1 Degree of disablement. 2 Likely prognosis for quality of life. 3 Relationship between injury and disability: – Degree attributable to brain damage. – Degree attributable to psychic trauma of the accident. – Degree attributable to mere manipulation.

REFERENCES AND FURTHER READING Bennett DA, Wilson RS, Schneider JA et al. (2002) Natural history of mild cognitive impairment in older persons. Neurology 59, 18. Bouman WP, Pinner G (2002) Use of atypical antipsychotic drugs in old age psychiatry. Adv. Psychiatr. Treat. 8, 49. Bullock R, Hammond G (2003) Realistic expectations: the management of severe Alzheimer disease. Alzheimer Dis. Assoc. Disord. 17, s80. Burns A, Dening T, Baldwin R (2001) Care of older people: mental health problems. BMJ 322, 789. Butler R, Fleminger S (2001) Creutzfeldt–Jacob disease and its implications for psychiatric management. Adv. Psychiatr. Treat. 7, 50. Clifford DB (2002) AIDS dementia. Med. Clin. North Am. 86, 537. Coffey CE, Cummings JL (1994) Textbook of Geriatric Neuropsychiatry. American Psychiatric Press, Washington, DC.


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Cohen-Mansfield J (2001) Nonpharmacologic interventions for inappropriate behaviors in dementia. Am. J. Geriatr. Psychiatry 9, 361. Copeland JRM, Davidson IA, Dewey ME et al. (1992) Alzheimer’s disease, other dementias, depression and pseudodementia: prevalence, incidence and three year outcome in Liverpool. Br. J. Psychiatry 161, 230. Cummings JL (1985) Organic delusions: phenomenology, anatomical correlations and review. Br. J. Psychiatry 146, 184. Cummings JL (1986) Subcortical dementia: neuropsychology, neuropsychiatry and pathophysiology. Br. J. Psychiatry 149, 682. DeLaGarza VW (2003) Pharmacologic treatment of Alzheimer’s disease: an update. Am. Fam. Physician 68, 1365. DiCarlo A, Baldereschi M, Amaducci L et al. (2002) The ILSA Working Group. Incidence of dementia, Alzheimer’s disease, and vascular dementia in Italy: the ILSA Study. J. Am. Geriatr. Soc. 50, 41. Dik MG, Jonker C, Comijs HC et al. (2001) Memory complaints and APOE-4 accelerate cognitive decline in cognitively normal elderly. Neurology 57, 217. Doody RS, Stevens JC, Beck C et al. (2002) Practice parameter: management of dementia (an evidence-based review). Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 56, 1154. Dore GJ, McDonald A, Li Y et al. (2003) Marked improvement in survival following AIDS dementia complex in the era of highly active antiretroviral therapy. AIDS 17, 1539. Ely EW, Margolin R, Francis J et al. (2001) Evaluation of delirium in critically ill patients: validation of the Confusion Assessment Method for the Intensive Care Unit (CAM-ICU). Crit. Care Med. 29, 1370. Ely E, Stephens RK, Jackson JC et al. (2004) Current opinions regarding the importance, diagnosis, and management of delirium in the intensive care unit: a survey of 912 healthcare professionals. Crit. Care Med. 32, 106. Fassbender K, Stroick M, Bertsch T et al. (2002) Effects of statins on human cerebral cholesterol metabolism and secretion of Alzheimer amyloid peptide. Neurology 59, 1257. Ferris SH, Yan B (2003) Differential diagnosis and clinical assessment of patients with severe Alzheimer disease. Alzheimer Dis. Assoc. Disord. 17, s93. Francis PT, Palmer AM, Snappe M et al. (1999) The cholinergic hypothesis of Alzheimer’s disease: a review of progress. J. Neurol. Neurosurg. Psychiatry 66, 137. Gleason OC (2003) Delirium. Am. Fam. Physician 67, 1027. Gusella JF, MacDonald ME, Ambrose CM et al. (1993) Molecular genetics of Huntington’s Disease. Arch. Neurol. 50, 1157. Hardy J, Selkoe DH (2002) The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science 297, 353. Hedera P, Turner RS (2002) Inherited dementias. Neurol. Clin. 20, 779. Holtzman DM, Bales KR, Tenkova T et al. (2000) Apolipoprotein E isoform-dependent amyloid deposition and neuritic degereration in a mouse model of Alzheimer’s disease. Proc. Natl. Acad. Sci. USA 97, 2892. Kazui H, Mori E, Hashimoto M et al. (2000) Impact of emotion on memory: controlled study of the influence of emotionally charged material on declarative memory in Alzheimer’s disease. Br. J. Psychiatry 177, 343. Kerwin R (2003) Preventing suicide. Br. J. Psychiatry 182, 366. Kivipelto M, Helkala EL, Hanninen T et al. (2001) Midlife vascular risk factors and late-life mild cognitive impairment: a population-based study. Neurology 56, 1683. Koponen S, Taiminen T et al. (2002) Axis I and II psychiatric disorders after traumatic brain injury: a 30-year follow-up study. Am. J. Psychiatry 159, 1315. Leverenz JB, McKeith IG (2002) Dementia with Lewy bodies. Med. Clin. North Am. 86, 519. Lovestone S, Phipot M, Connell J (2002) Genetics, molecular biology, neuropathology and phenotype of frontal lobe dementia: a case history. Br. J. Psychiatry 180, 455.

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Marzuk PM, Tierney H, Tardiff K et al. (1988) Increased risk of suicide in persons with AIDS. JAMA 259, 1333. Mayou R, Bryant B (2002) Psychiatry of whiplash neck injury. Br. J. Psychiatry 180, 441. McKeith IG (2002) Dementia with Lewy bodies. Br. J. Psychiatry 180, 144. Misra S, Ganzini L (2003) Delirium, depression, and anxiety. Crit. Care Clin. 19, 771. Morris JC, Storandt M, Miller P et al. (2001) Mild cognitive impairment represents early-stage Alzheimer’s disease. Arch. Neurol. 58, 397. O’Brien JT, Erkinjuntti T, Reisberg B et al. (2003) Vascular cognitive impairment. Lancet Neurol. 2, 89. Pisani MA, McNicoll L, Inouye SK (2003) Cognitive impairment in the intensive care unit. Clin. Chest. Med. 24, 727. Romain GC (2002) Vascular dementia revisited: diagnosis, pathogenesis, treatment, and prevention. Med. Clin. North Am. 86, 477. Rosenburg RN (2000) Wartenberg Lecture. The molecular and genetic basis of AD: the end of the beginning. Neurology 54, 2045. Roth M (1986) The association of clinical and neurobiological findings and its bearing on the classification and aetiology of Alzheimer’s disease. Br. Med. Bull. 42(1), 42. Schupf N, Sergievsky GH (2002) Genetic and host factors for dementia in Down’s syndrome. Br. J. Psychiatry 180, 405. Sharma N, Standaert DG (2002) Inherited movement disorders. Neurol. Clin. 20, 759. Shumaker SA, Legault C, Rapp SR et al. (2003) Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women. The Women’s Health Initiative memory study: a randomized controlled trial. JAMA 289, 2651. Skegg K (1993) Multiple sclerosis presenting as a pure psychiatric disorder. Psychol. Med. 23, 909. Skuster DZ, Digre KB, Corbett JJ (1992) Neurologic conditions presenting as psychiatric disorders. Psychiatr. Clin. North Am. 15, 311. St George-Hyslop PH, Haines JL, Ferrer LA et al. (1990) Genetic linkage studies suggest that Alzheimer’s disease is not a single homogeneous disorder: FAD Collaborative Study Group. Nature 347, 194. Stanton LR, Coetzee RH (2004) Down’s syndrome and dementia. Adv. Psychiatr. Treat. 10, 50. Stevens T, Livingston G, Kitchen G et al. (2002) Islington study of dementia in the community. Br. J. Psychiatry 180, 270. Stevens T, Livingston G, Kitchen G et al. (2002) Islington study of dementia subtypes in the community. Br. J. Psychiatry 180, 270. Sy MS, Gambetti P, Wong B (2002) Human prion disease. Med. Clin. North Am. 86, 551. Terry RD, Masliah E, Salmon DP et al. (1991) Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann. Neurol. 30, 572.

Psychiatric aspects of epilepsy and sleep disorders

14

EPILEPSY Epilepsy is a term used to describe a persistent neurological condition characterized by sudden, discrete and recurrent abnormalities in electrical activity (seizures) of the brain resulting in behavioural, motor or sensory changes or changes in consciousness. CLASSIFICATIONS Classification may be according to:

• • •

Symptoms and signs of the seizure. Anatomical and electrophysiological evidence of the source of the seizure. Aetiology or precipitant of seizures.

Classification of seizure type is more straightforward than classification of ‘the epilepsies’. International league against epilepsy classification 1 Partial (focal) seizures (beginning locally in one hemisphere) a. Simple partial seizures (consciousness not impaired). i. With motor signs (‘Jacksonian’). ii. With somatosensory or special sensory symptoms. iii. With autonomic symptoms. iv. With psychic symptoms (e.g. perceptual or mood changes). b. Complex partial seizures (with impaired consciousness). i. Beginning as simple partial (‘aura’) and progressing to impaired consciousness. ii. With impaired consciousness at onset – either alone or with automatisms (‘psychomotor seizures’). c. Partial seizures secondarily generalized (to tonic–clonic). 2 Generalized seizures (begin bilaterally symmetrical, no local onset) a. Absence seizures (‘petit mal’). Atypical absence seizures (‘petit mal variant’).

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PSYCHIATRIC ASPECTS OF EPILEPSY AND SLEEP DISORDERS

b. Myoclonic seizures. c. Clonic seizures. d. Tonic seizures. e. Tonic–clonic seizures (‘grand mal’). f. Atonic seizures (‘drop attacks’). 3 Unclassified seizures. EPIDEMIOLOGY

• • • • •

Lifetime prevalence – About 10 per cent of the population will experience at least one seizure in their lifetime. About 3–4 per cent will develop epilepsy. Prevalence of active epilepsy is 5 per 1000. It is more prevalent in males; M:F ⫽ 1.5:1. Highest incidence is in young children and the elderly. Estimated 29 per cent of people with epilepsy overall show conspicuous psychological problems (50 per cent if temporal lobe epilepsy).

Age at onset 0–10 years – 30 per cent. 11–20 years – 25 per cent. 21–30 years – 20 per cent.

• • •

Seizure type Partial – 60 per cent (mostly complex, 90 per cent arising in temporal lobes). Generalized – 35 per cent. Mixed – 13 per cent.

• • •

AETIOLOGY

• • • •

Post-traumatic – 7 per cent. Cerebrovascular – 9 per cent. Other – 9 per cent. Unknown – 75 per cent.

PROGNOSIS Eighty per cent of those having a first seizure will have further seizures. Fifty per cent of those will have 10 or fewer seizures, usually as a short burst over a few months. If free for 5 years on medication, they have 30 per cent chance of having further fits if medication is stopped. There is an increased risk of death due to accidents, especially drowning. The risk of unexplained sudden death is 20 times greater than that of the general population. GENETIC COUNSELLING The recurrent risk is 1 in 25 if one parent has had epilepsy, 1 in 10 if parent and grandparent do. Certain epilepsies have a strong genetic component (e.g. juvenile myoclonic epilepsy).

EPILEPSY

177

FEATURES AND DIAGNOSIS PREICTAL PHASE

• •

Prodromal features: – Irritability, tension, insomnia, restlessness, occasionally suicidal depression. – May occur days or hours before fit. Aura: – Usually precedes a fit by only a few seconds, and lasts a few seconds – acute perceptual change, depersonalization, acute mood change, etc. – In itself a focal fit, reflecting abnormal electrical discharge. – Indicates focal disturbance in cerebral cortex. – Temporal lobe aura typically a rising epigastric feeling; déjàvu.

ICTAL PHASE: AUTOMATISMS The commonest source is temporal lobe structures – may also be frontal parietal, uncal or cingulate. There is a state of clouded consciousness which occurs during or immediately after a seizure. The individual retains control of posture and muscle tone but performs simple or complex movements and actions without being aware of what is happening. The phase lasts 5 minutes or less in 80 per cent, rarely more than 1 hour.

• • •

Early features – staring, slumping, ‘dazed’. Midpoint – Repetitive movements, blinking, smacking lips, chewing. Terminal (integrated) – wandering, paranoid ideas, confusion.

Diagnosis This is essentially on clinical grounds. An abnormal EEG may confirm, but a normal EEG in-between episodes does not exclude. Seek evidence from a witness – sudden onset, impaired awareness. • There is no retrograde amnesia. • If an offence is committed, seek evidence that it was unpremeditated and there was no attempt at concealment.

•

Differential diagnosis Hysterical amnesia and fugue. (Often covert conflict with purposeful escape. Amnesia of longer duration.) • Malingering (marked variability and inconsistency). • Stress reaction (inhibited individual exercising denial mechanisms). • Alcohol, drug intoxication. • Sleepwalking (stage IV; rarely repetitive or stereotyped; behaviour usually well integrated).

•

ICTAL PHASE: FUGUES

• • •

Prolonged states of altered behaviour, impaired consciousness, amnesia, tendency to wander. Complex partial status may give similar appearance. Less common than automatisms.

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ICTAL PHASE: TWILIGHT STATES

• • • • •

Occurrence of subjective abnormal experience rather than objective motor manifestations. Twilight states last from one to several hours (occasionally 1 week or more). Consciousness impaired with abnormal affective and perceptual experience. Psychomotor retardation with perseveration of speech and action. Foci most commonly temporal lobe.

POST-ICTAL PHASE

• • •

Automatism (see above). Twilight states. Transient paranoid–hallucinatory states (post-ictal psychosis).

INTER-ICTAL PERIODS Aggressive behaviour There is a higher prevalence of epilepsy in the British prison population but violence is not more common in epileptics than in other prisoners; automatism could not account for the majority of crimes. Possibilities are: 1 Organic brain disorder is responsible for both epilepsy and offence behaviour. 2 Organic brain disorder causes epilepsy with consequent social rejection and sense of inferiority, leading to offensive behaviour. 3 Adverse social factors lead to both epilepsy and antisocial behaviour (e.g. battered child). 4 A tendency to reckless and antisocial behaviour leads to offences and accidents which could injure the brain and cause post-traumatic epilepsy. Serious violence as an epileptic phenomenon is very rare; any violence is usually short-lived, fragmentary, unsustained, purposeless. ‘Episodic dyscontrol syndrome’ This is controversial. There are episodes of senseless, poorly remembered unprovoked violence. Temporal lobe EEG abnormalities may be present. It may be helped by carbamazepine. Depression and suicide These are possibly more common in non-dominant temporal lobe lesions. FlorHenry (1969) proposed that schizophreniform psychosis is more commonly associated with left-sided temporal lobe epilepsy. Onset may be severe and rapid and may show an inverse relation to fit frequency. The risk of suicide is increased in epilepsy. Schizophreniform psychosis and epilepsy There is an increased incidence of schizophrenia-like syndrome (usually paranoid type) among chronic epileptics compared to the general population. It usually develops 10–15 years after onset of epilepsy.

EPILEPSY

179

It is associated with:

• • • •

Increased incidence of neurological abnormalities. Negative family history for schizophrenia. ‘Warmer’ affect with less personality disintegration than schizophrenia. Temporal lobe epilepsies.

Suggested mechanisms Epiphenomena – ? There is a common brain disorder responsible for both schizophrenic symptoms and epilepsy. • Psychodynamic – ? Symptoms are a response to social rejection, etc., associated with epilepsy, and to abnormal mental experiences produced by it. • Pathophysiological – ? Schizophrenic symptoms are produced by physiological changes consequent on abnormal electrical or neurotransmitter activity.

•

Dementia A small proportion develop progressive decline in intellectual ability, with diffuse cerebral atrophy. This may develop after many years’ functioning at adequate level. It is also associated with deterioration in personality. Dementia is more common where epilepsy is secondary to a known brain lesion, and where epilepsy is early-onset, severe, chronic and temporal-lobe. Exclude:

• •

Effect of drug intoxication. Apparent dementia, where worsening of personality traits, neurotic withdrawal, chronic end-state of schizophreniform psychosis.

TREATMENT OF EPILEPSY Drug treatments Remember: 1 2 3 4 5

Every case is different. Be aware of the family, social and personal context. Assess and encourage compliance. Use one drug whenever possible. Phenytoin metabolism is saturable (zero-order kinetics), so monitor levels. Specific drugs:

• •

Partial seizures – carbamazepine, phenytoin, valproate, gabapentin, lamotrigine, tiagabine, topiramate, levetiracetam. Generalized seizures: – Tonic–clonic – valproate, carbamazepine, phenytoin, lamotrigine. – Tonic – valproate, felbamate, clonazepam. – Absence – ethosuximide, valproate, lamotrigine. – Myoclonic seizures – valproate, clonazepam.

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Surgery Consider temporal lobectomy for treatment-resistant epilepsy (after adequate trials) with a definite EEG focus. This usually requires extensive workup – neurophysiology and imaging. Up to 60–70 per cent are seizure-free after surgery. With other brain regions, up to 50 per cent are seizure-free afterwards (e.g. callosotomy). Vagus nerve stimulation This involves surgical implantation of an electrical nerve stimulator similar to a cardiac pacemaker, with electrodes attached to the left vagus nerve in the neck. This reduces seizures by 50 per cent in up to one-half of patients. Ketogenic diet By maintaining a ketoacidotic state, seizures may be suppressed by an unknown mechanism. However, it is difficult to maintain a ketogenic state. It has only been demonstrated to be effective in children. Psychosocial Be aware of the family, social and personal context.

• • •

Family – Overprotection may foster dependency. Personal – Is there poor self-esteem, inadequate social skills and social repertoire? Societal – Be aware of negative attitudes, discrimination.

NON-EPILEPTIC ATTACK DISORDER (PSEUDOSEIZURES) See also Chapter 16 (Psychophysiological, somatoform, dissociative and related disorders). Pseudoseizures may occur in those who also have true epileptic seizures. There is a variable attack pattern.

• • • • • • •

Often very frequent. Usually with others present. Usually occur indoors, at home. Often an emotional precipitant. Often gradual onset, rigidity with random struggling; rarely pass urine or injure self; often talk or scream during attack, which may last many minutes. May be ‘swoon’-like. EEG normal during attack. Serum prolactin not raised after attack.

SLEEP DISORDERS See Table 14.1. The normal physiology/normal sleep EEG is covered in Chapter 15.

INSOMNIA Insomnia is a symptom, not a disease. Thirty-five per cent of the population experience some insomnia; in 10–15 per cent it is clinically significant.

SLEEP DISORDERS

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Table 14.1 Classification of sleep disorders Dyssomnias Primary insomnia Primary hypersomnia Sleep–wake schedule disorders Jet lag Sleep delay Other Disorders of excessive sleep Breathing-related sleep disorder (obstructive sleep apnoea) Narcolepsy Parasomnias Nightmares Sleep terrors Sleepwalking REM sleep behaviour disorder Other Sleep disorder related to other mental disorder Sleep disorder related to general medical condition

Risk factors are: female, elderly, anxious, depressed, multiple health problems, lower social group. It is most prevalent in the elderly because of changes in the sleep pattern: ↓ REM, ↓ REM latency, ↑ number and duration of awakenings, ↑ shift through sleep stages, ↑ daytime napping; also increased physical and psychiatric morbidity. Forty per cent of insomniacs self-medicate with over-the-counter drugs or alcohol; 20 per cent take prescription sedatives/hypnotics. MANAGEMENT There should be a thorough initial evaluation to rule out secondary (physical/psychiatric) or situational (stress-related/environmental) causes. Sleep hygiene Encourage: regular bedtimes and rise times; a bedtime ritual (e.g. short read); diet (avoid hunger or overeating at night); avoid caffeine; avoid alcohol; no daytime naps; regular exercise. The bedroom should be dark, quiet, at normal temperature. Avoid ‘clock watching’ – use bed to sleep. Cognitive–behavioural therapy This is useful as a means of treating, possibly curing, primary insomnia as well as achieving discontinuation of hypnotic drug use. Drug therapy for temporary relief This should be cautious and ‘targeted’. Start with non-prescription hypnotics. Antidepressants with sedating qualities may be used.

•

Benzodiazepines (↓ REM and slow wave sleep, ↑ stage 2) – Short- or intermediateacting drugs cause less residual daytime sedation, but are more likely to cause

182

•


rebound insomnia with discontinuation (see Chapter 21). Abuse and dependency are problematic. Non-benzodiazepines: zolpidem and zopiclone – Although associated with lower abuse than benzodiazepines, those with a history of substance abuse or dependence, or psychiatric illness may be at increased risk to abuse these agents.

SLEEP AND PSYCHIATRIC ILLNESSES Sleep disturbance is a prominent symptom in many psychiatric disorders. There is no single sleep parameter with absolute specificity for any psychiatric disorder, but most prominent differences are seen with affective disorder.

• • • • • •

Depression – This reduces stages 3 and 4, reduces REM latency, and REM occurs earlier in the night. It is unclear as to the specificity to depression and prediction of treatment response. Sleep deprivation has been used as a treatment. Schizophrenia – There is reduced slow-wave sleep and REM. Anxiety – There is difficulty falling and staying asleep, increased stages 1 and 2, reduced efficacy of sleep, no characteristic REM changes as in depression. Panic disorder – There is increased sleep latency; other findings as in generalized anxiety. Alcoholism – There is increased ␦, REM sleep and ␣ activity. Alzheimer’s – ‘Sundowning’ (confusion, wandering), increased sleep, fragmentation, reduced sleep efficiency, Stages 3–4, and total REM.

NARCOLEPSY Narcolepsy has a population prevalence of about 0.05 per cent. The ‘narcoleptic tetrad’ is: 1 2 3 4

Hypersomnia. Cataplexy (sudden loss of muscle tone) in 80 per cent of cases. Sleep paralysis (marked loss of muscle tone on awakening). Hypnagogic hallucinations (i.e. on going to sleep) or hypnopompic (on waking).

Only 25 per cent of patients have the complete tetrad. Two-thirds have fallen asleep while driving, 80 per cent fallen asleep while at work. AETIOLOGY There is an abnormality on chromosome 6 (HLA DQB1 and DQA1 alleles) seen in over 85 per cent of patients. An association with human leukocyte antigen (HLA) allele suggests an autoimmune link. Neurochemical studies show absence of hypocretin in CSF. DIAGNOSIS Use the multiple sleep latency test (MSLT) EEG during the day – rapid onset of REM (⬍10 mins after onset of sleep), ⭓2 sleep-onset REM periods during MSLT is virtually diagnostic; also HLA testing.


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Table 14.2 Parasomnias Type

Incidence

Onset

Sleep stage Behaviour

Recall Treatment

Nightmares

Very frequent in children

Late in sleep

REM

Easily rousable, awareness

Usual Support

Night terrors

3% children, commonest in ages 4–7; often family history

First 1–2 hours of sleep

Non-REM, stage 4

Terrified, screaming, None thrashing, can’t be easily aroused, ‘trance-like’, may last 10–20 minutes

Reassurance and practical advice for parents; behavioural waking schedule if persistent

First 1–2 hours of sleep

Non-REM, stage 4

May last minutes to 1 hour

Safety precautions; avoid sleep deprivation

Sleepwalking 1–15%, normally 8–15 years old, but also in adults

None

From Shapiro (1993).

TREATMENT

• •

Allow only scheduled daytime naps. Use of stimulants – modafinil, dexamphetamine and methylphenidate. Cataplexy may be effectively treated with clomipramine or an SSRI.

OTHER CONDITIONS See also Table 14.2.

• •

Kleine–Levin syndrome – episodes of hypersomnia, pathological overeating. Also hypersexuality, hallucinations, mood disturbances. Disorder of hypothalamus. There is no specific treatment. Sleep apnoea (and pickwickian syndrome) – episodes of apnoea during sleep; disturbed noisy sleep; very tired during day. Causation may be central or peripheral.

REFERENCES AND FURTHER READING Baillargeon L, Landreville P, Verreault R et al. (2003) Discontinuation of benzodiazepines among older insomniac adults treated with cognitive–behavioural therapy combined with gradual tapering: a randomized trial. CMAJ 169, 1015. Blume WT (2003) Diagnosis and management of epilepsy. CMAJ 168, 441. Burneo JG, Martin R, Powell T et al. (2003) Teddy bears: an observational finding in patients with non-epileptic events. Neurology 61, 714. Currie S (2001) Cognitive–behavioural therapy may improve chronic primary insomnia. Evidence Based Healthcare 5, 144. Dagan Y (2002) Circadian rhythm sleep disorder (CRSD). Sleep Med. Rev. 6, 45. Flor-Henry P (1969) Psychosis and temporal lobe epilepsy: a controlled investigation. Epilepsia 10, 363. Glick TH (2002) The sleep-deprived electroencephalogram: evidence and practice. Arch. Neurol. 59, 1235.

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Goetz CG (2003) Textbook of Clinical Neurology, 2nd edn. WB Saunders, Philadelphia. Kalviainen R, Keranen T, Riekkinen PJ (1993) Place of newer antiepileptic drugs in the treatment of epilepsy. Drugs 46, 1009. Kaufman DM (2001) Clinical Neurology for Psychiatrists, 5th edn. WB Saunders, Philadelphia. Kryger MH, Walid R, Manfreda J (2002) Diagnoses received by narcolepsy patients in the year prior to diagnosis by a sleep specialist. Sleep 25, 36. Lefevre F, Aronson N (2000) Ketogenic diet for the treatment of refractory epilepsy in children: a systematic review of efficacy. Pediatrics 105, e46. Lin L, Hungs M, Mignot E (2001) Narcolepsy and the HLA region. J Neuroimmunology 117, 9. Littner M, Johnson SF, McCall WV et al. (2001) Practice parameters for the treatment of narcolepsy: an update for 2000. Sleep 24, 451. Olejniczak PW, Fisch BJ (2003) Sleep disorders. Med. Clin. North Am. 87, 803. Reuber M, Elger CE (2003) Psychogenic nonepileptic seizures: review and update. Epilepsy Behav. 4, 205. Schenck CH, Mahowald MW (2002) REM sleep behavior disorder: clinical, developmental, and neuroscience perspectives 16 years after its formal identification. Sleep 25, 120. Shneker BF, Fountain NB (2003) Epilepsy. Disease-a-Month 49, 426. Smith R, Ronald J, Delaive K et al. (2002) What are obstructive sleep apnea patients being treated for prior to this diagnosis? Chest 121, 164. Stores G (2003) Misdiagnosing sleep disorders as primary psychiatric conditions. Adv. Psychiatr. Treat. 9, 69. Szuba MP, Kloss JD, Dinges DF (2003) Insomnia Principles and Management. Cambridge University Press. Taheri S, Mignot E (2002) The genetics of sleep disorders. Lancet Neurol. 1, 242. Trimble MR (1992) Behaviour changes following temporal lobectomy: with special reference to psychosis. J. Neurol. Neurosurg. Psychiatry 55, 89. Vaughn BV, D’Cruz OF (2003) Obstructive sleep apnea in epilepsy. Clin. Chest Med. 24, 239.

EEG and brain imaging in psychiatry

15

ELECTROENCEPHALOGRAPHY (EEG) An EEG records regular and irregular oscillations of potentials between electrodes placed on the scalp. Repetitive waves reflect summated synaptic potentials generated by cortical pyramidal cells as response to rhythmic thalamic discharges. Amplitudes range from 5 to 150 microvolts. Frequencies (when regular) range from about 1 cycle/second (hertz) to ⭓40 Hz.

THE NORMAL EEG Frequency ranges • Delta – less than 4 Hz. May occur as regular waves or irregularly. Diffusely distributed over scalp in sleeping adults and in children but invariably abnormal in nonsleeping adults. • Theta – 4–7 Hz. Transient ␪ are components found in 15 per cent of the normal population. • Alpha – 8–13 Hz. Prominent over occipital region, accentuated by eye closure and attenuated by attention. A consistent difference of 1 Hz or more between hemispheres is pathological. Slowing seen in early phenytoin toxicity. • Beta – 14 Hz and above. Principally frontocentral. May be enhanced by anxiety, alcohol and some drugs (barbiturates, benzodiazepines). • Mu – Arch-like 7–11 Hz waves over precentral areas, attenuated by contralateral limb movements. • Lambda – Single sharp waves in occipital region, usually associated with visual ‘scanning’. • Vertex waves – Electronegative sharp waves over vertex, evoked by auditory stimulus. DEVELOPMENT Infants have slower and usually higher-amplitude rhythms. They are asynchronous at first and easily disturbed. Mature rhythms develop at between 2 and 6 years.

186

EEG AND BRAIN IMAGING IN PSYCHIATRY

Adults usually show either alpha posteriorly and beta anteriorly but generalized low-amplitude beta may be present – established by puberty. When the subject is drowsy, alpha becomes intermittent and theta appears. Alpha frequency tends to slow in old age, and delta activity is decreased; by 60 years, Stage 4 represents 10 per cent of total sleep. There is decreased rapid eye movement (REM) latency, with increased frequency and duration of nocturnal arousals. NEUROTRANSMITTERS AND SLEEP EEG

• • • • •

Histamine – active wakefulness, neurones in hypothalamus. Cholinergic – wakefulness, REM sleep. Adrenergic – decreased REM sleep (MAOIs, clonidine, propranalol). Serotonergic – increased non-REM sleep. Dopamine – increased REM sleep.

NORMAL SLEEP

• • • •

Stage 1 (lightest) – low-voltage, desynchronized activity and sometimes low voltage-regular activity at 4–6 Hz. Undulating low-frequency deflections seen due to rolling eye movements. Stage 2 – frequent spindle-shaped tracings at 13–15 Hz (sleep spindles) and highvoltage K complexes (high-voltage slow waves plus short episode of fast activity over vertex, response to sound). Stage 3 – high-voltage delta waves begin to appear. Stage 4 – delta waves occupy more than 60 per cent of record.

Features of normal sleep Sleep is cyclical, with four or five periods of emergence from stages 3 and 4 to a period lasting about 20 minutes – termed ‘paradoxical’ or ‘desynchronized’ (REM) sleep:

• • • • • • • • • •

Low-voltage asynchronous fast waves on cortical EEG. Rapid eye movements, conjugate. Irregular respiration. Slight tachycardia with increased blood pressure. Increased gastric motility. Increased cerebral blood flow. Absent tendon reflexes. Penile erection. Vivid and bizarre dreams. 15–30 per cent of sleep time spent in REM.

ABNORMAL EEG PATTERNS Abnormalities include:

• •

Reduced amount and amplitude of normal frequencies (generalized or localized). Increased slow frequencies (generalized or localized).

ABNORMAL EEG PATTERNS

•

187

Abnormal waveforms – spikes (duration less than 80 ms), sharp waves (duration 80–200 ms), spike and wave complexes.

Abnormal forms may occur spontaneously or may be provoked by photic stimulation, sleeping, or hyperstimulation. Diffuse abnormalities Rhythmic slowing. Occasionally periodic discharges.

• •

Focal abnormalities Polymorphic, arrhythmic unreactive delta. Periodic lateralized epileptiform discharges.

• •

Epilepsy Initial interictal EEG is abnormal in 75 per cent of suffers. With repeated recordings, 90–95 per cent will show abnormalities. 2 per cent of normal population have abnormalities considered to be epileptiform. Absence seizures: – 3/second spike and wave in infancy. – 4/second spike and wave in a juvenile. • Primary generalized tonic–clonic seizures: – Interictal – bursts of spike and wave. – Ictal – 10-Hz fast activity during tonic phase, followed by lower-frequency spike and wave complexes during clonic phase. – Postictal – generalized slowing ␦ range. • Myoclonic epilepsy: – Polyspike and wave. • Partial (focal) epilepsy: – Interictal – focal spikes or sharp waves. – Ictal – focal rhythmic discharge.

• • • •

Periodic complexes Herpes simplex encephalitis (look for localized temporal complexes). Creutzfeldt–Jakob disease (occurs in late stages). Subacute sclerosing panencephalitis.

• • •

Triphasic waves These indicate liver, renal, hypoxic or metabolic encephalopathies. Frontal intermittent rhythmic delta activity (FIRDA) Metabolic encephalopathy. Brain stem dysfunction.

• •

Alpha coma There is widespread, non-reactive alpha-range activity. It occurs in generalized encephalopathy.

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Burst-suppression There are high-voltage bursts, followed by periods of extreme suppression (flattening). It occurs with bihemispheric insult and deep anaesthesia.

USES OF THE EEG IN PSYCHIATRY DETECTION OF ORGANIC PSYCHOSIS In general, there is first a decrease in frequency and responsiveness of ␣ rhythm, progressing to increased amounts of activity at slower frequencies in both ␪ and ␦ ranges. Changes are usually diffuse and symmetrical, especially where there are extracerebral causes. Focal lesions usually produce localized abnormality. DIAGNOSIS OF SEIZURE AND SLEEP DISORDERS This is especially important to help identify atypical forms of epilepsy associated with psychotic experiences, sudden affective disturbance or behavioural change. Notes 1 The EEG showing ictal activity during a major or focal seizure is diagnostic of epilepsy. Absence of simultaneous EEG changes during the episodes therefore almost excludes a genuine fit. 2 An abnormal interictal EEG does not clinch a diagnosis of epilepsy. Taken together with a full and careful history, interictal spike and wave disturbances give support to a diagnosis of liability to epilepsy. 3 A normal interictal EEG does not exclude a diagnosis of epilepsy, which must be based on eyewitness accounts and history. 4 In temporal lobe epilepsy, a routine and a sleep EEG will reveal spike foci in about 90 per cent of patients. STUPOR Non-organic stupor due to depression, schizophrenia or hysteria shows a preservation of alpha rhythm.

BRAIN IMAGING See the diagram below. Brain imaging in psychiatry Structural

CT

MRI

Functional

SPECT

Xenon inhalation

PET

MEG

Blood flow

MRI

Spectroscopy

BRAIN IMAGING

189

STRUCTURAL INVESTIGATIONS (PRINCIPLES) COMPUTERIZED TOMOGRAPHY (CT) CT X-rays generate an image in a single plane. There is poorer grey–white tissue contrast than with MRI, but CT is better for examining bony structures/tissue calcification. CT is still clinically useful but increasingly being replaced by MRI (see below). MAGNETIC RESONANCE IMAGING (MRI) MRI images are generated from motion of tissue protons when excited within a magnetic field. MRI possesses superior anatomical resolution and multiplanar scanning capacity than CT. It allows for three-dimensional reconstruction and volumetric quantification. MRI tissue-relaxation parameters (T1 and T2) may also give information on tissue hydration status and iron or lipid metabolism. Recent developments Voxel-based quantitative morphometry, for more sophisticated volume measurements. • Shape morphometrics, for examining shape rather than volume. • Diffusion tensor imaging (DTI), which is MRI of myelin traits. • Magnetoencephalography (MEG) a very recent technique using measurement of alteration in cerebral magnetic fields to provide detailed information on cortical activity. It may be combined with MRI and is good for studying deeper brain structures.

•

MRI AND CT IN PSYCHIATRY MRI AND SCHIZOPHRENIA

• •

• • •

Confirmed ventricular enlargement (lateral ventricles, 4th ventricle) and cortical tissue loss or hypoplasia, as seen in CT studies or longitudinal studies, generally suggests a non-progressive nature, favouring a neurodevelopmental basis (see Chapter 3), but some patients show neuroprogression. There is an association with subtle anomalies (e.g. agenesis of corpus callosum, cavum septum pellucidum) of neurodevelopmental origin. Reduction in size of mesial temporal lobe and superior temporal gyrus (especially on the left) is correlated with positive symptoms. Other findings include smaller frontal lobes, and larger basal ganglia structures (probably medication-related). Improved (tissue segmentation) methodology has suggested more widespread grey matter cortical loss and findings consistent with generalized subtle tissue loss. T1 and T2 findings are inconsistent. There are associations of brain abnormalities with many clinical indices: poorer premorbid function, negative symptoms, obstetric complications, family history of schizophrenia, treatment resistance.

190


MRI AND AFFECTIVE DISORDERS

• • •

There is a high prevalence of white matter/hyperintensity lesions in bipolar patients, particularly in elderly depressives. Some studies report reductions in size of caudate and putamen nuclei in depression; others find only temporal lobe (right hippocampus) reduction. Neuroimaging findings are less pronounced than in schizophrenia. Late-onset depression has more brain changes than early-onset. Brain abnormalities on neuroimaging generally are associated with cognitive impairment, poorer outcome and higher mortality.

MRI AND ALZHEIMER’S DISEASE (AD)

• • • • • • •

Selective loss of hippocampal tissue may occur early in AD, and in mild cognitive impairment (MCI). Presence of apolipoprotein E gene is associated with more (and earlier) neuroimaging abnormalities. Both ventricular enlargement and cortical tissue loss show high prevalence in the ‘normal’ population after age 60. In Alzheimer’s disease, ventricular enlargement is marked and progressive and is of both diagnostic and prognostic significance. Cortical tissue loss is less clearly related. MRI or CT is useful to distinguish aetiology and type of dementia: ‘patchy’ atrophy and multiple lucencies in multi-infarct dementia; atrophy of caudate and frontotemporal region in Huntington’s chorea; hypodensities in basal ganglia in Wilson’s disease. There is severe, bilateral atrophy of anterior frontal (⫾ temporal) lobes in Pick’s disease; cortical and subcortical atrophy in Parkinson’s disease. Ventricular enlargement and cerebral atrophy is seen in chronic alcoholics. Cerebral atrophy is related to the extent of cognitive impairment. In some patients, abstinence is associated with reversibility of CT findings.

MRI AND SUBSTANCE ABUSE

• • • •

Reduction in cortical grey matter and T1 changes correlate with cognitive impairments in alcoholics. MRI detects neuropathological changes in Wernicke–Korsakoff ’s syndrome (WKS). Gadolinium-enhanced MRI indicates blood–brain barrier impermeability in WKS reduces after 1 week of thiamine treatment. Some report white matter hyperintensities in opiate addicts.

MRI AND AUTISM

• •

Generally larger brains are reported. Reports of hypoplasia of the 4th ventricle, cerebellar vermis and parietal tissue loss.

MRI AND GILLES DE LA TOURETTE’S SYNDROME (GTS) There are some reports of asymmetry and/or reduction in basal ganglia structures in GTS.

BRAIN IMAGING

191

FUNCTIONAL INVESTIGATIONS IN PSYCHIATRY Single photon emission (computerized) tomography (SPET; SPECT) uses single photon (␥-ray) emitting isotopes – e.g. xenon 133, technetium 99 – to examine regional cerebral blood flow (rCBF) or receptor pharmacology. SPECT AND SCHIZOPHRENIA

• •

A large number of studies have shown a pattern of functional underactivity, with reduced rCBF predominantly in the frontal regions – the ‘hypofrontality hypothesis’. SPECT has also been used to examine neuroanatomical correlates of psychotic symptoms and to determine the pattern of receptor binding of antipsychotics.

SPECT AND AFFECTIVE DISORDERS

• •

Some studies report hypofrontality less pronounced than that in schizophrenia, with reversal during antidepressant therapy. Studies also show different pattern of sadness in normal subjects compared with depressed patients.

SPECT AND ALZHEIMER’S DISEASE

• •

Decreased rCBF in posterior parietal and temporal regions correlates with neuropsychological deficits. Primary motor, sensory, and visual cortices are relatively unaffected until late in illness.

XENON INHALATION

• •

This is another index of rCBF. There is well-documented hypofrontality in schizophrenia, with failure of activation during performance of the Wisconsin Card Sorting Test (WCST). There have been similar reports in affective disorder, but this may be a less consistent finding.

POSITRON EMISSION TOMOGRAPHY (PET) Unstable isotopes (oxygen 15, fluorine 18, carbon 11), generated from a cyclotron, emit ␥-rays when penetrating tissue. These are then detected and an image based on complex kinetic models is reconstructed. Recently, overlay of MRI images has been used to achieve greater structural resolution. rCBF is measured indirectly via 15O utilization; local metabolism is measured with 18F-deoxy-D-glucose (18FDG). PET and schizophrenia Hypofrontality is studied in unmedicated and medicated states; related to negative symptoms and treatment resistance. • Activation studies to examine neuroanatomical specificity of psychotic symptoms, and studies of dopamine receptor occupancy, have been carried out (see Chapter 3).

•

192


PET and other disorders • PET studies in affective disorder and Alzheimer’s have shown similar findings to their respective SPECT research. • Decreased activity in the right parahippocampus has been demonstrated in panic disorder. Hypermetabolism in orbitofrontal cortex and caudate nucleus has been reported in OCD; it normalizes with treatment (see Chapter 5). MR SPECTROSCOPY (MRS) This uses similar principles to structural MRI, but the tuning of the head coil at particular frequencies will allow information to be obtained on phosphorus and ATP metabolism (31P-MRS), glutamate, N-acetyl asparate (1H proton MRS), or pharmacology (19F MRS for neuroleptics or fluoxetine; Li+ MRS for lithium concentration in brain).

• •

Schizophrenic patients show decreased phosphomonoesterases and ATP metabolism in dorsolateral prefrontal cortex. Alzheimer’s disease patients show increases in phosphomonoesterases, even early in the illness.

FUNCTIONAL MRI (fMRI) This is an adaptation of MRI using exogenous contrast agents (e.g. GdPTA) or the endogenous contrast agent effect of deoxyhaemoglobin in blood. It can achieve high spatial and temporal resolution images of brain activity. It is now the major technology for functional imaging available in clinical scanners. Overlay with structural images is possible. fMRI is used in the study of perception (e.g. patients with schizophrenia hearing voices have overactivity in temporal lobes), emotions (sadness, anger) and treatment response (drugs may alter and normalize blood flow in pretreatment/post-treatment comparisons).

CLINICAL APPLICATIONS OF NEUROIMAGING

• • • • • •

Unusual onset of psychosis/depression/personality change. Cognitive decline/suspected dementia. Confusion/delirium of unknown origin. Head trauma. Alcoholism (advanced); to rule out complications. Neuropsychiatric conditions.

RESEARCH APPLICATIONS OF NEUROIMAGING

• • •

Are there any structural or functional brain changes? Are they associated with particular symptoms, illness subtypes, course? Are they related to other aspects – e.g. genetics, familial risk, neurochemistry?


• • •

193

Do they change or worsen over the course of illness? Can treatment(s) improve or alter these changes? Can we predict illness and/or discriminate between illnesses based upon imaging findings?

REFERENCES AND FURTHER READING Bostwick JM, Philbrick KL (2002) The use of electroencephalography in psychiatry of the medically ill. Psychiatr. Clin. North Am. 25, 17. Bullmore E, Fletcher P (2003) The eye’s mind: brain mapping and psychiatry. Br. J. Psychiatry 182, 381. Burton EJ, Karas G, Paling SM et al. (2002) Patterns of cerebral atrophy in dementia with Lewy bodies using voxel-based morphometry. Neuroimage 17, 618. Chance SA, Esiri MM, Crow TJ (2002) Amygdala volume in schizophrenia: post-mortem study and review of magnetic resonance imaging findings. Br. J. Psychiatry 180, 331. Du AT, Schuff N, Amend D et al. (2001) Magnetic resonance imaging of the entorhinal cortex and hippocampus in mild cognitive impairment and Alzhiemer’s disease. J. Neurol. Neurosurg. Psychiatry 71, 441. Gilbert DL, Sethuraman G, Kotagal U, Buncher CR (2003) Meta-analysis of EEG test performance shows wide variation among studies. Neurology 60, 564. Gross-Isseroff R, Hermesh H, Zohar J, Weizman A (2003) Neuroimaging communality between schizophrenia and obsessive compulsive disorder: a putative basis for schizo-obsessive disorder? World J. Biol. Psychiatry 4, 129. Grossman R, Buchsbaum MS, Yehuda R (2002) Neuroimaging studies I post-traumatic stress disorder. Psychiatr. Clin. North Am. 25, 317. Hambrecht M, Lammertink M, Klosterkotter J (2002) Subjective and objective neuropsychological abnormalities in a psychosis prodrome clinic. Br. J. Psychiatry 181, s30. Hull AM (2002) Neuroimaging findings in post-traumatic stress disorder: a systematic review. Br. J. Psychiatry 181, 102. Kim J, Lee MC, Kim J et al. (2001) Grey matter abnormalities in obsessive–compulsive disorder: statistical parametric mapping of segmented magnetic resonance images. Br. J. Psychiatry 179, 330. Lacerda AL, Dalgalarrondo P, Caetano D et al. (2003) Elevated thalamic and prefrontal regional cerebral blood flow in obsessive–compulsive disorder: a SPECT study. Psychiatry Res. 123, 125. Lawrie SM, Whalley HC, Abukmeil SS (2002) Temporal lobe volume changes in people at high risk of schizophrenia with psychotic symptoms. Br. J. Psychiatry 181, 138. Lawrie SM, Whalley HC, Job DE, Johnstone EC (2003) Structural and functional abnormalities of the amygdala in schizophrenia. Ann. NY Acad. Sci. 985, 445. Martin R, Burneo JG, Prasad A et al. (2003) Frequency of epilepsy in patients with psychogenic seizures monitored by video-EEG. Neurology 61, 1791. O’Brien JT, Wiseman R, Burton EJ et al. (2002) Cognitive associations of subcortical white matter lesions in older people. Ann. NY Acad. Sci. 977, 436. Phan KL, Wager T, Taylor SF et al. (2002) Functional neuroanatomy of emotion: a meta-analysis of emotion activation studies in PET and FMRI. Neuroimage 16, 331. Raush SL (2003) Neuroimaging and neurocircuitry models pertaining to the neurosurgical treatment of psychiatric disorders. Neurosurg. Clin. North Am. 14, 213. Scheltens P, Fox N, Barkhof F, De Carli C (2002) Structural magnetic resonance imaging in the practical assessment of dementia: beyond exclusion. Lancet Neurol. 1, 13. Shergill SS, Brammer MJ, Fukuda R et al. (2003) Engagement of brain areas implicated in processing inner speech in people with auditory hallucinations. Br. J. Psychiatry 182, 525.

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Shneker BF, Fountain NB (2003) Epilepsy. Dis. Mon. 49, 426. Suddath RL, Christison GW, Torrey EF et al. (1990) Anatomical abnormalities in the brains of monozygotic twins discordant for schizophrenia. New Engl. J. Med. 322, 789. Surguladze S, Keedwell R, Phillips M (2003) Neural systems underlying affective disorders. Adv. Psychiatr. Treat. 9, 446. Thomas AJ, O’Brien JT, Davis S et al. (2002) Ischemic basis for deep white matter hyperintensities in major depression: a neuropathological study. Arch. Gen. Psychiatry 59, 785. Volkow ND, Hitzemann R, Wang GJ et al. (1992) Long-term frontal brain metabolic changes in cocaine abusers: a study with positron emission tomography. Br. J. Psychiatry 151, 641. Wykes T, Brammer M, Mellers J et al. (2002) Effects on the brain of a psychological treatment. Cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia. Br. J. Psychiatry 181, 144. Yang TT, Menon V, Reid AJ et al. (2003) Amygdalar activation associated with happy facial expressions in adolescents: a 3-D functional MRI study. J. Am. Acad. Child Adolesc. Psychiatry 42, 979.

Psychophysiological, somatoform, dissociative and related disorders

16

CONCEPTS These are disorders in which the onset and exacerbation of organic change are often seen in association with emotional distress – e.g. asthma. Before 1950, Alexander’s concept of psychosomatic medicine dominated: ‘a causal link between a specific constellation of unconscious conflicts, of psychological methods of coping with them … and the development of one of several organic diseases’. Psychophysiological disorders (involvement of autonomic nervous system, smooth muscles) were then separated from conversion disorders (sensorimotor, skeletal muscle). Between 1951 and 1965, the postulated ‘psychosomatic specificity hypothesis’ was tested against bronchial asthma, rheumatoid arthritis, ulcerative colitis, dermatitis, essential hypertension, peptic ulcer and thyrotoxicosis by the Chicago Institute for Psychoanalysis. Investigations concluded that it is possible to differentiate between illness on the basis of psychological patterns associated with them – but neither the specificity nor the direction of causality is established. Four possible models of the relationship are show in the diagram below. 1.

