Internal Medicine study notes Neuro/brain/psych Elevated intracranial pressure/ intracranial HTN o ICP>20 mm Hg o Causes: trauma, space-occupying lesions, hydrocephalus, impaired CNS venous outflow o Dx: diffuse headaches (worse in morning), N/V morning), N/V early in the day, vision changes, papilledema, changes, papilledema, CN deficit, somnolence, confusion, unsteadiness, cushings reflex (HTN and bradycardia) bradycardia) o Dx: CT or MRI Cavernous sinus thrombosis o Secondary to infection of the medial aspect of the face around the eyes and nose (can also be ethmoid or sphenoid sinus infections) infections) o Sx: headache, low grade fever, periorbital edema, cranial nerve palsies CN 3,4,5 (V1,V2, V3) all pass through the cavernous sinus and can be affected Headache d/t neuropathic pain d/t irritation of V1 and V2 Dx: MRI or CT w/ contrast of the orbits Tx: IV broad=spectrum antibiotic; anticoagulation, glucocorticoid, glucocorticoid, or surgery may be indicated Acoustic neuroma/ vestibular schwannoma o Typically unilateral o Sx: sensorineural hearing loss Craniopharyngioma o Tumor of the sella and suprasellar space o Sx: headache, focal neurologic changes, visual problems; can cause central diabetes insipidus (decreased ADH) Headaches o Dx: CT or MRI to exclude an intracranial mass lesion if the dx is unclear or the syndrome has recently started o Tension headache Most common type Dx of exclusion Tx: NSAIDs or other analgesics o Migraine headache Precipitants: emotions, food (chocolate, red wine, cheese), menses Sx: visual disturbance (flashes, sparks, stars, luminous hallucinations), photophobia, aura, N/V, headaches lasting 4-72 hrs (usually unilateral, pulsating quality) Other possible sx: aphasia, numbness, dysarthria, weakness Tx: IV antiemetics (chlorpromazine, (chlorpromazine, Prochlorperazine, or metoclopramide) +/- NSAIDS or triptans for acute migraine headaches; triptans or ergotamine Triptans must be started early in the course of the migraine before sx become severe in order to be of benefit Prophylactic (preventative) tx: propanolol (#1), calcium channel blockers, tricyclic antidepressants (amitriptyline), SSRIs, botulinum toxin injections o for pts with >3 migraine headaches/month headaches/month o cluster headaches M>F Sx: frequent short duration high intensity headaches Other possible sx: red tearing eye with rhinorrhea, horner syndrome Tx: triptans, ergotamine, 100% oxygen, prednisone, or lithium o giant cell (temporal) arteritis sx: visual sx (irreversible blindness), jaw claudication, scalp tenderness, headache; sx in other arteries (decreases arm pulses, bruits near clavicles, aortic regurgitation); systemic sx (muscle pain, fatigue, weakness) dx: elevated ESR and CRP; biopsy of artery (most accurate) tx: high dose prednisone (started before biopsy) o pseudotumor cerebri (benign/idiopathic intracranial HTN) communicating hydrocephalus; diagnosis of e xclusion a/w obesity, venous sinus thrombosis, thrombosis, vitamin A toxicity, medications (corticosteroids, (corticosteroids, OCPs), trauma sx: headache (pulsatile, wake pt from sleep, a/w pulsatile tinnitus; worse lying flat/ better standing up); mimics a brain tumor d/t elevated ICP (N/V, transient visual obscurations, blurry vision), papilledema w/ diplopia from 6 th cranial nerve (abducens) palsy vision loss, sluggish pupillary reflexes to light, papilledema, dx: CT or MRI to exclude an intracranial mass lesion (empty sella d/t downward herniation herniation of archnocele d/t high CSF pressure, slit like ventricles), lumbar puncture showing increased pressure (w/o CSF disturbances) note: papilledema is not a contraindication to an LP unless the pt has evidence of obstructive to noncommunicating hydrocephalus and/or space-occupying lesion +/- mass effect or midline shift tx: weight loss, acetazolamide (decreased CSF production), steroids, repeated lumbar puncture (rapidly lower ICP); ventriculoperitoneal ventriculoperitoneal shunt if medical therapy not sufficient Transient ischemic attack (TIA)/ stroke o #3 cause of death o Causes: carotid stenosis, cardioembolism, lipohyalinosis, small-vessel disease, atheroembolism from carotid artery Ischemia (85%), bleeding (15%) Embolic sources: carotid stenosis, heart (atrial fibrillation, valvular heart disease, DVT through patent foramen ovale) o Risk factors: HTN, diabetes, hyperlipidemia, hyperlipidemia, smoking Hypertensive stroke is most common in the putamen and adjacent internal capsule hemiparesis, hemiparesis, semi-sensory loss, homonymous hemianopsia o Sx: acute focal neuro deficits, amaurosis fugax Amaurosis fugax: transient monocular blindness; “gray shade being pulled down over the eye” d/t ischemia to the retinal arter y TIA: transient neuro deficit secondary to ischemia in a defined vascular territory that lasts <24 hr MCA stroke (90%) Sx: contralateral weakness/sensory loss, homonymous homonymous hemianopsia (loss of visual field on opposite side of stroke), eye deviation to side of lesion, aphasia, if speech center effected o Speech center on same side as “handedness” (if right handed L. side dominant Left sided speech center) Anterior cerebral artery (ACA) stroke
Sx: personality/cognitive defects, urinary incontinence, weakness leg >arm Posterior cerebral artery (PCA) stroke Sx: ipsilateral sensory loss of face & CN 9/10, contralateral sensory loss of limbs, limb ataxia Cerebellar hemorrhage: hemorrhage: ataxia, vomiting, occipital headache, gaze palsy (towards the lesion), facial weakness (opposite lesion) Lacunar stroke Occurs d/t microatheroma and lipohyalinosis lipohyalinosis (small (small vessel hyalinosis); type of ischemic stroke o RF: HTN, diabetes o Most common in the posterior internal capsule pure motor stroke Putamen hemorrhage: most common site of HTN hemorrhage; internal capsule lies adjacent to the putamen and is almost always involved hemiparesis; hemisensory loss, homonymous hemianopsia, hemianopsia, stupor, coma; eye are deviated away form the paralytic side o Dx: CT w/o contrast (best (best initial; differentiate ischemic from hemorrhagic stroke), MRI (most accurate) Determine etiology carotid duplex U/S or MRA to evaluate for carotid artery stenosis o tx: >70% stenosis + symptomatic cerebrovascular disease carotid endarterectomy > angioplasty w/ stenting >80% stenosis, asymptomatic, good surgical candidates carotid endarterectomy o consider carotid surgery for 50-60% stenosis o medical management with aspirin and statins <50% stenosis echocardiogram: damaged valves or thrombi o tx: surgically repair/replace damaged valves; heparin warfarin to INR of 2-3 for thrombi EKG: assess for atrial arrhythmia (fibrillation (fibrillation or flutter) o Holter monitoring if initial EKG is normal to r/o arrhythmia o Tx: warfarin to INR of 2-3 as long as arrhythmia persists o Tx: Non-hemorrhagic Non-hemorrhagic stroke (ischemic stroke) <3hr since onset thrombolytics (IV tPA) >3hr since onset aspirin; if pt was already on aspirin add dipyridamole or change to clopidogrel hemorrhagic stroke: no treatment control RFs: HbA1c<7%, control BP, LDL<100, smoking cessation Rankin score system for stroke o Measures the degree of disability or dependence n the daily activities of stroke pts (or other neuro disability) o 0= no sx o 1 - No significant disability. Able to carry out all usual activities, despite some symptoms. o 2 - Slight disability. Able to look after own affairs without assistance, but unable to carry out a ll previous activities. o 3 - Moderate disability. Requires some help, but able to walk unassisted. o 4 - Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted. o 5 - Severe disability. Requires constant nursing care and attention, bedridden, incontinent. o 6 - Dead. hypertensive encephalopathy o Sx: altered mental status (confusion), severe HTN, increased ICP, and/or seizures o Diff dx: drugs (cocaine, amphetamines), stroke, subarachnoid hemorrhage, meningitis, mass lesion, rebound HTN from meds (clonidine), pheochromocytoma o Tx: decreased BP in ICU (goal 100-110 mmHg systolic) Hematomas/hemorrhages o Note: hemorrhages appear as hyperdense areas on CT scan, whereas infarcts are hypodense parenchymal areas o Subarachnoid hemorrhage d/t rupture of an aneurysm (usually anterior circle of Willis) RFs of aneurysm: polycystic kidney diseases, smoking, HTN, hyperlipemia, high alcohol consumption Sx: “worst headache of my life”; su dden onset severe headache, meningeal irritation (stiff neck, photophobia), photophobia), fever, loss of consciousness (sudden increase in ICP), focal neurological complications Dx: CT w/o contrast, LP (blood, xanthochromic xanthochromic CSF; may have elevated WBC) WBC) WBC count should not exceed the normal ratio of 1 WBC for every 500-1000 RBCs; if elevated above this, consider meningitis EKG: may have large or inverted T waves (d/t excessive sympathetic activity) activity) Angiography to determine the site of aneurysm (CT angiography, catheter angiography, or MRA) Tx: nimodipine (calcium channel