No relationship

2.

Soma

Psyche

3.

Soma

Psyche Psyche

4.

Constitution Soma

Lipowski (1988) defined psychosomatic medicine as: 1 A science of the relationships between psychological, biological and social variables in relation to human health and disease. 2 An approach to the practice of medicine advocating the inclusion of psychosocial factors in the study, prevention, diagnosis and management of all diseases.

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PSYCHOPHYSIOLOGICAL, SOMATOFORM, DISSOCIATIVE AND RELATED DISORDERS

3 Clinical activities at the interface of medicine and the behavioural sciences, generally termed ‘consultation–liaison psychiatry’. RECENT CONCEPTS Recent concepts shift away from searching for psychodynamic formulations associated with specific organic pathology, rather to increased interest in social/environmental events and their effects on psychophysiological functioning, and relationship with onset, course and outcome of various diseases.

• • •

Murray Parkes (1970) has demonstrated vulnerability to physical illness in the first year after death of the spouse. Recent research demonstrates superior outcome in cancer therapy among patients who are psychologically minded and have less anxiety/depression (Spiegel, 2001). There is a large literature supporting a major role for depression in predicting morbidity and mortality in patients with ischemic heart disease (Blumenthal et al., 2003; Jiang et al., 2003).

Liaison psychiatry There has been growth of this concept in the last 60 years, facilitated by broader concepts of disease and location of psychiatric units in general hospitals (Kornfeld, 2002): 1 Diagnosis, prevention and management of mental illness in physically ill patients undergoing treatment. 2 Advice and mutual exchange of ideas on psychological aspects of care of the physically ill. 3 Management of psychopathological reactions to physical illness and injury (e.g. postoperative psychosis). 4 Prevention and management of deviant illness behaviour consequent upon, or part of, physical illness. 5 Advice and help in management of family problems related to illness and the individual. 6 Facilitation of adequate communication between patients and staff to avoid potential conflict and misunderstandings. 7 Education of staff in psychological aspects of illness. 8 Research. Recent emphasis includes: – Development of consultation (liaison psychiatry as sub-specialty). – Combined medical–psychiatric inpatient units in the general hospital.

PSYCHOLOGICAL REACTIONS TO PHYSICAL ILLNESS Physical and psychiatric disorders may coexist because:

• • • •

Both may have increased incidence in ‘vulnerable’ people. Psychiatric disorder may lead to physical disorder (e.g. alcoholism). Physical disorder may lead to psychiatric disorder (e.g. altered cerebral metabolism). Psychiatric drugs may lead to physical complications.

SOMATOFORM DISORDERS

• •

197

Medical drugs may lead to psychiatric complications. Physical illness may uncover a latent predisposition to psychiatric disorder.

FACTORS INFLUENCING RESPONSE TO PHYSICAL ILLNESS 1 Patient factors – Obsessional patients react to any doubt in the diagnosis. Narcissistic patients react to disfigurement. 2 The illness – The significance and meaning of the particular illness. Acute or chronic course. 3 The social environment – Financial or promotional threat. Illness may be welcomed if it resolves conflict (e.g. marital). PATTERNS OF RESPONSE

• • • • • • •

Therapeutic adaptation – to the symptoms. Anxiety – usually the first response. Depression – commonest psychiatric disorder in medical inpatients (see Chapter 4 for notes). Paranoid reaction – especially if deaf or blind. May blame relatives or doctors. Denial of illness – may be a helpful defence but may delay seeking help. Preoccupation with illness – ‘vigilant focusing’ on the symptoms. Prolongation of the sick role – for secondary gain.

SOMATOFORM DISORDERS See Table 16.1.

SOMATIZATION DISORDER There is repeated presentation of physical symptoms, with persistent requests for medical investigations, despite repeated negative findings and reassurances by doctors Table 16.1 ICD-10 and DSM-IV classification of somatoform disorders ICD-10 Neurotic, stress-related and somatoform disorders

DSM-IV Somatoform disorders

F44 Dissociative (conversion) disorder

Conversion disorder

F45 Somatoform disorders Somatization disorder Undifferentiated somatoform disorder Hypochondriacal disorder Somatoform autonomic disorder Persistent somatoform pain disorder

Somatization disorder Undifferentiated somatoform disorder Hypochondriasis Pain disorder

F48 Other neurotic disorders Neurasthenia

Body dysmorphic disorder

198


that the symptoms have no physical basis. If any physical disorders are present, they are insufficient to explain the severity of symptoms or patient distress/preoccupation. These people are extensive users of healthcare resources. For example, the management cost of treating chronic pelvic pain accounts for 0.6 per cent of UK health expenditure. Claims of gastrointestinal, dermatological, sexual or menstrual symptoms are most common. Prevalence rates vary. ECA reports 0.03–0.4 per cent (Escobar et al., 1987); approximately 10 per cent rate in medical outpatients. The male:female ratio is 1:20. There is a familial component. Between 10 and 20 per cent of first-degree female relatives are somatizers. First-degree male relatives are prone to substance abuse, antisocial personality disorder. It is associated with other psychiatric disorders: depression, substance abuse, antisocial and histrionic personality disorder. MANAGEMENT

• • • • •

It is a chronic disorder with a fluctuating course. Establish the absence of an underlying physical cause. Limit ‘window-shopping’ for doctors. Supportive psychotherapy is helpful. Pharmacotherapy is indicated for secondary complications (e.g. anxiety, depression) but has limited use otherwise (especially benzodiazepines because of potential for abuse).

CONVERSION DISORDER There is loss of motor or sensory function without an identifiable physical cause. Both primary and secondary gain encourage the persistence of the symptoms. ‘Classic’ conversion symptoms are those that suggest neurological disease, such as paralysis, aphonia, convulsions, coordination disturbances, etc. Vomiting as a conversion symptom may represent revulsion or disgust. Pseudocyesis (false pregnancy) may represent both a wish for, and fear of, pregnancy. Conversion symptoms can complicate true organic disease: Slater (1965) followed up 85 patients diagnosed as hysterical, after 9 years. One-third were found to have developed organic disease not initially detected, but probably having played a part in initial symptoms; 12 patients had died, of whom 3 had symptoms which could account for the previous ‘hysterical’ symptoms. Of 33 patients who had no significant organic disease, 13 had developed significant psychiatric illness. Conversion symptoms may be distinguished from organic symptoms by:

• • •

Their variability. A typical nature, often reflecting a patient’s concept of the disability. Inconsistency (e.g. apparently paralysed muscles may show synergistic power).

EPIDEMIOLOGY There is no definite information on age. Female:male ratio ⫽ 2–10:1. The condition accounts for about 3–4 per cent all psychiatric consultations.

SOMATOFORM DISORDERS

199

The estimated annual incidence is 11–22 cases per 100 000. Lower socioeconomic groups may be most affected (Stefansson). AETIOLOGY Genetics There is an incidence among first-degree relatives of about 5 per cent (lower in fathers, higher in mothers and daughters). This level most likely reflects family learning. There is some evidence of monozygotic twin-pair concordance, but not dizygotic. Psychophysiological aspects Evoked responses in patients with hysterical anaesthesias suggest two underlying mechanisms:

• •

A lowering of peripheral receptor sensitivity. A central mechanism of inhibition along different pathways.

Psychoanalytic aspects Repressed anxiety leads to hysterical symptoms, often having symbolic meaning and secondary gain. ‘Direct coping’ with conflict is avoided. Unresolved oedipal conflicts are often a prominent source of anxiety. Psychological/social aspects Both primary and secondary gain encourage the persistence of the symptoms. Hysterical symptoms have been viewed (Pilowsky) as a form of non-verbal communication in the doctor–patient relationship. (May particularly apply to those less effective in verbal communication, e.g. those perceiving themselves in a dependent inferior role.) COURSE AND PROGNOSIS The course is variable:

• •

Lewis – 40 per cent well and working 5 years later (Maudsley Hospital inpatients). Cater – 70 per cent well 4–6 years later (acute conversion reaction).

Good prognostic factors are acute onset, nature of conflict clear and resolvable. Poor factors are intractable personality problems and poor motivation on the part of the patient. TREATMENT

• • • •

Explain and reassure as to nature of the symptom. Investigate as far as necessary to exclude organic cause, not merely as a method of reassurance. Detect and treat associated emotional disorder, psychotherapy. Interviewing with sodium amytal administration is sometimes useful diagnostically as well as therapeutically.

200


PAIN DISORDER This is defined as the complaint of pain in the absence of adequate physical findings and in association with evidence of the aetiological role of psychological factors. Common sites are head and neck, abdomen, lower back and genitals. Patients may be any age, peaking around middle age. It is more common in women. The course is variable and depends on reinforcement factors, including secondary gain. CLINICAL FEATURES

• • • • • •

Inconsistent with anatomical distribution of the nervous system. Continuous over long periods by day. May prevent getting off to sleep but not cause wakening. May have symbolic significance; e.g. chest pain where father died of a heart attack. Insight into role of psychological factors is often restricted. Responds better to psychotropics than analgesics.

ASSESSMENT AND MANAGEMENT

• • • • • •

Exclude organic disease. Beware of ‘detecting’ psychological conflict in the absence of good evidence. Get a history from other witnesses if possible. Resolve current social stressors where possible. Earlier psychiatric illness may resemble current symptoms in course and precipitants. Earlier personality? Vulnerable aspects? Hypochondriasis? Pain threshold? Ethnic factors – some ethnic groups (e.g. Asian) have tendency to somatize problems.

The possibility of litigation is extremely important because resolution of the pain symptom is unlikely, and significant numbers of patients continue with chronic pain after settlement. Pain clinics often adopt a multidisciplinary approach with anaesthetist, physician and psychiatrist. Ensure adequate medical treatment where necessary. Antidepressants are better than placebo. Use behavioural methods of treatment where appropriate.

HYPOCHONDRIASIS The predominant disturbance is an unrealistic interpretation of physical signs or sensations as abnormal, leading to preoccupation with the fear of having a serious disease. The unrealistic fear persists despite medical reassurance and causes impairment in social or occupational functioning. It may present as primary hypochondriacal disorder, as a part of other syndromes, or as a form of personality disorder. Depressive illness presents more commonly with hypochondriacal/somatic features in non-European cultures. The condition may reach delusional intensity in depressive and schizophrenic illness.

DISSOCIATIVE DISORDERS

201

It is more common in men, young and old, in lower socioeconomic classes and those closely associated with disease. MANAGEMENT

• • •

Exclude organic pathology. If secondary to primary illness (e.g. depression), treat this. Hypochondriacal symptoms may then fade. If primary: – Follow firm policy regarding further investigations. – Educate over role of psychological factors in symptoms. Avoid equation of psychological with ‘faking’. Use cognitive and distraction techniques. – Search for meaning of symptoms in the social/family setting, where appropriate. – Exercise caution where symptoms serve a powerful defensive purpose. – Some advocate a trial of tricyclics in all patients.

PROGNOSIS The outcome is variable, but poor in more chronic and established cases. Those associated with depressive illness or anxiety disorder have better prognosis.

BODY DYSMORPHIC DISORDER (BDD) This typically begins in adolescence and is characterized by a preoccupation with an imagined physical defect or excessive concern over a minor physical flaw. Cases are often seen by non-psychiatrists, such as dermatologists and plastic surgeons. Individuals may isolate themselves, seek surgical interventions, or go to extremes to conceal their perceived physical defect. Preoccupation with the supposed defect causes clinically significant impairment in social, occupational, or other essential areas of functioning. EPIDEMIOLOGY The prevalence is between 0.7 and 2.3 per cent in the general population, 11.9 per cent in a dermatology setting (Phillips et al., 2000). There is a wide range of sex ratios, but probably M ⫽ F. Seventy-five per cent have never been married. TREATMENT The condition is often chronic and difficult to treat. BDD is thought by some to be a type of obsessive–compulsive disorder and treatment is similar. When patients agree to psychopharmacological treatment, improvement is seen with SSRI or SRI therapy. Cognitive–behavioural therapy has also been shown to help.

DISSOCIATIVE DISORDERS These are a spectrum of disorders involving a disturbance in the integration of consciousness, memory, identity or perception for which there are no demonstrable

202


organic findings, and which seem to have a psychological advantage or symbolic value. There is a strong presumption that the symptoms are a defence mechanism linked to unresolved internal conflict or stress, but the reaction appears to be at an unconscious level. Other features which may or may not be associated are:

• • • • •

Primary gain (conflict ‘resolved’, anxiety reduced). Secondary gain (attention of others). A choice of symptom modelled closely on recent experience in self or others. Manipulation of others and the environment. Personality type/disorder.

DISSOCIATIVE TYPES AND CLINICAL FEATURES Dissociative amnesia There is a sudden, temporary alteration in the function of memory usually associated with a traumatic or stressful event. There is an inability to recall important information, the extent of which is too great to be explained by ordinary forgetfulness. Dissociative fugue Like dissociative amnesia, there is a sudden alteration in memory, especially important personal information, which is also accompanied by unexpected travel away from the person’s usual setting. It is important to distinguish dissociative fugue from fugue states that may occur after head injury, in epilepsy, during depressive illness and in the context of heavy drinking (alcohol amnesic episodes). Often it is difficult to decide whether a fugue is an act of malingering or genuinely beyond the patient’s control. Dissociative identity disorder (DID) This is characterized by the presence of at least two separate identities or personalities, each of which may or may not know about the other and which can dominate individual behaviour. Individuals may report gaps in memory and lost time. Depersonalization disorder This is characterized by periods of feeling detached from one’s own body, identity or mental processes. Dissociative disorder not otherwise specified This covers dissociative symptoms not meeting the criteria for one of the above types. MANAGEMENT

• • •

Rule out any medical cause for the symptoms. In a supportive therapeutic relationship, memory usually returns with dissociative amnesia and dissociative fugue. With DID, long-term therapy is usually needed. Most dissociative disorders are not responsive to medications. With depersonalization disorder, SSRIs may be helpful.


203

CHRONIC FATIGUE SYNDROME (CSF) – NEURASTHENIA This is severe, disabling fatigue of uncertain aetiology associated with a variable extent of somatic and/or neuropsychiatric symptoms. Presentation is between ages 20 and 50 years, and females predominate. The prevalence is 7.4 per 100 000. There is no clear association with socioeconomic status. AETIOLOGY Patarca (2001) postulates immune dysfunction along with psychological vulnerability, but the evidence is inconclusive. There are immunological abnormalities, especially cell-mediated. T-lymphocyte mechanisms are common, but their significance is unclear. There is a high prevalence (⬎60 per cent) of antecedent/lifetime psychiatric illness, especially minor depression, anxiety and somatization. MANAGEMENT

• •

Cognitive–behavioural therapy has been beneficial (Whiting et al., 2001). There is no effective medical treatment. Medications are given for symptomatic treatment – antidepressants, analgesics. Non-steroidal anti-inflammatory agents are ineffective.

REFERENCES AND FURTHER READING Barsky AJ, Ahern DK, Bailey ED et al. (2001) Hypochondriacal patients’ appraisal of health and physical risks. Am. J. Psychiatry 158, 783. Barsky AJ, Fama JM, Bailey ED, Ahern DK (1998) A prospective 4- to 5-year study of DSM-III-R hypochondriasis. Arch Gen Psychiatry 55, 737. Blumenthal JA, Lett HS, Babyak MA et al. (2003) Depression as a risk factor for mortality after coronary artery bypass surgery. Lancet 362, 604. Breitbart W, Gibson C, Tremblay A (2002) The delirium experience: delirium recall and deliriumrelated distress in hospitalized patients with cancer, their spouses/caregivers, and their nurses. Psychosomatics 43, 183. Carson AJ, Best S, Postma K et al. (2003) The outcome of neurology outpatients with medically unexplained symptoms: a prospective cohort study. J. Neurol Neurosurg Psychiatry 74, 897. Crimlisk HL, Bhatia K, Cope H et al. (1998) Slater revisited: 6-year follow-up study of patients with medically unexplained motor symptoms. BMJ 316, 582. Escobar JI, Burnam MA, Karno M et al. (1987) Somatization in the community. Arch. Gen. Psychiatry 44, 713. Hickie I, Davenport T, Issakidis C, Andrews G (2002) Neurasthenia: prevalence, disability and health care characteristics in the Australian community. Br. J. Psychiatry 181, 56. Hollander E, Neville D, Frenkel M et al. (1992) Body dysmorphic disorder: diagnostic issues and related disorders. Am. J. Psychiatry 33, 156. Horwitz BJ, Fisher RS (2001) Current concepts. The irritable bowel syndrome. New Engl. J. Med. 344, 1846.

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Jiang W, Babyak MA, Ronzanski A et al. (2003) Depression and increased myocardial ischemic activity in patients with ischemic heart disease. Am. Heart J. 146, 55. Kornfeld DS (2002) Consultation–liaison psychiatry: contributions to medical practice. Am. J. Psychiatry 159, 1964. Lipowski ZJ (1988) Somatization: the concept and its clinical applications. Am. J. Psychiatry 145, 1358. Martin JB (2002) The integration of neurology, psychiatry, and neuroscience in the 21st century. Am. J. Psychiatry 159, 695. Medical Journal of Australia (2002) Clinical practice guidelines. Chronic fatigue syndrome. Med. J. Aust. 176, s23. Mehendale AW (2002) Fibromyalgia syndrome, idiopathic widespread persistent pain or syndrome of myalgic encephalomyelopathy (SME): what is its nature? Pain. Prac. 2, 35. Musselman DL, Tomer A, Manatunga AK et al. (1996) Exaggerated platelet reactivity in major depression. Am. J. Psychiatry 153, 1313. Ness DE (2002) Discussing treatment options and risks with medical patients who have psychiatric problems. Arch Intern. Med. 162, 2097. Nimnuan C, Rabe-Hesketh S et al. (2001) How many functional syndromes? J. Psychosom. Res. 51, 549. Patarca R (2001) Cytokines and chronic fatigue syndrome. Ann. NY Acad. Sci. 933, 185. Phillips KA, Dufresne RG (2002) Body dysmorphic disorder: a guide for primary care physicians. Prim. Care 29, 99. Phillips KA, Dufresne RG, Wilkel C et al. (2000) Rate of body dysmorphic disorder in dermatology patients. J. Am. Acad. Dermatol. 42, 436. Richards SC, Scott DL (2002) Prescribed exercise in people with fibromyalgia: parallel group randomised controlled trial. BMJ 325, 185. Roelofs K, Keijsers PJ et al. (2002) Childhood abuse in patients with conversion disorder. Am. J. Psychiatry 159,1908. Slater E (1965) The diagnosis of hysteria. BMJ 1, 1395. Spiegel D (2001) Mind matters: coping and cancer progression. J. Psychosom. Res. 50, 287. Van der Pompe G, Antoni MM, Duivenvoorden HJ et al. (2001) An exploratory study into the effect of group psychotherapy on cardiovascular and immunoreactivity to acute stress in breast cancer patients. Psychother. Psychosom. 70, 307. Wessely S, Pariante C (2002) Fatigue, depression and chronic hepatitis C infection. Psychol. Med. 32, 1. Whiting P, Bagnall AM, Sowden AJ et al. (2001) Interventions for the treatment and management of chronic fatigue syndrome: a systematic review. JAMA 286, 1360. Wise MG, Rundell JR (2002) Textbook of Consultation–Liaison Psychiatry: Psychiatry in the Medically Ill, 2nd edn. American Psychiatric Press, Washington, DC. Yudofsky SC, Hales RE (2002) Neuropsychiatry and the future of psychiatry and neurology. Am. J. Psychiatry 159, 1261.

Psychogeriatrics

17

PSYCHIATRIC DISORDER EPIDEMIOLOGY

• • • • •

In 2000, 15.6 per cent of the population of the UK was over 65 years of age, and is projected to be 20.4 per cent in 2025. In 2000, 12.4 per cent of the population of the USA was over 65 years of age, and is projected to be 18.2 per cent in 2025. 45 per cent aged over 65 live alone in the USA. About a 25 per cent increase in the population over 75 years of age is expected by the year 2025 in both the USA and the UK. Over one-quarter of the elderly have a mental disorder (16 per cent with a psychiatric disorder and 10 per cent with dementia). This number is expected to increase as the proportion of population over 65 years increases (Jeste et al., 1999; see also Table 17.1).

AFFECTIVE DISORDER EPIDEMIOLOGY

•

First admissions for affective disorders fall over 65 years, although inception rates for depressive psychosis in elderly men remain high.

Table 17.1 Psychiatric disorders over 65 years of age

Major depression Dysthymia Bipolar I Bipolar II Panic disorder Generalized anxiety disorder (GAD) Obsessive–compulsive disorder (OCD) Adapted from Jeste et al. (1999).

One-year prevalence (%)

Lifetime prevalence (%)

0.9 – 0.1 0.1 0.4 2.2 0.9

1.4 1.7 0.1 0.1 male 0.1, female 0.7 2.6–4.3 1.2

206

• • • •

PSYCHOGERIATRICS

44 per cent of over-65s score ‘depressed’ on the Zung rating scale. Only 20 per cent of elderly depressives are referred to a psychiatrist within the first 6 months of illness. Other forms of neurotic disorder may gradually change to depressive neurosis in late middle age, although obsessional and hysterical neurosis may well improve with age. Frequency of depressive episodes in those with a history of depression tends to increase with age. Also, episodes last longer.

AETIOLOGICAL FACTORS An increased prevalence is seen if:

• • • • • • • •

Female. Past psychiatric history – depressive or neurotic disorder. ‘Personality deviation’. Social isolation. Presence of physical ill-health. Early loss of parent. Smoking. Lack of satisfaction with life, loneliness.

Genetic factors There is much less evidence of familial incidence in late-onset (over 50) compared with early-onset (before age 40) depression. The risk of affective illness in relatives decreases with increasing age of the proband. Organic factors No aetiological connection with senile dementia has been confirmed, although depressive features may be a reaction to early dementia. Cerebrovascular disease may act as a precipitant of depression, but depressed patients may show increased incidence of cerebrovascular disease at follow-up. Depression may include a subgroup who have delayed auditory-evoked responses, evidence of ventricular dilatation on CT scan, more white matter hyperintensities on MRI, and a higher mortality rate than other depressives. In some cases depression may be a symptom of ‘general systems failure’. Causes of symptomatic depression include antihypertensive drugs, myxoedema, and potassium deficiency (see Chapter 4). Environmental factors It is widely held that environmental factors (bereavements, retirement, deprivation) are aetiological factors, yet there is little proof of causal relationships. A significant excess of losses in late-onset depression compared with early-onset has not been demonstrated. In the year following the death of a spouse there is increased incidence of suicide, death and psychiatric referral, but most elderly people adapt to the loss well: 16 per cent are still depressed at 13 months (Zisook and Shuchter, 1993). Prolonged grief

AFFECTIVE DISORDER

207

reaction is seen more commonly in the socially isolated, the poor and those with little experience of death in earlier life. Personality factors Unipolar neurotic depression may be related to obsessional premorbid personality. Psychotic depression is less clearly related to this personality type. CLINICAL FEATURES Agitation is much more common than retardation. The condition is often accompanied by:

• • • •

Histrionic, importunate behaviour. Hypochondriacal preoccupations or delusions. Delusions of guilt, poverty, nihilism, persecution. Pseudodementia – with a tendency to answer ‘Don’t know’ rather than confabulate.

Suicide is a particular danger in elderly depressed, socially isolated men (see Chapter 11). There is little evidence for a distinction between ‘reactive’ and ‘endogenous’ groups. Indeed, many with clear reactive features have marked ‘endogenous’ symptoms. Depression in the elderly is divided into:

• • • •

•

Agitated depression – characterized by apparently shallow affect, bizarre delusions, importunate behaviour, somatic interpretations of anxiety and a high risk of suicide. Senile melancholia – severe agitated depression with delusions of nihilism, guilt, grandiosity and hypochondriasis. Organic depression – depressive disorder precipitated or exposed by cerebral disease in a predisposed person. Depressive pseudodementia – depressive illness with perplexity, loss of interest, loss of concentration and low self-esteem, leading to approximate answers or lack of answers and the appearance of impaired awareness and memory. It is characterized by relatively acute onset, prominent complaints of cognitive difficulty, communication of distress, patchy deficits, inattention, mental slowing and absence of focal signs. Abreaction or sleep deprivation may clarify the diagnosis. Masked depression – depression expressed as physical symptoms or worsening of longstanding neurotic symptoms. There is little apparent depressive affect but many somatic symptoms of depression (anorexia, sleep disturbance, poor concentration, etc.).

This may be a useful descriptive classification but it does not carry aetiological implications. Apathetic depression is also seen, in which self-neglect, loss of interest and social withdrawal are marked features. Manic–depressive psychosis • Very rarely presents initially at ages over 65 years (Young, 1992). • 5 per cent of affective episodes in over-65s are diagnosed as mania or hypomania. Mixed affective states are more common. • Hypomania in the elderly is characterized by: – Irritability. – Garrulousness, anecdotal speech with little flight of ideas.

208

•

PSYCHOGERIATRICS

– Paranoid or sexual delusions or preoccupations. – Claims to be happy but tense appearance, irritable and miserable, often without any infectious gaiety – ‘miserable mania’. May present as ‘confusion’ and possibly delirium.

MANAGEMENT Hospital admission is necessary if the patient is agitated and a suicide risk. Make a full assessment of social factors, isolation, housing, family support. Investigate and treat any intercurrent physical illness which may form a focus of distress as well as a possible aetiological factor. Drug treatment Response to SSRI antidepressants is often very effective for the depression. Lower dosages and careful timing of doses may be indicated. Introduction of medication should be careful and increase should be gradual. Explanation and reassurance are especially necessary. Delusional depression does not respond well to SSRI therapy and usually requires additional antipsychotic therapy. Electroconvulsive therapy (ECT) ECT is likely to lead to a more rapid response. It is especially effective in delusional/ psychotic/resistant depression. Social therapies Rehabilitation measures are vital in all cases. Occupational therapy, home assessment, improvement of social support and development of ‘second careers’ are all of great importance. Support of the family and reassurance and discussion with them is necessary. Slow discharge with increasing periods at home to build confidence is indicated. Day hospital, day centre or residential home supervision may be indicated. PROGNOSIS Overall, there is a similar pattern to depression in younger patients.

• • •

88 per cent are discharged from hospital, but only 30 per cent remain symptomfree for 6 years. 17 per cent remain chronically depressed; i.e. initial prognosis is good but relapse rate is high. 30 per cent die within 6 years. Poor prognosis indicators are:

• • • • •

Onset after age 70. Organic brain disease. Serious physical illness. Senile habitus. Uninterrupted depression for more than 2 years. MRI brain changes carry a higher mortality risk.

PARANOID SYNDROMES

209

PARANOID SYNDROMES There is much debate concerning the relationship between pure paranoid psychosis and schizophrenia. Paranoid psychoses developing in late life may be distinguishable from paranoid schizophrenia and are often called ‘paraphrenias’. EPIDEMIOLOGY

• • •

4 per cent of schizophrenic disorders in men and 14 per cent in women arise after age 65. 5.6 per cent of all psychiatric first admissions after age 65 are for paranoid psychosis. Prevalence – 0.2–0.3 per cent of the population aged over 65 are affected. It is more common in females.

AETIOLOGY Genetics There is an increased risk of schizophrenia in relatives of late paraphrenics when compared with the general population, but a reduced risk compared with early-onset schizophrenia. There is an increased incidence of personality disorder in families, but not of manic–depressive psychosis. Sensory defects Between 30 and 40 per cent of paranoid psychotics have impaired hearing. There is an increased prevalence of visual defects also. Organic causes Cerebral lesions, especially of temporal lobe and diencephalon, are more common (e.g. cerebrovascular disease). Other physical disorders may present with paranoia; e.g. Parkinson’s disease, Huntington’s chorea and other dementias, metabolic disorders. Personality features Sufferers are often withdrawn and suspicious, with sensitive premorbid personality – paranoid or schizoid type. • Occasionally there is a history of schizophreniform illness in earlier life with personality defect since then. • Patients are socially isolated, usually unmarried. They frequently live in selfcreated social isolation. • They are said to have been cold, unloving parents.

•

Environmental factors Factors which appear to be precipitants are often merely uncovering pre-existing psychosis. The condition occasionally does seem to be precipitated by life events. There may be a sudden paranoid reaction to stress in a sensitive personality.

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CLINICAL FEATURES

• • • • •

Usually, there is insidious onset of increasingly secluded, isolated and suspicious personality with episodes of bizarre behaviour, abuse of neighbours, self-neglect, complaints to police, suicide attempt, etc. Often, once recognized, a well-organized paranoid delusional system is found to be present. This often concerns plots to kill the patient, who may feel hypnotized, drugged, spied upon and show other passivity phenomena. Hallucinations may not be present or may be bizarre (e.g. taste or smell of poison, gases, etc.). Mood is often congruous, may be angry and excited or fearful and depressed. Seventy per cent of paranoid patients appear depressed. Personality is frequently well preserved.

Differential diagnosis Depression – especially if associated with ideas of guilt and retribution. Organic cerebral disease – especially if associated with marked misinterpretations, lack of systematized delusions and visual hallucinations.

• •

PROGNOSIS The natural course is of chronic illness with only minor fluctuations in intensity. The person may become mute, withdrawn, flat, characterless. With treatment the illness usually becomes less florid, though the delusional system is often maintained, but may not interfere with life.

• •

Best prognosis – short duration of illness, good initial response. Worse prognosis – severe personality difficulties, deafness, cerebrovascular disease, non-compliance with medication.

TREATMENT

• • • • • • •

Investigate and treat any intercurrent physical illness which may be an aetiological factor. Hospital admission may be necessary if the patient is disorganized, lacks capacity of self-care, or is at risk for harm to self or others. Antipsychotics, atypicals have a lower side-effect burden and require lower doses. Consider cognitive–behavioral therapy or supportive psychosocial therapy. Social/environmental assessment is required. Modify the environment where necessary. Provide education and support for the care-giver.

DEMENTIA See Chapter 13, Organic psychiatry.

GENERAL ASPECTS OF PSYCHOGERIATRIC MANAGEMENT

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GENERAL ASPECTS OF PSYCHOGERIATRIC MANAGEMENT PRINCIPLES 1 Early correct and full diagnosis of medical and social aspects: – Assess at home, take a full history from patient, relatives, friends, co-workers, etc. – Assess the problem where it presents, and assess local resources. – Fewer than 50 per cent of those visited at home are admitted to hospital. 2 Keep the patient at home as long as possible. This reduces confusion and the danger of institutionalization and encourages utilization of local resources. Major risk factors which predict institutionalization for the elderly are: – Extreme old age. – Living in retirement housing. – Recent hospitalization. – No spouse or partner. Family support is the most important factor here, and families must themselves be supported, with their problems explained and discussed. High rates of physical and psychiatric illness occur among carers. Maximize home support with community nurses, social workers, practical help (meals on wheels, home helps, laundry service, attendance allowance) and ensure correct accommodation (warden-controlled flats, residential home, etc.). However, when dementia patients cannot be managed on their own at home, support in this circumstance paradoxically accelerates institutionalization (O’Connor et al., 1990). Outpatient clinic support of patient and relatives may be very helpful. Day hospital, day centre or luncheon club attendance is beneficial. The day hospital needs to have a high staff/patient ratio and multidisciplinary input. However, cost-effectiveness is somewhat disputed. Admission to a short-stay psychogeriatric unit for full physical, psychological and mental state assessment may be indicated.

TREATMENT POSSIBILITIES Use of drugs • Beware of overmedication or undertreatment. • Assess the physical condition (heart, lungs, kidneys, liver) and presence of other drugs (including alcohol). • Treat with the lowest effective dose. • Use a limited range of familiar drugs. • Introduce medication slowly and carefully, to avoid side-effects and to increase compliance. Assess with plasma drug levels if available. • If at home, give small quantities with each prescription and supply large written instructions. • Explain the treatment to the patient and carers and involve relatives as appropriate.

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Use of psychotherapy • The person may need longer-term therapy, but with shorter individual sessions than for younger age-groups. • Cognitive–behavioural therapy is effective in the elderly. • There is an increased need for support and encouragement, attention to selfesteem and practical issues. Inpatient issues Aim for a high staff/patient ratio. Build and maintain morale and interest in the unit. Treat patients with respect, and avoid institutionalization.

ORGANIZATION OF SERVICES FOR THE ELDERLY

• •

•

Define those to be helped and their numbers. Define the components of the multidisciplinary service: – Domiciliary service – consultant, nurse, social worker. – Outpatient service to be offered. – Day centre liaison in district and other local authority facilities present. – Day hospital service offering assessment, short-term treatment and rehabilitation. – Inpatient beds for acute admission and assessment, in conjunction with geriatric service. – Inpatient beds for long-stay patients – includes elderly, chronic hospitalized patients (e.g. chronic schizophrenics), old people with functional mental disorders and old people with dementia. – Inpatient beds for terminal care if necessary. Define other responsibilities of service: – Support own staff and members of the multidisciplinary team. – Support families and workers in the community. – Teaching – of staff, of students and of local community. – Liaison with colleagues and other disciplines. – Research, for personal and general improvement of services. – Campaigning for more and proper resources.

Further comments on service delivery There is a need for an integration of mental health services with primary care services in order to improve access and utilization of mental health services among the elderly. Increased support, advocacy, training and in-home help for informal care-givers of those with Alzheimer’s may delay or prevent costly nursing home placements.

REFERENCES AND FURTHER READING Administration on Aging (2001) Older Adults and Mental Health Issues and Opportunities. Department of Health and Human Services, Rockville, MD. Beekman ATF, Geerlings SW, Deeg DJH, Smit JH et al. (2002) The natural history of late-life depression. Arch. Gen. Psychiatry 59, 605.


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Benbow SM, Jolley D (2002) Home assessments in old age psychiatry. Adv. Psychiatr. Treat. 8, 316. Blazer DG (2003) Depression in late life: review and commentary. J. Gerontol. A. Biol. Sci. Med. Sci. 58, 249. Bouman WP, Pinner G (2002) Use of atypical antipsychotic drugs in old age psychiatry. Adv. Psychiatr. Treat. 8, 49. Brodaty H, Sachdev P, Koschera A et al. (2003) Long-term outcome of late-onset schizophrenia: 5-year follow-up study. Br. J. Psychiatry 183, 213. Brown GK, Bruce ML, Pearson JL et al. (2001) High risk management guidelines for elderly with suicidal patients in primary care settings. Int. J. Geriatr. Psychiatry 16, 593. Bruce ML, McAvay GJ, Raue PJ et al. (2002) Major depression in elderly home health care patients. Am J. Psychiatry 159, 1367. Burns A, Dening T, Baldwin R (2001) Care of older people: mental health problems. BMJ 322, 789. Burns A, Lawlor B, Craig S (2002) Rating scales in old age psychiatry. Br. J. Psychiatry 180, 161. Cohen-Mansfield J (2001) Nonpharmacologic interventions for inappropriate behaviors in dementia. Am. J. Geriatr. Psychiatry 9, 361. Dewey ME, Saz P (2001) Dementia, cognitive impairment and mortality in personas aged 65 and over living in the community: a systematic review of the literature. Int. J. Geriatr. Psychiatry 16, 751. Evans M, Mottram P (2000) Diagnosis of depression in elderly patients. Adv. Psychiatr. Treat. 6, 49. Furniss L (2002) Use of medicines in nursing homes for older people. Adv. Psychiatr. Treat. 8, 198. Geller B, Craney JL, Bolhofner K et al. (2002) Two-year prospective follow-up of children with a prepubertal and early adolescent bipolar disorder phenotype. Am. J. Psychiatry 159, 927. Hybels CF, Blazer DG (2003) Epidemiology of late-life mental disorders. Clin. Geriatr. Med. 19, 663. Jeste DV, Alexopoulos GS, Bartels SJ et al. (1999) Consensus Statement on the Upcoming Crisis in Geriatric Mental Health: research agenda for the next 2 decades. Arch. Gen. Psychiatry 56, 848. Kawas CH, Brookmeyer R (2001) Aging and the public health effects of dementia. New Engl. J. Med. 344, 1160. Lawlor B (2002) Managing behavioural and psychological symptoms in dementia. Br. J. Psychiatry 181, 463. Lenze EJ, Dew MA, Mazumdar S, Begley AE (2002) Combined pharmacotherapy and psychotherapy as maintenance treatment for late-life depression: effects on social adjustment. Am. J. Psychiatry 159, 466. Mather AS, Rodriguez C, Guthrie MF et al. (2002) Effects of exercise on depressive symptoms in older adults with poorly responsive depressive disorder: randomised controlled trail. Br. J. Psychiatry 180, 411. Nebes RD, Vora IJ, Meltzer CC et al. (2001) Relationships of deep white matter hyperintensities and apolipoprotein E genotype to depressive symptoms in older adults without clinical depression. Am. J. Psychiatry 158, 878. O’Connor DW, Pollitt PA, Roth M et al. (1990) Problems reported by relatives in a community sample of dementia. Br. J. Psychiatry 156, 835. Olin JT, Katz IR, Meyers BS et al. (2002) Provisional diagnostic criteria for depression of Alzheimer disease. Am J. Geriatr. Psychiatry 10, 129. Ormel J, Oldehinkel AJ, Brilman E et al. (2001) The interplay and etiological continuity of neuroticism, difficulties, and life events in the etiology of major and subsyndromal, first and recurrent depressive episodes in later life. Am. J. Psychiatry 158, 885. Ostling S, Skoog I (2002) Psychotic symptoms and paranoid ideation in a nondemented populationbased sample of the very old. Arch. Gen. Psychiatry 59, 53. Oyebode J (2003) Assessment of carer’s psychological needs. Adv. Psychiatr. Treat. 9, 45. Richardson B, Orrell M (2002) Home assessments in old age psychiatry. Adv. Psychiatr. Treat. 8, 59.

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Salib E, El-Nimr G (2003) Gender in elderly suicide: analysis of coroner’s requests of 200 cases of elderly suicide in Cheshire 1989–2001. Int. J. Psychiatry Clin. Pract. 18, 1082. Smith D, Dempster C, Glanville J et al. (2002) Efficacy and tolerability of venlafaxine compared with selective serotonin reuptake inhibitors and other antidepressants: a meta-analysis. Br. J. Psychiatry 180, 396. Snowden J, Arie T (2002) Old age psychiatry services: long-stay care facilities in Australia and the UK. Psychiatr. Bull. 26, 24. Spector A, Thorgrimsen L, Woods B et al. (2003) Efficacy of an evidence-based cognitive stimulation therapy programme for people with dementia: randomised controlled trail. Br. J. Psychiatry 183, 248. Unutzer J, Patrick DL, Marmon T, Simon GE, Katon WJ (2002) Depressive symptoms and mortality in a prospective study of 2558 older adults. Am. J. Geriatr. Psychiatry 10, 521. Waern M, Runeson BS, Allebeck P, Beskow J et al. (2002) Mental disorder in elderly suicides: a case – control study. Am. J. Psychiatry 159, 450. Whalley LJ (2002) Brain ageing and dementia: what makes the difference? Br. J. Psychiatry 181, 369. Wilson KCM, Mottram PG, Ashworth L, Abousaley MT (2003) Older community residents with depression. Long-term treatment with sertraline: a randomised, double-blind, placebocontrolled study. Br. J. Psychiatry 182, 492. Wolfson C, Wolfson DB, Asgharian M et al. (2001) A reevaluation of the duration of survival after the onset of dementia. New Engl. J. Med. 344, 1111. Young RC (1992) Geriatric mania. Clin. Geriatr. Med. 8, 387. Zisook S, Schucter SR (1993) Uncomplicated bereavement. J. Clin. Psychiatry 54, 365.

Forensic psychiatry

18

ANTISOCIAL PERSONALITY DISORDER (ASP) See Table 18.1. HISTORICAL DEVELOPMENT

• • • •

Pinel (1801) – Manie sans délire: – Disturbance of emotions and volition; reason intact. Rush (1812) – Moral derangement: – Innate, constitutional moral depravity, amenable to medical treatment. Pritchard (1835) – Moral insanity: – Intellectually unimpaired, but affective and moral faculties disturbed. Koch (1891) – Psychopathic inferiority: – Constitutional predisposition to mental disturbances of all kinds.

Table 18.1 ICD-10 and DSM-IV diagnostic criteria ICD-10

DSM-IV

Dissocial personality disorder Gross disparity between behaviour and social norms; i.e.: (a) callous unconcern for others (b) gross, persistent irresponsibility, disregard for social norms/rules/obligations (c) incapacity to sustain relationships (d) low frustration tolerance and low threshold for aggression (e) inability to experience guilt/benefit from experience (f) blames others/society for behaviour and its consequences

Antisocial personality disorder (a) current age ⭓18 (b) incidence of conduct disorder with onset ⬍15 (c) pervasive pattern of disregard since 15 as shown by ⭓3 of: 1. repeated unlawful behaviour 2. irritability and aggressiveness 3. consistent irresponsibility (work, finances) 4. impulsivity/failure to plan ahead 5. deceitfulness 6. reckless disregard for safety (self or others) 7. lack of remorse (d) antisocial behaviour is not exclusively during the course of schizophrenia or manic episode

216

• • • •

• • •

FORENSIC PSYCHIATRY

Kraepelin (1909) – Psychopathic traits: – Degenerative disorders of personality, separate from neuroses or psychosis (his views changed in later years). Schneider (1927) – Psychopathic personalities: – People who either suffer themselves or cause society to suffer (this introduced the concept of deviance). Partridge (1930) – Sociopath: – Emphasized primary effect on society rather than on the individual (the American perspective). Henderson (1939) – Psychopathy: – Three types described – creative, inadequate, aggressive. – Separate from neuroses. – Selfish, lack of empathy, impulsive, low stress threshold, do not learn from mistakes. Scott (1960): – Absence of other psychiatric illness/defect, antisocial behaviour, persistence since early youth; requires a specialized form of handling by society. Cleckley (1966) – the mask of sanity: – Considered sociopathy equivalent to antisocial personality disorder: pernicious, insightless, affectless. Lewis (1974): – Antisocial personality too general; may apply to ‘normal’ persons who ‘struggle to make a dishonest living’; insufficient regard for the possible neuropsychiatric basis of this behaviour.

EPIDEMIOLOGY There is a 2–3 per cent lifetime prevalence in Western societies (Coid, 2003a). Males are more affected than females (ratio 5:1), and urban dwellers more than rural. Highest rates are in 25- to 44-year-olds. AETIOLOGY Organic causes Twin studies – MZ:DZ concordance ⫽ 60%:30%. Adoption studies confirm a genetic component. There is an excess of obstetric complications, minor physical anomalies, neuropsychological impairments – a form of minimal brain damage or dysmaturation? • EEG abnormalities: – Generalized slow-wave ␪ abnormalities (but normal in 50 per cent of aggressive criminals) which may be localized to the temporal region. – Posterior slow and sharp waves. – Immature ‘EEG’. • Corpus callosum abnormalities may reflect atypical neurodevelopmental pressesses and help explain abnormal interhemispheric transfer seen in psychopathic individuals (Raine et al., 2003). • Low serotonin is found in impulse disorders/ASP.

• • •

VIOLENCE IN THE CONTEXT OF MENTAL ILLNESS

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Sociocultural factors • Lower socioeconomic status families, single/divorced parents. • History of parental sociopathy. • Physical/sexual abuse. Psychodynamic factors Interference with early bonding may result in defective socialization and immaturity of emotional and moral development. Defective superego development may result in:

• • •

Abnormal, stereotyped antisocial behaviour under stress. Excessive anxiety at any perceived threat, so that all anxiety is ignored and there is a lack of anxiety to reinforce morality. Failure to acquire social behaviour at critical learning periods.

MANAGEMENT Primary prevention Prenatal care can lessen intrauterine insults to the brain. Parenting classes can establish a nurturing environment in infancy as well as effective parenting styles. • Early identification of at-risk children (i.e. conduct disorder) can lead to intervention in the home or at school.

• •

Active management Pharmacological – control of aggressive and sexual impulses; treatment of co-morbid illness (depression, DSH, substance abuse). • Psychological: – Supportive psychotherapy; advice to help avoid stressful situations; environmental manipulation. – Cognitive–behavioural therapy to heighten awareness of consequences of behaviour; reshape to appropriate behaviour.

•

Hospitalization Psychiatric hospitalization is of little benefit. More appropriate is a specialized inpatient or day care unit. A therapeutic prison (e.g. Grendon Underwood, UK) may be effective for aggressive psychopaths. Incarceration limits damage to society by the offender. PROGNOSIS The more numerous the risk factors in early life, the greater likelihood of antisocial personality developing. ‘Protective factors’ may offset risk factors; i.e. positive social orientation, good family support system, structure and rules in the household. Patients may become less aggressive and antisocial in later life. They tend to become depressed and self-blaming later. There is an increased incidence of alcoholism and suicide.

VIOLENCE IN THE CONTEXT OF MENTAL ILLNESS The relationship between violence and mental illness is poorly understood and overestimated by the public and media. In societies, violent behaviour is the result of

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FORENSIC PSYCHIATRY

Table 18.2 Swedish epidemiological study of violence Likelihood above normal population rate

Males with major mental disorder (schizophrenia/affective disorder) Females with major mental disorder Males with mental retardation Females with mental retardation

Criminal offence

Violent offence

2.5 5 3 4

4 27 5 25

Adapted from Hodgins (1992).

excessive motivation towards violence together with insufficient self-control. Possibly it therefore occurs in the under-controlled under any stress and in the over-controlled under extreme stress (leading to extreme violence). The peak age for violent offenders is 17–21 years. Fifty per cent of violent crimes occur in or near public houses or in domestic disputes. In 26 per cent of cases, the victim is regarded as having actively precipitated violence.

• • • •

Dangerousness (Scott) – ‘A dangerous concept’; an ‘unpredictable and untreatable tendency to inflict or risk serious irreversible injury or destruction or to induce others to do so’. Violence and psychiatric patients (Tardiff, 1992) – In societies where rates of crimes by the general population and crimes by substance abusers are very high, the mentally disordered and intellectually handicapped account for a very small proportion of offences. Swedish epidemiological study (Hodgins, 1992) – The likelihood (above the normal population rate) of police registration for violent offenses is shown in Table 18.2. 10 per cent of patients in general psychiatric hospital have a history of violence. In general: – Schizophrenia is the most common diagnosis, then organic brain disorders, mania, substance abuse and antisocial personality disorder. – Schizophrenia – related to delusions, hallucinations; often co-morbid substance abuse; violence occurs usually during relapse of illness. The ‘threat–control– override syndrome’. – Mania – less violent than in schizophrenia; early in treatment. – Substance abuse – may be due to disinhibition effect or secondary to delirium or personality-related; associated with alcohol, cocaine (especially crack) and PCP.

PATIENT ASSESSMENT Assessment is difficult, but detailed evaluation is essential.

• • • •

Obtain collateral, old records, police reports, etc. Evaluate carefully the extent and timing of violent episodes: precipitating, perpetuating factors, severity of injury or intended injury, history of previous violence. Past history of violence is best predictor of subsequent violence. Blood and urine screen for alcohol and drug abuse. EEG, CT/MRI may be indicated.

FEATURES OF VIOLENT CRIMES

• • • • • • • •

219

May depend on type and quality of violence. Aggressive sex offenders and the morbidly jealous are particularly liable to reoffend with violence. Threats of violence and frequent violence when drunk may indicate further danger. Repeated violence implies further violence. May depend on environmental factors – if stress remains or if potential victims are still available. Disinhibiting factors (e.g. alcohol, drugs, fatigue) which may occur must be assessed. Lack of remorse may indicate increased dangerousness. Widespread aggressive behaviour appearing at an early age (arson, cruelty to animals) and continuing, especially if also present in the family, indicates recurrence. Fear engendered in the examiner may well indicate dangerousness. Regressive, infantile behaviour during and after an offence may indicate dangerousness. Sadistic fantasy life is an ominous finding.

FEATURES OF VIOLENT CRIMES Violent crimes account for 5 per cent of all indictable offences.

KILLING DEFINITIONS

• • • •

Murder – unlawful killing with malice aforethought (‘mens rea’). Manslaughter – unlawful killing without malice aforethought. Found if there is provocation, diminished responsibility, suicide pact or involuntary killing, or negligence. Infanticide – unlawful killing of a child of less than a year by the mother, who must show postnatal mental disorder. Homicide – encompasses murder, manslaughter and infanticide.

EPIDEMIOLOGY

• • • • • • • • •

500 per year in England and Wales. Murderers have a male:female ratio of 11:1. 75 per cent of victims have a previous relationship with their murderer. 50 per cent of victims are a relative or lover. In the USA, homicide is the 11th most common cause of death. Up to 30 per cent of homicide suspects kill themselves following murder (especially women). Alcohol is involved in up to 50 per cent of cases. 50 per cent of murderers are mentally abnormal – particularly with severe personality disorder. Fewer than 1 per cent recommit murder.

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Thus the most common combination of factors leading to murder are: an irritable and violent husband, alcohol and family disharmony. Sadistic murderers are described as: usually male, under 35, solitary, emotionally blunted, reserved, with a rich fantasy life (fascism, black magic, sadistic pornography).

RAPE DEFINITION Rape is sexual intercourse (i.e. penetration) with a woman who does not consent, the man knowing that she did not consent or being reckless as to whether or not she consented. A CLASSIFICATION

• • • •

Aggressive aim – sexual assault is primarily destructive and sadistic. May be displaced anger (e.g. to mother). May humiliate the victim. Sexual aim – aggression with the aim of achieving sexual intercourse. Part of general hedonism. Explosive – forcible expression of sexual drives in an over-controlled man. May have compulsive quality. Aggressive and sexual aim – resistance and humiliation are essential for sexual satisfaction.

EPIDEMIOLOGY Most rapists are aged under 25 years, single, have a record of non-sexual crime and are not mentally disordered. There is an increased incidence in summer, in the first half of night and at weekends. Thirty per cent of victims are neighbours or acquaintances. Twenty per cent of victims have a criminal record (especially soliciting). OUTCOMES

• • •

80 per cent of rapists are sentenced to prison. 85 per cent of aggressive rapists later commit non-sexual crimes and 20 per cent recommit sexual offences. 28 per cent of non-aggressive rapists later commit non-sexual crimes and 3 per cent recommit sexual offences.

ARSON DEFINITION Arson is to damage or destroy any property by fire, without lawful excuse. A CLASSIFICATION

•

Motivated arson: – No psychotic disorder; insurance fraud, bankruptcy, revenge, political, to cover up another crime, vagrant. – Suicidal.


•

•

221

– Result of boredom, desire to impress. – Juvenile fire (firesetting, fireplay). Motivated by mental illness: – Schizophrenia (approx 8 per cent of convicted arsonists), probably in response to voices, delusions. – Depression, possibly due to morbid delusion, or in manic excitement. – Drug or alcohol-induced psychosis, diminished responsibility. – Mental retardation. – Dementia. Motiveless arson: – Primary interest is the fire is the excitement, sexual arousal, desire to be the hero, release of tension. – Repeated offenders (‘firebugs’) fall into this category.

EPIDEMIOLOGY Arson accounts for 0.1 per cent of all serious crime (one-third the incidence of murder or rape). There is a peak incidence at 17 years in men, at 45 years in women (85 per cent of offenders are men). There is an increased incidence of mental retardation (up to 50 per cent) and alcoholism. OUTCOMES

• •

Fewer than 4 per cent repeat arson. There is an increased likelihood of recurrence with: – History of previous arson. – Presence of psychosis, severe abnormality or dementia. – Marked pleasure or sexual excitement associated. – Awareness by arsonist of overwhelming urge to start fires to relieve tension.

NON-ACCIDENTAL INJURY TO CHILDREN DEFINITIONS

• • •

In 1962 Kempe introduced the term battered child syndrome to describe the signs and symptoms characteristic of physical abuse. In 1972 Caffey introduced the term shaken baby syndrome to describe the signs and symptoms of violent shaking of an infant that results in tearing of intracranial veins with the degree of brain damage corresponding to the intensity of shaking. An overall definition is ‘the killing of, physical violence towards, persistent abuse of or neglect of a child, by those in charge of the child’.

A CLASSIFICATION (SCOTT)

• • • • •

Elimination – of an unwanted encumbrance. Euthanasia – mercy killing (e.g. of handicapped child). Psychotic – the result of delusions. Displaced anger – from elsewhere on to the child. Anger – arising from within the child–parent relationship.

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EPIDEMIOLOGY Possibly 0.5 per cent of children aged under 3 years are involved (considerable underreporting). Underweight and ill children are particularly likely to be battered.

• • • • •

1 in 1000 children aged under 4 years suffers major injury each year in England and Wales. The death rate is 10 per cent in 2 years, and 25 per cent are intellectually damaged. 2–4 per cent of children are in subnormality hospitals. There is a 60 per cent chance of further battering. 19 per cent of siblings have also been battered.

CLINICAL FEATURES TO AROUSE SUSPICION In the child Bruises, burns or lacerations of different ages. Multiple fractures (or any fracture in child under 2 years). Subperiosteal haematomas, epiphyseal separations. Subdural haematoma, retinal injury, rupture of abdominal viscera or any bizarre injury. • Failure to thrive of unknown aetiology. • ‘Frozen watchfulness’ towards parents. • ‘Reverse caring’ (child shows over-anxious concern for parents). In parents • Delayed reporting. • Parents do not volunteer information. • Contradictory stories. • ‘Mechanical handling’ of child, lacking warmth and confidence.

• • • •

Associated features In child • Illegitimacy. • Early separation from parents. In parents • Lower social class. • Young maternal age. • Unmarried or father absent. • Subnormality in mother. • Very rarely (3 per cent) psychotic mother. • Criminal record and/or personality disorder in father. • Family is socially isolated. • Parents often victims of battering themselves. PREVENTION 1 2 3 4

A high level of awareness of the problem is needed in baby clinic, by GPs, etc. There should be good communication between services, with easy availability of help. Emergency action (e.g. Place of Safety order) should be rapidly available. ‘At risk’ case registers must be held by local authorities.


223

5 Case conferences should be held, with designation of a ‘key worker’. 6 Supportive family therapy should be considered to correct unrealistic expectations of having a child, reduce resentment and improve marital understanding.

PAEDOPHILIA Paedophilia is the erotic attraction to children. There are three characteristic groups:

• • •

Immature adolescents. Middle-aged men with marital difficulties. Elderly, socially isolated men.

Fifty per cent of perpetrators are relatives or friends. Once discovered, most do not reoffend.

INCEST There is a variable extent of sexual activity, from fondling to intercourse. In 75 per cent cases it is between a father/stepfather and daughter. Five per cent of the adult female population report being abused by their father. Forty-four per cent of incest perpetrators have also committed extrafamilial offences. Characteristics of the offender • No specific traits. • High rates of alcohol abuse. • 30 per cent sexually and/or physically abused as a child. • Often a pattern of poor marital relationships. Characteristics of the abused Females ⬎⬎ males.

CHILD SEXUAL ABUSE (CSA) Child sexual abuse is a general term that includes incest. A range of definitions results in wide reported prevalence rates: 12–36 per cent of females and 3–29 per cent of males report some sexual abuse in childhood. CSA may occur at any age, but the peak occurrence is after age 12 years. The mean duration of abuse before detection is 2 years. Boys tend to be abused at an earlier age, and the offender is more likely to be a stranger. Absence of one or both parents and the presence of a stepfather in the home conveys greater risk of CSA. Poverty is associated with greater reporting of CSA but not necessarily greater incidence. Presentation of CSA by child There are diverse manifestations, such as sexualized behaviour, self-mutilation, childhood substance abuse and depression.

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EVALUATION

• • • • • •

Attempt to confirm CSA. Many cases of ‘suspected abuse’ demonstrate incomplete evidence, and the family declines investigation. Use of anatomical dolls is controversial. There is overlap in play behaviour of nonabused and abused children, so this is not a good diagnostic tool. If CSA is confirmed in a minor, or strongly suspected by a health professional, social services must by law be informed in the UK and USA. Children as witnesses – Younger children are suggestible; overall, children are competent witnesses; most do not lie. Multidisciplinary evaluation – Legal involvement must be early on to protect the child from ongoing CSA.

MANAGEMENT This must be multimodal:

• • • •

Cognitive–behavioural therapy. Social skills education, stress management. Family intervention therapy, if appropriate. Legal action and a programme to prevent further CSA.

OUTCOMES There is a drop-out rate of 18 per cent for incest families in therapy. However, with therapy, 60 per cent of families are safe from further abusive behaviours. Long-term sequelae for the abused child Emotional: Anxiety/fear, low self-esteem, anger, guilt. Psychiatric: • Depression, deliberate self-harm. • Personality disturbance (borderline, multiple personality). • Substance abuse. • PTSD symptoms. • Eating disorders. • Somatization. Behavioural: Early sexual activity. Promiscuity, teenage prostitution. Adult sexual dysfunctional disorders.

• • •

NON-VIOLENT OFFENDERS (SHOPLIFTING) There are several groups of shoplifters: • Professionals who steal as a livelihood. • Shoplifters with severe psychiatric disorder. • Reactive shoplifters – as a transient stress reaction.

LEGAL ASPECTS

• •

225

Young shoplifters – the majority. Those with abnormal learned behaviour – repetitive theft.

EPIDEMIOLOGY Figures in the early 1970s showed that most offenders were women. Ninety per cent did not reoffend when caught. Fifteen per cent of British-born offenders showed a psychiatric disorder. Recent changes • There has been an increase in young shoplifters (ages 10–18) – now the majority. • There has also been an increase in male shoplifters – now the majority. • The incidence of psychiatric disorder is reduced – now estimated at 5 per cent. • The offence may be regarded by some as an ‘accepted perk’ of shopping. Approximately 5 per cent shoplift at each shop they visit.

LEGAL ASPECTS PREPARING COURT REPORTS Plan of report – Name, address and age of person charged. – Charge. – When and where interviewed. – All other sources of information (notes, other doctors, relatives, etc.). – Short description of person charged. – Concise, relevant family history. – Concise, relevant personal history. – Past medical, psychiatric and criminal history. – Brief account of circumstances of offence and any relevant psychiatric disturbances, sources of tension, etc. – Findings at interview, including assessment of personality. – Findings of further investigations (EEG, psychological testing, etc.). – Opinion – All the above information is merely an explanation of the basis of the opinion. Comment on fitness to plead, responsibility for offence, mitigating factors, prognosis. – Recommendations – for treatment and further management, if appropriate. – Psychiatrist’s name, qualifications, professional address and approval under the Mental Health Act. Aim at accuracy, understandability, relevance and impartiality.

PSYCHIATRIC DEFENCES (APPLIES TO UK ONLY) Unfit to plead (at the time of trial) This is decided by a jury. It results in admission to a special hospital until fit to plead, as decided by the Home Secretary.

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The person charged must be: 1 2 3 4 5

Unable to understand the charge or the significance of the plea; or Unable to challenge a juror; or Unable to instruct counsel; or Unable to examine a witness; or Unable to follow the progress of the trial.

Not guilty by reason of insanity (‘special verdict’) McNaughten rules: ‘Labouring under such a defect of reason, from disease of the mind, as not to know the nature and quality of the act he was doing, or if he did know it, that he did not know that what he was doing was wrong.’ This is less used in murder cases since abolition of the death penalty by the Homicide Act (1957). If the ‘special verdict’ is found, the defendant is detained in hospital and his/her time of release is decided by the Home Secretary. Diminished responsibility This defence can be used only if the charge is murder. If found, it reduces the charge of murder (carrying a mandatory life sentence) to manslaughter (sentencing at the discretion of the judge). The defendant must be suffering from ‘such abnormality of mind … as substantially to impair his mental responsibility for his acts’. ‘Abnormality of mind’ is a state of mind so different from that of ordinary human beings that the reasonable person would term it abnormal. It could include severe personality disorder, extreme intoxication, etc. Possible results at sentencing • The law takes its normal course – prison, fine, etc. • Conditional or absolute discharge – possibly with voluntary psychiatric treatment. • Probation order, under Powers of Criminal Courts Act 1973. An approved psychiatrist (s.12 of the Mental Health Act) takes on the responsibility for treatment, as an inpatient or outpatient. The offender must agree to this. • Detention in hospital under s.60 of the Mental Health Act, with or without s.65. • Offenders aged under 17 years may be committed to the care of the local authority.

CRIMINAL RESPONSIBILITY (APPLIES TO UK ONLY) AGE

• • •

A child under 10 years is held to be incapable of forming a guilty intent (mens rea). A child of 10–13 years is so capable if he/she is able to discern good from evil. A child of 14 years and over is presumed to be fully responsible for his/her actions.

INTENT Some offences require that specific guilty intent (mens rea) be proved present as well as the unlawful act (actus reus) – e.g. murder, arson, rape, assault with intent to cause grevious bodily harm. Other offences do not require proof of guilty intent – e.g. manslaughter, indecent assault, assault occasioning actual bodily harm.

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Complicating factors • Multiple intention. • Unconscious intention. • Changing intention during the crime. • Overwhelming tension, stress or emotion. • Amnesia, including that due to alcohol. • Alien intention (as in schizophrenic passivity). • Self-induced intoxication Simple drunkenness is no defence. A person may not, however, be held to have committed a crime requiring mens rea if that person was too drunk to form an intent. The person may, however, be held to have committed a crime not requiring proof of mens rea.

TESTAMENTARY CAPACITY (APPLIES TO UK ONLY) A person may make a will if he/she is ‘of sound disposing mind’ and: 1 Knows the nature and extent of his/her property. 2 Knows the persons having a claim on it and the relative strengths of their claims. 3 Can express himself/herself clearly and without ambiguity.

COMPETENCE TO CONSENT TO TREATMENT (APPLIES TO UK ONLY) INFORMED CONSENT Informed consent, which may be verbal or written, includes: 1 2 3 4 5

Disclosure of information. Competency. Understanding. Voluntariness. Decision.

COMPETENCY Does the patient understand: 1 2 3 4

The condition for which treatment is proposed? The nature and purpose of the treatment? The risks and benefits of undergoing the treatment? The risks and benefits of not undergoing the treatment?

NEGLIGENCE Negligence results in unintentional wrong to a person. To be found it requires the Four D’s: 1 2 3 4

A duty to a client. A dereliction (breach) of duty. The breach is a direct cause of the damage. Actual damages result from the breach of duty.

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Duty is accepted as the usual standard of care, as assessed by a responsible body of medical opinion. Common causes of action against psychiatrists include: suicide, injury to a third party and treatment with medication (lethal overdose, side-effects, tardive dyskinesia, benzodiazepine dependency).

TARASOFF DOCTRINE In the USA, courts have decided that a psychiatrist who knows or should know of a patient’s dangerousness to a third person must take all reasonable steps to protect (not just inform) potential victims.

INVOLUNTARY COMMITMENT There is wide variation across countries and mental health systems on terms and procedures for commitment. Common elements include:

• • • •

Commitment due to the presence of mental disorder which poses grave and imminent risk to self or others. Certification by a health professional (not exclusively by a psychiatrist). Limitation on duration of involuntary hold. A review process (tribunal, court, etc.) prior to the end of the time limitation, linked to patient appeal process.

Commitment must be for a defined mental disorder. Sexual deviancy, immorality, excesses of drugs/alcohol, violence (without mental disorder ⫽ legal problem) are not mental disorders and reasons per se for commitment. Commitment represents a delicate balance between the protection of society and protecting personal autonomy. In some systems, commitment procedures allow containment only for assessment, there being a separate (secondary) procedure for involuntary treatment. Most systems invoke both assessment and treatment. Most commitment statutes are for inpatient hospitalization, but there is a growing trend towards outpatient commitment. The patient is ordered to follow a ‘community treatment order’, or else revocation of community tenure with rehospitalization. This is difficult to enforce and monitor. New initiatives There is a broad move to enhance appropriate diversion of mentally ill offenders into mental heath care rather than jails. In a jail diversion programme, for example, mental health professionals might be called out to assist police at the time of disturbance of the peace due to a patient’s psychotic behavior; the patient receives hospitalization rather than jail. Mental health courts are another initiative.

PSYCHIATRIC ADVANCED DIRECTIVES Two types of directive are available to specify the wishes of an individual should he/she no longer have the capacity to make decisions on his/her own behalf.

MANAGEMENT OF DANGEROUS MENTALLY DISTURBED PERSONS

• •

229

Living will – provides specific information about treatment concerns. Proxies or healthcare powers of attorney – designates an individual to act as a surrogate decision-maker.

MENTAL ILLNESS IN PRISONS There is a high prevalence of psychiatric illnesses in prisoners (Fazel and Danesh, 2002):

• •

• • •

Males: – 3.7 per cent psychotic disorder. – 10 per cent major depression. – 65 per cent personality disorder. Females: – 4 per cent psychotic disorder. – 12 per cent major depression. – 42 per cent personality disorder. The high prevalence of mental illness in prison has various causes, including: Small likelihood of early release. Small likelihood of being granted probation. High rates of revocation of probation.

MANAGEMENT OF DANGEROUS MENTALLY DISTURBED PERSONS AT A POLITICAL LEVEL Possible policies 1 Mental hospitals should provide secure facilities on an area or regional basis; i.e. a return to traditional roles. 2 There should be better provision for the mentally disturbed within prisons. This requires a change of policy: prisons are for punishment, hospitals for treatment. Grendon Underwood, for people with severe personality disorders, is the only such prison in England and Wales. – Between 20 and 40 per cent of prisoners are found to be psychiatrically disturbed (2 per cent are psychotic, 11 per cent have alcohol and drug addictions, 14 per cent are mentally handicapped), and the suicide rate is three times higher than normal. In Western societies the size of the prison population is inversely related to the size of the mental hospital population. 4 There needs to be more provision of special hospitals (e.g. Broadmoor, UK). But these may be expensive, institutionalized and have difficulty discharging patients because other hospitals will not accept them. They are part of the Health Service and are under the direct control of the Secretary of State for Health. 5 There can be provision of regional secure units and, more recently advocated, development of smaller, more widely distributed units: 1500 medium secure units and 750 long-term medical secure beds are recommended for England and Wales (Reed Report; UK Government, 1992).

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AT WARD LEVEL Architectural considerations • Adequate but unobtrusive security. • Ease of arousal of alarm. • Available space for exercise, expression of anger, etc. Staff policies Develop a clear violence-prevention policy of which all staff are aware. Adequate training of staff in coping with violent behaviour. Adequate numbers of staff (1:1 ratio) in units with violent patients. Acceptance of responsibility of dealing with violence by all staff, teamwork. Effective communication of dangers. Rapid availability of more staff and of medical staff.

• • • • • •

Management of the violent incident Raise the alarm. Free any victim, remove weapons as soon as possible. Assess diagnosis (e.g. alcohol, psychosis). Remain calm and non-critical. Use minimum necessary force; avoid force if possible. ‘Talk patient down’ – done by the most skilled staff member or member most trusted by the patient. Involves listening, agreeing, reassuring. • If force is necessary, ensure adequate numbers of staff. • If sedation is needed (IV or IM), use carefully. Can be given even to informal patients in an emergency. • Ensure adequate reporting and ward discussions afterwards.

• • • • • •

LONG-TERM MANAGEMENT Psychotherapy Detainees need a place to call at times of stress. There should be attention to self-esteem and masculinity. Exploration of violent fantasies in a controlled setting can be beneficial. Increase the patient’s understanding of feelings behind violence. Counselling and behavioural techniques may help the patient to avoid stressful situations.

• • • • •

Drug therapy Numerous drugs are claimed to be anti-aggressive (Corrigan et al., 1993): lithium, antipsychotics, valproate, carbamazepine. Use of benzodiazepines may result in paradoxical aggression due to disinhibition.

REFERENCES AND FURTHER READING American Psychiatric Association (2002) Psychiatric Services in Jails and Prisons: a Report of the Task Force to Revise the APA Guidelines on Psychiatric Serviecs in Jails and Prisons. American Psychiatric Association, Washington, DC. Applebaum P (2001) Thinking carefully about outpatient commitment. Psychiatr. Serv. 52, 347. Blair RJR (2003) Neurobiological basis of psychopathy. Br. J. Psychiatry 182, 5. Bluglass R (1990) Forensic Psychiatry: a Comprehensive Textbook. Churchill Livingstone, Edinburgh.


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Buchanan A, Leese M (2001) Detention of people with dangerous severe personality disorders: a systematic review. Lancet 358, 1955. Buckley PF, Noffsinger SG, Smith DA et al. (2003) Treatment of the psychotic patient who is violent. Psychiatr. Clin. North Am. 26, 231. Carpenter WT (1999) The challenge to psychiatry as society’s agent for mental illness treatment and research. Am. J. Psychiatry 156, 1307. Chen YH, Aria AM, Anthony JC (2003) Firesetting in adolescence and being aggressive, shy, and rejected by peers: new epidemiologic evidence from a national sample survey. J. Am. Acad. Psychiatry Law 31, 44. Coid J (2003a) Epidemiology, public health and the problem of personality disorders. Br. J. Psychiatry 182, s3. Coid J (2003b) Formulating strategies for the primary prevention of adult antisocial behaviour: ‘high risk’ or ‘population’ strategies? In: Farrington DP, Coid JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 32–78. Cambridge University Press, Cambridge. Coid J, Petruckevitch A, Bebbington P et al. (2002a) Ethnic differences in prisoners. 1: Criminality and psychiatric morbidity. Br. J. Psychiatry 181, 473. Coid J, Petruckevitch A, Bebbington P et al. (2002b) Ethnic differences in prisoners. 2: Risk factors and psychiatric service use. Br. J. Psychiatry 181, 481. Corrigan PW, Yudovsky SC, Silver JM (1993) Pharmacological and behavioural treatments for aggressive psychiatric patients. Hosp. Commun. Psychiatry 44, 125. Cottle CC, Lee RJ, Heilbrun K (2001) The prediction of criminal recidivism in juveniles. Crim. Just. Behav. 28, 367. Dolan M, Millington J, Park I (2002) Personality and neuropsychological function in violent, sexual and arson offenders. Med. Sci. Law 42, 34. Earthrowl, M, O’Grady J, Birmingham L (2003) Providing treatment to prisoners with mental disorders: development of a policy: selective literature review and expert consultation exercise. Br. J. Psychiatry 182, 299. Fazel S, Danesh J (2002) Serious mental disorders in 23,000 prisoners: a systematic review of 62 surveys. Lancet 349, 545. Feeney A (2003) Dangerous severe personality disorder. Adv. Psychiatr. Treat 9, 349. Gesch CB, Hammond SM et al. (2002) Influence of supplementary vitamins, minerals and essential fatty acids on the antisocial behaviour of young adult prisoners: randomised, placebocontrolled trial. Br. J. Psychiatry 181, 22. Glasser M, Campbell KD, Glasser A et al. (2001) Cycle of child sexual abuse: links between being a victim and becoming a perpetrator. Br. J. Psychiatry 179, 482. Gordon H, Grubin D (2004) Psychiatric aspects of the assessment and treatment of sex offenders. Adv. Psychiatr. Treat. 10, 73. Haque Q, Cumming I (2003) Intoxication and legal defences. Adv. Psychiatr. Treat 9, 144. Harty MA, Thomas S, Parrot J (2001) HM prison healthcare needs assessment. J. Forens. Psychiatry 12, 639. Hawkins JD, Herrenkohl TI (2002) Prevention in the school years. In: Farrington DP, Coid JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 265–291. Cambridge University Press, Cambridge. Herpertz SC, Wenning B, Mueller B et al. (2001) Psychophysiological responses in ADHS boys with and without conduct disorder: implications for adult antisocial behavior. J. Am. Acad. Child Adolesc. Psychiatry 40, 1222. Hill J (2003) Early identification of individuals at risk for antisocial personality disorder. Br. J. Psychiatry 182 (Suppl. 44), s11. Hodgins S (1992) Mental disorder, intellectual deficiency, and crime: evidence from a birth cohort. Arch. Gen. Psychiatry 49, 476. Honberg RS (2003) Advance Directives. www.nami.org/Content/ContentGroups/Legal/ Advance_Directives.htm (accessed 28 December 2003).

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Kennedy HG, Ivenson RC, Hill O (1999) Violence, homicide and suicide: strong correlation and wide variation across districts. Br. J. Psychiatry 175, 462. Lamb HR, Bachrach LL (2001) Some perspectives on deinstitutionalization. Psychiatr. Serv. 52, 1039. Lane WG (2003) Diagnosis and management of physical abuse in children. Clin. Fam. Pract. 5, 493. Litwack TR (2001) Actuarial versus clinical assessments of dangerousness. Psychol. Pub. Pol. Law 7, 409. Macpherson R, Cornelius F, Kilpatrick D, Blazey K (2002) Outcome of clinical risk management in the Gloucester rehabilitation service. Psychiatr. Bull. 26, 449. Monahan J, Bonnie RJ, Applebaum PS et al. (2001) Mandated community treatment: beyond outpatient commitment. Psychiatr. Serv. 52, 1198. Monahan J, Steadman H, Silver E et al. (2001) Rethinking risk assessment: the MacArthur study of mental disorder and violence. Oxford University Press, New York. Mowbray CT, Grazier KL, Holter M (2002) Managed behavioral health care in the public sector: will it become the third shame of the States? Psychiatr. Serv. 53, 157. Munro E, Rumgay J (2000) Role of risk assessment in reducing homicides by people with mental illness. Br. J. Psychiatry 76, 116. Nestor PG (2002) Mental disorder and violence: personality dimensions and clinical features. Am. J. Psychiatry 159, 1973. Putnam FW (2003) Ten-year research update review: child sexual abuse. J. Am. Acad. Child Adolesc. Psychiatry 42, 269. Raine A (2002) Biosocial studies of antisocial and violent behavior in children and adults: a review. J. Abnorm. Child Psychol. 30, 311. Raine A, Lentz T, Taylor K et al. (2003) Corpus callosum abnormalities in psychopathic antisocial individuals. Arch. Gen. Psychiatry 60, 1134. Ramchandani P, Jones DPH (2003) Treating psychological symptoms in sexually abused children: from research findings to service provision. Br. J. Psychiatry 183, 484. Reed J (2003) Mental health care in prisons. Br. J. Psychiatry 182, 287. Roberts LW (2002) Informed consent and the capacity for voluntarism. Am J. Psychiatry 159, 233. Rock M (2001) Emerging issues with mentally ill offenders: causes and social consequences. Admin. Policy Ment. Health 28, 165. Rutter M (2003) Causal processes leading to antisocial behaviour (commentary). Dev. Psychol. 39, 372. Tardiff K (1992) The current state of psychiatry in the treatment of violent patients. Arch. Gen. Psychiatry 49, 493. Taylor JL, Thorne I, Robertson A, Avery G (2002) Evaluation of a group intervention for convicted arsonists with mild and borderline intellectual disabilities. Crim. Behav. Ment. Health 12, 282. Taylor PY, Leese M, Williams D et al. (1998) Mental disorder and violence. Br. J. Psychiatry 172, 218. Tremblay RE, Japel C (2003) Prevention during preganancy, infancy and the preschool years. In: Farrington DP, Coid JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 205–242. Cambridge University Press, Cambridge. Trowell J, Kolvin I, Weeramanthri H et al. (2002) Psychotherapy for sexually abused girls: psychopathological outcome findings and patterns of change. Br. J. Psychiatry 180, 234. UK Government (1992) Review of Health and Social Services for Mentally Disordered Offenders and Others Requiring Similar Services (Reed Report). HMSO, London. Uting D (2003) Prevention through family and parenting programmes. In: Farrington DP, Coid JW (eds), Early Prevention of Adult Antisocial Behaviour, pp. 243–264. Cambridge University Press, Cambridge. Volavka J (2002) The Neurobiology of Violence. American Psychiatric Press, Washington, DC. Walsh E, Buchanan A, Fahy T (2002) Violence and schizophrenia: examining the evidence. Br. J. Psychiatry 180, 490. Wasserman GA (2003) Mental health assessments in juvenile justice: report on the consensus conference. J. Am. Acad. Child Adolesc. Psychiatry 42, 752. Wettstein RM (2002) Ethics and forensic psychiatry. Psychiatr. Clin. North Am. 25, 623. World Health Organization (2002) World Report on Violence and Health. WHO, Geneva.

Child psychiatry

19

OVERVIEW EPIDEMIOLOGY The Mental Health Evaluation and Community Consultation Unit at the University of British Columbia (2002) reported on the prevalence of mental disorders in youth and found a 15 per cent prevalence of any type of mental disorder. Of these, 6.5 per cent had an anxiety disorder, 3.3 per cent conduct disorder, 3.3 per cent attentiondeficit/hyperactivity disorder (ADHD), 2.1 per cent depression. DIFFICULTIES DIAGNOSING THE YOUNG

• • • • • • •

There is only a limited life history. Children are in the process of developing. Symptoms overlap with other disorders. There tends to be co-morbidity of diagnoses. Multiple informants are needed – school, family, clinician. Reports of symptoms vary. Substance use and trauma must be ruled out.

TREATMENT CONSIDERATIONS Psychopharmacology Research on psychopharmacology in the young is limited. There is frequent ‘off label’ use of prescribed medications, frequently treat target symptoms. • Appropriate consent for treatment is needed. • Extended-release medications avoid school dosing. • Children require lower dosing of dopamine antagonists. • There is highly efficient hepatic metabolism in the young.

• •

Other considerations Need for family involvement in assessment and treatment. Role of peer influence. School teachers/counsellors are important.

• • •

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Table 19.1 Main groups of childhood psychiatric disorders as classified in ICD-10 and DSM-IV ICD-10

DSM-IV

F80 Specific developmental disorders of speech and language F81 Specific developmental disorders of scholastic skills F82 Specific developmental disorders of motor function F83 Mixed specific developmental disorder F84 Pervasive developmental disorder F90 Hyperkinetic disorders

Learning disorders Communication disorder

F91 Conduct disorders F92 Mixed disorders of conduct and emotion F93 Emotional disorders with onset specific to childhood F94 Disorder of social functioning with onset specific to childhood and adolescence F95 Tic disorders F98 Other behavioural/emotional disorders with onset usually in childhood/adolescence

Motor skills disorder Pervasive developmental disorder Disruptive behaviour and attention-deficit disorders

Other disorders of infancy, childhood or adolescence Feeding and eating disorders of infancy or early childhood Tic disorders Elimination disorder

CLASSIFICATIONS OF CHILDHOOD PSYCHIATRIC DISORDERS See Table 19.1.

MATERNAL DEPRIVATION Bowlby has expounded the theory that a warm, intimate and continuous mother–child relationship is essential for subsequent mental health of the child. There are two components: 1 Bonding describes the relationship formed between mother and baby, usually over the first few days of life. This process may be impaired by illness, separation, ambivalence towards the pregnancy, etc. 2 Attachment describes the relationship of child to mother. This is presumed not to be formed until after the first 6 months. ‘Maternal deprivation’ is a loose term covering those experiences in which the attachment process with mother is disrupted through death or other distortions. It is important to discriminate between basic variables combined under the term ‘maternal deprivation’, such as:

• • •

Lack of opportunity to form attachments is different from their being broken. Physical separation is different from deprivation of maternal care (which could be provided by someone else). Separation by death differs from separation through a broken home.

PERVASIVE DEVELOPMENTAL DISORDER (‘AUTISM’)

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Rutter (1972) distinguishes between them thus:

• • • •

Short-term separation (e.g. hospitalization). Consequences are the ‘distress syndrome’: – Protest (tears, etc.). Despair (apathy and misery). Detachment (apparent contentment, indifference on mother’s return). Long-term maternal deprivation. Consequences are: – Antisocial behaviour. – Poor development of IQ and language. – ‘Affectionless psychopathy’. – Poor physical growth (‘deprivation dwarfism’). – Depression.

PERVASIVE DEVELOPMENTAL DISORDER (‘AUTISM’) CLINICAL FEATURES

• • • • •

Onset before 30 months of age. Major deficits in language development (echolalia, pronomial reversal, perseveration). Disturbance of normal social interaction. Bizarre responses to environment; e.g. resistance to change, irrational attachment to various objects, rituals and routines. Absence of delusions, hallucinations, loosening of associations as in schizophrenia.

Associated features Unpredictable fears, screaming or laughter. Abnormal movements (stereotypies, etc.). Hyperkinesis. Self-destructive behaviour. Difficulties learning manipulative tasks. Isolated skills (e.g. rote memory). Up to two-thirds have IQs in the MR range.

• • • • • • •

EPIDEMIOLOGY

• • • • •

By definition, onset is before age 30 months. Boy:girl ratio ⫽ 3.8:1. There is a normal socioeconomic distribution. There are 34 cases per 10 000 in the USA (Yeargin-Allsopp et al., 2003). There are 62.6 cases per 10 000 in the UK (Chakrabarti and Frombonne, 2001).

AETIOLOGY Genetics Concordance rate – MZ:DZ twins ratio ⫽ 36:0. There is a 3 per cent prevalence among siblings of autistics. About 5 per cent of autistic patients have fragile X syndrome.

• • •

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Non-genetic factors Autism is (uncommonly) associated with PKU, congenital rubella, tuberous sclerosis, Rett’s syndrome. There is a high prevalence of mental retardation and cognitive impairments, even in ‘mild’ autistics. One-third of autistics develop seizures during adolescence. Neurochemistry • Increased CSF HVA associated with autistic stereotypies. • Increased 5-HIAA associated with symptom severity. Other factors There is an excess of perinatal complications, minor physical anomalies, abnormal dermatoglyphics – suggesting a neurodevelopmental basis. Some MRI findings (cerebellar hypoplasia, polymicrogyria) are consistent with this, although there has been overall inconsistency in neuroimaging findings to date. Psychosocial factors Emotional factors are not causative. The hypothesis of ‘refrigerator parents’ is now discounted. DIFFERENTIAL DIAGNOSIS Exclude: deafness, childhood schizophrenia, mental retardation with behavioural symptoms, disintegrative psychosis, developmental language disorder, CNS disorders (tuberous sclerosis, etc.). COURSE AND PROGNOSIS The condition is chronic. IQ and development of language skills are related to prognosis:

• • •

Severely handicapped – about 66 per cent. Fair adjustment – about 17 per cent. Adequate social adjustment – about 17 per cent.

MANAGEMENT There is no ‘specific’ treatment. Modalities cover:

• • • •

Counselling and support for parents; self-help groups. Educational placement. Behaviour modification – social behaviour, language skills, etc. Drug treatments.

No drug is specifically recommended. Atypical antipsychotics probably decrease behavioural symptoms. Antiepileptics have been shown experimentally to help some autistic patients.

MOOD DISORDERS IN CHILDREN/ADOLESCENTS

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OTHER DEVELOPMENTAL DISORDERS ASPERGER’S DISORDER Asperger’s disorder begins in the third year of life. Males are affected more than females (6:1 ratio). There are not the cognitive or verbal deficits as seen in autism. There is abnormal social reciprocity – the child often appears odd or eccentric. He/she often exhibits restricted obsessional, ritualistic or idiosyncratic interests/activities. This disorder is said to have a better social prognosis than autism, but their separate status is disputed by some.

CHILDHOOD-ONSET SCHIZOPHRENIA Twenty-five per cent of schizophrenia has an onset before age 15 years. There are prominent brain changes on MRI. Medication treatment is complicated by the greater sensitivity to antipsychotic medication side-effects, so lower doses are indicated. The prognosis is poor.

DISINTEGRATIVE PSYCHOSIS There is severe and sustained impairment in social relationships, speech and language. Onset is after 24 months.

MOOD DISORDERS IN CHILDREN/ADOLESCENTS See also Chapter 4. There is major concern about the diagnosis and possibly increasing incidence of bipolar illness and depression in children.

BIPOLAR DISORDER This is often a controversial diagnosis in adolescents, and especially so in young children. The diagnosis is made difficult by the variability in presentation, overlap of symptoms with other disorders, the low incidence rate, medication-induced mania (SSRIs, steroids), and substance abuse.

• • •

Severe or psychotic depression may precede mania. Psychosis is often part of mania in the young. Mixed states and rapid (sometimes ultra rapid) cycling are common.

There are serious lifelong implications with poorer prognosis if the parents have psychiatric disorders: increased rates of substance use, suicide attempts/completions, legal difficulties and academic difficulties.

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MANAGEMENT As with adults, manage with mood stabilizers, atypical antipsychotics, or a combination of atypical antipsychotics with a mood stabilizer. However, treatment resistance is common.

DEPRESSION AND SUICIDE Depressive symptoms are common in emotionally disturbed children, but earlier studies suggested that typical depressive disorder of adulthood was uncommon. Rutter et al. (1970) found depressive disorders in only 1–2 children per 1000 of 10- to 11-year-olds. A broader view suggests that masked depression (presenting as behaviour disorders) and depressive equivalents (presenting with somatic symptoms) are much more common. However, these concepts are so over-inclusive that nearly all childhood disorders could be included. There are high rates (40 per cent) of co-morbidity, especially of anxiety disorder and conduct disorder.

• • •

Depression, irritability and social withdrawal are prominent features. Childhood depression is usually self-limiting, but may become chronic and presage recurrent depression in adulthood. Suicide is extremely rare before puberty, but the incidence rises during adolescence.

DIAGNOSIS, MANAGEMENT AND PROGNOSIS Use of self-report schedules (e.g. CDI) or semi-structured interviews (e.g. K-SADS) may aid diagnosis. Antidepressants may be started with low doses but, with close monitoring, adult dosage may be required to achieve a therapeutic blood level. Non-specific social and psychological treatments and cognitive approaches are also helpful but need further research evaluation. Early-onset bipolar disorder carries a poor prognosis. Typical characteristics of a suicidal child Above-average intelligence. Disturbed family. Recent involvement in antisocial behaviour and non-attendance at school. Close experience of similar behaviour in peers. An apparently depressed mental state with marked guilt. Recent humiliation or imminent disciplinary action. Feels alienated socially.

• • • • • • •

Actual suicide in children and early adolescents is rarely impulsive, and frequently warnings are given.

ANXIETY DISORDERS IN CHILDREN – OVERVIEW See also Chapter 5.

SCHOOL REFUSAL

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Anxiety in a child may be developmentally appropriate (e.g. stranger anxiety, separation anxiety) and becomes a disorder only when it occurs beyond developmental norms, and causes distress and impairment. Anxiety disorder may be difficult to diagnose in the young due to ‘normalization’ of behavior, and minimalization of impairment. The young rarely present with a subjective report of ‘feeling anxious’. Instead, somatic complaints are common. Treatment is similar to that in adults: cognitive–behavioural therapy, SSRIs, etc.

SCHOOL REFUSAL School refusal is a persistent reluctance or refusal to go to school in order to stay with a major attachment figure. See the diagram and Table 19.2. Not at home (truancy) Domestic reasons Child not at school

Kept at home Emotional disturbance in parent

At home School refusal

Separation anxiety

Fear of travel

General social withdrawal

Specific fears at school

The term ‘school phobia’ is now rarely used. Some classify school refusal under ‘separation anxiety disorders’ (ICD-10). Probably it is not an entity – possibly in some cases it is a variant of childhood depression. Other features • Anxiety symptoms are seen more often than depressive symptoms. • Onset is more often gradual than sudden. • The child may be timid and fearful outside, demanding and wilful at home. • Academic attainments good or superior. EPIDEMIOLOGY Age at presentation is most commonly 11 years but is distributed over a wide range. Boys and girls are equally affected. They tend to be in a higher social class. They account for 3 per cent of all child psychiatric referrals. Table 19.2 Features distinguishing truancy and school refusal Truancy

School refusal

Other antisocial features Family history of psychopathy Poor school performance

Lacks antisocial traits, passive good child Parents have neurotic traits/agoraphobia Average/above-average student of childhood

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AETIOLOGY There are three broad categories: 1 Separation anxiety, mainly in younger children. 2 True phobia of aspects of school or travel. 3 General social withdrawal, e.g. in older children with high standards and fragile self-esteem. Important features are:

• • • •

Mothers are frequently overprotective. Fathers are passive. There is a history of psychiatric illness in 20 per cent of mothers (especially anxiety disorder). It is often precipitated by the move from junior to senior school or a change of class.

COURSE AND PROGNOSIS The treatment of school refusers also involves parents and teachers. A graded return to school is most beneficial. Follow-up has shown good, moderate and poor outcomes in equal proportions. A good prognosis is associated with:

• • •

Younger age. Stability of the home. ‘Psychological sophistication’ of the parents.

Probably one-third of school refusers later present as adult ‘neurotics’. Twenty per cent of agoraphobics interviewed had had ‘school phobia’, but this is the same as in neurotics in general.

INAPPROPRIATE SOILING ENURESIS Enuresis is repeated involuntary voiding of urine by day or at night, after an age at which continence is expected. It is not due to a physical disorder, or a physiological effect of a medication. By definition, the age of onset is at least 5 years (for nocturnal).

• •

Primary – if not preceded by period of urinary continence for at least 1 year. Secondary – if preceded by 1 year of continence.

ASSOCIATED FEATURES The majority do not have a coexisting mental disorder, but psychiatric disorder is twice as common in this group as the general population (especially among girls). With functional encopresis, sleepwalking and night terrors may also be present. Typically, disturbance occurs during the first third of the night, during non-REM sleep.

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Urinary-tract-infection (UTI) Five per cent of enuretics (usually girls) have significant bacteriuria. Fifteen per cent of children with UTI are consequently enuretic. EPIDEMIOLOGY

• • • • •

Primary after age 4 years, secondary between ages 5 and 8. Boys are more affected than girls (3:1 ratio, but varies with age). Lower social classes are over-represented. At age 7 – about 7 per cent for boys, 3 per cent for girls. At age 15 and older – 2 per cent for boys, almost non-existent for girls.

AETIOLOGY Any hypothesis must explain the following facts:

• • • • • • • • • •

Greater concordance in MZ than DZ twins. Higher incidence in relatives. Higher incidence in social classes IV and V. Larger families. Institutional upbringing. Male predominance. Below-average IQ. Stress events in early childhood (illness and hospitalization, maternal death). Small functional bladder capacity. No association with any specific syndrome, except encopresis.

Possible mechanisms Enuresis is secondary to a psychiatric disorder; or The same factors (e.g. stress) produce both psychiatric disorder and enuresis; or Psychiatric disorder is secondary to negative parental reactions to enuresis.

• • •

MANAGEMENT AND PROGNOSIS

• • • • •

Reassure and advise. Exclude UTI, diabetes, neurological/urological disorders. A star chart is effective for about one-third of children. A bell and pad is effective in 80–90 per cent, if done correctly and persisted with over time. Tricyclics (imipramine, amitriptyline) are helpful, but there is a high relapse rate on stopping the drug. Treat any psychiatric disturbance if present.

Most children become continent by adolescence; but in some the disorder continues into adulthood.

ENCOPRESIS Encopresis is the repeated voluntary or involuntary passage of faeces of normal, or near-normal, consistency in inappropriate places. By definition it starts after age 4 years.

242

• •

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Primary – after age 4 years. Secondary – if preceded by faecal continence for at least 1 year.

Encopresis is associated with inadequate, inconsistent toilet training and psychosocial stress (e.g. family and school). Management includes reducing tensions in the family, and behaviour modification to reinforce appropriate defecation as well as continence. MANAGEMENT

• • •

Exclude physical reasons for soiling, such as retention, constipation with overflow leakage (possibly due to anal fissure, Hirschsprung’s disease) and/or diarrhoea. Reassure the child and support the parents, with explanations. Start retraining if necessary.

NIGHT-TIME INCIDENTS SLEEPWALKING See also Chapter 14. Sleepwalking is repeated episodes of arising from bed during sleep, walking about for several minutes and remaining unresponsive to the efforts of others to influence sleepwalking, or to communicate. The child can be awoken only with great difficulty, and is amnesic on waking. It usually occurs between 30 and 180 minutes after onset of sleep (EEG: delta activity, stages 3 and 4). Between 1 and 4 per cent of children experience the disorder at some time. Isolated episodes are even more frequent. Adolescence usually sees the disorder disappear.

NIGHT TERRORS See also Chapter 14. Night terrors are repeated episodes of abrupt awakening lasting 1–10 minutes, occurring between 30 and 180 minutes after onset of sleep (typically occurs during stages 3 and 4). They usually begin with a panicky scream. There are then signs of autonomic arousal – tachycardia, rapid breathing, dilated pupils, etc. There is confusion, disorientation and perseveration of movements. The person is relatively unresponsive to others.

SPECIFIC READING RETARDATION (SRR) SRR applies to children whose reading ability falls significantly below the average for their age, schooling and IQ. It must be distinguished from ‘reading backwardness due

ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD)

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to low IQ’. There is a prevalence of 4–10 per cent (higher in inner-urban areas), with a male predominance of 3–4:1. It is a broader concept than dyslexia, which implies localized cerebral immaturity. ASSOCIATED FEATURES

• • • •

Large family size. Low socioeconomic status. Poor concentration and attention. Increased prevalence in epileptic children, but overall no overt prevalence of neurological abnormalities.

Conduct disorder One-third of 10-year-olds with SRR in an Isle of Wight study were diagnosed as ‘conduct disorder’. There was a family history of reading difficulties, spelling difficulties, speech delay, clumsiness and poor left–right differentiation. AETIOLOGY AND OUTCOME Developmental, neurological, constitutional, family and emotional factors all contribute. The prognosis is poor, even with remedial education.

ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD) This is the leading neurobehavioural disorder among the young. Some will improve with maturity, others persist into adulthood. Criteria include:

• • • • •

There is inattention and/or hyperactivity–impulsivity. Behaviour occurs in at least two settings, e.g. home and school. It causes impairment in social, academic, or occupational functioning. Symptoms are evident before age 7 years. Behaviour is not due to other another disorder. ADHD is classified into three subtypes:

1 Predominantly inattentive. 2 Predominantly hyperactive–impulsive. 3 Combined. ASSOCIATED FEATURES

• • • • • • •

Dyssocial behaviour, difficulty disciplining, temper episodes. Family discord. Injuries. Low self-esteem. Low frustration threshold. Learning difficulties common. Under-achiever at school even when IQ is taken into account.

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•

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Soft neurological signs (motor coordination, perceptual and attention tests), EEG abnormalities (dysmaturation EEG) have been described.

DIFFERENTIAL DIAGNOSIS There is much overlap. Chief differentials are:

• • • •

Pervasive developmental disorder. Conduct disorder and oppositional defiant disorder (ODD). Inattention/overactivity associated with anxiety/depressive disorders of childhood. Extreme end of normal childhood behaviour.

EPIDEMIOLOGY Onset is typically before age 3 years, though it may not present before school age. Boys outnumber girls (3:1 ratio). Prevalence estimates in school-aged children range from 3 to 7 per cent. AETIOLOGY The aetiology is probably multifactorial. The heterogeneity view suggests a group of syndromes which have a common clinical phenotype. Genetics It seems to be biological, although adoptive parents of hyperactive children show increased rates of alcoholism and sociopathy. Biological fathers were likely to have been overactive. Recent risk analysis studies suggest a shared familial vulnerability for ADHD and affective disorders. Other factors Neurological soft signs, EEG, clinical evidence of maturational lags (e.g. associated learning disabilities) may suggest in utero damage. • fMRI studies indicate subnormal acitivation in prefrontal brain regions as well as decreased putaminal blood flow (Yitzchak and Pavlakis, 2001). • Noradrenergic dysfunction has been demonstrated. • Other neurotransmitters are implicated.

•

It has been hypothesized that such children have under-aroused CNS with insufficient cortical inhibitory control. Hence, stimulants are said to stimulate the reticular activating system (RAS) and increase cortical inhibition. COURSE AND PROGNOSIS These are variable. Three patterns of course and outcome are proposed: 1 All symptoms persist into adolescence and adult life, especially attention deficit; or 2 There is attenuation of symptoms with maturity; or 3 The condition is self-limiting, with disappearance of symptoms at puberty.

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MANAGEMENT The main focus for treatment is to maximize functioning.

• • • • • •

Psychostimulation – Methylphenidate and dextroamphetamine (short-, intermediateand long-acting variations) are first-line treatments (American Academy of Pediatrics, 2002). Antidepressants – Imipramine, desipramine and bupropion, and the nonpsychostimulant selective norepinephrine reuptake inhibitor atomoxetine, are secondline medications (ibid.). Behavioural regimens in classroom and home have proven to be effective. Remedial education. Counselling – of child and/or family. Dietary measures are expensive, lack scientific basis and are usually ineffective.

‘SYMPTOMATIC’ DISORDERS TICS Tics are rapid, sudden purposeless movements of a functionally related group of muscles, frequently occurring in the same part of the body. They can be suppressed voluntarily, but only at the expense of mounting tension and anxiety. Most commonly the tics are facial (blink, grimace). Vocal tics appear as grunts and coprolalia in Gilles de la Tourette syndrome. Tics increase with anxiety and disappear during sleep. They may be attenuated during periods of sustained attention. DIFFERENTIAL DIAGNOSIS

• • • • • • •

Choreiform movements – uncoordinated, irregular, non-repetitive. Athetiod movements – slow, writhing and irregular, frequently in fingers and toes. Myoclonic movements – brief, shock-like muscle contractions that may affect part or whole of a muscle (not muscle groups). Dystonic movements – slower, more sustained movements. Dyskinesias – especially those such as tardive dyskinesia, which are oral, buccal, lingual masticatory movements in the face and choreoathetiod movements in the limbs. Hemiballismic movements – coarse, intermittent and unilateral movements of the limbs. Spasmodic torticollis.

ASSOCIATED FEATURES

• • •

Development disorders. Other psychiatric disorders. IQ normally distributed.

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EPIDEMIOLOGY Age at onset is nearly always during childhood and adolescence and may be as early as 2 years. Boys are more affected than girls (3:1 ratio). Between 10 and 20 per cent of children are reported as having transient tic-like movements at some stage. There is a normal social class distribution (?). AETIOLOGY There is association with other developmental disorders. Stress, temperamental features and psychiatric disorder may act as precipitants. COURSE AND PROGNOSIS The prognosis is generally good. At 8-year-old follow-up, one study suggested 40 per cent completely recovered and 53 per cent improved, though with overall increased rate of emotional symptomatology. There is a poor prognosis for established Gilles de la Tourette syndrome. MANAGEMENT

• • •

Relaxation exercises, with massed practice, have been proposed. Evidence for their effectiveness is unclear. Minor tranquillizers and haloperidol are sometimes effective. Individual and family counselling, including reassurance, is aimed at minimizing stress.

GILLES DE LA TOURETTE SYNDROME (GTS) This is a disorder characterized by multiple motor and at least one vocal tic. Onset is before age 21 years. The site, frequency and pattern of tics change over time. There is substantial overlap between GTS and obsessional disorders. About 40 per cent of GTS patients exhibit obsessive–compulsive behaviours. First-degree relatives of GTS patients have high rates for diagnosis of oppositional defiant disorder (ODD). EPIDEMIOLOGY The exact prevalence is unknown but a figure of 0.5 per 1000 has been suggested. There are no known associations with race or social class. Males are more affected than females (4:1 ratio). AETIOLOGY Genetics A major autosomal dominant gene is likely. Linkage studies show preliminary evidence: 18 per cent of first-degree relatives have GTS. Non-genetic factors • EEG abnormalities (non-specific) are seen in 10–40 per cent of GTS cases. • PET and SPECT show hypermetabolism in frontal and basal ganglia regions.

CONDUCT DISORDER

•

247

Dopaminergic abnormalities are implicated from: – Decreased HVA in CSF in some studies. – Efficacy of antipsychotics. – Adverse effects of stimulants. – A similar syndrome to GTS seen with neuroleptic use.

Dopamine D1/D2 imbalance has been suggested. Noradrenergic and cholinergic systems are also implicated, but with less evidence. Recent interest has been shown in serotonergic systems in GTS. CLINICAL FEATURES

• • • • • • •

Age at onset is 2–15 years, with mean 7 years. Vocal tics have mean age at onset of 11 years. Motor tics are most commonly facial. Others are squatting, jumping, gait abnormalities. Vocal tics may be coughing, barking, throat-clearing grunting. Coprolalia (shouting obscenities) is seen in 30 per cent of GTS cases; mean onset 13–14 years. Echolalia is seen in 20–40 per cent. 40 per cent of GTS patients show associated disturbances, including attention deficits, aggressive, antisocial or inappropriate sexual behaviour, and deliberate self-harm.

COURSE AND PROGNOSIS There have been no long-term follow-up studies. It appears to be a lifelong disorder, but with some tendency for features to wax and wane. There is marked psychosocial impairment.

CONDUCT DISORDER Conduct disorder is characterized by persistent and excessive behaviour which attracts social disapproval. It may be stealing, disobedience, lying, truancy, setting fire or aggressive behaviour or promiscuity. The behaviour must be associated with disturbances of personal functioning or subjective happiness to be labelled ‘conduct disorder’, and to distinguish it from ‘delinquency’. Classification has been problematic because antisocial behaviour is a heterogeneous construct and is seen in conduct disorder, ADHD (less commonly) and ODD. ODD is the presence of markedly defiant/disobedient behaviour but with absence of more severe aggressive acts. It is debated whether this is a milder form of conduct disorder. Subclassification 1 Socialized – behaviour is viewed as normal within the context of the child’s subcultural group (e.g. truancy and gang membership).

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2 Unsocialized – behaviour is antisocial by any standards. This is more frequently associated with abnormalities in personality, and absence of adequate social bonds. 3 Mixed disorder – antisocial behaviour accompanied by marked emotional disturbance. EPIDEMIOLOGY Onset is usually before puberty for the unsocialized type, and pubertal or postpubertal for the socialized type. There is a 5 per cent point prevalence in middle childhood. It was the most common psychiatric disorder in an Isle of Wight study. It is far more common in boys than girls (ratios range from 4:1 to 12:1). Lower social classes appear to be most affected. AETIOLOGY Possible important factors:

• • • • •

Unsocialized type – parental rejection, inconsistent management with harsh discipline, early institutionalization, frequent change of parent figures (e.g. fostering) and being illegitimate. Socialized type – large family size, membership of a gang, absent father. Generally – disorder more common in children of alcoholic parents and parents with antisocial personality disorder. Child factors – male, biological vulnerability, difficult temperament (see Chapter 6), early behavioural problems, school failure. One-third show severe retardation of reading.

COURSE AND PROGNOSIS A proportion in the socialized group achieve adequate adjustment as adults. A large proportion in the unsocialized group develop antisocial personality disorder as adults. MANAGEMENT Management is aimed at reversing significant aetiological factors:

• • • •

Conjoint family therapy; behavioural training for parents. Remedial teaching. Individual counselling or group counselling. Alternative peer-group provision (e.g. adventure clubs, etc.).

CHILDHOOD/TEENAGE SUBSTANCE ABUSE See also Chapters 9 and 10. Intoxication can lead to injuries and death, and impairment in social, educational and psychological development and wellbeing. There is variability over time in the popularity of different substances. Surveys show that half of 12- to 15-year-olds have consumed alcohol. By age 15, almost two-thirds


249

had tried cigarettes and about one-quarter had tried marijuana. Over half of 12th-graders indicated they had used an illicit drug. The most commonly used substances from greatest to least are as follows: (Kaul and Coupey, 2002): marijuana; amphetamines; inhalants; hallucinogens; ecstasy; barbiturates; tranquilizers; cocaine; heroin. RISK FACTORS

• • • • • • • •

Behavior and mood disorders at an early age. Previous diagnosis of ADHD, conduct disorder, personality disorder. A history of sexual or physical abuse. Inherited genetic factors. Association with drug-using peers. No after-school supervision. Broken family. Poverty.

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Cote S, Tremblay RE, Nagin DS et al. (2002) Childhood behavioral profiles leading to adolescent conduct disorder: risk trajectories for boys and girls. J. Am. Acad. Child Adolesc. Psychiatry 41, 1086. Dale RC, Heyman I (2002) Post-streptococcal autoimmune psychiatric and movement disorders in children. Br. J. Psychiatry 181, 188. Dalsgaard S, Mortensen PE et al. (2002) Conduct problems, gender and adult psychiatric outcome of children with attention-deficit hyperactivity disorder. Br. J. Psychiatry 181, 416. Dekker MC, Koot HM, van der Ende J, Verhulst FC (2002a) Emotional and behavioral problems in children and adolescents with and without intellectual disability. J. Child Psychol. Psychiatry 43, 1087. Dekker MC, Nunn RJ, Koot HM (2002b) Psychometric properties of the revised developmental behaviour checklist scales in Dutch children with intellectual disability. J. Intellect. Disabil. Res. 46, 61. Delbello MP, Schwiers ML, Rosenberg HL, Strakowski SM (2002) A double-blind, randomized, placebo-controlled study of quetiapine as adjunctive treatment for adolescent mania. J. Am. Acad. Child Adolesc. Psychiatry 41, 1216. Dunn DW, Kronenberger WG (2003) Attention-deficit/hyperactivity disorder in children and adolescents. Neurologic Clinics 21, 933. Egger HE, Costello EJ, Angold A (2003) School refusal and psychiatric disorders: a community study. J. Am. Acad. Child Adolesc. Psychiatry 42, 797. Emslie GJ, Mayes TL (2001) Mood disorders in children and adolescents: psychopharmacological treatment. Biol. Psychiatry 49, 1082. Emslie GJ, Mayes TL, Laptook RS, Batt M (2003) Predictors of response to treatment in children and adolescents with mood disorders. Psychiatr Clin North Am. 26, 435. Essex MJ, Klein MH, Cho E, Kraemer HC (2003) Exposure to maternal depression and marital conflict: gender differences in children’s later mental health symptoms. J. Am. Acad. Child Adolesc. Psychiatry 42, 728. Fishman L, Rappaport L, Schonwald A, Nurko S (2003) Trend in referral to a single encopresis clinic over 20 years. Pediatrics 111, e604. Fombonne E, Tidmarsh L (2003) Epidemiological data on Asperger disorder. Child Adolesc. Psychiatr. Clin. North Am. 12, 15. Ford T, Goodman. R, Meltzer H (2003) The British Child and Adolescent Mental Health Survey 1999: the prevalence of DSM-IV disorders. J. Am. Acad. Child Adolesc. Psychiatry 42, 1203. Frombonne E, Wostear G, Cooper V, Harrington R, Rutter M (2001) The Maudsley long-term follow-up of child and adolescent depression. 1: Psychiatric outcomes in adulthood. Br. J. Psychiatry 179, 210. Frombonne E, Wostear G, Cooper V, Harrington R, Rutter M (2001) The Maudsley long-term follow-up of child and adolescent depression. 2: Suicidality, criminality and social dysfunction in adulthood. Br. J. Psychiatry 179, 218. Geller B, Craney JL, Bolhofner K et al. (2002) Two-year prospective follow-up of children with a prepubertal and early adolescent bipolar disorder phenotype. Am. J. Psychiatry 159, 6. Goodman T, Ford T, Meltzer H (2002) Mental health problems of children in the community: 18 month follow-up. BMJ 324, 1496. Goodyer IM (2002) Social adversity and mental functions in adolescents at high risk of psychopathology: position paper and suggested framework for future research. Br. J. Psychiatry 181, 383. Grella CE, Hser Y-I, Joshi V, Rounds-Bryant J (2001) Drug treatment outcomes for adolescents with comorbid mental and substance use disorders. Mental Dis. 189, 384. Guilleminault C, Palombini L et al. (2003) Sleepwalking and sleep terrors in prepubertal children: what triggers them? Pediatrics 111, e17. Hazell PL, Stuart JE (2003) A randomized controlled trial of clonidine added to psychostimulant medication for hyperactive and aggressive children. J. Am. Acad. Child Adolesc. Psychiatry 42, 886.


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Hofstra MB, van der Ende J, Verhulst FC (2002) Child and adolescent problems predict DSM-IV disorder in adulthood: a 14-year follow-up of a Dutch epidemiological sample. J. Am. Acad. Child Adolesc. Psychiatry 41, 182. Kaminski KM, Garber J (2002) Depressive spectrum disorders in high-risk adolescents: episode duration and predictor of time to recovery. J. Am. Acad. Child Adolesc. Psychiatry 41, 410. Kaul P, Coupey SM (2002) Clinical evaluation of substance abuse. Pediatr. Rev. 23, 85. Keenan K, Wakschlag LS (2002) Can a valid diagnosis of disruptive behavior disorder be made in preschool children? Am. J. Psychiatry 159, 351. King M, Coxell A, Mezey G (2002) Sexual molestation of males: associations with psychological disturbance. Br. J. Psychiatry 181, 234. Klin A, Warren J, Schultz R et al. (2002) Defining and quantifying the social phenotype in autism. Am. J. Psychiatry 159, 153. Kolvin I, Ounsted C, Humphrey M et al. (1971) Studies in the childhood psychoses. II: The phenomenology of childhood psychoses. Br. J. Psychiatry 118, 385. Kowatch RA, Suppes T, Carmody TJ et al. (2000) Effect size of lithium, divalproex sodium, and carbamazepin in children and adolescents with bipolar disorder. J. Am. Acad. Child Adolesc. Psychiatry 39, 713. Kuperman S, Schlosser SS, Kramer JR et al. (2001) Developmental sequence from disruptive behavior diagnosis to adolescent alcohol dependence. Am. J. Psychiatry 158, 2022. Kurlan R, Como PG, Miller B et al. (2002) The behavioral spectrum of tic disorders: a community-based study. Neurology 59, 414. Kurlan R, McDermott MP, Deeley C et al. (2001) Prevalence of tics in school children and association with placement in special education. Neurology 57, 1383. Lord C, Volkmar F (2002) Genetics of childhood disorders: XLII. Autism part 1: diagnosis and assessment in autistic spectrum disorders. J. Am. Acad. Child Adolesc. Psychiatry 41, 1134. McCracken JT, McGough J, Shah B et al. (2002) Risperidone in children with autism and serious behavioral problems. New Engl. J. Med. 347, 314. Meltzer H, Gatward R, for the Office for National Statistics (2000) Mental Health of Children and Adolescents in Great Britain. The Stationery Office, London. Mental Health Evaluation and Community Consultation Unit (2002) Prevalence of Mental Disorders in Children and Youth. University of British Columbia, Vancouver. Available online at www.mheccu.ubc.ca/publications/cy/MHECCU_Prevalence_Oct02.pdf (accessed 10 November 2003). Michelson D, Allen AJ, Busner J et al. (2002) Once-daily atomoxetine treatment for children and adolescents with attention-deficit hyperactivity disorder: a randomized, placebo-controlled study. Am. J. Psychiatry 159, 1896. Moreau D, Weissman MM (1992) Panic disorder in children and adolescents: a review. Am. J. Psychiatry 149, 1306. Pappadopulos E, Jensen S, Schur SB et al. (2002) ‘Real world’ atypical antipsychotic prescribing practices in public child and adolescent inpatient settings. Schizophr. Bull. 28, 111. Pappadopulos E, MacIntyre JC, Crismon ML et al. (2003) Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY): II. J. Am. Acad. Child Adolesc. Psychiatry 42, 145. Patel NC, Sanchez RJ, Johnsruc MT, Crismon ML (2002) Trends in antipsychotic use in a Texas Medicaid population of children and adolescents: 1996 to 2000. J. Child Adolesc. Psychopharmacol. 12, 1219. Pickles A, Rowe R, Somonoff E et al. (2001) Child psychiatric symptoms and psychosocial impairment: relationship and prognostic significance. Br. J. Psychiatry 179, 230. Rosenberg DR, MacMillan SN, Moore GJ (2001) Brain anatomy and chemistry may predict treatment response in paediatric obsessive–compulsive disorder. Int. J. Neuropsychopharmacol. 4, 179. Rutter M (2002) The interplay of nature, nurture, and developmental influences: the challenge ahead for mental health. Arch. Gen. Psychiatry 59, 996.

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Rutter M, Caspi A, Moffitt TE (2003) Using sex differences in psychopathology to study causal mechanisms: unifying issues and research strategies. J. Child Psychol. Psychiatry 44, 1092. Sayal K, Taylor E et al. (2002) Pathways to care in children at risk of attention-deficit hyperactivity disorder. Br. J. Psychiatry 181, 43. Schur SB, Sikich L, Findling RL et al. (2003) Treatment recommendations for the use of antipsychotics for aggressive youth (TRAAY). I: A review. J. Am. Acad. Child Adolesc. Psychiatry 42, 132. Silberg J, Rutter M, D’Onofrio B, Eaves L (2003) Genetic and environmental risk factors in adolescent substance use. J. Child Psychol. Psychiatry 44, 664. Simpkin DR (2002) Adolescent substance use disorders and comorbidity. Pediatr. Clin. North Am. 49, 463. Stein MA, Sarampote CS, Waldman ID et al. (2003) A dose–response study of oral methylphenidate in children with attention-deficit/hyperactivity disorder. Pediatrics 112, e404. Szatmari P, Merette C, Bryson SE et al. (2002) Quantifying dimensions in autism: a factoranalytic study. J. Am. Acad. Child Adolesc. Psychiatry 41, 467. Tourette’s Syndrome Study Group (2002) Treatment of ADHD in children with tics. Neurology 58, 527. Trowell J, Kolvin I, Weeramanthri T et al. (2002) Psychotherapy for sexually abused girls: psychopathological outcome findings and patterns of change. Br. J. Psychiatry 180, 234. Tuchman R (2003) Autism. Neuro Clin. 21, 915. US Department of Health and Human Services (2001) Mental Health: Culture, Race and Ethnicity (supplement to Mental Health: a Report of the Surgeon General). Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health; Rockville, MD. Volkow ND, Wang G, Fowler JS et al. (2001) Therapeutic doses of oral methylphenidate significantly increase extracellular dopamine in the human brain. J. Neuroscience 21, rc121. Wagner KD, Ambrosini P, Rynn M (2003) Efficacy of sertraline in the treatment of children and adolescents with major depressive disorder: two randomized controlled trials. JAMA 290, 1033. Wakefield JC, Pottick KJ, Kirk SA (2002) Should the DSM-IV diagnostic criteria for conduct disorder consider social context? Am. J. Psychiatry 159, 380. Watson S, Porter R, Birmaher B et al. (2002) The role of hypothalamic–pituitary–adrenal axis dysfunction in the attenuated growth hormone response in adolescents with familial loading for affective disorder. Arch. Gen. Psychiatry 59, 186. Weiner DA, Abraham ME, Lyons J (2001) Clincial characteristics of youths with substance use problems and implications for residential treatment. Psychiatr. Serv. 52, 793. Yeargin-Allsopp M, Karapurkar RC, Boyle DN et al. (2003) Prevalence of autism in a US metropolitan area. JAMA 289, 49. Yitzchak F, Pavlakis SG (2001) Brain imaging in neurobehavioral disorders. Pediatr. Neurol. 25, 278. Zito JM, Safer DJ, dosReis S et al. (2000) Trends in the prescribing of psychotropic medications to preschoolers. JAMA 283, 1025.

Mental retardation

20

OVERVIEW DEFINITIONS World Health Organization • Impairment – any loss or abnormality of psychological, physiological or anatomical structure or functions. • Disability – any reduction or lack (resulting from impairment) of ability to perform an activity in the manner or within the range considered normal for a human being. • Handicap – a disadvantage for the individual, resulting from impairment or disability, that limits the fulfilment of a role that is normal (depending on age, sex, culture) for that individual. May be in dimensions of physical independence, mobility, occupations, social integration, economic self-sufficiency, orientation or other. ICD-10 Mental retardation (MR) A condition of arrested or incomplete development of the mind, which is especially characterized by impairment of skills manifested during the developmental period, which contribute to the overall level of intelligence; i.e. cognitive, language motor and social abilities. DSM-IV-TR A B C

Subaverage intellectual functioning, IQ ⬍70 Concurrent deficits in ⬎2 skills areas: communications, self-care, home living, social/interpersonal skills, use of community resources, self-direction, academic skills, leisure, work, health and safety Onset before age 18 years

Coding See Table 20.1. The criteria are those of social competence. Precise classification by IQ is not always possible. IQ of less than 50–55 usually denotes major impairment,

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Table 20.1 Coding of mental retardation (MR) IQ range (ICD-10 and DSM-IV-TR) Mild MR Moderate MR Severe MR Profound MR

55–60 to 70 35–40 to 50–55 20–25 to 35–40 ⬍20–25

but 10–20 per cent become economically independent. An IQ of between 50 and 70 may denote impairment if accompanied by social incompetence. EPIDEMIOLOGY

• • •

Severe impairment has a prevalence of 3·5 per 1000 population. Between 2 and 3 per cent of the population have an IQ less than 70. It is more common in males, who have a larger variance in IQ. Of inpatient populations: – 10 per cent have severe psychiatric disorders. – 20 per cent have defects of vision or hearing. – 20 per cent have severe speech defects.

AETIOLOGY Severe impairment Nearly all cases have gross cerebral pathology at post mortem. Between 33 and 85 per cent have an organic aetiology diagnosed during life. 33 per cent are due to Down syndrome. 19 per cent are due to other inherited conditions or associated congenital malformations. • 18 per cent are due to perinatal injury. • 14 per cent are due to infections. • 4 per cent are due to biochemical disorders (inborn error of metabolism). • 15 per cent are of unknown aetiology.

• • • •

Mental impairment Fewer than 33 per cent have an organic aetiology diagnosed during life. Mental impairment shows a ninefold increase in the lower social class. A proven organic aetiology is more likely if the handicapped child is from a higher social class.

• • •

Social factors (i.e. ‘subcultural problems’, poor education, poor home environment, poor diet, etc.) therefore play a much larger part in the aetiology of impairment than of severe impairment. The lower end of the normal distribution curve of IQ (excluding the excess caused by organic disease) will account for a proportion of the handicapped group.

CHROMOSOMAL ABNORMALITIES

255

CHROMOSOMAL ABNORMALITIES TRISOMIES TRISOMY 13–15: PATAU’S SYNDROME There is severe handicap and facial abnormalities. Those affected rarely live longer than 6 months. TRISOMY 17–18: EDWARDS’ SYNDROME There is severe handicap, with facial and skeletal abnormalities. Those affected rarely live longer than 3 months. It is most common in females. TRISOMY 21 (22): DOWN SYNDROME Five per cent of cases result from translocation. The incidence is 1·8 per 1000 live births (1 per 50 if mother older than 45). It is most common in males. Features Low birthweight; small round head, epicanthic folds of eyelids, Brushfield spots on iris, cataracts, strabismus, small nose and ears, high arched palate, protruding tongue, short neck, short limbs, hypotonic muscles, umbilical hernia common, single palmar crease in one-third, pathogenic dermatoglyphic patterns, significant deafness in two-thirds. Severe handicap is usual but not invariable. Associated conditions There is increased incidence of: congenital heart disease; gastrointestinal atresia; Hirschsprung’s disease; respiratory infections; Alzheimer’s dementia (found in 95 per cent of those over 40 years); epilepsy (12 per cent aged over 40 years). Recurrence likelihood • Regular trisomy – 1 per cent. • Translocation 21/21 – 100 per cent. • Other translocations – 5–20 per cent. DELETIONS Deletion of short arm of 5: ‘cri du chat’ syndrome Most common in females. There is a characteristic cry, facial abnormalities, severe handicap, spasticity. Compatible with adult life. Deletion of short arm of 4: Wolf syndrome There is severe handicap, facial abnormalities, epilepsy. Partial deletion of long arm of 18 There is severe handicap, small size, facial abnormalities. Partial deletion of long arm of 21 This is described as ‘antimongolism’. SEX CHROMOSOME ABNORMALITIES Increasing numbers of X chromosomes lead to increased degree of handicap, in males and females.

•

XXX – 1 in 1000 females. – Slight mental handicap, no physical abnormalities.

256

•

• •

MENTAL RETARDATION

XXY (Klinefelter’s syndrome) – 1 in 500 men. – The most common of the sex chromosome abnormalities. – Tall, slightly reduced IQ, lack of male secondary sexual characteristics. Barr body is present (⫽chromatin positive) because of extra X. Any more X chromosomes (e.g. XXXY) have an extra Barr body each per X chromosome. XYY – 1 in 700 men. – Tall, not notably handicapped, possibly show more criminal behaviour of nonviolent sort than normal controls. XO – Dull normal IQ, short stature, webbed neck in 50 per cent. Lack of secondary sexual characteristics, gonadal dysgenesis, coarctation of aorta in 35 per cent.

FRAGILE X SYNDROME Fragile X syndrome is the second most common known cause of MR in males; it is thought to account for 6 per cent of severe MR, 10 per cent of mild MR in males.

• • • •

Diagnosis is confirmed on fragility test of X chromosome in folate-deficient medium. Chromosome analysis for fragile site (Q 27–28) on X chromosome (Young, 1993; Warren and Nelson, 1994). There is an association with autism; about 20 per cent of autistics have fragile X abnormality (Turk, 1992). There is a suggested clinical association with attention deficit disorders.

Clinical features These include MR, floppy ears, prognathism, macro-orchidism, hypertelorism, blue eyes, single palmar crease. Female carriers have physical stigma and somewhat reduced IQ.

GENETIC ABNORMALITIES

• • • •

Tuberous sclerosis – Autosomal dominant with variable penetrance. Variable handicap (mild to severe), epilepsy and skin changes – adenoma sebaceum after 4 years old, café-au-lait spots, shagreen patches. Sclerotic brain nodules, lung cysts. Apert’s syndrome – Autosomal dominant with poor penetrance. Mental handicap, tower skull, protruberant eyes, abnormalities of fingers and toes. Craniofacial dysostosis – Autosomal dominant with poor penetrance. Low incidence of handicap, tower skull. First arch syndromes – Autosomal dominant. – Berry–Franceschetti syndrome of mandibulofacial dysostosis, with sheep-like face, deafness and variable degree of handicap. – Hallerman–Streiff syndrome of mandibulo-oculofacial dyscephaly with severe subnormality and facial abnormalities.

INBORN ERRORS OF METABOLISM

• • • • • • •

257

Hypertelorism – May be autosomal dominant or recessive. Severe handicap is usual, with wide-set eyes and broad bridge to the nose. True microcephaly – Autosomal recessive. 1 in 1000 live births, males more common. Severe handicap with a normal size face but very small cranial vault, short stature, epilepsy common. Velo–cario–facial syndrome (VCFS) – Most commonly (85 per cent cases) 22q11 microdeletion. High prevalence of psychiatric disorders, especially psychosis and mood disorders. Virchow–Seckel dwarf – Autosomal recessive. Small stature, facial and skeletal abnormalities, mild or moderate handicap. Ataxia telangiectasia: Louis–Bar syndrome – Autosomal recessive. Gradual mental deterioration after age 3 years with development of facial telangiectasia, café-au-lait spots and cerebellar and extrapyramidal signs. Deficiency of IgA leads to infections and lymphocytic neoplasia. Laurence–Moon–Biedl syndrome – Autosomal recessive. Severe handicap, obesity, hypogenitalism, polydactyly, retinitis pigmentosa. Marinesco–Sjögren syndrome – Autosomal recessive. Severe handicap, microcephaly, cataracts, cerebellar signs, skeletal abnormalities.

X-LINKED DISORDERS ASSOCIATED WITH SUBNORMALITY

• • • • • • • • • •

X-linked hydrocephalus – with aqueduct of Sylvius stenosis. X-linked spastic paraplegia. Menkes’ ‘kinky hair’ syndrome. Lesch–Nyhan syndrome. Lowe’s syndrome. Pseudo-pseudohypoparathyroidism (Albright’s syndrome). Diffuse cerebral sclerosis. Mucopolysaccharidosis type 2 (Hunter’s syndrome) Nephrogenic diabetes insipidus. Hyperammonia syndrome.

POSSIBLY GENETIC DISORDERS

• • • •

de Lange syndrome with handicap – Characteristic facial and skeletal abnormalities, dwarfism and excessive body hair. Sturge–Weber syndrome (‘port wine syndrome’) – Facial angiomatous naevus with corresponding intracranial abnormality leading to contralateral hemiparesis, handicap and epilepsy. Prader–Willi syndrome – Gross obesity, hypogonadism, mild to severe handicap and outbursts of anger. Possibly hypothalamic disorder. Autism – see Chapter 19.

INBORN ERRORS OF METABOLISM Most are autosomal recessive except Hunter’s and Lesch–Nyhan syndromes and nephrogenic diabetes insipidus, which are X-linked.

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DISORDERS OF PROTEIN METABOLISM OVERFLOW AMINOACIDURIAS

•

• • •

Phenylketonuria – This is the most common inborn metabolic error (1 per 12 000 live births). Phenylalanine hydroxylase deficiency leads to build-up of phenylalanine in blood and phenylpyruvate in urine. All newborn babies in the UK are tested (Guthrie test) at 6–14 days for phenylalanine, which promotes the growth of Bacillus subtilis in a quantitative fashion. Subjects tend to be fair-haired, blue-eyed and prone to eczema. They may be epileptic and severely handicapped if untreated. Treat with a phenylalanine-free diet. Homocystinuria – There is a deficiency of cystathionine synthetase leading to raised homocystine and methionine. Clinically there is fair hair and skin, eye and skeletal abnormalities, poor peripheral circulation, liver degeneration, epilepsy and mental deterioration. Treat with a methionine-free diet. Argininosuccinic acidura – There is deficiency of argininosuccinase leading to raised argininosuccinic acid and ammonia. Subjects have short brittle hair, epilepsy, chorea and variable handicap. Maple syrup disease – There is a deficiency of ketoacid decarboxylase leading to abnormalities of branched chain amino acids. There is epilepsy, spasticity, paralysis and very early death if untreated. Treat with a diet low in leucine, isoleucine and valine.

RENAL AMINOACIDURIA (HARTNUP’S DISEASE) There is deficiency of transport of amino acids across gut and renal membranes, leading particularly to low tryptophan absorption and abnormal amino acids in urine. There is handicap, confusion, ataxia, photosensitive skin and pellagra. Some improvement is shown with a high-protein diet and nicotinamide.

DISORDERS OF CARBOHYDRATE METABOLISM

• •

Galactosaemia – There is deficiency of phosphogalactose-uridyl transferase. There is vomiting, lethargy, jaundice in the neonatal period leading to handicap and early death if untreated. Treat early with a galactose-free diet. Idiopathic hypoglycaemia – Leucine ingestion leads to hypoglycaemia and raised insulin levels. Epilepsy and handicap occur unless treated early with a leucinefree diet.

DISORDERS OF LIPID METABOLISM AND CONNECTIVE TISSUE

• •

Tay–Sachs disease – There is deficiency of hexosaminidase A, leading to excess ganglioside. It occurs especially in Ashkenazi Jews. There is optic atrophy with ‘cherryred spot’ on the macula, epilepsy, spasticity, mental deterioration and early death. There is no treatment, but it can be detected antenatally with amniocentesis. Niemann–Pick disease – There is deficiency of sphingomyelinase. Clinically it is like Tay–Sachs, but also enlarged liver and spleen owing to Niemann–Pick cells.

NON-GENETIC CAUSES OF MENTAL RETARDATION

• •

259

Gaucher’s disease – There is deficiency of cerebroside-beta-glucosidase leading to Gaucher cell (cerebroside) accumulations in many tissues. Mental deterioration is rapid. There is no treatment, but it can be detected at amniocentesis. Refsum’s disease – There is deficiency of phytanic acid oxidase with loss of myelin. Onset is in childhood, with mental deterioration, visual and auditory loss, cerebellar signs and weakness. Treat with a phytanic-acid-free diet and vitamin A.

MUCOPOLYSACCHARIDOSES

• • •

Type 1: Hurler’s syndrome – gargoylism, progressive mental and physical deterioration with corneal clouding. Type 2: Hunter’s syndrome (X-linked recessive) – gargoylism, deterioration is slower than Hurler’s and there is no corneal clouding. Type 3: Sanfilippo’s syndrome – mild physical signs but severe mental deterioration.

OTHER METABOLIC DISORDERS

• •

• •

Hypothyroidism (cretinism) – Deficiency of thyroxine leads to lethargy, large tongue and feeding problems, puffy skin, protuberant abdomen (often with umbilical hernia), mental handicap. Treat with thyroxine as early as possible. Infantile hyperuricaemia: Lesch–Nyhan syndrome (X-linked recessive) – Disturbance of purine metabolism leads to hyperuricaemia. There is development of spasticity, choreoathetosis, self-mutilation and severe mental handicap. Early death can be expected. It is partially treatable with allopurinol. It can be detected by amniocentesis. Nephrogenic diabetes insipidus (X-linked recessive) – Renal tubules do not respond to antidiuretic hormone; thus dehydration, epilepsy and handicap ensue. Treat with large fluid intake, ethacrynic acid and potassium chlorate. Rett’s syndrome – Affects females only, with onset at 7–24 months. There is loss of acquired hand skills and speech; stereotypies; lack of social interaction; later development of ataxia, apraxia, kyphoscoliosis and seizures; MR is usually severe.

NON-GENETIC CAUSES OF MENTAL RETARDATION

•

•

Nutritional/toxic: – Placental insufficiency. – Malnutrition. – Infantile hypoglycaemia. – Fetal alcohol syndrome (20–50 per cent risk with alcoholic mother). – Lead encephalopathy. Anoxia: – Perinatal. – In infancy.

260

•

• •

•

MENTAL RETARDATION

Maternal infection: – Rubella at up to 16 weeks of pregnancy. Leads to microcephaly, eye, ear and head abnormalities and subnormality. – Cytomegalovirus. – Syphilis. – Toxoplasmosis. – Listeria. Child infection: – Encephalitis. – Meningitis. Trauma: – Non-accidental injury – possibly one of the most important causes of mental handicap. – Accidental injury. – Birth trauma. Rhesus factor incompatibility.

PSYCHIATRIC DISORDER IN THE MENTALLY HANDICAPPED FACTORS CONNECTING PSYCHIATRIC DISORDER AND HANDICAP

• • • • • • • • •

Reaction of the individual to the stigma of subnormality. Reaction of others (family, fellow employees, etc.) to the handicap. Psychiatric disorder as a consequence of the psychological abnormalities associated with handicap (e.g. lack of social skills, impaired attention). Possible genetic aetiology for both psychiatric disorder and handicap. Organic brain disease as a cause of both. Iatrogenic consequences of either (e.g. drugs, institutionalization). Psychiatric disorder may lead to lowered IQ in later years. Persons with handicap as well as psychiatric disorder are more likely to come to the attention of services. Prevalence of mental illness in 165 MR adults (Holden and Gitlesen, 2003): – Depression – 30.0 per cent. – Anxiety – 21.3 per cent. – Hypomania – 8.4 per cent. – Psychosis – 15.5 per cent.

The prevalence of psychiatric disorder is greater in MR patients with challenging behaviour – i.e. aggression, self-injury, destruction of property, sexual acting out.

INDIVIDUAL SYNDROMES Schizophrenia Between 3 and 6 per cent of handicapped inpatients suffer with schizophrenia. They are characterized by childish behaviour and stereotypies, poverty of thought, perplexity and ‘confusion’, loss of drive and ill-formed hallucinations and delusions.

SERVICES REQUIRED

261

Manic depressive psychosis Between 1 and 6 per cent of handicapped inpatients or outpatients suffer. Depression is characterized by agitation or withdrawal, apathy, somatic complaints and compulsive behaviour. Mania presents as episodic excitation and overactivity. Neurotic disorders Hysterical symptoms tend to be more common than in the normal population. Bereavement and adjustment reactions are underestimated. Epilepsy Epilepsy is found in 30 per cent of the severely handicapped. Hypsarrhythmia, Lennox–Gastaut syndrome and West’s syndrome are associated. Incidence generally reduces with age but may develop later in autism, Down’ syndrome and progressive disorders (e.g. lipidoses).

SERVICES REQUIRED OVERALL GUIDELINES 1 Developmental principle – Mentally handicapped people will continue to grow and develop given an appropriate environment. 2 Principles of rights – The mentally handicapped are worthy of all the dignity and rights of any citizens. 3 The dignity of risk – The concept of learning through risk-taking and avoiding overprotection. 4 Principle of normalization – The availability of everyday, normal conditions of life. 5 Principle of generic environments and services – wherever possible. Services should be community based, comprehensive, continuous, coordinated, dignified and of high quality. The responsibilities of the multidisciplinary team are:

• • •

Official – to develop and maintain the best standards of care. Legal – clarification and recording of individual legal responsibilities. Interpersonal – support and communication between members.

ASSESSMENT SERVICES Mental handicap is often impossible to assess at ages of less than 6 months. Medical assessment includes neurological and general examination, details of any family history, pathological screening of blood count and film, thyroid function tests, amino acid chromatography of blood and urine, calcium levels, lead levels, blood sugar, serological tests for syphilis, skull radiograph, electroencephalogram and chromosomal analysis.

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MENTAL RETARDATION

Developmental assessment includes tests of general IQ and tests of special functions as well as assessment of developmental milestones. General assessment must be made of the child and his/her family and social circumstances. This is to be done by the multidisciplinary team: psychiatrist, psychologist, general practitioner, social workers, physiotherapist, paediatrician, teacher, occupational therapist. All assessments must be repeated and the assessment is under constant review as the child grows and his/her needs and abilities change.

EDUCATIONAL SERVICES These are the responsibility of the local education authority, no matter how handicapped the child is, if under 19 years. There is considerable debate about whether handicapped children are best taught in special schools or in ordinary schools, integrated with normal children (‘mainstreaming’). Structured, active teaching with precise measurable goals is most effective, based on careful developmental assessment. Behaviour modification techniques are particularly useful for severely handicapped people. Prolonged face-to-face care and teaching are important and more time needs to be spent with the child. Education may need to go on for longer (e.g. into early 20s). After this, sheltered workshops are often needed. Adult training and social education centres provide continuing assessment and training for adults.

RESIDENTIAL SERVICES Inpatient units are likely to continue to be needed for:

• • • •

Severe behavioural problems (including violence). Severe epilepsy. Severe physical handicaps. Major psychiatric illness.

In a population of 100 000 there will be about 100 severely handicapped children (aged under 16): 70 per cent live at home, 20 per cent live in hospital care and 10 per cent need residential care. There will also be 375 severely handicapped adults: 12 per cent living at home and 88 per cent living in hospitals or hostels. The emphasis is now on the use of ordinary housing (staffed homes, group homes). Fifty per cent of the adult severely handicapped are regarded as employable.

MANAGEMENT PRINCIPLES MEDICAL Medical management is rarely useful, as in phenylketonuria and cretinism. Severe physical handicaps may required medical or surgical treatment.

PREVENTION OF MENTAL RETARDATION

263

PSYCHIATRIC Psychotropic medication may be required for agitation, depression, etc. Individual and family psychotherapy may be appropriate. Behaviour therapy may be useful. Behavioural modification involves detailed analysis of unwanted behaviour and the supplying of immediate appropriate rewards for required behaviour. ROLE OF THE PSYCHIATRIST The psychiatrist must be:

• • • • • • • •

Trained in taking extensive histories. Able to negotiate with parents, staff, etc., to affect attitudes. Able to take a long-term view, tolerant of limited success. Skilled at understanding threatening events and suffering. Skilled at assessing subtle loss of intellectual skills. Able to support other staff. Concerned with maximizing personal growth. Able to use psychotropic medication appropriately. The psychiatrist may have therapeutic areas (e.g. a ward) for admission.

GUIDANCE FOR PARENTS The parents will need to be supplied with factual information about the disorder, cause, prognosis and management. They will also need reassurance, discussion and advice concerning the prognosis, likely disabilities and ways of helping with the child. Genetic counselling may be appropriate. Practical help (e.g. house alteration) will be needed. Occasionally family therapy will be appropriate.

PREVENTION OF MENTAL RETARDATION PRIMARY PREVENTION

• • •

Avoid development of the condition. Give genetic counselling. Manipulate the environment.

SECONDARY PREVENTION Detect and treat the condition early. TERTIARY PREVENTION Avoid additional disability by good care and early intervention. 1 Genetic counselling: – Unknown-cause severe handicap – 30 per cent recurrence risk. – Balanced translocation – mother, 20 per cent risk; father, 5 per cent risk.

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MENTAL RETARDATION

– – – – 2

3 4 5 6 7 8 9 10 11 12 13 14 15

Dominant – 50 per cent risk. Recessive – 25 per cent risk. X-linked – 50 per cent of sons affected; 50 per cent of daughters carriers. Neural tube malformation – 5 per cent risk if one child affected; 12 per cent if two children affected. Amniocentesis – Down’ syndrome, open neural tube defects (with alpha-fetoprotein) and certain biochemical abnormalities are especially detected by this method. Amniocentesis is offered if parents have an affected child, a positive family history or the mother is over 35. Abortion is offered if the fetus is affected. Now selective screening for amniocentesis. Prenatal screening – PKU galactosaemia, Tay–Sachs disease. Rhesus-negative screening – Kernicterus is prevented by the use of anti-D antibody, amniocentesis and exchange transfusion. Neonatal blood sample screening for phenylketonuria and other metabolic disorders. Rubella immunization in all adolescent girls. Maternal syphilis screening and treatment. Improvement of obstetric care (avoidance of harmful drugs in pregnancy, improved surveillance of pregnancy and delivery, improved neonatal care). Folate supplement in pregnancy to prevent neural tube defects. Prevention of malnutrition. Improved social and educational standards. Avoidance of maternal drug and alcohol abuse (fetal alcohol syndrome). Detection and early treatment of psychiatric disturbance in MR. Support for family. Bereavement counselling for MR individuals after loss of parent, etc.

REFERENCES AND FURTHER READING Aman MG, Collier-Crespin A, Lindsay RL (2000) Pharmacotherapy of disorders in mental retardation. Eur. Child Adolesc. Psychiatry 9, 98. Chechlacz M, Gleeson JG (2003) Is mental retardation a defect of synapse structure and function? Pediatr. Neurol. 29, 11. Deb S, Thomas M, Bright C (2001a) Mental disorder in adults with intellectual disability. 1: The rate of behaviour disorders among community based population aged between 16 and 64 years. J. Intellect. Disabil. Res. 45, 495. Deb S, Thomas M, Bright C (2001b) Mental disorder in adults with intellectual disability. 2: The rate of behaviour disorders among community based population aged between 16 and 64 years. J. Intellect. Disabil. Res. 45, 506. Dekker MC, Koot HM (2003a) DSM-IV disorders in children with borderline to moderate intellectual disability. I: Prevalence and impact. J. Am. Acad. Child Adolesc. Psychiatry 42, 915. Dekker MC, Koot HM (2003b) DSM-IV disorders in children with borderline to moderate intellectual disability. II: Child and family predictors. J. Am. Acad. Child Adolesc. Psychiatry 42, 923. Dykens E (2001) Introduction to the special issue on behavioral phenotypes. Am. J. Ment. Retard. 406, 1. Holden B, Gitlesen JP (2003) Prevalence of psychiatric symptoms in adults with mental retardation and challenging behaviour. Res. Dev. Disabil. 24, 323.


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Ivanov D, Kirov G, Norton N et al. (2003) Chromosome 22q11 deletions, velo-cardio-facial syndrome and early-onset psychosis: molecular genetic study. Br. J. Psychiatry 183, 409. Kahng SW, Iwata BA, Lewin AB (2000) Behavioral treatment of self-injury, 1964 to 2000. Am. J. Ment. Retard. 107, 212. Linhorst DM, Bennet L, McCutchen T (2002) Development and implementation of a program for offenders with developmental disabilities. Ment. Retard. 40, 41. McCarthy J, Boyd J (2001) Psychopathology and young people with Down syndrome: childhood predictors and adult outcome of disorder. J. Intellect. Disabil. Res. 45, 99. Moss SC, Emerson E, Kiernan C et al. (2000) Psychiatric symptoms in adults with learning disability and challenging behaviour. Br. J. Psychiatry 177, 452. Murphy KC, Owen MJ (2001) Velo-cardio-facial syndrome: a model for understanding the genetics and pathogenesis of schizophrenia. Br. J. Psychiatry 179, 397. Sanderson TL, Doody GA, Best GA et al. (2001) Correlations between clinical and historical variables and cerebral structural variables in people with mild intellectual disabilities. J. Intellect. Disabil. Res. 45, 89. Schupf N (2002) Genetic and host factors for dementia in Down’s syndrome. Br. J. Psychiatry 180, 405. Simpson MK, Hogg J (2001) Patterns of offending among people with intellectual disabilty: a systematic review. I: Methodology and prevalence data. J. Intellect. Disabil. Res. 45, 384. Surgeon General (2001) Closing the Gap: a National Blueprint to Improve the Health of Persons with Mental Retardation. Washington, DC. Szymanski L, King GH (1999) Practice parameters for the assessment and treatment of children, adolescents, and adults with mental retardation and comorbid mental disorders. J. Am. Acad. Child Adolesc. Psychiatry 38, s5. Thompson CL, Reid A (2002) Behavioural symptoms among people with severe and profound intellectual disabilities: a 26-year follow-up study. Br. J. Psychiatry 181, 67. Thorpe L, Davidson P, Janicki M (2001) Healthy ageing – adults with intellectual disabilities: biobehavioural issues. J. Appl. Res. Intellect. Disabil. 14, 218. Turk J (1992) The fragile X syndrome: on the way to a behavioural phenotype. Br. J. Psychiatry 160, 24. Van Narrden Braun K, Yeargin-Allsopp M, Schendel D, Fernhoff P (2003) Long-term developmental outcomes of children identified through a newborn screening program with a metabolic or endocrine disorder: a population-based approach. J. Pediatrics 143, 236. Warren ST, Nelson DL (1994) Advances in molecular analysis of fragile X syndrome. JAMA 271(7), 536. Young ID (1993) Diagnosing fragile X syndrome. Lancet 342, 1004.

Drug therapy

21

PHARMACOKINETICS AND PHARMACODYNAMICS

• •

Pharmacokinetics – What the body does to the drug. Time-course of drug absorption (distribution, metabolism, excretion) and drug transport (to and from receptors). Pharmacodynamics – What the drug does to the body. Relationship between drug concentration and efficacy (tolerability, drug effects at receptor level.)

ABSORPTION Absorption depends on: 1 Nature of the drug – Particle size, diluents, coating materials, etc., affect rate of absorption. 2 Gastric emptying and gut motility – Anticholinergic effects of many psychotropic drugs slow absorption. 3 Gut mucosa – Malabsorption syndromes. 4 Liver enzymes – May be inhibited (e.g. by MAOIs) or induced (e.g. by barbiturates). All drugs absorbed from the GI pass through the liver first and are partly destroyed (about 15 per cent chlorpromazine reaches systemic circulation). Compare IV, IM or sublingual preparations, which quickly reach the brain. PROTEIN BINDING Most drugs bind to plasma and tissue proteins. Only unbound drug is biologically active. Binding may be influenced by: 1 Displacement by other drugs. 2 Change in concentration of plasma proteins. METABOLISM Metabolism is mostly in the liver, but also in lung, gut, kidney and placenta. Metabolism in the liver is mostly through the cytochrome P450 hepatic microenzyme system (e.g. CYP2D6, CYP3A3/4).

PHARMACOKINETICS AND PHARMACODYNAMICS

267

Liver metabolism produces derivatives of increasing polarity, which are less lipidsoluble and so more readily excreted by the kidney. The rate of metabolism is an important factor in influencing serum levels. DRUG EXCRETION This is mostly through the kidney by passive diffusion. Some drugs, particularly glucuronide conjugates, are excreted in bile. OTHER FACTORS AFFECTING PHARMACOKINETICS See Table 21.1.

• • •

Age (increasing age reduces liver metabolism, affects cerebral circulation, reduces renal clearance). Sex. Proportion of body fat.

IMPORTANT DRUG INTERACTIONS Absorption The rate of gastric emptying is slowed by anticholinergic drug effects. Colloidal antacids slow drug absorption. Hepatic enzymes See Table 21.2.

Table 21.1 Pharmacokinetics in select populations

Young Old Pregnant Renal disease Liver disease

Renal clearance

Hepatic metabolism

Protein binding

↑ ↓ ↑ ↓ ⫽↓

↑ ⫽↓ ⫽ ↓↑ ↓ ↓

⫽ ⫽ ⫽↓ ↓ ⫽↓

Table 21.2 Enzyme inducers and inhibitors Enzyme inducers (reduces drug level)

Enzyme inhibitors (increases drug level)

Omeprazole Carbamazepine Phenytoin Barbiturates

MAOIs Fluoxetine, fluvoxamine, paroxetine Nefazodone ‘Azole’ antifungals (ketoconazole) Co-trimoxazole Macrolides Cimetidine Quinidine Cigarettes

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Genetic polymorphisms • CYP2D6 – poor metabolizers, autosomal recessive, more in Asians. – N-acetyltransferase – slow acetylators, autosomal recessive, more in Caucasians. PHARMACOGENETICS Pharmacogenetics is the study of genetically based, interindividual variability in response to drugs and in susceptibility to drug-induced adverse effects. It focuses on genetic polymorphisms influencing structure or function of proteins for which a given gene codes. Examples include:

• •

Polymorphism of dopamine D3 receptor gene exists – homozygotes (serine–serine; glycine–glycine) versus heterozygotes (serine–glycine) – DRD3 glycine–glycine phenotype associated with higher risk of tardive dyskinesia with antipsychotic therapy (Lerer et al., 2002). Genetic variation in serotonin transporter gene predicts response to antidepressant (especially SSRIs; see page 275) therapy (Lever and Marciardi, 2002) – still at research stage but likely to influence clinical practice in coming years.

PRESCRIBING IN PREGNANCY RISKS TO FETUS

• • •

Increased incidence of dysmorphogenesis, especially cardiac anomalies with lithium. Possible increased risk with other psychotropics, but no clear evidence. Do not use any drug during pregnancy, especially in first 12 weeks, except when risks of relapse outweigh other risks. If necessary, give a minimum dosage.

RISKS TO NEWBORN

• • • •

May be born ‘flat’. May show withdrawal symptoms if mother dependent on opiates or alcohol. May be limp or goitrous if mother takes lithium. Most drugs cross the placental barrier. This is probably unimportant in phenothiazines, tricyclics, hypnotics and anticonvulsants. Avoid breast feeding with lithium and high doses of diazepam.

ANTIPSYCHOTIC DRUGS CLASSES OF ANTIPSYCHOTIC DRUGS

• • •

Typical antipsychotic classes – see Table 21.3. Atypical antipsychotic classes – see Table 21.4. Differences between atypicals and typicals – see Table 21.5.

ANTIPSYCHOTIC DRUGS

269

Table 21.3 Typical antipsychotics Typical antipsychotic classes

Example

Phenothiazine – Aliphatic class – Piperidine class – Piperazine class Butyrophenone Thiozanthene Diphenylbutylpiperidine Substituted benzamide

Potency

Chlorpromazine Thioridazine Trifluoperazine Haloperidol Fluphenthixol Pimozide Sulpiride

100 100 10 5 ? 1 ?

Potency ⫽ milligrams of drug equivalent to 100 mg chlorpromazine.

Table 21.4 Atypical antipsychotics Atypical antipsychotic classes

Example

Dibenzodiazepine Benzisoxazole Thienobenzodiazepine Dibenzothiazepine Benzisothiazolyl Phenylindol Phenylindol Dibenzothiepine

Clozapine Risperidone Olanzapine Quetiapine Ziprasidone Aripiprazole Sertindole Zotepine

Table 21.5 Differences between atypicals and typicals

Extra-pyramidal side-effects Hyperprolactinaemia Mesolimbic D2 binding Improves negative symptoms Improves cognitive symptoms Improves depressive symptoms Lessens suicide

Atypical

Typical

⫹/– ⫹/– ⫹⫹ ⫹⫹ ⫹ ⫹ ⫹

⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹ – ⫹/– ⫹/–

EVIDENCE FOR DOPAMINE BLOCKADE AS MECHANISM OF ACTION

• • • • •

Amphetamine, which promotes dopamine (DA) release, induces a schizophrenialike psychosis. Antipsychotics (typicals) block DA D2 receptors, the extent of which is a measure of their potency. cis-Fluphenthixol isomer (which blocks D2 receptors), but not trans-fluphenthixol (inert isomer), is an effective antipsychotic. Homovanillic acid is the metabolite of dopamine and its plasma level is correlated with response to antipsychotic agents. PET studies confirm the need for antipsychotics to achieve above 60 per cent D2 receptor blockage to be clinically effective, yet EPS occurs at 74 per cent receptor

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occupancy and above. Binding of atypical antipsychotics is more complex (e.g. quetiapine rapidly dissociates from D2 receptors; aripiprazole is a D2 partial agonist). SCHEME OF RECEPTOR ANTAGONISTIC BINDING PROFILE OF ANTIPSYCHOTICS See Table 21.6. EXTRAPYRAMIDAL SIDE-EFFECTS (EPS) OF ANTIPSYCHOTICS See Table 21.7. Table 21.6 Scheme of receptor antagonistic binding profile of antipsychotics Drug

D2

5-HT2A

H1

Alpha-1

ACh

Haloperidole Thioridazine Trifluperazine Amisulpride Clozapine Risperidone Olanzapine Quetiapine Sertindole Aripiprazoleaa Ziprasidone Zotepine

⫹⫹⫹ ⫹ ⫹⫹ ⫹ ⫹/– ⫹ ⫹ ⫹/– ⫹ ⫹ ⫹ ⫹

– ⫹ – – ⫹⫹ ⫹⫹⫹ ⫹⫹ ⫹/– ⫹ ⫹⫹ ⫹⫹⫹ ⫹

–/⫹ ⫹ –/⫹ – ⫹⫹⫹ – ⫹⫹ – – – – –

⫹ ⫹⫹ ⫹/– – ⫹ ⫹ ⫹ ⫹⫹ ⫹ – ⫹⫹ ⫹

–/⫹ ⫹⫹ ⫹⫹ – ⫹⫹ – ⫹⫹ – – – – –

D2 ⫽ dopamine D2 receptor; 5-HT2A ⫽ 5-hydroxytryptamine receptor, type 2A; H1 ⫽ histamine H1 receptor; Alpha-1 ⫽ alpha-1 adrenoceptor; ACh ⫽ acetylcholine receptor; ⫺ ⫽ no significant receptor binding antagonism; ⫹/⫺ ⫽ or ⫺/⫹ ⫽ minimal receptor antagonism; ⫹ ⫽ receptor antagonism; ⫹⫹ ⫽ moderate antagonism; ⫹⫹⫹ ⫽ strong antagonism. a displays partial agonist properties at dopamine and serotonin receptors.

Table 21.7 Extrapyramidal side-effects (EPS) of antipsychotics EPS

Mechanism

Risk factors

Treatment

Acute dystonia – oculogyric crisis – torticollis – dysarthria – dysphagia

Acute hypodopaminergic in basal ganglia

Young, male, high dose, high potency, typical antipsychotics

Immediate: Oral/IM anticholinergic Subsequent: decrease dosage, add anticholinergic, or change to atypical.

Parkinsonism – tremor – cog-wheel rigidity – bradykinesia

Basal ganglia D2 blockage

Dose related, more with typical antipsychotics

Reduce dose or add oral anticholinergic, or change to atypical.

Akathisia – subjective and motor restlessness

Basal ganglia D2 blockage Low iron also relevant?

Low serum iron Dose related, more with typical antipsychotics

Reduce dose, or add benzodiazepines or betablocker. Change to atypical.

ANTIPSYCHOTIC DRUGS

271

Tardive dyskinesia (TD) This involves abnormal involuntary movements primarily involving the mouth and tongue (but can involve the trunk and limbs). It is thought to occur after long-term use of antipsychotics when postsynaptic dopamine receptors become hypersensitive to dopamine. There is a 5 per cent incidence per year in the young; higher rates are seen in the elderly. Risk factors Female; advanced age; organic brain disease; mood disorder; prominence of negative symptoms; long duration and high doses of typical antipsychotics. Management Change to an atypical antipsychotic. Clozapine has an indication for TD. Vitamin E or amantidine may help. Neuroleptic malignant syndrome (NMS) This is an idiosyncratic reaction, primarily to typical antipsychotics, characterized by pyrexia, muscle rigidity, altered consciousness, autonomic instability, elevated CPK. Incidence Eighty per cent are over 40 years of age; male:female ratio ⫽ 2:1. Risk factors Rapid neuroleptic titration or depot injection; pre-existing dehydration; pre-existing agitation; organic brain disease. Aetiology Unclear, but occurs within days or years after blockade of central dopamine receptors. Vulnerability is hypothesized to be related to a defect of intracellular calcium regulation in the sympathetic nervous system (Gurrera, 2002). Treatment Hospitalization. Stop antipsychotic administration; supportive treatment; change to atypical antipsychotic 2 weeks after resolution of NMS.

NON-NEUROLOGICAL SIDE-EFFECTS OF ANTIPSYCHOTICS See Table 21.8.

Table 21.8 Non-neurological side-effects of antipsychotics Side-effect

Treatment

Orthostatic hypotension – antiadrenergic effect Anticholinergic effects – blurred vision, dry mouth, constipation Hyperprolactinaemia – amenorrhroea, galactorrhoea, gynaecomastia Sexual dysfunction – impotence, ejaculatory delay/failure, anorgasmia Sedation Seizures (clozapine lowers Sz threshold) Weight gain Diabetes mellitus (hyperglycaemia is a potential side-effect of all atypicals) Cardiac arrhythmias – increased risk with thioridazine

Lower dose, change drug. Lower dose, change to atypical. Change to prolactin-sparing atypical. Rule out medical cause, change medication. Lower dose, change medication. Slow dose titration, reduce dose, add antiepileptic. Dietary assistance, exercise, antiobesity agents. Treat diabetes accordingly. Weight management may help. Change to lower-risk antipsychotic.

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Table 21.9 Antipsychotic safety and tolerability Item

Typ

Clz

Ris

Olz

Qtp

Zip

EPS TD Somnolence Prolactin Weight Dyslipidaemia DM QTc Orthostatic BP↓

⫹ – ⫹⫹⫹ ⫹⫹⫹ ⫾ – ⫹⫹⫹ ⫹⫹⫹ ⫾ ⫾ ⫾ ⫾ ⫾

⫾ ⫾ ⫹⫹⫹ ⫾ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹ ⫹⫹⫹

⫾ – ⫹⫹⫹a ⫾–⫹ ⫾ ⫹⫹⫹ ⫹ ⫹ ⫹ ⫹ ⫹⫹

⫾ – ⫹a ⫾(?) ⫹ ⫾ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹ ⫹

⫾ ⫾(?) ⫹⫹ ⫾ ⫹⫹ ⫹⫹ ⫹⫹ ⫹ ⫹⫹

⫾ – ⫹a ⫾(?) ⫾ ⫾ ⫾ ⫾ ⫾ ⫹⫹ ⫾

Typ ⫽ typical antipsychotics; Clz ⫽ clozapine; Ris ⫽ risperidone; Olz ⫽ olanzapine; Qtp ⫽ quetiapine; Zip ⫽ ziprasidone; a ⫽ dose-related; ⫾ ⫽ none to minimal; ⫹ ⫽ mild; ⫹⫹ ⫽ moderate; ⫹⫹⫹ ⫽ marked compared with placebo rate.

ANTIPSYCHOTIC SAFETY AND TOLERABILITY See Table 21.9.

ANTIDEPRESSANT DRUGS The pharmacological action of antidepressant drugs (a few hours) does not correlate with mood effect (2–4 weeks). The exact mechanism of altering mood is uncertain, but the therapeutic effect occurs after manipulation of central neurotransmitters. Unlike the older TCAs and MAOIs, most of the newer antidepressants have high therapeutic indexes. Ensure maximum dose and adequate length of trial before abandoning a particular agent/class. Side-effects can be used as therapeutic effects. SIDE-EFFECTS General All antidepressants – with the exception of mirtazapine, bupropion and nefazodone – have sexual side-effects which include impotence, anorgasmia and delayed ejaculation. There have been rare cases of priapism with trazodone. Gastrointestinal upset is associated to some degree with almost all antidepressants except mirtazapine, TCAs and MAOIs. Serotonin syndrome With overstimulation of central serotonin receptors, the patient my appear agitated, confused, and exhibit myoclonus, diaphoresis, nausea, vomiting, diarrhoea, syncope, tachycardia and elevated blood pressure. Ventricular tachycardia, seizures, disseminated intravascular coagulation, renal failure, coma and hypotension are complications seen in severe cases. Aetiology Caused by serotonergic medication use – additive effect. Treatment Discontinue serotonergic agents. With supportive treatment the syndrome will usually resolve within 24 hours.

ANTIDEPRESSANT DRUGS

273

Table 21.10 Characteristics of antidepressants Antidepressant class

Re-uptake inhibition

ACh blockade

Activating

Sedating

Half-life (h)

Dosage (mg/d)a

SSRIs Fluoxetine Paroxetine Fluvoxamine Sertraline Citalopram Escitalopram

S S S S S S

– ⫹ – – – –

⫹⫹⫹ ⫹ ⫹ ⫹⫹ ⫾ ⫾

– ⫹ ⫹ ⫾ ⫾ ⫾

330 21 16 26 35 27–32

20–80 20–50 100–300 50–200 10–60 10–20

Other Bupropion Trazodone Nefazodone Mirtazapine Venlafaxine

D, N, S S N, Sb Nb, Sb D, N, S

– ⫾ – – –

⫹⫹⫹ – ⫾ – ⫹⫹

– ⫹⫹⫹ ⫹⫹ ⫹⫹ ⫹

20 6 3 30 5

150–450 300–800 100–600 15–45 75–350

TCAs 2nd Desipramine Nortriptyline

N N, S

⫹⫹ ⫹⫹

⫾ –

⫹⫹ ⫹⫹

14–25 18–35

50–300 20–150

TCAs 3rd Amitriptyline Clomipramine Doxepine Imipramine

N, S N, S N, S N, S

⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹

– – – –

⫹⫹⫹ ⫹⫹⫹ ⫹⫹⫹ ⫹⫹

9–25 19–37 6–8 8–16

50–300 50–300 50–300 50–300

MAOIs Phenelzine Tranylcypromine

␮ ␮

⫹⫹ ⫹⫹

⫾ ⫹

⫹ –

␮ ␮

15–90 20–90

D ⫽ dopamine; N ⫽ norepinephrine; S ⫽ serotonin; – ⫽ none; ⫾ ⫽ none to minimal; ⫹ ⫽ mild; ⫹⫹ ⫽ moderate; ⫹⫹⫹ ⫽ marked compared with placebo rate; a may be in divided doses, long-acting formulations have different maximums, see package insert; b ⫽ receptor antagonist; ␮ ⫽ inhibits monamine oxidase with maximal effect occurring in 5–10 days.

CHARACTERISTICS OF A RANGE OF ANTIDEPRESSANTS See Table 21.10.

SELECTIVE SEROTONIN RE-UPTAKE INHIBITORS (SSRIs) These are the first-line medical treatment for depression. They have a more favourable side-effect profile than TCAs and MAOIs and a negligible mortality risk in overdose. A report of increased suicidal ideation/behaviour in children is under investigation. USES OF SSRIs

• • • •

Depression. OCD. Bulimia nervosa. PTSD.

274

• • • •

DRUG THERAPY

Social phobia. Generalized anxiety disorder. Panic disorder. Premenstrual dysphoric disorder.

Side-effects of SSRIs Nausea; loose stools; headache; insomnia (best given in morning dosage regime); nervousness, agitation; sweating; weight gain; withdrawal syndrome (associated with agents with short half-lives).

OTHER ANTIDEPRESSANT COMPOUNDS Bupropion Bupropion primarily inhibits the re-uptake of dopamine and norepinephrine, and serotonin to a lesser extent. It has no sexual side-effects, so it is used as an adjunct to SSRIs to counter those side-effects. It has been associated with weight loss. Otherwise, the sideeffects are similar to those of SSRIs.

• • • •

Lower rates of mania induction. Higher rate of seizures than SSRIs, especially at higher doses, therefore contraindicated in patients with seizure disorder and eating disorder because of lower seizure threshold in these patients. Sustained-release form decreases incidence of seizures and also has an indication for smoking cessation. Used in ADHD with positive results.

Trazodone Blocks 5-HT2 receptors at low dosage, stimulates at higher dosage, and is a weak inhibitor of serotonin re-uptake. • Low therapeutic index due to sedation. • Low anticholinergic effect, and reported to be non-cardiotoxic (mixed agonist effects). • Side-effects include sedation, orthostatic hypotension, dizziness, headache, dry mouth.

•

Nefazodone Similar to trazodone – weak inhibitor of norepinephrine and serotonin reuptake and blocks 5-HT2 serotonin receptors. Side-effects also similar to trazodone, with the exception of less sedation/sexual side-effects. Mirtazapine • Antagonizes ␣2-adrenergic and serotonin 5-HT2 receptors. • Moderate therapeutic index owing to sedation. • Has significant antihistamine activity, which accounts for its sedating effects – more so at lower doses. • No sexual or SSRI-like side-effects. • Side-effects include sedation, increased appetite and weight gain, dizziness, dry mouth, constipation. • Rare cases of blood dyscrasias reported, but all recovered after cessation of this drug.

ANTIDEPRESSANT DRUGS

275

Venlafaxine • Inhibits re-uptake of serotonin at low doses and norepinephrine and dopamine at high doses. • Extended-release formulation is indicated for generalized anxiety disorder as well as depression. • Side-effect profile similar to SSRIs. • Monitor for increased blood pressure (dose related).

TRICYCLICS: TERTIARY AMINES (AMITRIPTYLINE, IMIPRAMINE) Tricyclics preferentially block uptake of 5-HT. Demethylated metabolites are secondary amines which preferentially block dopamine and noradrenaline. Tricyclics have a lower therapeutic limit for serum levels; 90 per cent is plasma- or protein-bound. Major tranquillizers prescribed concurrently inhibit metabolism, so increase serum levels. Tricyclics infrequently prescribed because of their side-effect profile. Some use in chronic pain – superior to placebo in somatoform pain disorder. May have a direct effect on nerve conduction, treat affective component or enhance effects of analgesics. SIDE-EFFECTS OF TRICYCLICS

• • • •

• • • • • •

Anticholinergic (dry mouth, blurred vision, worsening glaucoma, urinary hesitancy, constipation). Hypotension (central effect – anti-␣1-noradrenergic). Drowsiness, sedation (anti-histamine/ ⫾ anti-acetylcholine). Cardiovascular: – Palpitations. – Tachycardia. – ECG changes (‘R on T phenomenon’), quidine-like effect; QT prolongation, decreased ST interval; myocardial sensitization to catecholamines. – Ventricular tachyarrhythmias. – Cardiomyopathy or heart failure (decreased inotropic effect following depletion of catecholamines from myocardium). – Distal conduction defects in bundle of His following overdosage. Weight gain/increased appetite (serotonergic ?). Confusional reactions in the elderly – probably due to anticholinergic effects, especially where phenothiazine (weak anticholinergic) and a strong antiparkinson drug are combined. Tremor. Convulsions (rare). Sexual dysfunction, impotence, anorgasmia (especially clomipramine), delayed ejaculation. Withdrawal syndrome – symptoms of noradrenergic and cholinergic ‘overdrive’.

276

DRUG THERAPY

TRICYCLICS: CONTRADICTIONS AND PRECAUTIONS Cardiovascular • Acute myocardial infarction. • Presence of intraventricular or bundle block. • Presence of multifocal premature contractions. • Unexplained blackouts. Neurological Elderly patients treated for Parkinson’s disease with anticholinergic drugs. Epilepsy.

• •

Other Prostatic hypertrophy. Narrow-angle glaucoma.

• •

Pregnancy Evidence for dysmorphogenesis equivocal. Drug interactions Competition for plasma- and protein-binding – phenytoin, aspirin, phenylbutazone; alcohol; antihypertensives (not beta-blockers); sympathomimetics; MAOIs; anticholinergics; neuroleptics (same catabolic pathway); oral contraceptives (slow metabolism). TRICYCLICS: SECONDARY AMINES Nortriptyline and desipramine are secondary amines. Desipramine is the least sedative. They preferentially block uptake of noradrenaline. OTHER TRICYCLICS

• • •

Dothiepin – derivative of amitriptyline, with fewer autonomic side-effects. Doxepin – derivative of amitriptyline, strongly anxiolytic, with less cardiotoxicity. Mianserin – blocks ␣2-adrenergic receptors; effectively no re-uptake blocking activity or anticholinergic activity. Minimal cardiotoxicity. Rarely causes convulsions; risk of leucopenia requires careful monitoring.

MONOAMINE OXIDASE INHIBITORS (MAOIs) Monamine oxidase is an enzyme that degrades tyramine, serotonin, dopamine and norepinephrine, and its inhibition causes an increase in these monamines. MAO inhibition reaches a maximum in 5–10 days. Restoration of MAO stores takes 2 weeks after stopping MAOIs. Drug and dietary restrictions are necessary to avoid hypertensive crises (see below). MAOIs are thought to be effective in refractory and atypical depressive states – especially those with mixed anxiety, phobic, obsessional features. SIDE-EFFECTS OF MAOIs

• • •

Anticholinergic. Postural hypotension. Tremor.

MOOD STABILIZERS USED IN BIPOLAR ILLNESS

• • • •

• • • •

277

Ankle oedema. Paraesthesia in limbs. Confusional states and possible precipitation of mania. Hypertensive crisis: – Headache and neck pain. – Throbbing neck veins. – Palpitations. – Hyperpyrexia. – Convulsions, coma, death. – Reverse with phentolamine 5–10 mg IV; chlorpromazine (PO) also used. Insomnia. Nausea. Myoclonus. Tranylpromine has amphetamine-like properties.

MAOIs: CONTRAINDICATIONS AND PRECAUTIONS 1 Cardiac failure, hypertension, infective hepatitis, obstructive jaundice or cirrhosis. 2 Avoid food high in tyramine: meat or yeast extracts, pickled herring, cheeses, alcohol (including wines), broad bean pods, chicken liver. 3 Drugs: – Sympathomimetic amines (may be present in proprietary cold-relieving agents and anaesthetics). – Antihypertensive drugs. – Antihistamines. – Sensitivity to insulin increased. – Oral antidiabetic agents. – Morphine and meperidine. – Metabolism of many drugs by liver, including barbiturates, phenytoin.

MOOD STABILIZERS USED IN BIPOLAR ILLNESS Mood stabilizers used for bipolar illness include lithium, antiepileptic drugs (AED) and, more recently, atypical antipsychotics. These agents are used with varying success to delay or treat the onset of mood episodes. Lithium has long been known to exert suicide-protective effects in bipolar patients. Recent studies also suggest that AED mood stabilizers are associated with reduced suicide ideation and attempts (Yerevanian et al., 2003). Atypical antipsychotics have been shown to be useful both alone and in combination with mood stabilizers in the treatment of acute mania. Benzodiazepines are also useful in the treatment of acute mania.

LITHIUM Lithium is prescribed in the form of its simple salts. It was introduced into medicine in 1859 as a treatment for gout, but later abandoned because of toxicity. It was reintroduced

278

DRUG THERAPY

as a treatment for mania by John Cade in 1949, in Australia. Its use was generally established by 1965. KINETICS OF LITHIUM Absorption is rapid following an oral dose and complete within 6–8 hours. Plasma level peaks in 30 minutes to 2 hours. It is distributed in total body water, shifting slowly to cells. There is no protein-binding. The therapeutic index is low due to neurotoxicity. There is no metabolism – the substance is excreted unchanged by the kidney. Between one- and two-thirds of the oral dose appears in urine after 8–12 hours; the rest is excreted slowly over days. Once lithium therapy is established, the clearance rate is fairly constant. Rates of lithium clearance between different persons may differ fourfold. It depends on renal function: the amount of fluid passing through the kidney and its sodium content. Lithium tends to follow sodium in reabsorption at proximal tubules; hence:

• • •

Increased sodium intake produces decreased reabsorption, with decreased reabsorption of lithium. A sodium-restricted diet produces increased reabsorption, and lithium levels may become toxic. Thiazide diuretics decrease lithium clearance by 24 per cent, owing to compensatory reabsorption of sodium in proximal tubules.

ACTIONS OF LITHIUM The therapeutic action is not understood, but the following effects have been noted. Neurotransmitters • Synapses – Lithium is thought to increase presynaptic destruction of catecholamines, inhibit release of neurotransmitter, decrease sensitivity of postsynaptic receptors. • Ions – Lithium influences sodium and calcium ion transfer across cell membranes. These ions affect neurotransmitter release and receptor activity. • Cyclic AMP – Lithium inhibits prostaglandin E-stimulated cyclic AMP. • Lithium stimulates sodium and magnesium-dependent ATPase. Cations and water Lithium stimulates exit of sodium from cells, probably by stimulating the pump mechanism, where intracellular Na is elevated (as in depression). Lithium stimulates entry of sodium into cells where intracellular Na is low (as may be the case in mania). Cell membranes Lithium may interact with both calcium and magnesium and increase cell membrane permeability. Other actions • Lithium restores diurnal rhythm of corticosteroids to normal in mania (but may simply reflect changes in behaviour as mania ameliorates). • In depressed patients, there is restoration of normal slow-wave EEG rhythms during sleep, and decreases in stage 1 and REM sleep correlate with plasma levels. • Changes in magnesium and calcium may be the secondary effects of altered carbohydrate metabolism. Lithium influences this by releasing insulin and increasing transport of glucose and muscle glycogen formation. This may be the cause of weight gain.


279

PLASMA LEVEL AND STABILIZATION OF DOSE Take a blood sample 12 hours after the last dose because of ‘peaking’ of level. Therapeutic and toxic ranges refer to this ‘basal’ level. Give smaller doses more frequently rather than large doses infrequently, because large interpeak troughs are associated with renal side-effects. Slow-release preparations also smooth out peaks.

• •

Acute treatment: 0.9–1.4 mEq/L. Maintenance: 0.6–0.8 mEq/L (some researchers suggest as low as 0.4 mEq/L).

USES OF LITHIUM 1 2 3 4 5

Control of mania (3–4 days for therapeutic effect). Prophylaxis of recurrent bipolar and unipolar disorder. Schizoaffective disorder. Augmentation of antidepressant therapy. Treatment of impulsive and aggressive behaviour.

There are significant reductions in aggressive behaviour among prisoners and mentally retarded on lithium compared with placebo treatment. SIDE-EFFECTS OF LITHIUM Early Nausea, vomiting, diarrhoea (related to ‘peak’ serum levels). Tremor, especially on voluntary movement. Dryness of mouth, slight thirst. Fatigue, drowsiness. Stuffy nose, metallic taste in mouth.

• • • • •

At any time Toxicity – tremor, ataxia, incoordination, slurred speech, confusion, disorientation convulsion, coma and death. Symptoms begin to appear with blood levels ⬎2.0 mmol/L. Longer-term • Nephrogenic diabetes insipidus. Polyuria and polydipsia may occur at therapeutic plasma concentrations. The distal tubule becomes resistant to the influence of antidiuretic hormone (ADH), possibly owing to blockade of ADH-sensitive adenyl cyclase. This is reversible but may take weeks. – Treatment: Reduce/stop lithium; use indomethacin or amiloride. • Hypothyroidism occurs in about 3 per cent of chronic lithium-takers, females more than males. The lithium ion interferes with production of thyroid hormones and the action of TSH. This is reversible but will recur on restarting lithium. • Oedema. • Weight gain (not accounted for by water retention). • Neurological – choreoathetosis, ataxia, dysarthria, tardive dyskinesia (rare), neurotoxicity with neuroleptics or carbamazepine, NMS. • Cardiac T-wave flattening on ECG. • Arrhythmias – possibly caused by reduction of intracellular potassium. • Poor memory short-term. • Nephropathy – association unclear; 5–10 per cent develop nephropathy, but this does not invariably cause ‘clinical’ renal insufficiency.

280

• •

DRUG THERAPY

Dermatological/alopecia. SLE/myasthenia gravis.

DRUG INTERACTIONS AND CAUTIONS 1 Avoid in association with: – Low salt diet. – Diarrhoea/vomiting. – Pregnancy. – Dehydration. 2 Use cautiously in association with: – Major tranquillizers. – Renal insufficiency. – Diuretics. – NSAIDs. MONITORING

• •

Baseline – examination; routine lab tests including urea, electrolytes, creatinine, urine tests, thyroxine and TSH; weight; ECG; pregnancy test, if female of childbearing age. During treatment: – Lithium – 8-weekly once stabilized. – Chemistry, T4, TSH, creatinine, urea, urine – 6–12 months. – ECG examination – annually.

VALPROIC ACID The therapeutic level for bipolar disorder is 50–100 micrograms for both maintenance and acute mania. It is better tolerated than lithium. It is equal to lithium in the treatment of acute mania, and more effective for rapid cycling and mixed states. The mechanism of action is unknown, but it is shown to increase central GABA levels by inhibiting its degradation/enhancing its synthesis. Valproic acid has a moderate therapeutic index gastrointestinal symptoms and neurotoxicity. It is metabolized in the liver. USES OF VALPROIC ACID

• • • • • •

Acute mania. Maintenance therapy for bipolar illness. Preferred for rapid cycling and mixed episodes. Treatment-resistant bipolar illness. Epilepsy. Migraine prophylaxis.

SIDE EFFECTS OF VALPROIC ACID Gastrointestinal (nausea, vomiting, diarrhoea); headache; ear ringing; weight gain; hair loss; polycystic ovarian syndrome (due to weight gain?); neural tube/craniofacial defects during pregnancy; pancreatitis, liver damage (rare).


281

CARBAMAZEPINE Carbamazepine inhibits limbic kindling. The therapeutic level is 8–12 micrograms. It has a low therapeutic index due to neurotoxicity. Carbamazepine is metabolized in the liver, where it induces its own metabolism. It is excreted in the kidney. Caution is needed with use of oral contraceptives and some antibiotics. It is contraindicated with MAOIs. USES OF CARBAMAZEPINE

• • • • • •

Acute mania. Prophylaxis of bipolar illness. Rapid cycling mania – more effective than lithium. Trigeminal neuralgia. Epilepsy. Alcohol withdrawal.

SIDE-EFFECTS OF CARBAMAZEPINE Dizziness, sedation, ataxia, dry mouth; generalized erythematous rash (Steven Johnson syndrome); leucopenia/agranulocytosis occurring in early stages of treatment; hyponatremia; neural tube/craniofacial defects during pregnancy.

LAMOTRIGINE Lamotrigine is used for maintenance therapy in bipolar disorder. It delays the onset of manic/hypomanic as well as depressive episodes in bipolar illness. It is not effective for acute mania. Lamotrigine is thought to work by stabilization of neurons via inhibition of sodium and calcium channels in presynaptic cell membranes. It does not require serum level monitoring like lithium, valproic acid and carbamazepine. Valproic acid increases lamotrigine levels while carbamazepine lowers levels. It is not associated with weight gain. USES OF LAMOTRIGINE

• •

Maintenance therapy for bipolar illness. Epilepsy.

SIDE-EFFECTS OF LAMOTRIGINE Headache; nausea; insomnia; rash (higher risk with rapid titration, higher doses, younger age).

OTHER AEDs USED AS MOOD STABILIZERS Gabapentin, tiagabine, oxcarbazepine and topiramate are used for mood stabilization with promising reports, but studies do not fully support their use in this manner.

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DRUG THERAPY

SEDATIVES AND ANXIOLYTICS BENZODIAZEPINES See Table 21.11. MODE OF ACTION There is enhancement of GABA effects, probably via benzodiazepine (bz) receptors localized on neurones throughout brain, but with highest density in cortical and limbic areas. The bz receptors are closely tied to GABA receptors, which explains the CNS inhibitory actions of the benzodiazepines. Benzodiazepines are safe in overdoses, producing drowsiness or stupor, and rebound insomnia in the next few days. USES OF BENZODIAZEPINES

• • • • • • • • •

Anxiety disorders. Insomnia. Withdrawal symptoms. Psychosis induced by hallucinogens. Status epilepticus. Abreactive techniques. Premedication and minor operative procedures. Muscle relaxant. Acute agitation.

SIDE-EFFECTS OF BENZODIAZEPINES

• •

Sedation. Ataxia/motor impairment. Table 21.11 Benzodiazepines Select bz drugs

Half-life (h)

Active metabolite

Long-acting Clorazepate Chlordiazepoxide Clonazepam Diazepam Flurazepam

40–50 24–30 30–40 20–100 47–100

Nordiazepam Desmethylchlordiazepoxide None Nordiazepam N-hydroxyethyl-flurazepam

Intermediate-acting Estazolam Lorazepam Oxazepam Temazepam

10–24 13 6–11 3.5–18.4

4-hydroxy estazolam (weak) None None None

Short-acting Alprazolam Triazolam

11.2 1.5–5.5

None None

SEDATIVES AND ANXIOLYTICS

• • • • • • •

283

Cognitive blunting. Memory impairment. Apnoea on IV administration. Slight respiratory depression (important in patients with obstructive airways disease). Dependency – psychological and physical, associated with chronic use. Amnesia in large doses. Confusion in the elderly.

WITHDRAWAL EFFECTS On withdrawal (placebo-controlled) of long-term normal-dose benzodiazepine treatment, there is:

• • •

Rebound insomnia, REM rebound. Tremor, anxiety, restlessness. Weight loss, appetite disturbance, sweating.

Symptoms usually subside after several days, but may last months in some cases. Withdrawal is possibly aided by substituting long-acting bz, gradual titration, and supportive/counselling measures. Convulsions have been reported on abrupt withdrawal of long-term, very-high-dose treatment.

NON-BENZODIAZEPINE HYPNOTICS See Table 21.12. These agents have a chemical structure unrelated to the benzodiazepines but share many of the same pharmacological effects. The mechanism of action is via selective interaction with only one GABA–bz receptor complex, resulting in sedation. Side effects are similar to benzodiazepines and abuse potential is present. Table 21.12 Non-benzodiazepines Non-bz hypnotics

Half-life (hours)

Active metabolite

Zaleplon Zolpidem Zopiclone

1 2.6 3.5–6.5

None None None

AZAPIRONES (BUSPIRONE) Azapirones are unrelated to benzodiazepines and are anxioselective. Buspirone is a full agonist of presynaptic dorsal raphe 5-HT1A receptors and partial agonist of 5-HT1A receptors in the hippocampus and cortex. It is rapidly absorbed: peak plasma concentration in 40–90 minutes; half-life 2–11 hours. It is metabolized in the liver. It is relatively non-sedative and does not interact with bz or alcohol. Side-effects are mild and can include light-headedness, headache, drowsiness. There is no liability of abuse. The anxiolytic effect may take 1–2 weeks to achieve.

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BARBITURATES Barbiturates are rarely used now because of the high risk of psychological and physical dependence. There is tolerance and liver enzyme induction, drug accumulation causing confusional states (especially in the elderly). Respiratory depression is another drawback, as is the withdrawal syndrome (see Chapter 10). Barbiturates are used sometimes in abreaction, for narcosis in a severely disturbed patient.

ADRENERGIC AGENTS ALPHA AGONISTS The mechanism of action involves stimulation of central ␣-adrenoreceptors which results in reduced sympathetic outflow. USES OF ALPHA AGONISTS

• • • • • • •

Hypertension. Opioid withdrawal – suppresses autonomic activity. Adjunct in treatment of ADHD for highly activated children. Aggression in children. Akathisia. Tic disorder. PTSD.

SIDE-EFFECTS OF ALPHA AGONISTS Sedation; dry mouth; hypotension; headache; constipation; dizziness; rebound hypertension. CAUTIONS AND CONTRAINDICATIONS

• • • • •

History of cardiac or cardiovascular disorder. Combining with other drugs. History of medication non-compliance. Taper during discontinuation. Autonomic hyperarousal with sudden cessation.

BETA BLOCKERS Depending on the particular agent, the mechanism of action attained by selectively or non-selectively blocking of ␤-adrenergic receptors throughout the body. USES OF BETA BLOCKERS

• •

Hypertension. Familial and other tremors.

STIMULANTS

• • • •

285

Control of autonomic aspects of anxiety. Impulsive aggression. Akathisia. Opiate withdrawal.

SIDE-EFFECTS OF BETA BLOCKERS Bradycardia, light-headedness; tinnitus, rashes, purpura; insomnia, nausea. CAUTIONS AND CONTRAINDICATIONS

• • • • •

May precipitate heart failure. Diabetes – prevents early recognition of hypoglycaemia and interferes with metabolism of glycogen. Obstructive airways disease – may precipitate bronchospasm. Presence of second- and third-degree heart block. Exercise caution in patients with poor cardiac reserve.

DISULFIRAM FOR ALCOHOLISM If disulfiram is taken with alcohol, the person experiences severe headache, nausea, facial flushing and general malaise. Severe reaction can be treated by oxygen, dextrose drip or parenteral antihistamine. Effectiveness is limited by compliance issues. Disulfiram interferes with metabolism of other drugs, especially barbiturates, phenytoin, warfarin and paraldehyde. Citrated calcium carbimide has fewer side-effects and milder reaction. SIDE-EFFECTS OF DISULFIRAM Nausea, constipation, fatigue; breath odour, metallic taste in mouth; psychotic and confusional states; reduction in libido; hypothyroidism. CONTRAINDICATIONS

• • •

Cardiac failure or ischaemic heart disease. Pregnancy. Psychosis (may exacerbate schizophrenic psychosis).

STIMULANTS PSYCHOSTIMULANTS Psychostimulants cause CNS excitement by increasing the activity of the catecholamines dopamine and/or noradrenaline. The prototype stimulants are dextroamphetamine and methylphenidate (milder). There are also mixed salt amphetamine/dextroamphetamine formulations. All have generally comparable efficacies. Intermediate- and long-acting variations are available in order to avoid multiple daily dosing.

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Pemoline has similar effects but is structurally different from the prototype stimulants and sees only limited use because of excessive morbidity and mortality associated with liver complications. USES OF PSYCHOSTIMULANTS

• • • •

ADHD (first-line treatment). Narcolepsy. Obesity. Augmentation of antidepressants.

SIDE-EFFECTS OF PSYCHOSTIMULANTS Insomnia; appetite suppression; growth suppression; unmasking of latent tic disorder; hallucinations; agitation, excitement; tolerance and dependency; rebound depression on stopping or after prolonged use; paranoid psychosis; hypertension. CAUTIONS AND CONTRAINDICATIONS

• • • •

Cardiovascular disease. Tic disorder. History of substance abuse. Glaucoma.

NON-PSYCHOSTIMULANTS (ATOMOXETINE) Used in ADHD, atomoxetine’s mechanism of action is thought to be selective inhibition of presynaptic norepinephrine re-uptake. It has the advantage of once-a-day (morning) dosing and full-day coverage. Therapeutic effect is not seen until 2 weeks. It has fewer side-effects than classic stimulants. It is not a controlled substance and there is no abuse potential.

PHARMACOECONOMICS Pharmacoeconomics examines drug utilization, risks and benefits, access, and affordability in mental health delivery systems. It is increasingly playing a role in availability/ rationing of new (invariably more expensive) medications.

REFERENCES AND FURTHER READING Ahrens B, Muller-Oerlinghausen B (2001) Does lithium exert an independent antisuicidal effect? Pharmacopsychiatry 34, 132. American Psychiatric Association (2002) Practice guideline for the treatment of patients with bipolar disorder (revision). Am. J. Psychiatry 159 (Suppl. 4), 1. Anderson IM (2003) Drug treatment of depression: reflections on the evidence. Adv. Psychiatr. Treat. 9, 11.


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Baldwin D, Mayers A (2003) Sexual side-effects of antidepressants and antipsychotics. Adv. Psychiatr. Treat. 9, 202. Bauer M, Whybrow PC, Angst J et al. (2002) World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders. 1: Acute and continuation treatment of major depressive disorder. World J. Biol. Psychiatry 3, 5. Bowden CL, Calabrese JR, Sachs G et al. (2003) A placebo-controlled 18-month trial of lamotrigine and lithium maintenance treatment in recently manic or hypomanic patients with bipolar I disorder. Arch. Gen. Psychiatry 60, 392. Brambilla P, Barale R, Soares JC (2003) Atypical antipsychotics and mood stabilization in bipolar disorder. Psychopharmacology 166, 315. Brimes P, Coppin D, Schmitt L et al. (2003) Serotonin syndrome: a brief review. CMAJ 168, 1439. Calabrese JR, Bowden CL, Sachs G et al. (2003) A placebo-controlled 18-month trial of lamotrigine and lithium maintenance treatment in recently depressed patients with bipolar I disorder. J. Clin. Psychiatry 64, 1013. Carney S, Geddes J, Davies C et al. (2001) Duration of treatment with antidepressants (Cochrane Review). J. Psychopharmacology 15 (Suppl. 3), a10. Caroff SN, Mann SC, Campbell EC, Sullivan KA (2002) Movement disorders associated with atypical antipsychotic drugs. J. Clin. Psychiatry 63 (Suppl. 4), 12. Davis JM, Chen N, Glick ID (2003) A meta-analysis of the efficacy of second-generation antipsychotics. Arch. Gen. Psychiatry 60, 553. Garside S, Rosebush PI (2003) Serotonin syndrome: not a benign toxidrome. CMAJ 169, 543. Gilmore ML, Owens MJ, Nemeroff CB (2002) Inhibition of norepinephrine uptake in patients with major depression treated with paroxetine. Am. J. Psychiatry 159, 1702. Goldsmith DR, Wagstaff AJ, Ibbotson T, Perry CM (2003) Lamotrigine: a review of its use in bipolar disorder. Drugs 63, 2029. Goodwin GM (2003) Evidence-based guidelines for treating bipolar disorder: recommendations from the British Association for Psychopharmacology. J. Psychopharmacology 17, 149. Grauso-Eby NL, Goldfarb O, Feldman-Winter LB, McAbee GN (2003) Acute pancreatitis in children from valproic acid: case series and review. Pediatr. Neurol. 28, 145. Grunze H, Kasper S, Goodwin G et al. (2003) The World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Biological Treatment of Bipolar Disorders. I: Treatment of bipolar depression. World J. Biol. Psychiatry 3, 115. Grunze H, Kasper S, Goodwin G et al. (2003) The World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for the Biological Treatment of Bipolar Disorders. II: Treatment of mania. World J. Biol. Psychiatry 4, 5. Gurrera RJ (2002) Is neuroleptic malignant syndrome a neurogenic form of malignant hyperthermia? Clin. Neuropharmacol. 25, 183. Hajak G, Muller WE, Wittchen HU et al. (2003) Abuse and dependence potential for the nonbenzodiazepine hypnotics zolpidem and zopiclone: a review of case reports and epidemiological data. Addiction 98, 1371. Ihara M, Kohara N, Urano F (2002) Neuroleptic malignant syndrome with prolonged catatonia in a dopa-responsive dystonia patient. Neurology 59, 1102. Ikebe S, Harada T, Hashimoto T et al. (2003) Prevention and treatment of malignant syndrome in Parkinson’s disease: a consensus statement of the malignant syndrome research group. Parkinsonism Relat. Disord. 9, s47. Kawanishi C (2003) Genetic predisposition to neuroleptic malignant syndrome: implications for antipsychotic therapy. Am. J. Pharmacogenomics 3, 89. Keller MB, Hirshfeld RM, Demyttenaere K, Baldwin DS (2002) Optimizing outcomes in depression: focus on antidepressant compliance. Int. Clin. Psychopharmacol. 17, 265. Khan A, Leventhal RM, Khan RK et al. (2002) Severity of depression and response to antidepressants and placebo: an analysis of the Food and Drug Administration database. J. Clin. Psychopharmacol. 22, 40.

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Kohen D (2004) Psychotropic medication in pregnancy. Adv. Psychiatr. Treat. 10, 59. Lambert M, Conus P, Lambert T, McGorry PD (2003) Pharmacotherapy of first-episode psychosis. Expert Opin. Pharmacother. 4, 717. Lerer B, Macciardi F (2002) Pharmacogenetics of antidepressant and mood-stablizing drugs: a review of candidate-gene studies and future research directions. Int. J. Neuropsychopharmacol. 5, 255. Lerer B, Segman RH, Fangerau H et al. (2002) Pharmacogenetics of tardive dyskinesia: combined analysis of 780 patients association with D3 receptor gene ser9Gly Polymorphism. Neuropsychopharmacology 27, 105. Licht RW (2002) Limits of the applicability and generalizability of drug trials in mania. Bipolar Disord. 4 (Suppl. 1), 66. Lin K, Smith MW, Ortiz V (2001) Culture and psychopharmacology. Psychiatr. Clin. North. Am. 24, 523. Mason PJ, Morris VA, Balcezak TJ (2000) Serotonin syndrome: presentation of two cases and review of the literature. Medicine 79, 201. Meltzer HY, Alphs L, Green AI et al. (2003) Clozapine treatment for suicidality in schizophrenia: International Suicide Prevention Trail. Arch. Gen. Psychiatry 60, 82. Michelson D, Adler L, Spencer T et al. (2003) Atomoxetine in adults with ADHD: two randomized, placebo-controlled studies. Biol. Psychiatry 53, 112. Michelson D, Faries D, Wernicke J et al. (2001) Atomoxetine in the treatment of children and adolescents with attention-deficit/hyperactivity disorder: a randomized, placebo-controlled, dose–response study. Pediatrics 108, e83. Paton C, Okocha C (2004) Risperidone long-acting injection: the first 50 patients. Psychiatr. Bull. 28, 12. Pickar D (2003) Pharmacogenomics of psychiatric drug treatment. Psychiatr. Clin. North Am. 26, 303. Schatzberg AF, Nemeroff CB (2001) Essentials of Clinical Psychopharmacology. American Psychiatric Press, Washington, DC. Smith D, Dempster C, Glanville J et al. (2002) Efficacy and tolerability of venlafaxine compared with selective serotonin reuptake inhibitors and other antidepressants: a meta-analysis. Br. J. Psychiatry 180, 396. Terzano MG, Rossi M, Palomba V et al. (2003) New drugs for insomnia: comparative tolerability of zopiclone, zolpidem, and zaleplon. Drug Safety 26, 261. Thase ME (2002) Comparing the methods used to compare antidepressants. Psychopharmacol. Bull. 36 (Suppl. 1), s1. Thase ME, Bhargava M, Sachs GS (2003) Treatment of bipolar depression: current status, continued challenges, and the STEP-BD approach. Psychiatr. Clin. North Am. 26, 495. Yatham LN, Grossman F, Augustyns I et al. (2003) Mood stabilizers plus risperidone or placebo in the treatment of acute mania: international, double-blind, randomized controlled trial. Br. J. Psychiatry 182, 8. Yerevanian BI, Koek RJ, Mintz J (2003) Lithium, anticonvulsants and suicidal behavior in bipolar disorder. J. Affect. Disord. 73, 223. Zarate CA, Quiroz JA (2003) Combination treatment in bipolar disorder: a review of controlled trails. Bipolar Disord. 5, 217. Zhang Z, Yao Z, Liu W et al. (2004) Effects of antipsychotics on fat deposition and changes in leptin and insulin levels: magnetic resonance imaging study of previously untreated people with schizophrenia. Br. J. Psychiatry 184, 58. Zimmerman M, Posternak MA (2002) Are subjects in pharmacological treatment trials of depression representative of patients in routine clinical practice? Am. J. Psychiatry 159, 469.

Physical treatments

22

ELECTROCONVULSIVE THERAPY (ECT) HISTORY Camphor-induced convulsions were first used by W. Oliver in 1785 for melancholia. The effect was slow and produced fits inconsistently. In the 1930s, Meduna used IV injections of metrazol, based on a belief that there is an antagonism between schizophrenia and epilepsy. Cerletti, on the basis of the same notion in 1938, administered an electrically induced fit to a catatonic vagrant found wandering in a Rome railway station. Later, anaesthesia was introduced and convulsions modified using muscle-relaxing agents. PRESENT INDICATIONS In depressive illness • Poor response to adequate pharmacotherapy. • Person unable to tolerate side-effects of pharmacotherapy (especially the elderly). • Depressive stupor, not eating or drinking. • Severe suicide risk. • ‘Severe’ depression with delusions, psychomotor retardation. • Severe post-partum depression. The presence of delusions and severe psychomotor agitation or retardation are the main ‘reliable’ clinical predictors of response to ECT. Numerous studies of real ECT versus simulated ECT confirm the therapeutic efficacy of ECT. It is more effective than antidepressant medications (UK ECT Review Group, 2003). Up to 90 per cent show improvement in depressive symptoms. In mania Quicker response and ‘better social response’ in ECT-treated patients. Equally efficacious but more rapid response with ECT ⫹ neuroleptics. Use generally reserved for acute treatment-‘refractory’ mania.

• • •

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PHYSICAL TREATMENTS

Schizophrenia ECT is useful when schizophrenia is superimposed with catatonia or major depression. SIDE-EFFECTS OF ECT Early reported side-effects are:

• • • •

Headache. Slight and temporary confusion. Short-term memory loss, increasing with the number used. Tachycardia and hypertension immediately after ECT.

At 6 months after the course, there is no significant difference in memory between those receiving ECT and those receiving simulated ECT. MORTALITY Deaths are estimated 4.5 per 100 000 ECT treatments – similar to rates for minor anaesthesia. The majority of deaths have been caused by cardiovascular complications (arrhythmias, sudden cardiac arrest secondary to vagal inhibition). CAUTION AND CONTRAINDICATIONS There is no absolute contraindication, other than raised intracranial pressure, and risks of treatment must always be weighed against risks of illness.

• • • • •

Cardiac infarct in preceding 3 months. Other cardiac disease including arrhythmias. History of cerebral infarction. Brain tumour. Pulmonary disease.

ADMINISTRATION OF ECT Before administration 1 Full physical examination. 2 Discuss any significant organic pathology with the anaesthetist. 3 Ensure an empty stomach in patient, and full resuscitatory equipment for the anaesthetist. Application of anaesthetic 1 Induction – methohexitole (most commonly). 2 Atropine – reduces secretions, counters cholinergic effects of muscle relaxants. 3 Muscle relaxant – succinylcholine; rarely, prolonged paralysis produced due to pseudocholinesterase deficiency. 4 Oxygenate – will also facilitate seizure activity. Application of electrical stimulation The modern approach is to use brief square-wave pulses of 1–2 ms duration. This has similar efficacy to a sine-wave stimulus, but with less memory disturbance. The voltage stimulus needs to be in excess of seizure threshold to achieve an effect, but this is also related to cognitive deficits. The degree to which this stimulus exceeds

ELECTROCONVULSIVE THERAPY (ECT)

291

the seizure threshold is critical for efficacy in unilateral ECT in particular, and for the speed of response in unilateral or bilateral ECT. If there is no convulsion, repeat the stimulation up to a maximum of three times (ensure good skin contact, oxygenation). Increasing the stimulation, decreasing concomitant benzodiazepines, and giving caffeine will help to maximize seizure activity in a seizure-refractory patient.

• •

Unilateral – on non-dominant hemisphere, produces less cognitive impairment: – Between frontotemporal and mastoid region. – Lancaster position – between frontotemporal position and vertically to vertex. Bilateral – frontotemporal position.

Post-ictal 1 Oxygenate. 2 Nurse in prone position with airway in situ. 3 Reassure the patient during recovery of consciousness. Do not prescribe ECT in set courses, although the average number is 6–8. Continue applications twice to three times weekly (UK and US practices respectively) until euthymic, up to a maximum of 10–12. Transient elevation of mood on recovery after the first 1–2 treatments predicts good response. If no response whatsoever by the sixth treatment, then prognosis is poor. Daily application does not improve response, and seriously increases memory disturbance. Maintenance treatment is usually pharmacological; but some recent evidence suggests reduced relapses with maintenance ECT. EFFECTS OF ECT Cardiovascular • Brief asystole on passage of current. • Bradycardia during the tonic phase, tachycardia during the clonic phase and occasional arrhythmias in the post-ictal period. • Brief blood pressure decrease during the early tonic phase followed by a rapid rise above normal level. The rise persists through the clonic phase. • Blood pressure rise apparently is centrally stimulated, independent of peripheral convulsive activity. It is exacerbated by atropine. ?? Related to memory impairment. Neurological Immediate loss of consciousness (if given without anaesthesia). Flattening of EEG, followed by slow waves, and waves reappear as consciousness recovers, with gradual return to normal pattern over 30 minutes. Frontal areas are slowest in resuming normal activity. • Very rarely post-ictal automatisms.

• •

Neuropathological (neuroendocrine) There are complex effects, and the overall mechanism of action is unclear. Increase in blood–brain barrier permeability and capillary leakage in CNS: transitory cerebral oedema. Absence of MRI changes disputed.

• •

292

• • • •

PHYSICAL TREATMENTS

Depletion of CNS noradrenaline (NA) – subsequent increase and turnover of NA? Increased dopamine, serotonin turnover – increased receptor sensitivity? Release of oxytocin-associated neurophysin – extent is predictive of eventual response. ? Increased sensitivity of dopamine and other receptor sites.

Sleep and other changes Decreased amount of time spent in REM sleep. Decrease in number of eye movements during REM sleep – ? change in reticular activity. • Water retention. • Occasional menstrual irregularities. • Transient increases in plasma sodium, potassium, chloride, calcium, lymphocytes and neutrophils. • Eosinopenia. • Rise in plasma hydroxycorticosteroid levels. • Transitory rise in plasma glucose and in insulin secretion.

• •

UNILATERAL VERSUS BILATERAL ECT Unilateral ECT to the non-dominant hemisphere produces less post-treatment confusion and memory loss. However, there is no clear consensus of therapeutic efficacy of unilateral versus bilateral ECT. ‘Dose’ of ECT is also important in studies comparing unilateral versus bilateral, especially for side-effects. Bilateral treatment is quicker, and better in the elderly.

• •

Royal College of Psychiatrists (1989) recommends bilateral but recognizes alternative of unilateral. American Psychiatric Association (APA, 1990) gives greater preference to unilateral.

ETHICAL AND LEGAL ASPECTS Treatment with ECT requires informed written consent. The doctor must also sign to the effect that a full explanation of ‘the procedure, benefits and dangers of ECT’ has been given (Royal College of Psychiatrists, 1989). Preferably obtain consent from a relative also. The patient may withhold consent at any time during the course of treatment. There has been improved care in delivery of ECT in response to Royal College of Psychiatrists guidelines (1989). However, there is still insufficient consultant participation and training of juniors (Pippard, 1992). US guidelines are rigorous (APA, 1990). EEG monitoring is required, and specialist training and periodic recertification is necessary. Patient refusal What happens if the patient refuses treatment or is unable to understand what is proposed? The patient’s right to refuse treatment must be weighed against his/her right to receive treatment, where the ability to make a rational decision about his/her wellbeing is impaired.

PSYCHOSURGERY

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Under s.58 of the Mental Health Act 1983, ECT is a treatment requiring consent or a second opinion, in the case of detained patients. A second opinion must be sought if the patient is unable to give informed consent, refuses or withdraws consent. The opinion is given by a medical practitioner appointed by the Mental Health Commission.

OTHER FORMS OF PHYSICAL STIMULATION VAGUS NERVE STIMULATION (VNS) This affects concentrations of serotonin, norepinephrine, ␥-aminobutyric acid and glutamate. VNS has been shown to significantly improve depressive symptoms in treatment-resistant depression in about one-third of patients. Response is usually seen after about 6 weeks of stimulation. The greater the treatment-resistance (i.e. non-responders to ECT, higher number of unsuccessful trails of antidepressants), the less likely is the patient to improve with VNS. SIDE-EFFECTS OF VNS

• • •

Mild voice hoarseness (related to the electric current intensity); headache; dysphagia; neck pain; coughing; dyspnoea on exertion (related to the electric current intensity). Overall, VNS is well tolerated and the side-effects not related to current intensity resolve after time in the majority of patients. Unlike ECT, VNS has no associated cognitive side-effects.

DEEP BRAIN STIMULATION (DBS) DBS is used for the treatment of tremor in Parkinson’s disease. Electrodes are implanted into the subthalamic nucleus or thalamus. Stimulation is via a pacemakerlike device inserted on the anterior chest wall. High-frequency electrical stimulation deactivates basal ganglia regions.

TRANSCRACNIAL MAGNETIC STIMULATION (TMS) This provides non-invasive electrical stimulation of the brain, is well tolerated and has been shown to improve depressive symptoms in numerous studies. A recent study on bipolar depression showed no separation from sham treatment (Nahas et al., 2003). Research continues into the treatment parameters and patient populations for TMS.

PSYCHOSURGERY DEFINITIONS

•

WHO – The selective surgical removal or destruction … of nerve pathways … with a view to influencing behaviour.

294

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PHYSICAL TREATMENTS

US National Commission for the Protection of Human Subjects of Biomedical and Behavioural Research – Brain surgery on (i) normal brain tissue of an individual who does not suffer from any physical disease, for the purpose of changing or controlling the behaviour or emotions of such individual; or (ii) diseased brain tissue of an individual, if the primary object of the performance of such surgery is to control, change or affect any behavioural or emotional disturbance of such individual.

HISTORY

• • •

• • •

1875 – Ferrier removed frontal lobes of monkeys and noticed marked changes in animal’s ‘disposition’ and ‘character’ with no effect on motor or sensory abilities. 1936 – Moniz performed a localized division of prefrontal tracts in a series of 20 patients. There was a claimed reduction in severe and chronic agitation without marked side-effects. 1942 – Freeman and Watts introduced the ‘standard’ cut leucotomy involving wider severing of prefrontal connections. It was an imprecise, nearly ‘blind’ operation, with serious side-effects: epilepsy, incontinence, marked apathy with flattened affect, disinhibition, intellectual impairment and aggression. Mortality was 6 per cent. – At least 10 000 were performed between 1942 and 1952 in the UK, usually for chronic illness with disturbed behaviour, unresponsive to other treatments – 66 per cent schizophrenia, 33 per cent affective disorder. – ‘Modified’ operations were later designed to ablate more specific brain targets without producing side-effects associated with the cruder ‘standard’ procedure. 1949 – Scoville introduced orbital undercutting. A modified form was used extensively in the UK by Knight, who restricted orbital undercut to medial half of lobe. 1950s – The advent of effective psychotropic drugs with fuller documentation of side-effects led to rapid decline of psychosurgery. 1961 – Only 11 British hospitals reported performing more than 10 leucotomies.

MODERN PROCEDURES Modern surgery is highly selective, most often using radioisotopes (yttrium implants), ultrasound, or electrocautery under stereotactic guidance by MRI and CT.

• • • •

Procedures for anxiety/OCD – cingulotomy, subcaudate tractotomy, limbic leukotomy, capsulotomy. Procedure for depression with anxiety – subcaudate tractotomy. Procedures for Parkinson’s disease – thalamotomy, pallidotomy. Also for Parkinson’s disease – transplantation of embryonic mesencephalic or genetically engineered autologous cells into the basal ganglia which synthesize tyrosine hydroxylase.

INDICATIONS FOR PSYCHOSURGERY It is rarely appropriate and is the treatment of last resort, after:

• • • • •

Failed, adequate pharmacological treatment. Failed ECT (in refractory depression). Failed behavioural therapies (in refractory OCD). Failed psychosocial interventions. Failed pharmacotherapy for Parkinson’s.


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Chronic intractable OCD is currently the main indication. There must be comprehensive presurgical evaluation including further pharmacological trials if indicated. Psychosurgery is contraindicated if there is substance abuse, organic brain damage, co-morbid personality disorder, insufficient evaluation or prior treatment. PROGNOSIS AND OUTCOME The prognosis is good if cases are carefully selected. Pharmacological and behavioural treatments are usually continued, so that the apparent efficacy may reflect the primary effect of surgery and/or synergism with ongoing treatments. There have been insufficient controlled trials because they are ethically difficult to do.

• • • • • • •

Improvement may be gradual for even the first 2 years. 50–70 per cent show improvement. Fewer than 3 per cent get worse. No mortality now (high mortality in the 1950s and 1960s). 1 per cent epilepsy rate – controllable with medication. 6 per cent apathy/amotivation. 6 per cent personality change.

ETHICAL AND LEGAL ASPECTS Under the UK Mental Health Act 1983, psychosurgery is considered a ‘treatment which gives rise to special concern’ – this applies to formal and informal patients. It requires consent and a second opinion by an independent doctor (appointed by the Mental Health Commission) who must consult the nurse and other team member (neither doctor nor nurse) involved with treating the patient.

REFERENCES AND FURTHER READING American Psychiatric Association Task Force on ECT (1990) The Practice of ECT: Recommendations for Treatment, Training and Privileging. APA, Washington, DC. (Summary of recommendations in Convulsive Therapy (1990) 6, 85–120.) Bridges PK, Bartlett JR, Hale AS (1994) Psychosurgery: stereotactic subcaudate tractomy, an indispensable treatment. Br. J. Psychiatry 165, 599. Brodaty H, Berle D, Hickie I, Mason C (2001) ‘Side effects’ of ECT are mainly depressive phenomena and are independent of age. J. Affec. Disord. 66, 237. Conway CR, Chinbnall JT, Li X, George MS (2002) Changes in brain metabolism in response to chronic vagus nerve stimulation in depression. Biol. Psychiatry 51, 85. Cosgrove GR, Rauch SL (2003) Stereotactic cingulotomy. Neurosurg. Clin. North Am. 14, 225. Dougherty DD, Baer L, Cosgrove GR et al. (2002) Prospective long-term follow-up of 44 patients who received cingulotomy for treatment-refractory obsessive–compulsive disorder. Am. J. Psychiatry 159, 269. Eranti SV, McLoughlin DM (2003) Electroconvulsive therapy: state of the art. Br. J. Psychiatry 182, 8. George MS, Nahas Z, Bohning DE et al. (2002) Vagus nerve stimulation therapy: a research update. Neurology 59 (Suppl. 4), s56. George MS, Nahas Z, Lisanby SH et al. (2003) Transcranial magnetic stimulation. Neurosurg. Clin. North Am. 14, 283. Gershon AA, Dannon PN, Grunhaus L (2003) Transcranial magnetic stimulation in the treatment of depression. Am. J. Psychiatry 160, 835.

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Gilbody S, Whitty P, Grimshaw J, Thomas R (2003) Educational and organizational interventions to improve the management of depression in primary care: a systematic review. JAMA 289, 3145. Greenberg BD, Murphy DL, Rasmussen SA (2000) Neuroanatomically based approaches to obsessive–compulsive disorder: neurosurgery and transcranial magnetic stimulation. Psychiatr. Clin. North Am. 23, 671. Hoppe C, Helmstaedter C. Schermann J, Elger CE (2001) No evidence for cognitive side effects after 6 months of vagus nerve stimulation in epilepsy patients. Epilepsy Behav. 2, 351. Katona CL (2001) Psychotropics and drug interactions in the elderly patient. Int. J. Geriatr. Psych. 16 (Suppl. 1), s86. Lomarev M, Denslow S, Nahas Z et al. (2002) Vagus nerve stimulation (VNS) synchronized BOLD fMRI suggests that VNS in depressed adults has frequency and/or dose dependent effects. J. Psychiatry Res. 36, 219. Marangell LB, Rush AJ, George MS et al. (2002) Vagus nerve stimulation (VNS) for major depressive episodes: one year outcome. Biol. Psychiatry 51, 280. Mathews K, Eljamel MS (2003) Status of neurosurgery for mental disorder in Scotland: selective literature review and overview of current clinical activity. Br. J. Psychiatry 182, 404. Mathews K, Eljamel MS (2003) Vagus nerve stimulation and refractory depression: please can you switch me on doctor? Br. J. Psychiatry 183, 181. Nahas Z, Kozel FA, Li X et al. (2003) Left prefrontal transcranial magnetic stimulation (TMS) treatment of depression in bipolar affective disorder: a pilot study of acute safety and efficacy. Bipolar Disord. 5, 40. Philpot M, Treloar A, Gormley N, Gustafson L (2002) Barriers to the use of electroconvulsive therapy in the elderly: a European survey. Eur. Psych. 17, 41. Pippard J (1992) Audit of electroconvulsive treatment in two National Health Service regions. Br. J. Psychiatry 160, 621. Raoul S, Faighel M, Rivier I et al. (2003) Staged lesions through implanted deep brain stimulating electrodes: a new surgical procedure for treating tremor or dyskinesias. Mov. Disord. 18, 933. Rasmussen KG, Rummans TA, Richardson JW (2002) Electroconvulsive therapy in the medically ill. Psychiatr. Clin. North Am. 25, 177. Rocchi L (2002) Effects of deep brain stimulation and levodopa on postural sway in Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry 73, 267. Rose D, Fleischmann P, Wykes T et al. (2003) Patients’ perspectives on electroconvulsive therapy: systematic review. BMJ 326, 1363. Royal College of Psychiatrists (1989) The Practical Administration of Electroconvulsive Therapy. Gaskell, London. Russel E (2001) Running an ECT department. Adv. Psychiatr. Treat. 7, 57. Sackeim HA, Rush AJ, George MS et al. (2001) Vagus nerve stimulation (VNS) for treatmentresistant depression: efficacy, side effects and predictors of outcome. Neuropsychopharmacology 25, 713. Schuurman PR, Bruins J, Merkus MP et al. (2002) A comparison of neuropsychological effects of thalamotomy and thalamic stimulation. Neurology 59, 1232. UK ECT Review Group (2003) Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet 361, 799. Van der Wurff FB, Stek ML, Beekman ATF, Hoogendijk WJG (2003) The efficacy and safety of electroconvulsive therapy in depressed elderly. The Cochrane Library, issue 2.

Psychotherapy

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GENERAL ASPECTS Psychotherapy is the development of a trusting relationship, which allows free communication and leads to understanding, integration and acceptance of self. COMMON FEATURES OF PSYCHOTHERAPIES (JEROME FRANK) 1 An intense, emotionally charged relationship with a person or group. 2 A rationale or myth explaining the distress and methods of dealing with it. 3 Provision of new information about the future, the source of the problem and possible alternatives which hold a hope of relief. 4 Non-specific methods of boosting self-esteem. 5 Provision of success experiences. 6 Facilitation of emotional arousal. 7 Takes place in a locale designated as a place of healing. DIFFERING LEVELS OF PSYCHOTHERAPY Informal As between friends and relatives and in self-help groups. Formal • Supportive – to restore or maintain the status quo. Useful in: – Those in crisis for whom change is not desired. – The emotionally severely handicapped who are not expected to improve greatly. • Dynamic – to effect change in the individual. Uses: – Confrontation of defences. – Clarification. – Interpretations – new formulations of problems.

PSYCHOANALYSIS DEFINITIONS AND KEY TERMS

•

Psychoanalysis – both (i) a psychological theory of the mind and (ii) a psychotherapeutic treatment method.

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•

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Libido – now used to mean overall mental ‘energy’ or drive. Love object – person or thing towards which the libido is directed (or ‘cathected’). Actual neurosis – caused by physical damming-up of sexual urges (e.g. neurasthenia). Psychoneurosis – caused by psychological damming-up of fundamental instinctive urges in a conflict situation (e.g. hysteria). Dream work – the process which turns the hidden ‘latent dream thoughts’ into the reported ‘manifest content of the dream’. It consists of: – Condensation – the manifest content shows ‘over-determinism’. – Displacement. – Dramatization. – Symbolization. – Secondary elaboration. Parapraxes – apparent errors or omissions in everyday life which symbolize underlying attitudes. They may be: – Symptomatic – the emotional urge is not repressed at all. – Disturbed – incomplete repression is present. – Completely inhibited – with complete repression. The ego – that part of the individual which is in direct touch with reality. Ego functions: – Relationships with reality: adaptive; reality testing; maintenance of a sense of reality. – Regulation and control of drives (‘libido theory’). – Relationships with other people (‘object relations theory’). – Cognitive. – Defensive. – Synthetic – the ability to hold together as a person. – Autonomous – derived from autonomous energies of the ego. Ego defence mechanisms – habitual, unconscious and sometimes pathological mental processes which are employed to resolve conflict between instinctive needs, internalized prohibitions and external reality. – Repression – the basic ego defence mechanism; refusal to recognize internal reality; prevents the perception of instincts and feelings, with unconscious inhibition of the conflicting impulse. – Denial – refusal consciously to recognize external reality. – Projection – attribution of one’s own unacknowledged feelings to others. May be of delusional strength. – Distortion – grossly reshaping external reality to suit inner needs. – Reaction formation – feeling or behaving in a way which is the opposite of unacceptable instinctual impulses. – Turning against the self – unacceptable aggression towards others is expressed, indirectly, towards the self. Seen in passive aggressive individuals and hypochondriasis. – Displacement – redirection of feelings towards a less cared-for object. – Projective identification – dissociation of unacceptable parts of the personality and projection on to another, resulting in identification with the other. – Acting out – direct expression of an unconscious impulse in order to avoid awareness of the accompanying affect.

PSYCHOANALYSIS

• • • •

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– Intellectualization – thinking about rather than feeling instinctive desires. – Sublimation – a healthy coping mechanism; indirect expression of instincts without adverse consequences. – Splitting – the positive and negative fantasized relationships remain alternatively in consciousness, with the alternative dissociated. – Isolation – the separation of an idea from its associated affect. Transference – a repetition of the past which is inappropriate to the present. Transfer of unconscious memories into consciousness. So, in therapy, transference is the shifting of an emotional attitude from a past object or person on to the therapist. Countertransference – the therapist’s emotional attitudes towards the patient. Therapeutic or working alliance – the normal, adult relationship between therapist and patient. The therapeutic alliance leads to the transference neurosis which leads to the countertransference. The transference neurosis is interpreted to the patient; the countertransference may or may not be. ‘Working through’ – repeatedly experiencing a conflict, in the transference situation, so that it may be resolved.

Mental states associated with ego defence Hysteria – denial, projection, identification. Obsessional conditions – isolation, magic undoing, reaction formation. Paranoia – projection and splitting. Depression – turning on the self. Phobias – displacement of affect.

• • • • •

Components of repression Dissociation from the self of the unconscious idea leads to – Failure of comprehension of the enacted idea, so there is then – Unresponsiveness to feedback, and acts are not regulated (leading to repetition compulsion).

• • •

But there is still the:

•

Abnormal motivational state – since unconscious motivation still drives the acts.

There is also:

•

Repression of memory – but the data are preserved in the unconscious and normal forgetting is prevented.

PSYCHOANALYTIC TECHNIQUES FOR UNDERSTANDING THE UNCONSCIOUS

• • •

Free association – of words and thoughts. Interpretation of dreams. Exploration of parapraxes.

Suitability for dynamic psychotherapy 1 The patient’s problem must be understandable in psychological terms. 2 The patient must be willing and able to understand his/her problems in psychological terms. A test interpretation may be used to assess the patient’s response.

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Table 23.1 Stages of sexual development Age

Stage

0–1 years

Oral

1–3 years

Anal

Transitional object leads to: 3–5 years Phallic (Oedipal) 5–12 years 12–20 years 20⫹ years

Latency period Puberty Adult sexual development

Breast is the love object Gratification is by oral means Basic trust develops Gratification is achieved by control over defecation A sense of self develops

Genital gratification leads to Oedipal mother and father object relationships Sexual drives reawoken by hormonal changes

3 The patient must have adequate ‘ego strength’ – the ability to cope with the tensions arising from inner conflict. 4 The patient must be able to form and sustain a psychotherapeutic relationship. SEXUAL DEVELOPMENT See Table 23.1.

• •

Oedipal complex – after the Greek tragedy in which Oedipus unknowingly killed his father and married his mother. Signifies rivalry between son and father for mother’s affection. The son imagines he will be castrated as a punishment. Electra complex – equivalent rivalry between daughter and mother, arising out of daughter’s fear that she has been castrated.

Castration anxiety in males resolves the Oedipal complex and leads to the latency period. Castration anxiety in females begins the Electra complex.

• •

Primary process thinking is unconscious and is based on the pleasure principle (the libidinal drive for satisfaction). Secondary process thinking is conscious and is based on the reality principle (which takes into account the social pressures).

There are two basic theories: instinct (libido) theory versus object relations theory; i.e. the need to reduce instinctual drives versus the importance of the subject’s need to relate to objects.

IMPORTANT PSYCHOANALYTICAL THEORISTS EARLY THEORISTS Freud (1856–1939) Development of his theories: 1 The cathartic model (‘psychic abscess’) – therapy releases the blocked emotions. See Studies in Hysteria (Breuer and Freud, 1895).

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2 The topographical model – unconscious, preconscious and conscious levels of the mind. See The Interpretation of Dreams (Freud, 1900) and The Psychopathology of Everyday Life. 3 The structural model – id, ego and superego. The balance of these three makes up the character structure. This model also includes Eros, the life instinct, and Thanatos, the death instinct. See Mourning and Melancholia, Beyond the Pleasure Principle and The Ego and the Id (Freud, 1923). Adler (1870–1937): School of Individual Psychology Adler propounded theories of:

• • •

Organ inferiority and psychic compensation. Fictive goals. Drive for superiority – importance of power and social significance in psychodynamics.

Adler’s work was integrated into schools of ego psychology. Jung (1875–1961): School of Analytical Psychology Jung propounded three levels of psyche:

• • •

Conscious – includes the persona. Personal unconscious. Collective unconscious (racial, universal).

The persona is the outer crust of the personality, which is the opposite of the personal unconscious on dimensions of:

• • •

Thinking/feeling. Sensuousness/intuition. Extrovert/introvert (related to direction of flow of mental energy).

Archetypes are generalized symbols and images within the collective unconscious. They include:

• •

Animus – the unconscious, masculine side of the woman’s female persona. Anima – the unconscious, feminine side of the man’s male persona.

A complex is a group of interconnected ideas which arouse associated feelings and effect behaviour. Wilhelm Reich • Neurosis results from sexual frustration. • Body armour. Orgone energy accumulator. • Recently developed into bioenergetics. Otto Rank Neurosis originates in the trauma of birth.

•

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NEO-FREUDIANS (USA) Neo-Freudians were influenced by Adler to shift emphasis from:

• • •

Biological to social processes. Intrapsychic to interpersonal processes. Past history to ‘here and now’.

Horney Horney attributed sexual difficulties (especially female difficulties) to social rather than biological causes. Fromm/Stack-Sullivan The self consists of:

• •

The ‘reflected appraisals’ of others. The roles it has to play in society.

In therapy there is ‘consensual evaluation’ – therapist and patient interact to validate each other’s experience.

BRITISH SCHOOLS These are particularly involved with child analysis. Anna Freud • Ego psychology and the importance of ego defence mechanisms. • Psychotherapeutic relationship with the child is more educational. Melanie Klein Worked with pre-oedipal children using play analysis. Ego and its defence mechanisms are present from birth and the superego before the age of 2 years. • Paranoid position develops first. There is splitting of good and bad aspects. The good aspects of mother are introjected but are threatened by the externalized bad aspects – leads to rage, fear and hatred. • Depressive position develops next. The realization that mother is both good and bad leads to guilt and fear of destroying the loved one with the hatred.

•

Bowlby Bowlby’s work on maternal depreviation pointed to the importance of separation anxiety, with stages of:

• • •

Protest. Despair. Detachment.

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POST-FREUDIANS AND THE NEW PSYCHOTHERAPIES (‘GROWTH THERAPIES’, ‘HUMAN POTENTIAL MOVEMENT’) Winnicot (1896–1971) • Development of object relations theory, with Fairbairn, Guntrip and others. Satisfaction is sought in relationships, not only in sexual relief. • Personality develops from internalized early relationships, particularly with the mother (‘good-enough mother’). Transitional objects are intermediate between oral eroticism and true object relationships. Erikson Erikson underlined the importance of psychosocial development and the adolescent identity crisis. Rogers (1951): client-centred therapy and the Encounter movement The therapist, by use of (i) genuineness, (ii) unconditional positive regard and (iii) accurate empathy shows his/her acceptance of the client’s real self, thus leading to reduction of the client’s discrepancy between real self and ideal self. In Encounter groups, non-directive acceptance leads to exposure of emotions, leading to ‘basic encounters’ in which there is emotional and intellectual contact between individuals. Perls: Gestalt therapy The therapist emphasizes awareness of here-and-now needs and how they are blocked, by the use of various techniques (e.g.‘hot seat’ work,‘doing a round’). The client may thus experience himself/herself as an organized whole (‘Gestalten’). See Perls et al. (1973). Berne (1964): transactional analysis The therapist explores, with the client, the ‘games’ that he/she plays with others and the ‘scripts’ which he/she has made for his/her life. Based on a view of the personality as consisting of parent, adult and child ego states. Frankl: existential logotherapy The therapist seeks to bring spiritual realities to awareness and uses paradoxical intention. This is based on the view that the individual is searching for meaning and purpose. Others • Ellis – rational–emotive therapy. • Assagioli – psychosynthesis. • Moreno – psychodrama. • Janov – primal therapy. • Maslow – self-actualization.

THE INTERNATIONAL APPROACH An international approach has developed from the ideas of Adler, Stack-Sullivan and Bateson and also from studies of control systems in physics and physiology.

304

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Cybernetics – theory of control and communication between the individual and machine. This developed into – General systems theory (von Bertalanffy) – used particularly in family therapy, with the concept of concentric and overlapping systems and subsystems of interacting individuals.

System process 1 Within a system there is maintenance of homeostasis whenever possible. But there may be – 2 Crisis due to external challenge. This may lead to – 3 Exploration of the problems. This may lead to – 4 Reorganization and a new homeostasis. Family therapists Family therapists may be: • Conductors – acting as authority figures to alter family systems by persuasion or criticism. • Reactor analysts – experiencing the family conflicts by entering into them, to attain greater understanding. • Systems purists – analysing the subsystems and family rules and feeding this back to the family without becoming involved. Crisis intervention developed from this model. At the time of crisis there is maximum possibility for a change of the system for the better. Key names Haley, Minuchin, Ackerman, Satir, Laing. Crisis intervention (Caplan) Common features of the crisis intervention: 1 2 3 4

Fast provision of service. Intensive short-term work, with rapid withdrawal of help. Here-and-now therapy, specific goals, exploration of all possibilities. A more active, confronting therapeutic style.

This may operate by phone service, walk-in centre, self-help centre or multidisciplinary domiciliary teams.

GROUP THERAPIES Groups may be simply supportive self-help groups and social clubs.

ANALYTIC GROUPS Analysis in the group This is treatment of the individual within a group setting. Analysis of the group (Tavistock Institute groups) The leader is inactive and interprets purely the transference relationship of the whole group to himself/herself. Two writers on this type of group are Bion and Ezriel.

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Bion Two methods of working: • Work groups – consciously working on a task. • Basic assumptions group – defensive group cultures block the work of the group. These cultures are: – Dependency – the assumption that solutions are provided by the leader. – Fight–flight – the assumption of threat to the group. – Pairing – the assumption that a new leader will arise. Ezriel Common group tensions are based on three levels of relationship with the leader: 1 Required (superficial). 2 Avoided. 3 Calamitous (in fantasy). Analysis through and of the group (Institute of Group Analysis: Foulkes) Groups function at three levels: 1 Current adult relationships. 2 Individual multipersonal transference relationships. 3 Hared feelings and fantasies. CURATIVE FACTORS IN GROUPS (YALOM, 1985)

• • • • • • • • • • • •

Interpersonal learning. Catharsis. Group cohesiveness. Insight. Development of socializing techniques. Existential awareness. Universality. Instillation of hope. Altruism. Corrective recapitulation of primary family group. Guidance. Imitative behaviour.

THERAPEUTIC COMMUNITIES In these there is open communication and shared examination of problems.

• • •

Main, of the Northfield Clinic, made first use of the term in 1946. Maxwell-Jones – Henderson Hospital. Rapoport – basic features are: – Democratization – abolition of hierarchy. – Permissiveness – tolerance of disturbed behaviour. – Reality confrontation – regular feedback to individuals of the results of their behaviour. – Communalism – equal shares for all.

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BEHAVIOURAL TREATMENTS There are two basic theories: 1 Pavlovian – classic conditioning: association of conditioned stimulus (CS) with unconditional stimulus (UCS) to produce the response. 2 Skinnerian – operant conditioning: alteration of the frequency of a piece of spontaneous behaviour by reward or punishment. These two strands were brought together by Mowrer: the double learning theory (see diagram below). UCS

Response (fear)

Avoidance

Reduction of fear

CS

Reward Pavlovian

Skinnerian

BEHAVIOURAL TREATMENTS These involve:

• • • • • • •

Learning theory principles. Precise observation of behaviour. Concentration on symptoms. An empirical approach. Directive treatment methods. Clear goals. Objective evaluation of results.

USES OF BEHAVIOURAL TREATMENTS They have been shown to be useful in:

• • • • • • • •

Single phobias – desensitization and flooding. Obsessional states – response prevention. Marital problems – contract therapy. Sexual inadequacy – Masters and Johnson techniques. Sexual deviancy – aversion, covert sensitization. Chronic schizophrenia – token economy. Mental subnormality – ‘behaviour modification’. Enuresis – ‘pad and bell’.

SOME PRINCIPLES Premack principle Any frequently performed piece of behaviour can be used as a positive reinforcer of the desired behaviour.

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Intermittent reinforcement This is more resistant to extinction than continuous reinforcement. Shaping This involves successive approximations to the required behaviour, with contingent positive reinforcement.

COGNITIVE THERAPY See also Chapter 4. Like behaviour therapy, cognitive therapy uses directive methods and deals with present problems. Unlike behaviour therapy, it regards inner attitudinal factors as vitally important and seeks to change these. Maladaptive internal habits of thought and self-statements are identified and alternatives suggested and ‘tried out’ in fantasy (Meichenbaum). Irrational beliefs may be exposed and strongly confronted with ‘reason’ (‘rational–emotive’ therapy of Ellis). Beck in particular has introduced cognitive theory and therapy into the understanding and treatment of depression. COGNITIVE THEORY OF DEPRESSION Depression results from a network of negative attitudes to the self, the future and the world. Such cognitive distortions (‘silent assumptions’) arise from early traumatic experiences and show four basic types of error:

• • • •

Arbitrary inference – always drawing the worst conclusions from a situation. Selective abstraction – focusing on the worst aspects of a situation. Over-generalization – drawing general conclusions about personal worth from one example. Minimization and magnification – performance is underestimated and errors are overestimated.

Such errors confirm attitudes of self-blame and hopelessness. As a description of thinking in a depressive episode, this has much validity; but as a causal theory it is not proven. Between episodes these errors may not be present. ‘COGNITIVE RESTRUCTURING’ Depressive cognitions (‘automatic thoughts’) are identified from present or recent experiences. The patient is then encouraged to challenge those assumptions and express alternatives. The person keeps a record of automatic thoughts and possible alternatives. Reality testing, graded test assignments, role rehearsal (trying out the new cognitions and behaviour), activity scheduling with experience of success and social skills training are all used to support the cognitive restructuring. COGNITIVE–BEHAVIOURAL THERAPY (CBT) This is now an established modality in depression (Chapter 4), anxiety disorders (Chapter 5), eating disorders (Chapter 7), and in schizophrenia (Chapter 3) to treat persistent symptoms and to improve compliance (‘compliance therapy’).

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VARIATIONS Interpersonal therapy (IPT ) Initially developed for depression (see Chapter 4). The focus is on grief, interpersonal role disputes, interpersonal skill, life role and transitions; also useful in bulimia nervosa. Dialectic behavioral therapy (DBT) A form of cognitive behavioural therapy used for borderline personality disorder (see Chapter 6). The focus is on emotional regulation, distress tolerance and validation. Motivational enhancement therapy (MET) Used for substance abuse (see Chapters 9 and 10). The focus is on the client’s motivation to change and plan for change.

PSYCHOTHERAPY RESEARCH

• •

‘Outcome’ research is assessment of results of psychotherapy. ‘Process’ research is examination of how results are achieved.

METHODOLOGICAL PROBLEMS Methodological problems have proven almost insuperable. There are many possible confounding variables:

• • •

Patients – diagnosis, severity, age, IQ, culture, personality type, motivation, expectation of therapy, attendance, current life circumstances, spontaneous recovery rates. Appropriate controls are required. Therapists – precise techniques used, personality type, level of experience, length of therapy. The interaction of patient and therapist variables. Outcome – assessed by whom (patient, therapist, observer) and how (self-report, family report, video observation, MMPI, PSE, etc.)? Length of follow-up?

Multicentre trials particularly have failed either because of insufficient standardization or because rigorous standardization has prevented progress (e.g. Maudsley/ Tavistock study of 1972). Several large-scale ‘meta-analyses’ of outcome research have been published.

OUTCOMES Given the above provisos, all forms of psychotherapy seem to give a general remission rate of 65 per cent. Bloch (1979) suggests seven factors are predictive of good progress in therapy: 1 A reasonable degree of personality integration and functioning. 2 Motivation for change. 3 Realistic expectations based on psychological mindedness (this can be improved by preparatory interviews). 4 At least average intelligence. 5 Neuroses and mild personality disorders (not psychoses). 6 Strong affect is present (especially anxiety or depression). 7 Life circumstances are free of unresolvable crises.

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Compare this list with the traditional (YAVIS): young, attractive, verbal, intelligent, successful. Freud and others advocated a ‘trial interpretation’ to assess acceptance. Sloane et al. (1975) conducted a comparative trial of (i) behaviour therapy, (ii) psychoanalysis and (iii) waiting list in anxiety states. Behaviour therapy showed 93 per cent improved at the end of therapy. Short-term psychoanalysis showed 73 per cent improved. On the waiting list, again, 73 per cent improved. In 101 studies of outcome of psychotherapy up to 1970, 81 showed favourable outcome and 20 did not. Eysenck (1952) reported a spontaneous remission rate of 70 per cent in 2 years. Analysts’ recovery rates were between 44 and 64 per cent in 2 years. Malan (1977) proposed that ‘spontaneous remission’ after a first interview may be due to:

• • • •

Insight gained. Realization of personal responsibility. Genuine reassurance. Joining with ‘significant other’.

THE PROCESS Most studies show the personality, enthusiasm and involvement of the therapist and the therapist–patient interaction to be far more important than the theoretical form of therapy. Therapist skills A trained analyst may do no better than concerned, intelligent, thoughtful people (e.g. college professors). Accurate empathy, unconditional positive regard and genuineness (congruity) are said to be related to good outcome, but are unreliably measured (Truax and Carkhuff, 1967). Yalom (1985) found negative group therapy factors: ‘aggressive stimulator’ type of leader, attack by the leader, rejection by the group. Exploitiveness and disinterest from the therapist are negative factors. Transference Malan found early development of therapist/parent transference, encouraged by interpretations relating to early parent relationships, to predict good outcome. Working through termination of therapy is important. Arousal Sifneos and other proponents of brief psychotherapy regard emotional arousal as vital to success. Jerome Frank has pointed to its relevance in all forms of psychotherapy. Assessment by patients Malan wrote that patients valued warmth and individual attention. Patients disliked therapists who did not support or advise. No patient remembered an analytic-group interpretation.

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REFERENCES AND FURTHER READING Bateson G (1972) Steps to an Ecology of Mind: Collected Essays. Paladin, London. Beck AT (1976) Cognitive Therapy and the Emotional Disorders. International Universities Press, New York. Beck AT, Rush AJ, Shaw BF, Emery G (1979) Cognitive Therapy of Depression. Guilford Press, New York. Beck AT, Sokol L, Clark DA, Berchick R et al. (1992) A crossover study of focused cognitive therapy for panic disorder. Am. J. Psychiatry 149, 778. Berne E (1964) Games People Play. Grove Press, New York. Bion WR (1961) Experiences in Groups. Tavistock, London. Blay SL, Vel Fucks JS, Barruzi M et al. (2002) Effectiveness of time-limited psychotherapy for minor psychiatric disorders: randomised controlled trial evaluation of immediate v. longterm effects. Br. J. Psychiatry 180, 416. Bloch S (1977) Supportive psychotherapy. Br. J. Hosp. Med. 18, 63. Bloch S (1979) Assessment of patients for psychotherapy. Br. J. Psychiatry 135, 193. Bloch S, Crouch E (1985) Therapeutic Factors in Group Psychotherapy. Oxford University Press, New York. Bowlby J (1977) The making and breaking of affectional bonds. I: Aetiology and psychotherapy. Br. J. Psychiatry 130, 201. Breuer J, Freud S (1895) Studies on Hysteria. Standard edn, Vol. 2. Hogarth, London. Brown D, Pedder J (1979) Introduction to Psychotherapy. Tavistock, London. Brown JAC (1961) Freud and the Post-Freudians. Penguin, Harmondsworth. Casacalenda N, Perry JC, Looper K (2002) Remission in major depressive disorder: a comparison of pharmacotherapy, psychotherapy, and control conditions. Am. J. Psychiatry 159, 1354. Chesser ES (1976) Behaviour therapy: recent trends and current practice. Br. J. Psychiatry 129, 289. Clark DH (1977) The therapeutic community. Br. J. Psychiatry 131, 553. Eysenck HJ (1952) The effects of psychotherapy: an evaluation. J. Consult. Psychol. 16, 319. Ezriel H (1950) The psychoanalytic approach to group treatment. Br. J. Med. Psychol. 23, 59. Fava GA, Rafanelli C, Grandi S et al. (2001) Long-term outcome of panic disorder with agoraphobia treated by exposure. Psychol. Med. 31, 891. Fordham F (1953) An Introduction to Jung’s Psychology. Penguin, Harmondsworth. Frank JD (1973) Persuasion and Healing, revised edn. Johns Hopkins Press, Baltimore. Freud S (1900) The Interpretation of Dreams. Standard edn, Vols 4 and 5. Hogarth, London. Freud S (1923) The Ego and the Id. Standard edn, Vol. 19. Hogarth, London. Goddard A (1982) Cognitive behaviour therapy and depression. Br. J. Hosp. Med. 27, 248. Gomes-Schwartz B (1982) Negative change induced by psychotherapy. Br. J. Hosp. Med. 28, 248. Hobson RP (2003) Between ourselves: psychodynamics and the interpersonal domain. Br. J. Psychiatry 182, 309. Kennedy E (2002) Evidence in the psychological therapies: a critical guide for practitioners. Br. J. Psychiatry 181, 262. Kingdom D, Turkington D, John C (1994) Cognitive behaviour therapy of schizophrenia. Br. J. Psychiatry 164, 581. Main TF (1957) The ailment. Br. J. Med. Psychology 30, 129. Malan D (1977) The Frontier of Brief Psychotherapy. Plenum, New York. Marks IM (2002) The maturing of therapy: some brief psychotherapies help anxiety/depressive disorders but mechanisms of action are unclear. Br. J. Psychiatry 180, 200. Montgomery C (2002) Role of dynamic group therapy in psychiatry. Adv. Psychiatr. Treat. 8, 34. Murphy GE, Guze SB (1960) Setting limits: management of the manipulative patient. Am. J. Psychother. 14, 30.


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Olfsen M, Marcus SC, Druss B, Pincus HA (2002) National trends in the use of outpatient psychotherapy. Am. J. Psychiatry 159, 1914. Perls F, Hefferline RF, Goodman P (1973) Gestalt Therapy. Penguin, Harmondsworth. Pilkonis PA, Imber SD, Lewis P, Rubinsky P (1984) A comparative outcome study of individual, group and conjoint psychotherapy. Arch. Gen. Psychiatry 41, 431. Rogers CR (1951) Client Centred Psychotherapy. Houghton-Mifflin, Boston. Ryle A (1976) Group psychotherapy. Br. J. Hosp. Med. 15, 239. Sandler J, Dare C, Holder A (1973) The Patient and the Analyst: the Basis of the Psychoanalytic Process. Allen & Unwin, London. Schulberg HC, Raue PJ, Rollman BL (2002) The effectiveness of psychotherapy in treating depressive disorders in primary care practice: clinical and cost perspectives. Gen. Hosp. Psychiatry 24, 203. Segal H (1964) Introduction to the Works of Melanie Klein. Heinemann, London. Shear MK, Pilkonis PA, Cloitre M, Leon AC (1994) Cognitive behavioural treatment compared with nonprescriptive treatment of panic disorder. Arch. Gen. Psychiatry 51, 395. Skynner ACR (1976) One Flesh: Separate Persons. Constable, London. Sloane RB, Staples FR, Cristol AH et al. (1975) Psychotherapy versus Behaviour Therapy. Harvard University Press, Cambridge, MA. Soldz S, Budman S, Demby A, Feldstein M (1990) Patient activity and outcome in group psychotherapy: new findings. Int. J. Psychother. 40, 53. Truax CB, Carkhuff R (1967) Towards Effective Counselling and Psychotherapy. Aldine, Chicago. Vaillant GE (1971) Theoretical hierarchy of adaptive ego mechanisms. Arch. Gen. Psychiatry 24, 107. Waldron G (1984) Crisis intervention: is it effective? Br. J. Hosp. Med. 31, 283. Walton H (1971) Small Group Psychotherapy. Penguin, Harmondsworth. Whitfield G, Williams C (2003) The evidence base for cognitive–behavioural therapy in depression: delivery in busy clinical settings. Adv. Psychiatr. Treat. 9, 21. Willner P (1984) Cognitive functioning in depression: a review of theory and research. Psychol. Med. 14, 807. Yalom ID (1985) The Theory and Practice of Group Psychotherapy, 3rd edn. Basic Books, New York.

Community-orientated psychiatry

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HISTORICAL REVIEW Large institutions were initially a humanitarian response to appalling conditions of private madhouses, prisons and workhouses where the community ‘cared’ for its mentally ill. Originally, the concept of an asylum was as a place of ‘sanctuary’. There was an early optimistic phase of non-restraint – ‘moral’ treatment. PROBLEMS WITH LARGE INSTITUTIONS

• • •

They were isolated from the communities they served, with a self-sufficient subculture of their own. There was selective intake of chronically ill, behaviourally disturbed and socially unsupported individuals. Institutionalization (Wing and Brown, 1970): – Social understimulation – encourages inactivity and social withdrawal. – Restriction of independence – leads to lack of initiative and drive. – Authoritarianism and pauperism – underline individuals’ status as bottom of the social hierarchy. – Loss of skills – little training in domestic, practical or social skills. – Depersonalization – loss of sense of individual identity.

DECARCERATION The modern concept of reorientation of care away from large institutions was based on principles of community mental health care:

• • • •

Locally based, accessible services. A comprehensive and integrated range of therapeutic interventions and resources for range of mental health needs. Services delivered by locally based community mental health teams (CMHT). Multidisciplinary teamwork involves medical and nursing staff, behaviour therapists, psychologists, occupational therapists and social workers. Mental health teams work closely with, or integrated with, primary care teams.

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RECENT DEVELOPMENTS IN COMMUNITY CARE 1 ‘Assertive outreach’ models incorporating intensive community follow-up and home treatment programmes, continued ‘down-sizing’ of mental hospitals, and expansion of daycare facilities. 2 Targeting of resources to patients with enduring psychiatric illness. 3 Fully operational key worker programmes – incorporated in the UK into the ‘Care Programme Approach (CPA). A named keyworker is responsible for a range of agreed treatment objectives. Also, development in the UK of care management: a worker supervises care for particularly vulnerable individuals across a range of resources. 4 Users and carers have a crucial role in the planning, development and management of mental health services through patient advocacy groups. 5 Promotion of the recovery model: – Focus on patients’ strengths, not their disabilities. – Focus on patients’ life aspirations. – Focus less on the medical. – Hope, autonomy and desire are key elements. – Recognize the value of peer support and peer treatment programmes in helping patients recover. 6 Training in the Community Living Programme (Stein and Test) and the successor Programme of Assertive Community Treatment (PACT). Developed in Madison, Wisconsin – embraces most of the principles of modern community mental health care noted above. The assertive community treatment (ACT) model is the most effective. ACT components include: – High staff:patient ratio. – 24-hour availability. – Outreach to patient, with frequent (daily, or 3–5 visits/week) contact. – Functional outcomes (patient satisfaction, level of social/vocational activities, continued community tenure without rehospitalization) more important than symptom outcomes. 7 Home-based treatment projects. Most are a development of the Stein and Test model. Muijen et al. (1992) showed that at 3-month follow-up, the experimental home-treatment group had fewer admissions, shorter length of stay, improved clinical and social outcome compared with control groups offered standard treatment. Home treatment was preferred (but only marginally) by patients and relatives. There were similar findings in other programmes (Sparkbrook, UK; Sydney, Australia).

POLICY INITIATIVES State hospital beds in the USA have been declining in number:

• • •

1955 – 339 per 100 000 population. 1992 – 41 per 100 000 population. 1998 – 24 per 100 000 population.

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An estimate of inpatient bed requirements per 100 000 population in the UK is:

• • • •

Acute – 25. Substance abuse – 3. Medium-stay – 8. Long-stay and rehabilitation – 20.

Resources (as a percentage of gross domestic product) have not changed dramatically:

• •

In the UK – 0.26 per cent in 1960, 0.33 per cent in 1985. In the USA – 0.33 per cent in 1960, 0.32 per cent in 1985.

Mental disorders are a major cause of morbidity. They account for 14 per cent reported days off work and for 23 per cent of British National Health Services inpatient costs. There are national and international efforts to:

• • • • • •

Reduce the incidence of suicide. Detect and treat mental illness early in children. Change health behaviour and public awareness to decrease drug and alcohol abuse. Better integrate mental health and physical medicine services. Provide more community-based residential alternatives to reduce excess of mentally ill (the ‘transtutionalized’) in nursing homes, jails, long-stay facilities, acute inpatient beds, and reduce homelessness. Continue to combat the stigma of and discrimination against mental illness.

OTHER IMPORTANT ISSUES IN COMMUNITY PSYCHIATRY

• • • • • • • •

Continuity of care. Implementation of evidence-based mental health best practice. Cost containment and resource allocation (distinguishing clinical ‘effectiveness’ from efficacy). Providing integrated (mental health and addiction) services for persons with dual diagnosis (co-occurring mental disorder and alcohol/drug addiction). Development and integration of recovery model services, including peer support programs. Multidisciplinary teamwork with the consultant seen as a fundamental part of the service. Need for more community psychiatric nurses and clinical psychologists. Need for greater integration of social workers and occupational therapists within the multidisciplinary team.

HOMELESSNESS Cohen and Thompson (1992) – Is it that the mentally ill are homeless or that the homeless are mentally ill?

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There are high rates of psychiatric and physical morbidity. Marshall (1989) reported that 29/46 hostel residents in Oxford showed psychosis. Susser et al. (1989) reported that 17 per cent of new arrivals at New York shelters were psychotic and 58 per cent were substance abusers. NEEDS ANALYSIS Needs are multifaceted. Steps in care include: 1 Identification of those in need through outreach programmes. 2 Systematic evaluations – mental and physical health, support, familial needs. 3 Integration of care – treatment of psychosis, depression, substance abuse, physical conditions. 4 Housing requirements. 5 Continued support and rehabilitative care. 6 Continued research and audit. 7 Refinement of local and national policy. At present, care is poorly coordinated. In the USA, the case management system is not focused towards the homeless; a bureaucratic process of health delivery ‘discourages’ re-entry of the homeless into the health system (Bachrach, 1992). Many homeless people deny any mental illness, are non-compliant with medication and avoid mental health care. The US system protects personal rights, possibly aggravating the plight of the homeless. An alternative view maintains that mental health systems cannot understand the real needs of these individuals without adopting their perspective.

REHABILITATION ASSESSMENT 1 To determine the kinds of mental and physical disability present and their severity. 2 To discover potential talents that could be developed. 3 To specify short-term and longer-term objectives and design plans to achieve them. In the UK, operation of care programme and care management approaches. 4 To seek appropriate forms of professional, voluntary and family help and involvement of patient advocacy. 5 To monitor progress and tailor care plans as necessary. 6 Specifically to assess: – Chronic symptoms and liability to relapse (psychiatrist, community psychiatric nurse (CPN)). – Behavioural analysis (nurses, occupational therapist (OT), psychologist). – Self-care and domestic skills (OT). – Occupational skills and work assessment (work rehabilitation programmes). – Social skills training (develop interpersonal skills and ability to develop and maintain relationships).

PSYCHIATRY AND GENERAL PRACTICE/PRIMARY CARE Primary care physicians or general practitioners (GPs) are in a prime position to detect and begin early treatment of psychiatric illness. Twenty-five per cent of GP attenders

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have a psychiatric element to their consultation, yet only 43 per cent of GPs have had training or experience in a psychiatric setting. Emphasis is on the role of primary care physicians in multidisciplinary teams, and joint models of such care are now being practised.

REFERENCES AND FURTHER READING Bachrach LL (1992) Psychsocial rehabilitation and psychiatry in the care of long-term patients. Am. J. Psychiatry 149, 1455. Berzins KM, Petch A, Atkinson JM (2003) Prevalence and experience of harassment of people with mental health problems living in the community. Br. J. Psychiatry 184, 526. Christensen RC (2002) The ethics of cost shifting in community psychiatry. Psychiatr. Serv. 53, 921. Clark C, Rich AR (2003) Outcomes of homeless adults with mental illness in a housing program and in case management only. Psychiatr. Serv. 54, 78. Cohen CI (2003) The future of community psychiatry. Commun. Ment. Health J. 39, 459. Cohen CI, Thompson KS (1992) Homeless mentally ill or mentally ill homeless? Am. J. Psychiatr. 149, 816. Compton SN, Swanson JW, Wagner HR et al. (2003) Involuntary outpatient commitment and homelessness in persons with severe mental illness. Ment. Health Serv. Res. 5, 27. Davies S (2002) Compulsory treatment in the community: current legal powers. Adv. Psychiatr. Treat. 8, 180. Desai MM, Rosenheck RA, Kasprow WJ (2003) Determinants of receipt of ambulatory medical care in a national sample of mentally ill homeless veterans. Med. Care 41, 275. Drury LJ (2003) Community care for people who are homeless and mentally ill. J. Health Care Poor Underserved 14, 194. Felton BJ (2003) Innovation and implementation in mental health services for homeless adults: a case study. Commun. Ment. Health J. 39, 309. Fiander M, Burns T et al. (2003) Assertive community treatment across the Atlantic: comparison of model fidelity in the UK and USA. Br. J. Psychiatry 182, 248. Gilmer TP, Folsom DP, Hawthorne W et al. (2003) Assisted living and use of health services among Medicaid beneficiaries with schizophrenia. J. Ment. Health Policy Econ. 6, 59. Hassett A, George K (2002) Access to a community aged psychiatry service by elderly from nonEnglish-speaking backgrounds. Int. J. Geriatr. Psychiatry 17, 623. Jones K, Colson PW, Holter MC et al. (2003) Cost-effectiveness of critical time intervention to reduce homelessness among persons with mental illness. Psychiatr. Serv. 54, 884. Linsley K, Slinn R, Nathan R et al. (2001) Training implications of community-oriented psychiatry. Adv. Psychiatr. Treat. 7, 208. Manderscheld RW, Henderson MJ, for the Center for Mental Health Services (2000) Mental Health, United States 2000. DHHS, Washington, DC. Marshall M (1989) Collected and neglected: are Oxford hostels for the homeless filling up with disabled psychiatric patients? BMJ 299, 706. Marshall M, Creed F (2000) Assertive community treatment: is it the future of community care in the UK? Int. Rev. Psychiatry 12, 191. Marshall M, Lockwood A (2000) Assertive community treatment for people with severe mental disorders. Cochrane Database Syst. Rev. 2, CD-ROM. Metraux S, Marcus SC, Culhane DP (2003) The New York-New York housing initiative and use of public shelters by persons with severe mental illness. Psychiatr. Serv. 54, 67. Moncrieff J (2003) The politics of a new Mental Health Act. Br. J. Psychiatry 183, 8.


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Morrissey JP, Calloway MO, Thakur N et al. (2002) Integration of service system for homeless persons with serious mental illness through the ACCESS program. Psychiatr. Serv. 53, 949. Muijen M, Marks I, Connolly J et al. (1992) Home-based care and standard hospital care for patients with severe mental illness: a randomized controlled trial. BMJ 304, 749. Nose Michela, Garbui C (2003) Clinical interventions for treatment non-adherence in psychosis: meta-analysis. Br. J. Psychiatry 183, 197. Park MJ, Tyrer P, Elsworth E et al. (2002) The measurement of engagement in the homeless mentally ill: the Homeless Engagement and Acceptance Scale – HEAS. Psychol. Med. 32, 855. Pijl YJ, Sytema S, Barels R, Wiersma D (2002) Costs of deinstitutionalization in a rural catchment area in the Netherlands. Psychol. Med. 32, 1435. Prigerson HG, Desai RA, Liu-Mares W, Rosenheck RA (2003) Suicidal ideation and suicide attempts in homeless mentally ill persons: age-specific risks of substance abuse. Soc. Psychiatry Psychiatr. Epidemiol. 38, 213. Randolf F, Blasinsky M, Morrissey JP et al. (2002) Overview of the ACCESS program. Psychiatr. Serv. 53, 945. Readhead C, Henderson R, Hughes G, Nickless J (2002) Accredited accommodation: an alternative in-patient care in rural north Powys. Psychiatr. Bull. 26, 264. Roberts G, Wolfson P (2004) The rediscovery of recovery: open to all. Adv. Psychiatr. Treat. 10, 37. Rosenheack RA, Lam J, Morrissey JP et al. (2002) Service systems integration and outcomes for mentally ill homeless persons in the ACCESS program. Psychiatr. Serv. 53, 958. Simmons S, Coid J, Joseph P et al. (2001) Community mental health team management in severe mental illness: a systematic review. Br. J. Psychiatry 178, 497. Susser E, Conover M, Struering E (1989) Problems of epidemiologic method in assessing the type and extent of mental illness among homeless adults. Hosp. Commun. Psychiatry 40, 261. Swenson JR, Bradwejn J (2002) Mental health reform and evolution of general psychiatry in Ontario. Can. J. Psychiatry 47, 644. Trieman N, Leff J (2002) Long-term outcome of long-stay psychiatric in-patients considered unsuitable to live in the community: TAPS Project 44. Br. J. Psychiatry 181, 428. Turrer T, Priebe S (2002) Forget community care, reinstitutionalisaton is here. Br. J. Psychiatry 181, 253. Wing JK, Brown GW (1970) Institutionalism and Schizophrenia: a Comparative Study of Three Mental Hospitals 1960 to 1968. Cambridge University Press, Cambridge. Ziguras SJ, Stuart GW, Jackson AC (2002) Assessing the evidence on case management. Br. J. Psychiatry 181, 17.

Specific psychiatric problems of women

25

EPIDEMIOLOGY GENERAL There is an increasing focus on women’s healthcare needs. Systems of care arrange to promote comprehensive care to women – women’s Health Centers of Excellence – in which mental health services play a major role. In most Western societies, psychiatric disorders are more common in women. Suggested reasons for this include:

• • • •

Genetic differences. Societal pressures. Differences of rearing patterns. Cultural expectations.

In general practice, the prevalence of mental disorders in females is three times that in males. The inception rate is twice as high in females, suggesting a worse prognosis in females. SPECIFIC DISORDERS Neuroses Women have twice the risk of developing neurotic depression. Interpersonal problems are reported more commonly in women. Anxiety states and obsessional disorders are equally distributed, but anxiety states are more commonly reported by women.

• • •

Affective disorders The risk of developing unipolar psychotic depression is increased in women up to the age of 75 (male, 3.5 per cent; female, 5.8 per cent). • The risk of developing bipolar affective psychosis is evenly distributed. • Women tend to report more somatic and psychic anxiety and more general somatic symptoms.

•

EPIDEMIOLOGY

• •

319

Men tend to report more hypochondriacal fears and are more likely to lack insight. The oral contraceptive pill is not associated with a higher risk of depression in females.

Schizophrenia The lifetime risk is equal in males and females. There is increased incidence in females aged under 16 years compared with males under 16 and in females over 35 compared with males over 35. • There is an increased incidence in males aged 16–35 compared with females aged 16–35. • Process schizophrenia may be more common in men, while schizoaffective disorders may be more common in women.

• •

Suicidal behaviour Completed suicide is more common in men (11 per 100 000 per year) compared with women (6 per 100 000). • Deliberate self-harm is more common in women. • Repeated deliberate self-harm seems to be slightly more common in men. • The use of violent means of self-harm (knives, guns, etc.) is more common in men.

•

Anorexia nervosa More common in females (female:male ratio about 9:1). More severe and with worse prognosis in males.

• •

Mental handicap More common in males (male:female ratio ⫽ 4:3). Senile dementia More common in females, but this may be due to the greater longevity of women. Criminal behaviour Of children taken into care under the age of 13, 50 per cent of the boys have committed offences compared with 13 per cent of the girls. • Adult males are convicted nine times more commonly than women. This figure relates to reportability and sentencing policies as well as actual prevalence of crime. • Males commit more violent crime, while women tend to be convicted of offences related to prostitution.

•

Alcoholism Alcoholism is eight times more common in men (in a survey of south-east London).

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PREMENSTRUAL SYNDROME DEFINITIONS There is no universally agreed definition.

• •

Physical symptoms – feeling bloated, weight gain, tender breasts, headache, backache, cramps. Psychological symptoms – tension, irritability, depression, tiredness, forgetfulness.

There is recurrence of symptoms between ovulation and menstruation. They subside during menstruation and are absent between menstruation and ovulation. During this period there is said to be an increase in violent crimes, suicide and parasuicide, illness behaviour, accidents and poor academic performance. Many of these studies are methodically flawed. Mental hospital admissions for all forms of disorder are higher during the premenstrual period, suggesting that patients with pre-existing disorder feel worse at this time. The relationship (if any) to mental disorder is unclear (Halbreich, 1995). EPIDEMIOLOGY Prevalence ranges from 20 to 95 per cent in studies, demonstrating diagnostic unreliability. Premenstrual complaint is found more commonly in those with psychiatric illhealth. This may be because psychiatric distress sensitizes the women to the additional premenstrual changes (Clare, 1983). AETIOLOGY Various unproven theories include:

• •

A relative deficiency of progesterone, raised prolactin levels, fluid retention, excessive aldosterone, pyridoxine deficiency, raised MAO activity and ‘psychological’ effect. Premenstrual decline in circulating ␤-endorphin.

TREATMENT Selective serotonin re-uptake inhibitors have been shown to be effective in reducing the symptoms of severe premenstrual syndrome (Dimmock et al., 2000). Progesterones (e.g. dydrogesterone) show some improvement in symptoms. Supportive psychotherapy, information giving and relaxation therapy may be beneficial.

PSYCHOLOGICAL PROBLEMS IN PREGNANCY EPIDEMIOLOGY Women are less likely to be admitted to a psychiatric ward or to commit suicide during pregnancy than at other times. This is in spite of the major life event which pregnancy forms.

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Minor psychological symptoms are common, however. Two-thirds of women have some psychological symptoms during pregnancy, especially in the first and last trimesters. Anxiety is common, as is a tendency to irritability and minor lability of mood. Ten per cent of pregnant women become significantly depressed during pregnancy. This usually lasts less than 12 weeks and is more common in the first trimester. It is associated with: previous history of depression, previous history of abortion, the pregnancy being unwanted, marital conflict and anxieties about the fetus. It is characterized by fatigue, irritability, increased neuroticism scores and denial of the pregnancy. Depression in the last trimester may persist as a postnatal depression. MANAGEMENT

• • •

Increased support by medical, nursing and other services, as well as by family, may reduce the need to contact psychiatric services. Clear and informed reassurance, antenatal classes and discussion with other mothers should help. Interpersonal psychotherapy can be effective in the treatment of depression during pregnancy (Spinelli and Endicott, 2003). Conjoint marital therapy or separate counselling of the husband may be indicated.

Drugs Drug treatment with SSRIs or TCAs appears to be safe during pregnancy (Kohen, 2004). Between 10 and 35 per cent of women take psychotropic drugs at some time during their pregnancy. All psychotropics that can cross the blood–brain barrier (i.e. are lipophilic) can cross the placenta. Higher blood levels may develop in the fetus than in the mother. During the immediate antenatal period, psychotropics may lead to oversedation of the neonate.

POSTPARTUM PSYCHIATRIC DISORDERS PUERPERAL PSYCHOSIS EPIDEMIOLOGY Psychoses occur following 1.5 per 1000 deliveries. They are associated with primigravida status. A history of manic–depressive psychosis predicts 20 per cent chance of developing puerperal psychosis. Lack of specification of puerperal psychosis in ICD-10 and DSM-IV reflects continued confusion regarding the nosological status of puerperal disorders. AETIOLOGY

• •

Genetic factors appear to play a part, since a family history of major psychiatric disorder predisposes to puerperal psychosis. Biochemical causes have been postulated for the functional psychoses, relating the precipitation of psychosis to the effects of sudden decreases of progesterone and oestrogen on tryptophan metabolism.

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There has been little evidence of an excess of psychological stresses in the perinatal period in the psychotic mother, although death of the baby may be a clear precipitant. Psychodynamic factors may well be important and will include the patient’s relationship with her own mother, her feelings about the responsibility of motherhood, her reaction to this assertion of her female role, her relationship with her husband and his personality (over-passive or over-dominant).

The relationship between lack of effective ‘bonding’ between mother and baby (due to early separation, emotionally or physically) and the development of psychosis is unclear. CLINICAL FEATURES Puerperal psychoses are widely held not to be a distinct and unitary form of psychosis but to be divided into affective psychoses (70 per cent), schizophrenia (25 per cent) and organic psychoses (very rare now in the UK). The affective psychoses are primarily depressive. The few organic psychoses are particularly due to cerebral thrombophlebitis. The evidence for suggesting that puerperal psychoses are not a distinct entity is: 1 Family history of psychotic disorder is as commonly present as in non-puerperal psychosis. 2 There is an increased incidence of psychosis before and after the pregnancy and puerperal period also. 3 Manic depressives have 10 times the risk of developing a puerperal psychosis compared with the normal population. 4 The clinical syndromes resemble psychoses occurring at other times. However, suggestions remain that there is a distinct clinical picture of puerperal psychosis. This consists of: 1 A prodromal period, about 2 days after parturition, of insomnia, irritability, restlessness, refusal of food and depression. 2 This is rapidly followed by the acute onset of confusion, excitability, overactivity, hallucinations, fatiguability, very labile mood and preoccupations and delusions concerning the baby. Elation, grandiosity and schizophreniform symptoms are common. 3 Onset is almost always in the first 2 weeks. In character and timing the psychoses are very similar to postoperative psychosis. PROGNOSIS Seventy per cent recover fully, affective psychosis having a better prognosis than schizophrenic. The risk of psychosis in future puerperal periods is 14–20 per cent. The risk of psychosis at any future time is up to 50 per cent. Poor prognosis is indicated by a positive family history, schizophrenia, neurotic personality and the presence of severe marital problems.

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PUERPERAL DEPRESSION EPIDEMIOLOGY Ten per cent (range 3–16 per cent) of women develop a non-psychotic depressive disorder in the postpartum period. Onset is usually within the first postpartum month, often on return home and usually between day 3 and day 14. It is associated with increased age, childhood separation from the father, problems in relationships with mother- and father-in-law, marital conflict, mixed feelings about the baby, physical problems in the pregnancy and perinatal period, a tendency to more neurotic and less extroverted personalities. AETIOLOGY Possible aetiological factors include a postulated hormonal effect on tryptophan metabolism. Social and situational changes make the woman particularly vulnerable at this time. Having a baby is an important life event involving changes in financial, social and marital status. Lack of support from the partner or family may increase vulnerability to depression. CLINICAL FEATURES Typically, the woman is tearful and irritable. Associated symptoms may include feeling tired, despondent and anxious, with worry about ability to cope with baby, fear for own and baby’s health and feeling generally inadequate. There is often poor appetite, decreased libido and difficulty in sleeping. These patients often have difficulty concentrating and may complain of feeling confused, although cognitive testing is normal. PROGNOSIS Most symptoms (90 per cent) last less than 1 month, even without treatment. In 4 per cent of cases they last longer than a year.

POSTPARTUM ‘BLUES’ EPIDEMIOLOGY Fifty per cent of women have a short-lived emotional disturbance commencing on the third day and lasting for 1–2 days. It is more common in primigravidae and in those who complain of premenstrual tension. CLINICAL FEATURES Common features are: episodic weeping, feeling depressed and irritable, feeling separate and distant from the baby, insomnia and poor concentration. This coincides with sudden weight loss, decreased thirst and increased urinary sodium secretion. The syndrome would appear to have a biochemical basis.

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MANAGEMENT OF POSTPARTUM DISORDERS Postpartum disorders are important to detect. There should be an early high index of suspicion – don’t assume ‘baby blues’ – with use of rating scales (e.g. Edinburgh postnatal depression scale). Postnatal depression may have enduring emotional and cognitive sequelae for the infant. Young mothers particularly need support. PSYCHOSIS Admission to hospital is frequently required, owing to the potential danger to the baby (of violence, neglect or mishandling) and to the difficulty of dealing with a behaviourally disturbed and psychotic mother at home. Admission of both mother and baby together is always advisable, if possible (mother and baby units). This allows for the development of bonding, reduction in the emotional deprivation of the child and reduction in the guilt of the mother. It also allows for the supervision of mother and baby, and their relationship. By gentle advice, encouragement and reassurance the mother’s confidence can be built up. Breast-feeding can be continued where possible and desired. The father should be free to visit and keep his contact with his family. Mothers admitted with their babies tend to stay in hospital for less time and are less disturbed on discharge than mothers admitted without their babies. Drugs and other physical treatments should be given as appropriate to the symptoms. If the baby is breast-fed, major tranquillizers will be present in the milk and the baby should be observed for over-sedation. If this occurs, the needs of the mother for sedation and those of the baby for breast-feeding must be balanced. It may be necessary to stop breastfeeding for a short period while the mother’s symptoms are brought under control. Psychotherapy, usually of a supportive kind, is always required. Discussion will centre on the mother’s relationship with the baby and her feelings about herself. Her relationship with her partner and family may also be necessary to explore. Psychotherapy will be aimed at reducing her guilt and feelings of inadequacy and hostility and at fostering maternal feeling. Couple therapy is often a critical component of recovery. DEPRESSION Since this is usually self-limiting, supportive measures of encouragement and reassurance are usually all that are required. If the depression lasts for more than 1 month, an antidepressant may be indicated, as well as more active psychotherapy and marital therapy. ‘BLUES’ This does not require any more than simple reassurance and explanation, both to the mother and to her partner.

TERMINATION OF PREGNANCY About one in five pregnancies in the UK are terminated for therapeutic reasons. Sixtythree per cent of females seeking abortion are single, 32 per cent are aged 20–24 years.

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After abortion, transient psychological distress (anxiety, grief reactions) is common, but prominent or persistent psychiatric illness is uncommon (⬍10 per cent) (Zolese and Blacker, 1992). Risk factors: • Past psychiatric history. • Poor social support. • Young age. • Multiparous. • Sociocultural setting which discourages abortion.

STILLBIRTH Stillbirth is viewed variously as ‘an overlooked catastrophe’ or as a ‘non-event’. There is a risk of pathological grieving because there is no surviving child. There may be guilt and fear of failure as a woman.

STERILIZATION AND HYSTERECTOMY Psychiatric symptoms are rare after tubal ligation – 71–99 per cent are completely satisfied with the operation. Between 2 and 5 per cent greatly regret having the operation, especially if aged less than 26, with a small family size and under pressure to be sterilized. The incidence of psychiatric symptoms in the 18 months after sterilization is about 1 per cent and is no higher than the general population rate. Sterilization has been shown to improve the mental state, social adjustment, general health and marital and sexual relationships of the woman. Although it was originally reported that hysterectomy is associated with increased psychiatric illness, especially depression, subsequent studies have discounted this claim.

MENOPAUSE The menopause used to be regarded as an important aetiological factor in so-called ‘involutional melancholia’. There is now no evidence that this is a distinct entity, but merely one presentation of depression in late middle age and not consistently related to the menopause. Whether the hormonal changes of the menopause lead to psychiatric disorder is much debated. It is methodologically difficult to separate the hormonal aspects from the psychodynamic aspects of altered perception of the self and altered relationship with the partner. At this time, also, many other life events are happening (e.g. children are leaving home, parents are dying, husbands are retiring, etc.). The risk of depressive illness does not seem to be higher at the menopause than at other times.

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REFERENCES AND FURTHER READING Angst J, Sellaro R, Merikangas KR, Endicott J (2001) The epidemiology of perimenstrual psychological symptoms. Acta Psychiatr. Scand. 104, 110. Bhatia SC, Bhatia SK (2002) Diagnosis and treatment of premenstrual dysphoric disorder. Am. Fam. Physician 66, 1239. Birtchnell J (2001) The nature of grief: the evolution and psychology of reactions to loss. Br. J. Psychiatry 178, 580. Chandran M, Tharyan P, Muliyil J, Abraham S (2002) Post-partum depression in a cohort of women from a rural area of Tamil Nadu, India: incidence and risk factors. Br. J. Psychiatry 181, 499. Clare AW (1983) Psychiatric and social aspects of premenstrual complaint. Psychol. Med., Monograph Suppl. 4. Cooper PJ, Murray L et al. (2003) Controlled trial of the short- and long-term effect of psychological treatment of post-partum depression. 1: Impact on maternal mood. Br. J. Psychiatry 182, 412. Dimmock PW, Wyatt KM, Jones PW (2000) Efficacy of selective-serotonin-reuptake inhibitors in premenstrual syndrome: a systematic review. Lancet 356, 1131. Domoney CL, Vashisht A, Studd JW (2003) Premenstrual syndrome and the use of alternative therapies. Ann. NY Acad. Sci. 997, 330. Essex MJ, Klein MH, Miech R, Smider NA (2001) Timing of initial exposure to maternal major depression and children’s mental health symptoms in kindergarten. Br. J. Psychiatry 179, 151. Evans J, Heron J, Francomb H et al. (2001) Cohort study of depressed mood during pregnancy and after childbirth. BMJ 323, 257. Facchinetti F (2001) Female depression and menopause. Psychother. Psychosom. 70, 166. Girman A, Lee R, Kligler B (2003) An integrative medicine approach to premenstrual syndrome. Am. J. Obstet. Gynecol. 188, s56. Grady-Weliky TA (2003) Premenstrual dysphoric disorder. New Engl. J. Med. 348, 433. Halbreich U (1995) Premenstrual dystrophic disorders, anxiety and depressions: vulnerability traits or comorbidity? Arch. Gen. Psychiatry 52, 606. Howard LM, Goss C, Leese M, Thornicoft G (2003) Medical outcome of pregnancy in women with psychotic disorders and their infants in the first year after birth. Br. J. Psychiatry 182, 63. Huttner RP, Shepherd JE (2003) Gonadal steroids, selective serotonin reuptake inhibitors, and mood disorders in women. Med. Clin. North Am. 87, 1065. Iles S, Gath D (1993) Psychiatric outcome of termination of pregnancy. Psychol. Med. 23, 407. Kessler RC (2003) Epidemiology of women and depression. J. Affect. Disord. 74, 5. Kirkcaldy B, Siefen G, Furnham A (2003) Gender, anxiety-depressivity and self-image among adolescents. Eur. Psychiatry 18, 50. Kohen D (2003) Psychiatric illness in women: emerging treatment and research. Br. J. Psychiatry B, a460. Kohen D (2004) Psychotropic medication in pregnancy. Adv. Psychiatr. Treat. 10, 59. Korstein SG, Wojcik BA (2002) Depression. In: Kornstein SG, Clayton AH (eds), Women’s Mental Health: a Comprehensive Textbook. Guilford Press, New York. Lee DTS, Yip ASK, Leung TYS, Chung TKH (2004) Ethnoepidemiology of postnatal depression: prospective multivariate study of sociocultural risk factors in a Chinese population in Hong Kong. Br. J. Psychiatry 184, 34. Lehtinen V, Michalak E, Wilkinson C et al. (2003) Urban–rural differences in the occurrence of female depressive disorder in Europe: evidence from the ODIN study. Soc. Psychiatry Psychiatr. Epidemiol. 38, 283. Lovett KF (2001) PTSD and stillbirth. Br. J. Psychiatry 179, 367.


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MacArthur C, Winter HR, Bick DE et al. (2002) Effects of redesigned postnatal care on women’s health 4 months after birth: a cluster randomized controlled trial. Lancet 359, 378. Martin N (2001) Feminist bioethics and psychiatry. J. Med. Phil. 26, 431. Miller LJ (2002) Postpartum depression. JAMA 287, 762. Miller MN, Miller BE (2001) Premenstrual exacerbations of mood disorders. Psychopharmacol. Bull. 35, 135. Morris-Rush JK, Freda MC, Bernstein PS (2003) Screening for postpartum depression in an inner-city population. Am. J. Obstet. Gynecol. 188, 1217. Murray L, Cooper PJ et al. (2003) Controlled trial of the short- and long-term effect of psychological teatment of post-partum depression. 2: Impact on the mother–child relationship and child outcome. Br. J. Psychiatry 182, 420. Nonacs R, Cohen LS (2003) Assessment and treatment of depression during pregnancy: an update. Psychiatr. Clin. North Am. 26, 547. O’Connor TG, Heron J, Glover V (2002) Antenatal anxiety predicts child behavioral/emotional problems independently of postnatal depression. J. Am. Acad. Child Adolesc. Psychiatry 41, 1470. Petrou S, Cooper P et al. (2002) Economic costs of post-natal depression in a high-risk British cohort. Br. J. Psychiatry 181, 505. Reardon DC, Cougle JR, Rue VM et al. (2003) Psychiatric admissions of low-income women following abortion and childbirth. CMAJ 168, 1253. Ross LE, Steiner M (2003) A biopsychosocial approach to premenstrual dysphoric disorder. Psychiatr. Clin. North Am. 26, 529. Sajatovic M, Rosenthal MB, Plax MS et al. (2003) Mental illness and menopause: a patient and family perspective. J. Gend. Specif. Med. 6, 31. Spinelli MG, Endicott J (2003) Controlled clinical trial of interpersonal psychotherapy versus parenting education program for depressed pregnant women. Am. J. Psychiatry 160, 555. Steiner M, Born L (2002) Psychiatric aspects of the menstrual cycle. In: Kornstein SG, Clayton AH (eds), Women’s Mental Health: a Comprehensive Textbook. Guilford Press, New York. Stotland NL (2002) Psychiatric issues related to infertility, reproductive technologies, and abortion. Prim. Care 29, 13. Turton P, Hughes P, Evans CDH, Fainman D (2001) Incidence, correlates and predictors of posttraumatic stress disorder in the pregnancy after stillbirth. Br. J. Psychiatry 178, 556. Warnock JK, Clayton AH (2003) Chronic episodic disorders in women. Psychiatr. Clin. North Am. 26, 725. Wyatt K, Dimmock P, Jones P et al. (2001) Efficacy of progesterone and progestogens in management of premenstrual syndrome: systematic review. BMJ 323, 776. Zolese G, Blacker CVR (1992) The psychological complications of therapeutic abortion. Br. J. Psychiatry 160, 742.

Transcultural psychiatry

26

CULTURAL CONTEXT Two views are debated:

• •

Psychiatric universalist view – mental disorders show similar phenomenology in all cultures. Cultural determinist view – mental disorders show essential differences in different cultures.

Evidence exists for both views. Patterns of ‘pathological’ behaviour may mirror and exaggerate the patterns of normal behaviour in a culture, but still fall into the same very broad diagnostic categories in all countries – the ‘pathoplastic’ effect of culture. Delusions and hallucinations are recognized as abnormal in almost all cultures (e.g. Yoruba of Nigeria, West Indians, Asians). Inhabitants of developing countries tend to discriminate differently between different emotional states from inhabitants of developed countries. Reaction to mental disorder by the local community varies greatly; greater acceptance may reduce social incapacity.

SPECIFIC DISORDERS SCHIZOPHRENIA Schizophrenia was originally noted to have increased incidence in the USA compared with the UK, as well as reduced incidence in developing countries. Neither view is correct (see Chapter 3). Use of the PSE in the International Pilot Study of Schizophrenia showed that reliable diagnosis of schizophrenia could be made throughout the world by local psychiatrists in nine different countries, including India, Colombia, Nigeria, the Soviet Union, the USA and the UK. Prevalence was similar in all countries, although the USA

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and Soviet Union had apparently higher prevalence of locally (but not PSE-) diagnosed ‘schizophrenia’. Confusion, excitement, transient hallucinations and unsystematized (often paranoid) delusions are more common in Africa. Catatonic symptoms are more common in India. Outcome is consistently shown to be better in developing countries, in terms of reduced social disability and psychopathology, even when single acute episodes are discounted. The reason is unknown (Jablensky et al., 1992).

DEPRESSION Depression was originally thought to be almost absent in developing countries. Depression is probably widespread, but with differing symptomatology, making diagnosis imprecise. Many cultures do not have a word equivalent to ‘depression’. Africans tend to show more paranoia and hypochondriasis. South Asians tend to show more hypochondriasis, agitation and somatic complaints (e.g. stomach pains, sexual dysfunction in men). Patients in Christian cultures may exhibit guilt, selfdepreciation and suicidal tendencies.

NEUROSES Hysterical dissociation is more common in developing countries. Acute, dramatic trance states with disturbed behaviour and fearfulness are also more common.

‘CULTURE-BOUND’ DISORDERS In these disorders there is a relatively unique pattern of symptoms, usually a variant of a major psychosis or neurosis.

• • • • • •

Latah (Far East, North Africa) – dissociative state with echolalia and automatic obedience. Hysterical reaction to stress, usually in women. Windigo (North American Indians) – delusional belief that subject has turned into a cannibalistic monster; may attempt to act on this. Regarded as a form of depressive psychosis. Koro (Malaya, South China) – anxiety associated with fear of penis retracting into abdomen and resulting in death. Acute anxiety state. Amok (South East Asia) – depressive withdrawal followed by indiscriminate murderous frenzy. May kill self or others. Hysterical dissociation or depressive. Susto (Central and South America) – anxiety and fear attributed to loss of soul. Acute anxiety state, possibly due to individual’s inability to fulfil his/her expected social role. Dhat syndrome – ‘semen loss’, erectile dysfunction, fatigue, insomnia. An Asian psychosexual disorder associated most commonly with neurotic depression.

330

TRANSCULTURAL PSYCHIATRY

ORGANIC PSYCHOSYNDROMES Infectious and nutritional problems lead to increased incidence of acute confusional states. Such causes also alter the presentation of functional psychiatric disorders.

ASSESSMENT AND TREATMENT See Harrison (1991).

• • • • •

Interpreters – There is a need for skilful interpreters. Health services require a network of experienced interpreters and all information literature should be available in all locally common languages/dialects. Presentation – Allow for variations in the presentation of common disorders and for cultural differences in the meaning of words and concepts. Use the family to help wherever possible. Role of ‘ethnic’ health workers – In some cases mental health workers will offer invaluable insight into cultural differences and variations where they share similar ethnic backgrounds to patients. They also raise team ‘awareness’ of cultural issues. Stereotypes – Beware of racial or ‘cultural’ stereotypes. Somatization – Recognize somatic manifestations of mental disorder.

AFFECTS OF MIGRATION Do migrants have increased incidence of psychiatric disorder? Ødegaard (1932) demonstrated an increased incidence of admission to mental hospitals in Norwegian immigrants to the USA (over Americans and Norwegians in Norway), especially due to schizophrenia. This stimulated debate between:

• •

Social selection – mentally ill people or those prone to develop mental disorder tend to migrate. Social causation – environmental factors associated with migration tend to lead to mental disorder.

Ødegaard favoured social selection for schizophrenia, because (i) there was no particular association with time of migration, and an apparent tendency for ‘schizoid’ personality before migration; and (ii) the reasons for breakdown seemed unrelated to the migration. American social scientists (e.g. Srole et al., 1962; Mid-Town Manhattan Study) favoured social causation, particularly of neurotic disorders. A third possibility is that the increased incidence is caused by confounding variables (e.g. increased age, unmarried status or lower social class in migrants). However, not all migrants have an increased incidence of psychiatric disorder. Astrup and Ødegaard (1960) demonstrated that internal migrants (i.e. those not leaving the country) have a lower incidence of psychosis. Only migrants into the capital city had a higher incidence than non-migrants. British immigrants to Victoria, Australia, in 1960 showed lower risk compared with those from southern and eastern Europe. Thus each group of migrants and each disorder must be investigated separately.


331

FACTORS RELATING TO MIGRATION Before (i.e. culture of origin) • Prevalence of disorder in original community. • Attitude towards migration (betterment or desertion). • Characteristics of upbringing (is independence encouraged?). After (i.e. society of resettlement) • May refuse entry to psychiatrically ill. • May be tolerant or rejecting (both could lead to increased incidence). • Hostility and discrimination. • Size and cohesiveness of new community. • Language and cultural difficulties. The incidence of schizophrenia in second-generation Afro-Caribbean migrants in the UK has been found to increase six-fold (Harrison et al., 1988, 1997) compared with the ‘indigenous’ population. This finding has been replicated by others, although methodological pitfalls include greater ease of Afro-Caribbeans to ‘filter’ through the health services, confounding effects of substance abuse, diagnostic and cultural misinterpretations and social bias (‘labelling’). The increased rate of schizophrenia among Afro-Caribbean migrants may result from biological factors (e.g. virus exposure, obstetric complications), or be related to social adversity (Harrison and Eaton, 2002).

REFERENCES AND FURTHER READING Astrup C, Ødegaard O (1960) Internal migration and mental disease. Psychiatr. Q. Suppl. 34, 116. Baer RD, Weller SC, de Alba Garcia JG et al. (2003) A cross-cultural approach to the study of the folk illness nervios. Culture, Med. Psychiatry 27, 315. Bhui K, Stansfeld S, Hull S et al. (2003) Ethnic variations in pathways to and use of specialist mental health services in the UK: a systematic review. Br. J. Psychiatry 182, 105. Boydell J, van Os J, McKenzie K et al. (2002) Incidence of schizophrenia in ethnic minorities. I: London – ecological study into interactions with environment. BMJ 323, 1336. Caracci G, Mezzich JE (2001) Culture and urban mental health. Psychiatr. Clin. North Am. 24, 581. Coker EM (2003) Narrative strategies in medical discourse: constructing the psychiatric ‘case’ in a non-western setting. Social Sci. Med. 57, 905. Fabrega H (2001) Culture and history in psychiatric diagnosis and practice. Psychiatr. Clin. North Am. 24, 391. Fabrega H (2001) Cultural psychiatry: international perspectives. Epilogue. Psychiatr. Clin. North Am. 24, 595. Fabrega H (2001) Mental health and illness in traditional India and China. Psychiatr. Clin. North Am. 24, 555. Harrison G (1991) Migration and Mental Disorders. Med. Internat., 3978. The Medicine Group (UK). Harrison G, Eaton W (2002) Migration and the social epidemiology of schizophrenia. In: Hafner H (ed.), Risk and Protective Factors in Schizophrenia. Steinkopff, Darmstadt. Harrison G, Owens D, Holton T et al. (1988) A prospective study of severe mental disorder in Afro-Caribbean patients. Psychol. Med. 18, 643.

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Harrison G, Glazebrook C, Brewin J et al. (1997) Increased incidence of psychotic disorders in African Caribbean migrants to the UK. Psychol. Med. 27, 799. Jablensky A, Sartorius N, Ernberg G et al. (1992) Schizophrenia: manifestations, incidence and course in different cultures. A World Health Organization Ten-Country Study. Psychol. Med., Monograph Suppl. 20. Jaycox LH, Stein BD, Kataoka SH et al. (2002) Violence exposure, posttraumatic stress disorder, and depressive symptoms among recent immigrant schoolchildren. J. Am. Acad. Child Adolesc. Psychiatry 41, 1104. Johns LC, Nazroo JY, Bebbington P et al. (2002) Occurrence of hallucinatory experiences in a community sample and ethnic variations. Br. J. Psychiatry 180, 174. Karlsen S, Nazroo J (2002) Relation between racial discrimination, social class and health among ethnic minority groups. Am. J. Public Health 92, 624. Kendrick T (2003) Black people are more likely than white people to be detained in psychiatric wards in the United Kingdom [review]. Evidence Based Ment. Health 6, 76. Kleinman A (2001) Cross-cultural psychiatry: a psychiatric perspective on global change. Harvard Rev. Psychiatry 9, 46. Kulhara P, Chakrabarti S (2001) Culture and schizophrenia and other psychotic disorders. Psychiatr. Clin. North Am. 24, 449. Lee S (2002) Socio-cultural and global health perspectives for the development of future psychiatric diagnostic systems. Psychopathology 35, 152. Moldavsky D (2003) The implication of transcultural psychiatry for clinical practice. Isr. J. Psychiatry Relat. Sci. 40, 47. Nazroo JY (2003) The structuring of ethnic inequalities in health: economic position, racial discrimination, and racism. Am. J. Public Health 93, 277. Ødegaard O (1932) Emigration and insanity. Acta Psychiatr. Neurol. Scand. 4, 1–206. Olatawaru M (2001) Culture and child psychiatric disorders: a Nigerian perspective. Psychiatr. Clin North Am. 24, 497. Rohde LA (2002) ADHD in Brazil: the DSM-IV criteria in a culturally different population. J. Am. Acad. Child Adolesc. Psychiatry 41, 1131. Simon GE, Chisholm D, Treglia M et al. (2003) Course of depression, health services costs, and work productivity in an international primary care study. Dis. Mon. 49, 293. Skapinakis P, Lewis G, Mavreas V (2003) Cross-cultural differences in the epidemiology of unexplained fatigue syndromes in primary care. Br. J. Psychiatry 182, 205. Srole L, Langner TS, Michael ST et al. (1962) Mental Health in the Metropolis: the Mid-Town Manhattan Study. McGraw-Hill, New York. Stauffer WM, Kamat D, Walker PF (2002) Screening of international immigrants, refugees, and adoptees. Prim. Care 29, 879. Subramaniam H (2002) Cross-cultural training in psychiatry. Br. J. Psychiatry 180, 381. Trujillo M (2001) Culture and the organization of psychiatric care. Psychiatr. Clin. North Am. 24, 539.

Psychiatry and the Internet

27

MENTAL HEALTH ISSUES

• • •

Mental health is a very common focus of Internet searches by the public. The Internet is used increasingly for support and discussion groups, and for information on diseases and latest medications. Psychiatry is beginning to explore e-mental health which may be useful for: – Short-term therapies. – Counselling. – Prescription renewals. The Internet is also inappropriately used (e.g. Internet addiction).

USEFUL WEBSITES GOVERNMENTAL

• • • •

US National Library of Medicine, creator of MEDLINE/PubMed: – www.nlm.nih.gov National Institute of Mental Health (NIMH), the leading Federal agency for research on mental and behavioral disorders in the USA: – www.nimh.nih.gov Substance Abuse and Mental Health Services Administration, part of the US Department of Health and Human Services – www.samhsa.gov National Institute for Clinical Excellence (for clinical guidelines in UK): – www.nice.org.uk

NON-GOVERNMENTAL Advocacy/support sites Bazelon Center for Mental Health Law: – www.bazelon.org • National Alliance for the Mentally Ill (NAMI): – www.nami.org

•

334

• • • •

PSYCHIATRY AND THE INTERNET

National Mental Health Association (NMHA): – www.nmha.org Rethink: – www.rethink.org SANE: – www.sane.org.uk Schizophrenia.com: – www.schizophrenia.com

Other sites American Psychiatric Association: – www.psych.org • Expert Consensus Guidelines Series: – www.psychguides.com • Internet Mental Health: – www.mentalhealth.com • Mental Health InfoSource: – www.mhsource.com • Mental-Health-Matters.com: – www.mental-health-matters.com • Mental Help Net: – www.mentalhelp.net • Mental Wellness.com: – www.mentalwellness.com • Pharmacology Algorithm Project (Harvard): – http://mhc.com/Algorithms • PlanetPsych.com: – www.planetpsych.com • PSYweb.com: – www.psyweb.com • Refdesk.com Mental Health: – www.refdesk.com/mental.html • Royal College of Psychiatrists: – www.rcpsych.ac.uk

•

GENERAL INTERNET SEARCH ENGINES Search for ‘psychiatry’, ‘mental health’, etc.

• • •

www.google.com www.yahoo.com www.excite.com

REFERENCES AND FURTHER READING Baker L, Wagner TH, Singer S, Bundorf MK (2003) Use of the Internet and e-mail for health care information: results from a national survey. JAMA 289, 2400.


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Charlton JP (2002) A factor-analytic investigation of computer ‘addiction’ and engagement. Br. J. Psychol. 93, 329. Cline RJW, Haynes KM (2001) Consumer health information seeking on the internet: the state of the art. Health Educ Res. 16, 671. Farvolden P, McBride C, Bagby RM, Ravitz P (2003) A Web-based screening instrument for depression and anxiety disorders in primary care. J. Med. Internet Res. 5, e23. Greist JH, Marks IM, Baer L et al. (2002) Behaviour therapy for obsessive–compulsive disorder guided by a computer or by a clinician compared with relaxation as a control. J. Clin. Psychiatry 63, 138. Marks IM, Mataix-Cols D, Kenwright M et al. (2003) Pragmatic evaluation of computer-aided self-help for anxiety and depression. Br. J. Psychiatry 183, 57. Prasad V, Owens D (2001) Using the internet as a source of self-help for people who self-harm. Psychiatr. Bull. 25, 222. Pratarelli ME, Browne BL (2002) Confirmatory factor analysis of internet use and addiction. Cyberpsychol. Behav. 5, 53. Proudfoot J, Goldberg D, Mann A et al. (2003) Computerised, interactive, multimedia CBT reduced anxiety and depression in general practice: a RCT. Psychol. Med. 33, 217. Shaw LH, Gant LM (2002) In defense of the Internet: the relationship between Internet communication and depression, loneliness, self-esteem, and perceived social support. Cyberpsychol. Behav. 5, 157. Slater MD, Zimmerman DE (2002) Characteristics of health-related websites identified by common Internet portals. JAMA 288, 316. Stein DJ, Black DW, Shapira NA, Spitzer RL (2001) Hypersexual disorder and preoccupation with Internet pornography. Am. J. Psychiatry 158, 1590. Tantum D (2001) A guide to the Internet from psychotherapists. Psychiatr. Bull. 25, 29. Theodosiou L, Green J (2003) Emerging challenges in using health information from the Internet. Adv. Psychiatr. Treat. 9, 387. Whang LS, Lee S, Chang G (2003) Internet over-user’s psycholoigical profiles: a behavior sampling analysis on internet addiction. Cyberpsychol. Behav. 6, 143.


Index Page numbers in bold refer to tables

abnormal motivational state 299 absorption, drugs 266 acamprosate 119 accelerated tempo of thought 17 acetylcholine 48 affective disorders 48 Alzheimer’s disease 157 acetylcholinesterase inhibitors, Alzheimer’s disease 158 acquired immunodeficiency syndrome (AIDS) 167–8 adjustment disorders 168 aetiology of CNS effects 167–8 affective disorder 168 management 168 psychosis 168 see also HIV infection acting out 298 actual neurosis 298 actus reus 226 Addison’s disease 164 adjustment disorders, AIDS 168 adolescents anorexia nervosa 87 mood disorders 237–8 non-fatal deliberate self harm 138 suicide 137 adrenergic agents 284–5 antagonists see beta blockers sleep EGG 186 ␣-adrenergic agonists 284 adrenogenital syndrome 100 affect 18 affective disorders 43–59 aetiology 46–51 AIDS 168 bereavement reactions 55 childhood experiences 50 classifications 43–5 DSM-IV 44 ICD-10 44

clinical features 45–6 cognitive/behavioural theories 51 course 52 elderly patients see psychogeriatrics epidemiology 46 genetics 46–7 HIV 168 life event studies 51 mixed affective states 54 neurochemistry 47–9 neuroendocrine abnormalities 48 neuroimaging 49 MRI 190 PET 192 SPECT 191 neuropathology 49 neuropeptides 49 neurotransmitter abnormalities 47–8 organic causes 49–50, 49 pharmacology 53–4 poor outcome predictors 52 premorbid personality 51 primary/secondary 43 prognosis long-term 52 short-term 52 psychodynamics 50 psychological theories 50–1 psychotherapy 52–3 sociological theories 51 treatment 52–4 unipolar/bipolar 43 vulnerability factors 51 women 318–19 see also depression; manic states affectless states 18 agoraphobia 63, 65 AIDS dementia complex (ADC) 167–8 akathisia 270 Albright’s syndrome 257

338

INDEX

alcohol dependence 109–22 aetiology 112–13 biochemical factors 113 family studies 112 psychological factors 113 sociocultural factors 113 clinical features 113–14 complications 114–18 anaemia 117 cardiovascular 116 CNS 114–16 gastrointestinal 116 haematological 117 neoplasms 117 in pregnancy 117 psychiatric 116 respiratory 116 detection 118, 118 detoxification 119 DSM-IV criteria 109 economic effects 118 epidemiology 109–11, 110, 319 co-morbidity 110, 110, 119 ethic factors 110 sex 110 genetics 112 ICD-10 classification 109 management 118–20 drug therapy 119, 285 general guidelines 118–19 psychosocial rehabilitation 120 molecular genetics 112 prognosis 120 relapse 113, 114 sleep disorders 182 social effects 117–18 suicide 136 type I 112 type II 112 vulnerability markers 112 alcohol dependency syndrome 113–14 alcoholic dementia 115 alcoholic hallucinations 114 alcohol-related disabilities 114–18 alpha agonists 284 Alzheimer’s disease 155–9 aetiology 155–7 classification 157, 158 clinical features 157–8 Down’s syndrome 155 drug treatment 158

epidemiology 155 genetics 155–6 immunology 157 management 158 mild cognitive impairment 159 neurochemistry 157 neuroimaging CT 190 MRI 190 MR spectroscopy 192 PET 192 SPECT 191 neuropathology 156 prognosis 159 risk factors 156 sundowning 158, 182 aminoacidurias 258 amitriptyline 275–6 amniocentesis 264 amok 329 amphetamines 126 mechanism of action 269 amyloid ␤-peptide 156, 158 amyloid plaques 156 anakastic personality disorder 79 anatomical dolls 224 animal phobias 64 anorexia nervosa (AN) 87–91 aetiology 88–9 body image disturbance 88 clinical features 89, 90 complications 89 diagnostic criteria 90 differential diagnosis 89 epidemiology 87–8, 319 hypothalamic-pituitary -gonadal axis 89, 89 laboratory abnormality 89 management 89–90 predisposing factors 88 prognosis 90–1 anorgasmia (frigidity) 97 antidepressants side-effect 272 behaviour therapy 102 anoxia, mental retardation 259 anterior cerebral artery occlusion 153 anterograde amnesia, head injury 170–1 anti-aggressive drugs 230 anticonvulsants, epilepsy 179

INDEX

antidepressants 53, 272–7 attention-deficit/hyperactivity disorder 245 characteristics 273 childhood depression 238 pain disorder 200 side-effects 272 SSRIs see selective serotonin re-uptake inhibitors (SRRIs) tricyclics see tricyclic antidepressants antiepileptics 179–80 autism 236 antimongolism 255 antipsychotic medication 268–72 anorexia nervosa 90 atypical 269 atypical vs typical 269 autism 236 classes 268–9, 269 delusional disorder 38 dopamine blockade 269–70 mania 53 mechanism of action 269–70 receptor antagonistic binding profile 270 safety/tolerance 272 schizophrenia 34–5 side-effects extrapyramidal 270–1, 270 non-neurological 271 typical 269 antisocial personality disorder (ASP) 79, 215–17 aetiology 216–17 diagnostic criteria 215 epidemiology 216 historical development 215–16 hospitalization 217 management 217 organic causes 216 primary prevention 217 prognosis 217 psychodynamic factors 217 sociocultural factors 217 anxiety 18, 61 anxiety disorders 60–3 assessments 5 biological aspects 66–7 children 62, 238–9 complications 62 course 62 DSM-IV criteria 60 epidemiology 61

339

generalized 61, 69 genetics 62 ICD-10 classification 60 personality development 77 predisposing factors 62 pregnancy 321 psychosurgery 294 sleep disorders 182 treatment 62–3 ‘anxiety management’ training 62 anxiolytics 282–4 anxious personality disorder 79 apathetic depression 207 apathy 19 Apert’s syndrome 256 apolipoprotein E (APOE) 156 appearance disorders 13–15 approximate answers, syndrome of 146–7 argininosuccinic acidura 258 arson 220–1 classification 220–1 definition 220 epidemiology 221 arterial occlusion 153 Asperger’s disorder 237 assertive community treatment (ACT) 313 assertive outreach models 313 ataxia telangiectasia 257 atomoxetine 286 atropine 128 attachment, maternal-infant 234 attention 20 tests 20 attention-deficit/hyperactivity disorder (ADHD) 243–5 aetiology 244 associated features 243–4 atomoxetine 286 course 244 differential diagnosis 244 epidemiology 244 genetics 244 management 245 prognosis 244 subtypes 243 atypical depression see masked depression atypical grief 55 autism 235–6 aetiology 235–6 clinical features 235 course 236

340

INDEX

autism (contd) differential diagnosis 236 epidemiology 235 fragile X syndrome 256 genetics 235 management 236 MRI 190 neurochemistry 236 prognosis 236 automatic obedience 14 autoscopy 145 avoidant personality disorder 79 azapirones 63, 283 barbiturates 127, 284 liver enzyme induction 266, 284 basal syndrome 153 basilar artery occlusion 153 battered child syndrome 221 behavioural disorders 13–15 behaviour therapy 306–7 anorexia nervosa 90 double learning theory 306 intermittent reinforcement 307 mental retardation 262 obesity 87 Pavlovian 306 phobic disorders 65 premack principle 306–7 shaping 307 Skinnerian 306 uses 306 see also cognitive-behavioural therapy (CBT) belladonna 128 benzodiazepines 282–3, 282 alcohol dependence detoxification 119 anxiety disorders 63 insomnia 181–2 mode of action 282 phobic disorders 65 psychopharmacology 127 side-effects 282–3 substance abuse 129 uses 282 withdrawal effects 283 bereavement reactions 55 psychogeriatrics 206–7 stillbirth 324 termination of pregnancy 324 Berry–Franceschetti syndrome 256

beta blockers 284–5 anxiety disorders 63 contraindications 285 side-effects 285 uses 284–5 bias 4 binge-eating disorder 91 Binswanger’s chronic progressive subcortical encephalopathy 159 bipolar disorder children 237–8 DSM-IV criteria 44 ICD-10 classification 44 molecular genetics 47 mood stabilizers 277–81 body dysmorphic disorder (BDD) 201 bonding, maternal-infant 234 borderline personality disorder 79, 81 bovine spongiform encephalopathy 161 bradyphrenia 163 brain imaging see neuroimaging brainstem dysfunction 153 breast feeding 268, 324 Briquet’s syndrome 82 Broca’s area damage 151 bulimia nervosa 91–3 aetiology 91–2 clinical features 92, 92 drug treatment 93 epidemiology 91 management 92–3 prognosis 93 buprenorphine 129 bupropion 274 busipirone 283 cAMP signalling pathway, alcohol dependence 112 cannabis 127 children/teenagers 249 Capgras’ syndrome 144 carbamazepine 179, 281 affective disorders 53 alcohol dependence 119 side-effects 281 uses 281 carbohydrate craving 55 carbohydrate metabolism disorders 258 cardiovascular problems alcohol dependence 116 tricyclics side-effect 275

INDEX

Care Programme Approach (CPA) 313 case-note studies 4–6 castration anxiety 300 cataplexy 182 catego 25 caudate nucleus 71 census 4 cerebral artery occlusion 153 character 77 childhood-onset schizophrenia 237 children 233–52 anxiety disorders 238–9 assessments 6 depression 238 diagnosis difficulties 233 disorder classification 233 epidemiology 233 Huntington’ s chorea 161 inappropriate soiling 240–2 maternal deprivation 234–5 mood disorders 237–8 non-accidental injury see non-accidental injury school refusal 239–40, 239 substance abuse 248–9 suicide 238 treatment considerations 233 child sexual abuse (CSA) 223–4 behavioural outcomes 224 evaluation 224 management 224 personality disorders 82 presentation by child 223 psychiatric outcomes 224 cholinergic neurogransmission, Alzheimer’s disease 157 chromosomal abnormalities 255–6 alcohol dependence 112 deletions 255 narcolepsy 182 chronic fatigue syndrome (CSF) 202 cirrhosis 117 clang associations 17, 18 clinical trial design 10 clonidine alcohol dependence detoxification 119 substance abuse 129 clozapine schizophrenia 34 suicide prevention 138 cocaine 126

341

coenaesthopathic states 146 cognitive-behavioural therapy (CBT) 307 affective disorders 52 antisocial personality disorder 217 anxiety disorders 62 bulimia nervosa 92 insomnia 181 schizophrenia 35–6 cognitive impairment 172 cognitive therapy 307–8 automatic thoughts 307 restructuring 307 theory of depression 307 variations 308 coma 20 combat guilt 69 combat necrosis see post-traumatic stress disorder combination therapies 53 community mental health teams 312 community-orientated psychiatry 312–17 historical review 312 policy initiatives 313–14 recent developments 313–14 community treatment order 228 compensation necrosis 172 competency 227 compliance therapy 36 compulsions 70 compulsive phenomena 16 computerized tomography (CT) affective disorder 206 Alzheimer’s disease 190 Creutzfeldt–Jakob disease 161 Huntington’ s chorea 190 schizophrenia 33, 189 structural investigations 189 concentration 20 conduct disorder 243, 247–8 aetiology 248 course 248 epidemiology 248 management 248 prognosis 248 subclassifications 247–8 connective tissue metabolism disorders 258–9 consciousness 20 clouding 20 control group 4, 10

342

INDEX

conversion disorder 198–9 aetiology 199 course 199 epidemiology 198–9 genetics 199 prognosis 199 psychoanalytic aspect 199 psychophysiological aspect 199 social aspect 199 treatment 199 coprolalia 247 corpus callosum abnormalities 216 corticotropin releasing factor (CRF) 49 Cotard’s syndrome 148–9 countertransference 299 court report preparation 225 Couvade syndrome 146 crack-cocaine 126 craniofacial dysostosis 256 cretinism (hypothyroidism) 259 Creutzfeldt–Jakob disease (CJD) 161–2 aetiology 161 clinical features 161 neuroimaging 161 prognosis 162 cri du chat syndrome 255 crime, violent 219–24 criminal responsibility (UK only) 226–7 age 226 complicating factors 227 intent 226–7 crisis intervention 304 CT see computerized tomography culture-bound disorders 329 Cushing’s syndrome 164 cybernetics 304 cyclic AMP (cAMP) signalling pathway, alcohol dependence 112 cyclothymia 44, 44 dangerous patient management 229–30 long-term 230 political level 229 staff policies 230 ward level 230 decarceration 312 De Clérambault’s syndrome 145 decreased tempo of thought 17 deep brain stimulation (DBS) 293 de Lange syndrome 257 delayed ejaculation 272

deliberate self-harm (DSH), non fatal 138–40 associations 138–9 definition 134 epidemiology 138–9 management 139–40 post episode 139 pre episode 139 personality disorders 83 repetition 139 risk factors 138–9 suicide 139 delirium 154–5 aetiology 155 clinical features 150 ICD-10 criteria 154 management 155 delirium tremens 114 delusion(s) 16 delusional atmosphere 16 delusional disorders 37–8 differential diagnosis 38 DSM-IV criteria 38 hypochondriacal 146 management 38 subtypes 145–6 types 16 delusional misidentification 144–5 delusional mood 16 ‘delusions of doubles’ 144 dementia 150–1 alcoholic 115 clinical features 150 differential diagnosis 151 epilepsy 179 neuropsychiatric assessment 154 types 155–63 dementia praecox 24 denial 19, 298 dependent personality disorder 79 depersonalization 19 depersonalization disorder 202 depression 18–19 aetiology 46–51 agitated 207 arson 221 assessments 5 children 238 clinical features 45–6 cognition 45 cultural aspects 329

INDEX

DSM-IV criteria 44 ECT indications 289 elderly patients 207 epidemiology 46 epilepsy 50, 178 hypochondriasis 200 ICD-10 44 integrative models 51 masked (atypical) 55, 238 medication 50 MRI 190 pregnancy 321 psychosurgery 294 psychotic/retarded/endogenous 43–5, 45 sleep disorders 182 suicide 136 treatment-resistant 54 unipolar 47 see also affective disorders depression-allied syndrome 148–9 depressive pseudodementia 207 derealization 19 descriptive statistics 7–8 desipramine 276 desultory thinking 18 detoxification alcohol dependence 119 methadone 129 naltrexone 129 dexamethasone suppression test (DST) 48 dextroamphetamine 285 attention-deficit/hyperactivity disorder 245 Dhat syndrome 329 diabetes mellitus 271 Diagnostic and Statistical Manual of Mental Disorders IV criteria see DSM-IV criteria dialectic behavioural therapy (DBT) 308 diazepam agoraphobia 65 breast feeding 268 diencephalon dysfunction 153 diet ketogenic 180 obesity 87 dietary chaos syndrome see bulimia nervosa diffuse tensor imaging (DTI) 189 diminished responsibility 226

disability 253 disintegrative psychoses 237 dispersion measurements 8 displacement 298 dissociative amnesia 202 dissociative disorders 201–2 clinical features 202 management 202 types 202 dissociative fugue 202 dissociative identity disorder 147, 202 management 202 distortion 298 distress syndrome 235 disulfiram 119, 285 divalproex 119 donepezil 158 dopamine (DA) affective disorders 48 alcohol dependence 113 antipsychotic medication 269–70 Gilles de la Tourette’s syndrome 247 schizophrenia 32 dothiepin 276 ‘double’ depression 45 Down syndrome Alzheimer’s disease 155 associated conditions 255 features 255 recurrence likelihood 255 doxepin 276 dream work 298 drowsiness 20 drug excretion 267 drug interactions 267–8, 276 drug therapy 266–88 affective disorder 208 anti-aggressive 230 anxiety disorders 62–3 depression causing 50 epilepsy 179 obsessive-compulsive disorder 71–2 pharmacodynamics 266–8 pharmacoeconomics 286 pharmacogenetics 268 pharmacokinetics 266–8 phobic disorders 65 pregnancy 268 sexual dysfunction 103 toxic confusion 165 see also specific drugs, and disorders

343

344

INDEX

DSM-IV criteria affective disorders 44 alcohol dependence 109 anorexia nervosa 90 antisocial personality disorder 215 anxiety disorders 60 bipolar disorder 44 bulimia nervosa 92 child psychiatric disorders 233 cyclothymia 44 delusional disorder 38 depressive disorders 44 gambling, pathological 130 mental retardation 253–4 Münchausen syndrome 147 obsessive-compulsive disorder 60 panic disorder 60 personality disorders 79 phobic anxiety disorders 60 schizoaffective disorder 36 schizophrenia 26, 27, 28 sexual disorders 98 social anxiety disorder 60 somatoform disorders 197 stress reaction 60 substance abuse 123–4 substance dependence 123 duration of untreated psychosis (DUP) 32 dyskinesias 245 dysphasias 21 dysphoria 49 dysthymia 45 dystonia 270 eating disorders 86–96 assessments 5 echolalia 14 echopraxia 14 ecstasy (MDMA) 128 ecstasy states 19 Edwards’ syndrome (trisomy 17–18) 255 ego 298 ego defence mechanisms 298 associated mental states 299 ego functions 298 eidetic images 15 ejaculatory impotence 97 behaviour therapy 102 Ekbom’s syndrome 146 elderly patients see psychogeriatrics Electra complex 300

electroconvulsive therapy (ECT) 289–93 administration 290–1 anaesthetic application 290 bilateral 291 electrical stimulation application 290–1 post-ictal 291 pre treatment 290 unilateral 291 affective disorder 208 consent 292 contraindications 290 effects 291–2 cardiovascular 291 neurological 291 neuropathological 291–2 sleep 292 ethical/legal aspects 292–3 history 289–93 indications 289–90 mortality 290 patient refusal 292–3 prescription 291 schizoaffective disorder 37 schizophrenia 35 seizure threshold 290–1 side-effects 290 unilateral vs bilateral 292 electroencephalography (EEG) 185–8 abnormal patterns 186–8 alpha coma 187 burst-suppression 188 diffuse abnormalities 187 focal abnormalities 187 frontal intermittent rhythmic delta activity (FIRDA) 187 periodic complexes 187 triphasic waves 187 adults 185 antisocial personality disorder 216 Creutzfeldt–Jakob disease 161 developmental changes 185–6 frequency ranges 185 infant 185 normal 185–6 organic psychosis detection 188 psychiatric uses 188 seizure diagnosis 188 sleep 186 disorder diagnosis 188 neurotransmitters 186 stupor 188

INDEX

electrolyte disturbance 169 emotional blunting 19 emotional disorders 18–19 abnormal expression 19 abnormal reactions 18–19 predisposition 18 emotional incongruity 19 emotional incontinence 19 emotional indifference 19 emotional lability 19 encephalitis lethargy 167 encopresis 241–2 management 242 endocrine disorders 164 alcohol dependence 117 depression 50 enuresis 240–1 aetiology 241 associated features 240–1 epidemiology 241 management 241 prognosis 241 epigenesis 78 epilepsy 175–80 aetiology 176 classifications 175–6 depression 50 diagnosis 177 differential diagnosis 177 EEG 187 epidemiology 176 genetic counselling 176 ictal phase automatisms 177 fugues 177 twilight states 178 inter-ictal periods 178–9 aggressive behaviour 178 dementia 179 depression 178 schizophreniform psychosis 178–9 suicide 178 mental retardation 261 post-ictal phase 178 preictal phase 177 aura 177 prodromal features 177 prognosis 176 seizures 175–6 treatment 179–80 episodic dyscontrol syndrome 178

345

erectile dysfunction (impotence) 97 antidepressants side-effect 272 behaviour therapy 102 organic causes 101 erotomania 145 error 4, 6 euphoria 19, 49 evidence-based medicine (EBM) 11 excretion, drug 267 exhibitionism 103–5 aetiology 104 classification 104 epidemiology 104 management 104 prognosis 104–5 expressive behaviour disorders 14 expressive dysphasias 21 family therapy 304 fetal alcohol spectrum disorder (FASD) 117 fetal alcohol syndrome (FAS) 117 firebugs 221 first arch syndromes 256 flexibilitas cerea 15 flooding (implosion) 65 folie à deux 148 folie à plusieurs 148 folie simultanée 148 forensic psychiatry 215–32 competence to consent to treatment 227 court report preparation 225 criminal responsibility (UK only) 226–7 involuntary commitment 228 legal aspects 225–8 negligence 227–8 psychiatric defences 225–6 testamentary capacity 227 fragile X syndrome 256 Fregoli’s syndrome 144 frigidity see anorgasmia frontal lobe dementia 162 frontal lobe dysfunction 151 frontal lobe syndrome 162 frontal lobe syndrome of disinhibition 160 functional MRI (fMRI) 192 attention-deficit/hyperactivity disorder 244 GABA neurotransmission, Huntington’s cholera 160 gabapentin 179, 281

346

INDEX

galactosaemia 258 galantamine 158 gambling, pathological 130–1 addiction phases 131 classification 130 management 131 gamma hydroxybutyric acid (GHB) 128 Ganser’s syndrome 146–7 Gaucher’s disease 259 general paresis (GPI) 166 general practice care 315–16 genetic abnormalities, mental retardation 256–7 genetic counselling epilepsy 176 mental retardation 263–4 geriatric disorders see psychogeriatrics Gerstmann’s syndrome 152 Gilles de la Tourette’s syndrome (GTS) 246–7 aetiology 246–7 clinical features 247 course 247 epidemiology 246 genetics 246 MRI 190 obsessive-compulsive disorder 70, 246 prognosis 247 tics 247 glutamate neurotransmission Huntington’s cholera 160 schizophrenia 33 grand mal seizure 175 grief reaction atypical 55 chronic 55 psychogeriatrics 206–7 typical 55 group therapy 304–5 analytic groups 304–5 therapeutic communities 305 growth hormone 113 Hallerman–Streiff syndrome 256 hallucinations 15 alcoholic 114 narcolepsy 182 hallucinogens 127 haloperidol 246 handicap 253 Hartnup’s disease (renal aminoaciduria) 258

hashish 127 Hatchinski index 159 head injury diffuse 170 focal 170 medico-legal aspects 172 psychiatric sequelae 171–2 aetiology 171 classification 171–2 sequelae 170–2 hepatitis, alcoholic 117 hermaphroditism 100 heroin 126 herpes simplex encephalitis 167 high expressed emotion (HEE) 35 Hirano inclusion bodies 156 histamine, sleep EEG 186 HIV infection affective disorder 168 AIDS dementia complex 167 neurosyphilis 166 substance abuse 130 see also acquired immunodeficiency syndrome (AIDS) home based treatment 313 homelessness 314–15 homicide 219 homocystinuria 258 homosexuality 106 homovanillic acid 269 hospital admission affective disorder 208 alcohol dependence 110 puerperal psychosis 324 Hunter’s syndrome (mucopolysaccharidosis type 2) 257, 259 Huntington’ s chorea 160–1 aetiology 160 children 161 clinical features 161 CT 190 subcortical dementia 163 Hurler’s syndrome (mucopolysaccharidosis type 1) 259 hydrocephalus 162 5-HT see serotonin 17 hydroxysteroid deficiency 100 hyperparathyroidism 164 hyperprolactinemia 271 hypertelorism 257 hypertensive crisis 277

INDEX

hyperthyroidism 164 hyperuricaemia, idiopathic 259 hyperventilation syndrome 67 hypochondriasis 200–1 management 201 prognosis 201 hypofrontality hypothesis 191 hypoglycaemia, idiopathic 258 hypomanic states 45–6 behavioural features 45 elderly 207–8 seasonal affective disorder 55 hypoparathyroidism 164 hypopituitarism 164 hypothyroidism 164, 279 hypothyroidism (cretinism) 259 hysterectomy 325 hysteria-allied syndromes 146–8 ICD-10 classification affective disorders 44 alcohol dependence 109 anorexia nervosa 90 antisocial personality disorder 215 anxiety disorders 60 bipolar affective disorder 44 bulimia nervosa 92 child psychiatric disorders 233 delirium 154 depressive episode 44 manic episode 44 mental retardation 253 obsessive-compulsive disorder 60 pathological gambling 130 persistent mood disorders 44 personality disorders 79 post-traumatic stress disorder 68 recurrent depressive disorders 44 schizophrenia 26, 26, 28 sexual disorders 98 somatoform disorders 197 stress reaction 60 substance abuse 123–4 substance dependence 123 illness psychological reactions 196–7 response patterns 197 illness phobia 64 illusions 15 imipramine 275–6 immunology

347

affective disorders 49 Alzheimer’s disease 157 schizophrenia 33–4 impaired consciousness, head injury 170 impairment 253 implosion (flooding) 65 impotence see erectile dysfunction impulsive type personality disorder 79 inappropriate soiling 240–2 inborn errors of metabolism 257–9 incest 105, 223 offender characteristics 223 victim characteristics 223 indecent exposure 103 infanticide 219 infection 166–8 depression 50 mental retardation 260 inferential statistics 8–9 informed consent 227 insight 21–2 insomnia 180–2 drug therapy 181–2 management 181–2 risk factors 181 institutionalization 312 elderly 211 problems with 312 intellectual function disorders 20–1 intellectualization 299 intermetamorphosis, syndrome of 144 International Classification of Diseases, 10th edn see ICD-10 classification internet 333–5 search engines 334 interpersonal psychotherapy (IPT) 308 affective disorders 53 intersexual disorders 100 interventional strategies, schizophrenia 35, 35 interviews 4–6, 5–6 involuntary commitment 228 involutional melancholia 325 isolation 299 Jacksonian seizure 175 jail diversion programme 228 killing 219–20 definition 219 epidemiology 219–20

348

INDEX

Kleine–Levin syndrome 183 Klinefelter’s syndrome (XXY genotype) 100, 256 Klüver–Bucy syndrome 157 koro 329 Korsakoff ’s psychosis 115, 164 la belle indifférence 19 lamotrigine 179, 281 side-effects 281 uses 281 language function disorders 21 latah 329 Laurence–Moon–Biedl syndrome 257 lead toxicity 165 Lesch–Nyhan syndrome 259 leucotomy 294 levomethadyl acetate (LAAM) 129 Lewy-body (LB) 162 Lewy-body dementia 162 liaison psychiatry 196 libido 101, 298 lipid metabolism disorders 258–9 lithium 277–80 actions 278 affective disorders 53 breast feeding 268 cautions 280 dose stabilization 279 drug interactions 280 HIV-mania 168 kinetics 278 mental retardation 230 monitoring 280 plasma level 279 pregnancy 268 schizoaffective disorder 37 side-effects 279–80 suicide prevention 138, 277 uses 279 liver damage 117 liver enzymes 266, 267 liver failure 169 living will 229 logoclonia 14 lorazepam 119 Louis–Bar syndrome 257 love object 298 Lowe syndrome 257 lycanthropy 144 lysergic acid diethylamide (LSD) 127

‘made actions’ 17 magic mushrooms 127 magnetic resonance imaging (MRI) affective disorders 49, 190, 206 AIDS dementia complex 168 Alzheimer’s disease 190 autism 190, 236 childhood -onset schizophrenia 237 Creutzfeldt–Jakob disease 161 depression 190 Gilles de la Tourette’s syndrome 190 mild cognitive impairment 190 Pick’s disease 190 psychiatric uses 189–90 schizophrenia 33, 189 structural investigations 189 substance abuse 190 Wernicke–Korsakoff syndrome 190 magnetoencephalography (MEG) 189 manganese toxicity 165 manic-depressive psychosis 207–8 manic states 45–6 assessments 5 behavioural features 45 cognition 45 ECT indications 289 ICD-10 classification 44 management 53 mental retardation 261 rapid cycling 56 violence 218 manic stupor 54 mannerisms 14 manslaughter 219 maple syrup disease 258 Marchiafava–Bignami disease 116 Marinesco–Sjögren syndrome 257 masked (atypical) depression 207 children 238 Masters and Johnson technique 102, 103 maternal deprivation 234–5 McNaughten rules 226 MDMA (ecstasy) 128 melancholia 43 memantine 158 memory 20–1 Alzheimer’s disease 157 temporal lobe dysfunction 152 tests 21 Menkes ‘kinky hair’ syndrome 257 menopause 325

INDEX

mens rea 226 mental impairment 254 mental retardation 253–65 aetiology 254 assessment 6 developmental 262 general 262 medical 261 chromosomal abnormalities 255–6 coding 253–4, 254 definitions 253–4 educational services 262 epidemiology 254, 319 epilepsy 261 management principles 262–3 medical 262 parental guidance 263 psychiatric 263 manic depressive psychosis 261 neurotic disorders 261 non-genetic causes 259–60 prevention 263–4 tertiary 263–4 psychiatric disorders 260–1 residential services 262 schizophrenia 260 services required 261–2 assessment 261–2 guidelines 261 meperidine 126 mercury toxicity 165 mescaline psilocybin 127 metabolic disorders 169–70 depression 50 methadone 126, 129 methylphenidate 245, 285 mianserin 276 microcephaly 257 middle cerebral artery occlusion 153 mild cognitive impairment (MCI) 159 MRI 190 mirtazapine 274 miserable mania 208 mitgehen 14 mitmachen 14 mitral valve prolapse 66–7 modelling, phobic disorders 65 monoamine oxidase inhibitors (MAOIs) 276–7 affective disorders 53 anxiety disorders 63

349

contraindications 277 precautions 277 side-effects 276–7 monosymptomatic hypochondriacal psychosis 146 mood 18 mood disorders children 237–8 children/adolescents 237–8 delusional 16 depression 45 hypomanic/manic states 45 ICD-10 44 mood stabilizers 277–81 morbid jealousy 145 morphine 126 motivational enhancement therapy (MET) 308 alcohol dependence 120 motivational state, abnormal 299 motor cortex dysfunction 151 motor disorders (general behaviour) 13–15 mourning 55 movement disorders, adaptive 14 MRI see magnetic resonance imaging MR spectroscopy 192 mucopolysaccharidosis type 1 (Hurler’s syndrome) 259 mucopolysaccharidosis type 2 (Hunter’s syndrome) 257, 259 mucopolysaccharidosis type 3 (Sanflippo’s syndrome) 259 multiple personality disorder see dissociative identity disorder multiple sclerosis 170 multiple sleep latency test (MSLT) 182 Münchausen by proxy 148 Münchausen syndrome 147–8 clinical features 147–8 management 148 murder 219 myopathy, alcoholic 116 naltrexone alcohol dependence 119 substance abuse 129 narcolepsy 182–3 aetiology 182 clinical features 182 diagnosis 182 treatment 183

350

INDEX

nefazodone 274 negligence 227–8 nephrogenic diabetes insipidus 259 lithium side-effect 279 nephropathy 279 neurasthenia 202 neurofibrillary tangles (NFTs) 156 neuroimaging 188–92 clinical applications 192 functional investigations 191–2 research applications 192–3 schizophrenia 33 structural investigations 189 see also individual techniques neurokinin 1 49 neuroleptic malignant syndrome (NMS) 271 neuroleptics schizoaffective disorder 37 schizophrenia 34–5 neuropeptide Y (NPY) 112 neuroses cultural aspects 329 head injury 171 school refusal 240 women 318 neurosyphilis 166 neurotic depression 43–4 neurotic disorders 60–76 anxiety disorders 60–3, 60 mentally handicapped 261 neurotransmitters anxious patients 66 lithium 278 sleep EEG 186 nicotinic acid deficiency (pellagra) 163 Niemann–Pick disease 258 nightmares 183 post-traumatic stress disorder 68 night terrors 183, 242 night-time incidents 242 nihilistic delusions 148–9 non-accidental injury, children 221–3 classification 221 clinical features child 222 parents 222 prevention 222–3 definition 221 epidemiology 222 non-adaptive movements 14

induced movements 14 posture disorders 15 non-benzodiazepine hypnotics 283, 283 non-epileptic attack disorder 180 non-parametric statistics 8, 8 non-psychostimulants 286 non-violent offenders 224–5 noradrenaline affective disorders 48 Alzheimer’s disease 157 schizophrenia 33 nortriptyline 276 obesity 86–7 aetiology 86 management 87 obsessional phenomena 16 obsessions 70 obsessive-compulsive disorder (OCD) 69–72, 70 aetiology 70–1 anankastic type personality 71 assessments 5 body dysmorphic disorder 201 course 72 DSM-IV criteria 60 epidemiology 70 genetics 70 Gilles de la Tourette’s syndrome 246 ICD-10 classification 60 neuroanatomy 71 neurochemistry 71 PANDAs 71 PET 192 phenomenology 70 prognosis 72 psychosurgery 294, 295 theories 71 treatment 71–2 obstruction 14 occipital lobe dysfunction 153 Oedipal complex 300 opioids 126 alcohol dependence 113 oppositional defiant disorder (ODD) 246, 247 optic atrophy 116 orbital cortex 151 orbital undercutting 295 organic disorders 150–74 acute see delirium arterial occlusion 153

INDEX

brainstem dysfunction 153 cerebral function localization 151–3 chronic see dementia cultural aspects 330 diencephalon dysfunction 153 differential diagnosis 150 EEG 188 frontal lobe dysfunction 151 neuropsychiatric assessment 153–5 occipital lobe dysfunction 153 parietal lobe dysfunction 152 soft signs 154 temporal lobe dysfunction 152 orlistat 87 orofacial dyskinesia 14 Othello syndrome 145 outpatient clinics 211 oxazepam 119 oxcarbazepine 281 paedophilia 105, 223 pain disorder 200 assessment 200 clinical features 200 management 200 palilalia 14 pandysmaturation 32 panic disorder 61 clinical symptoms 61 DSM-IV criteria 60 hyperventilation syndrome 67 PET 192 parametric statistics 8, 8 paranoid personality disorder 79 paranoid syndromes 209–10 aetiology 209 clinical features 210 differential diagnosis 210 environmental factors 209 epidemiology 209 genetics 209 organic causes 209 personality features 209 prognosis 210 sensory defects 209 treatment 210 paraphilias 103–6 paraphrenias 209–10 parapraxes 298 parasomnias 183 parasuicide 134

351

pareidolia 15 parental absence 50 parietal lobe dysfunction 152 Parkinsonism 270 Parkinson’s disease deep brain stimulation 293 Lewy-bodies 162 psychosurgery 294 passivity phenomena 16–17 Patau’s syndrome (trisomy 13–15) 255 pediatric autoimmune neuropsychiatric disorders (PANDAs) 71 pellagra (nicotinic acid deficiency) 163 pemoline 286 pentazocine 126 perception disorders 15 performance anxiety 99, 101 perseveration 14, 21 personality 77 development theories 77–8 tests 5 personality changes pseudodepressive 151 pseudopsychopathic 151 personality disorders (PD) 78–83 aetiological theories 80–2 assessments 5, 80, 83 behavioural psychology 81 biopsychosocial model 80 borderline 81 childhood experiences 82 classification 80 DSM-IV 79 ICD-10 79 definitions 78–9 epidemiology 80 frontal lobe dysfunction 151 genetics 81–2 head injury 171 prognosis 83 psychodynamic theory 81 self-image 81 suicide 136 temperament 82 temporal lobe dysfunction 152 treatment 83 pervasive development disorder see autism PET see positron emission tomography petit mal seizure 175 petit mal variant seizure 175 phaeochromocytoma 164

352

INDEX

pharmacodynamics 266–8 pharmacogenetics 268 pharmacokinetics 266–8, 267 absorption 266 drug excretion 267 drug interactions 267–8 metabolism 266–7 phenomenology 13 phenylcyclidine (PCP) 127 phenylketonuria 258 phenytoin 179 phobic disorders 63–5 animal phobias 64 DSM-IV criteria 60 ICD-classification 60 illness phobia 64 social phobia 64 treatment 64–5 physical treatments 289–96 Pick’s cells 160 Pick’s disease 160, 190 pickwickian syndrome 183 placebo effect 9 polymorphisms, genetic 268 porphyria, acute intermittent 169–70 port wine syndrome (Sturge–Weber syndrome) 257 positron emission tomography (PET) 191–2 affective disorders 49, 192 Alzheimer’s disease 192 antipsychotic medication 269–70 Gilles de la Tourette’s syndrome 246 obsessive-compulsive disorder 71, 192 panic disorder 192 schizophrenia 33, 191 post-concussional syndrome 171 posterior cerebral artery occlusion 153 posterior inferior cerebral artery occlusion 153 postpartum ‘blues’ 323 management 324 postpartum psychiatric disorders 321–4 management 324 post-traumatic amnesia (PTA) 170–1 post-traumatic stress disorder (PTSD) 67–9 aetiology 68 clinical features 68 co-morbidity 68 drug treatment 69 ICD-10 classification 68 management 69 prevention 69

prognosis 69 posture disorders 15 power of attorney 229 Prader–Willi syndrome 257 praecox feeling 24 pregnancy 320–1 alcohol 117 drug prescribing 268 drug treatment 321 epidemiology 320–1 management 321 psychotropics 321 termination 324–5 tricyclics 276 premature ejaculation 97 behaviour therapy 102 premenstrual syndrome 320 premorbid personality affective disorders 51 obsessive-compulsive disorder 71 premotor cortex dysfunction 151 pressure of speech 17 priapism 101 prion disorder 161 prison inmates mental illness 229 suicide 137 progesterones 320 Programme of Assertive Community Treatment (PACT) 313 projection 298 projective identification 298 prolactin 47 propranolol 69 protein metabolism disorders 258 pseudocyesis (false pregnancy) 198 pseudohallucinations 15 pseudohermaphroditism 100 pseudoseizures 180 psychiatric advance directives 228–9 psychiatric defences (UK only) 225–6 diminished responsibility 226 not guilty by reason of insanity 226 special verdict 226 unfit to plead 225–6 psychic retardation 17 psychoanalysis 297–300 definition 297–9 theorists 300–4 British schools 302 early 300–1

INDEX

international approach 303–4 Neo-Freudians (USA) 302 post-Freudians 303 unconscious 299 psychogeriatrics 205–14 affective disorder 205–8 aetiology 206–7 clinical features 207–8 environmental factors 206–7 epidemiology 205–6 genetics 206 management 208 organic factors 206 prognosis 208 assessments 6 epidemiology 205, 205 home support 211 management 211–12 drug therapy 211 inpatient issues 212 principles 211 psychotherapy 212 paranoid syndromes 209–10 services organization 212 suicide 137 psychometric testing 6–7 psychoneurosis 298 psychopathology, descriptive 13–23 psychophysiological disorders 195–7 psychophysiological tests 7 psychosis affective 171 AIDS 168 head injury 171–2 schizophreniform 172 psychosocial treatment epilepsy 180 schizophrenia 35 psychosomatic specificity hypothesis 195 psychostimulants 285–6 attention-deficit/hyperactivity disorder 245 contraindications 286 side-effects 286 uses 286 psychosurgery 293–5 anxiety disorders 63 contraindications 295 definitions 293–4 epilepsy 180 ethical/legal issues 295

history 294 indications 294–5 obsessive-compulsive disorder 72 outcome 295 procedures 294 prognosis 295 psychotherapy 297–311 affective disorders 52–3 anorexia nervosa 90 anxiety disorders 62 common features 297 elderly patients 212 levels 297 mental retardation 230 obesity 87 obsessive-compulsive disorder 71 patient suitability 299–300 personality disorders 83 phobic disorders 65 psychoanalysis 297–300 research 308–9 arousal 309 methodological problems 308 outcomes 308–9 patient assessment 309 process 309 standardizations 308 therapist skills 309 schizophrenia 35–6 sexual dysfunction 103 see also specific modalities puerperal depression 323 management 324 puerperal psychosis 321–2 aetiology 321–2 biochemical causes 321 bonding lack 322 clinical features 322 epidemiology 321 genetics 321 management 324 prognosis 322 psychodynamic factors 322 punch-drunk syndrome 163 questionnaires 4–6 rape 220 rapid cycling mania 56 reaction formation 298 reactive depression 43–4

353

354

INDEX

reality testing 81 ‘recovery’ approaches, schizophrenia 35 recovery model 313 5␣-reductase deficiency 100 reduplicative paramnesia 144 Refsum’s disease 259 regional cerebral blood flow (rCBF) 191 rehabilitation assessment 315 relationship behaviour, normal 97 reliability 3 reliability paradox 3 renal aminoaciduria (Hartnup’s disease) 258 repression 298, 299 research design 2–3 research methodology 1–12 definitions 2–4 measurements 4–7 planning 1–2 sample selection 4, 10 statistics 7–9 trial design 10 research protocol 1–2 research publication review 10–11 retrograde amnesia 170 Rett’s syndrome 259 rhesus-negative screening 264 rivastigmine 158 sample selection 4, 10 Sanflippo’s syndrome (mucopolysaccharidosis type 3) 259 schizoaffective disorder 36–7 DSM-IV criteria 36 management 37 prognosis 37, 37 women 319 schizoid personality disorder 79 schizophrenia 24–42 aetiology 30–4 arson 221 assessments 5 childhood -onset 237 classification 25 cognitive impairment 29 concepts 24–5 controversies 27–9 cultural aspects 328–9 deficit syndrome 29 diagnostic criteria 25–9 DSM-IV 26, 27, 28 ICD-10 26, 26, 28

ECT indications 289 epidemiology 29–30, 319 family dynamics 34 first-rank symptoms 25 genetics 30–2, 30 immunology 33–4 life events 34 management 34–6 mental retardation 260 migration 330–1 neurochemistry 32–3 neurodegenerative 29 neurodevelopment 29 neuroimaging 33 CT 33, 189 functional MRI 192 MRI 33, 189 MR spectroscopy 192 PET 33, 191 SPECT 191 neuropathology 33 poor outcome predictors 36 positive/negative disorganization syndromes 28 prodromal studies 32 prognosis 36, 37 psychophysiology 33–4 psychosis continuum 29 relapse rates 35, 35 spectrum 31, 31 substance abuse 124 suicide 136 symptoms positive/negative 28 ranking 25 thought disorders 17–18, 17 type I/type II syndromes 28 violence 218 women 319 xenon inhalation 191 schizophrenia-like syndrome 178–9 school refusal 239–40, 239 aetiology 240 course 240 epidemiology 239 prognosis 240 seasonal affective disorder (SAD) 55–6 treatment 56 sedatives 282–4 seizures 175–6 EEG 188

INDEX

selective serotonin re-uptake inhibitors (SRRIs) 273–4 affective disorder 208 anxiety disorders 62–3 body dysmorphic disorder 201 bulimia nervosa 93 obsessive-compulsive disorder 71 phobic disorders 65 pregnancy 321 premenstrual syndrome 320 side-effects 274 uses 273–4 self-awareness disorders 19–20 self-mutilation, repeated 140 senile melancholia 207 sensate focus technique 102 sensory deceptions 15 sensory distortions 15 serotonin (5-HT) affective disorders 47 alcohol dependence 113 Alzheimer’s disease 157 bulimia nervosa 91 personality disorders 81 schizophrenia 32 suicide 137–8 serotonin syndrome 272 sex chromosome abnormalities 255–6 sexual abuse see child sexual abuse (CSA) sexual behaviour, normal 96–7 epidemiology 96 neurophysiology 97 physiology 97 relationship behaviour 97 sexual development 300 stages 300 theories 300 sexual dysfunction 97–106 aetiology 100–1 assessment 99–100 behaviour therapy 102 classifications 98–9, 98, 99 definitions 97–8 drug treatment side effects 103, 271, 272, 275 female 97 investigations 100 male 97 prognosis 103 psychotherapy 103 treatment 101–3

355

shaken baby syndrome 221 shell-shock syndrome see post-traumatic stress disorder shoplifting 224–5 epidemiology 225 sibutramine 87 single photon emission computerized tomography (SPECT) affective disorders 191 Alzheimer’s disease 191 Gilles de la Tourette’s syndrome 246 schizophrenia 191 sleep apnoea 183 sleep deprivation, affective disorders 54 sleep disorders 180–3 alcoholism 182 Alzheimer’s disease 158 # check ref #, 182 anxiety 182 classification 180 depression 182 EEG diagnosis 188 sleep EEG 186 neurotransmitters 186 sleep hygiene, insomnia 181 sleepwalking 183, 242 social phobia 64 social therapy, affective disorder 208 sodium lactate infusion response 66 somatization disorder 197–8 somatoform disorders 197–201 classification 197 conversion disorder 198–9 hypochondriasis 200–1 pain disorder 200 somatization disorder 197–8 specific reading retardation (SRR) 242–3 associated features 243 SPECT see single photon emission computerized tomography spectatoring 101 speech changes depression 45 hypomanic/manic states 45 splitting 299 standard deviation 8 statistics 7–9 descriptive 7–8 inferential 8–9 non-parametric 8, 9 parametric 8, 9 Steele–Richardson–Olszewski 163

356

INDEX

sterilization 325 sterotypies 14 Steven Johnson syndrome 281 stillbirth 325 stimulants 285–6 stress reaction DSM-IV criteria 60 ICD-10 classification 60 stroke victims 49 stupor 20 EEG 188 manic 54 Sturge–Weber syndrome (port wine syndrome) 257 subcortical dementia 163 sublimation 299 substance abuse (SA) aetiological theories 125–9 assessments 6 behavioural theories 125 children/teenage 248–9 co-morbidity 124 DSM-IV 123–4 epidemiology 124–5 genetics 125 HIV 130 ICD-10 123–4 management 129 MRI 190 pattern of abuse 125 physiological theories 125 prevention 130 prognosis 130 psychosocial treatments 129 theories 125–9, 126–8 violence 218 suicide 134–8 adolescents 137 AIDS 168 alcoholism 136 biological factors 137–8 children 238 definitions 134 deliberate self-harm 139 depression 136 drug prevention 277 elderly 137, 207 epidemiology 134–7, 135 epilepsy 178 genetics 138 hospital inpatients 137

hypothalamic-pituitary -adrenal axis 138 illness 136 management 138 neurochemistry 137–8 obsessive-compulsive disorder 70 personality disorders 136 pregnancy 321 prevention 138 prison inmates 137 psychiatric illness 135–8 schizophrenia 30, 136 victim characteristics 135 women 319 sundowning 158, 182 surgery see psychosurgery survey 4 susto 329 symptomatic disorders 245–7 syndrome of approximate answers 146–7 systemic desensitization 65 tabes dorsalis 166 tarasoff doctrine 228 tardive dyskinesia (TD) 271 Tay–Sachs disease 258 temporal lobe language functions 21 schizophrenia 33 temporal lobe dysfunction 152 termination of pregnancy 324–5 testamentary capacity (UK only) 227 testicular feminization syndrome (Y genotype) 100 therapeutic alliance 299 thiamine (B1) deficiency 163–5 Wernicke’s encephalopathy 114–15 thought blocking 18 thought broadcast 17 disordered forms of thinking 17–18 thought disorders 16–18 disordered content 16–17 schizophrenic 17–18, 17 thought insertion 17 thought stopping 71 thought withdrawal 17 thrombocytopenia 117 tiagabine 281 tics 14, 245–6 aetiology 246 associated features 245 course 246

INDEX

differential diagnosis 245 epidemiology 246 Gilles de la Tourette’s syndrome 247 management 246 prognosis 246 topiramate 281 toxic confusion 165 toxins 165 trait approach 80 transcranial magnetic stimulation (TMS) 293 transcultural psychiatry 328–32 assessment 330 migration 330–1 treatment 330 transference 299 research 309 transsexualism 106 transvestism 105 trauma, mental retardation 260 traumatic neurosis see post-traumatic stress disorder trazodone 274 treatment resistant depression, vagus nerve stimulation 293 tricyclic antidepressants 275–6 contraindications 276 drug interactions 276 enuresis 241 precautions 276 pregnancy 321 side-effects 275 trisomies 255–6 trisomy 13–15 (Patau’s syndrome) 255 trisomy 17–18 (Edwards’ syndrome) 255 trisomy 21 see Down syndrome tuberous sclerosis 256 Turner’s syndrome (XO genotype) 100, 256 turning against the self 298 Twelve-Step Facilitation (TSF) 120 ultraviolet light therapy 56 unfit to plead 225–6 uraemia 169 urinary tract infection, enuresis 241 vaginismus 97 behaviour therapy 102 vagus nerve stimulation (VNS) 293 epilepsy 180 side effects 293

357

validity 3 valproate (valproic acid) 280 affective disorders 53 epilepsy 179 schizoaffective disorder 37 side effects 280 uses 280 variables 2 variant Creutzfeldt–Jakob disease (vCJD) 161 vascular dementia (VaD) 159 velo-cario-facial syndrome (VCFS) 257 venlafaxine 63, 275 ventriculo-atrial shunts 162 violence epidemiology 218, 218 management 230 mental illness 217–19 patient assessment 218–19 repeated 219 violent crime 219–24 Virchow–Seckel dwarf 257 visuospatial functions 21 vitamin B12 deficiency 165 vitamin deficiencies 163–5 volatile substance abuse (VSA) 128 vomiting, conversion disorder 198 vulnerability-stress models 34 ‘waxy flexibility’ 15 websites 333–4 governmental 333 non-governmental 333–4 Wechsler Adult Intelligence Scale 6 weight phobia 88 Wernicke–Korsakoff syndrome 114–15 detoxification 119 MRI 190 Wernicke’s encephalopathy 114–15 thiamine deficiency 114–15, 163 windigo 329 Wisconsin Card Sorting Test (WCST), xenon inhalation 191 withdrawal alcohol dependence 113, 114 tricyclics side-effect 275 Wolf syndrome 255 women, psychiatric problems 318–27 epidemiology 318–19 affective disorders 318–19 alcoholism 319

358

INDEX

women, psychiatric problems (contd) anorexia nervosa 319 criminal behaviour 319 mental handicap 319 neuroses 318 schizoaffective disorder 319 schizophrenia 319 self harm 319 senile dementia 319 suicidal behaviour 319 hysterectomy 325 pregnancy 320–1 premenstrual syndrome 320 stillbirth 325 working alliance 299 working through 299

World Health Organization (WHO) mental retardation definition 253 psychosurgery definition 295 wrist-cutting, repeated 140 xenon inhalation 191 X-linked disorders 257 XO genotype (Turner’s syndrome) 100, 256 XXX genotype 255 XXY genotype (Klinefelter’s syndrome) 100, 256 XYY genotype 256 zidovudine (AZT) 168 zolpidem 182 zopiclone 182

Examination Notes in Psychiatry

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