blocker; prevents future ischemic stroke), e mbolization (coiling)> surgical clipping, ventriculoperitoneal ventriculoperitoneal shunt if hydrocephalus occurs, seizure prophylaxis with phenytoin Syncope o Transient LOC and postural tone w/ spontaneous recovery d/t transient global decrease in cerebral perfusion (not regional hypoperfusion like TIA) o causes: vasovagal: fainting d/t excessive vagal tone hypotension w/o reflex increase in HR or vasomotor tone; #1 cause of syncope prodromal sx: nausea, yawning, diaphoresis triggers: micturition, defecation, coughing, emotion (stress or fear), pain tx: if young pt w/no PMhx then just reassurance & D/C home carotid sinus hypersensitivity hypersensitivity occurs in old men; triggers (pressure on carotic sinus)= turning head, tight collar, shaving neck over area dx: carotid massage to massage to reproduce sx (auscultate 1 st to ensure no bruits) orthostatic hypotension: hypotension: decrease >20mm Hg with postural changes causes: diabetic neuropathy neuropathy (autonomic insufficiency), other peripheral neuropathy (alcoholic, nutritional, amyloid), parkinsonism, idiopathic dysautonomia, dysautonomia, hypovolemia, anti-HTN/ vasodilator drugs, neuro disorder (ShyDrager syndrome) physical deconditioning, sympathectomy, acute dysautonomia (guillain-barre syndrome variant) cardiac disease: arrhythmias or outflow obstruction (aortic stenosis, hypertrophic hypertrophic obstructive cardiomyopathy) cardiomyopathy) arrhythmias #1 cause of cardiac induced syncope (usually bradycardia) bradyarrhythmias: bradyarrhythmias: sinus bradycardia, sinoatrial block, s inus arrest, sinus syndrome, AV block
Sx: personality/cognitive defects, urinary incontinence, weakness leg >arm Posterior cerebral artery (PCA) stroke Sx: ipsilateral sensory loss of face & CN 9/10, contralateral sensory loss of limbs, limb ataxia Cerebellar hemorrhage: hemorrhage: ataxia, vomiting, occipital headache, gaze palsy (towards the lesion), facial weakness (opposite lesion) Lacunar stroke Occurs d/t microatheroma and lipohyalinosis lipohyalinosis (small (small vessel hyalinosis); type of ischemic stroke o RF: HTN, diabetes o Most common in the posterior internal capsule pure motor stroke Putamen hemorrhage: most common site of HTN hemorrhage; internal capsule lies adjacent to the putamen and is almost always involved hemiparesis; hemisensory loss, homonymous hemianopsia, hemianopsia, stupor, coma; eye are deviated away form the paralytic side o Dx: CT w/o contrast (best (best initial; differentiate ischemic from hemorrhagic stroke), MRI (most accurate) Determine etiology carotid duplex U/S or MRA to evaluate for carotid artery stenosis o tx: >70% stenosis + symptomatic cerebrovascular disease carotid endarterectomy > angioplasty w/ stenting >80% stenosis, asymptomatic, good surgical candidates carotid endarterectomy o consider carotid surgery for 50-60% stenosis o medical management with aspirin and statins <50% stenosis echocardiogram: damaged valves or thrombi o tx: surgically repair/replace damaged valves; heparin warfarin to INR of 2-3 for thrombi EKG: assess for atrial arrhythmia (fibrillation (fibrillation or flutter) o Holter monitoring if initial EKG is normal to r/o arrhythmia o Tx: warfarin to INR of 2-3 as long as arrhythmia persists o Tx: Non-hemorrhagic Non-hemorrhagic stroke (ischemic stroke) <3hr since onset thrombolytics (IV tPA) >3hr since onset aspirin; if pt was already on aspirin add dipyridamole or change to clopidogrel hemorrhagic stroke: no treatment control RFs: HbA1c<7%, control BP, LDL<100, smoking cessation Rankin score system for stroke o Measures the degree of disability or dependence n the daily activities of stroke pts (or other neuro disability) o 0= no sx o 1 - No significant disability. Able to carry out all usual activities, despite some symptoms. o 2 - Slight disability. Able to look after own affairs without assistance, but unable to carry out a ll previous activities. o 3 - Moderate disability. Requires some help, but able to walk unassisted. o 4 - Moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted. o 5 - Severe disability. Requires constant nursing care and attention, bedridden, incontinent. o 6 - Dead. hypertensive encephalopathy o Sx: altered mental status (confusion), severe HTN, increased ICP, and/or seizures o Diff dx: drugs (cocaine, amphetamines), stroke, subarachnoid hemorrhage, meningitis, mass lesion, rebound HTN from meds (clonidine), pheochromocytoma o Tx: decreased BP in ICU (goal 100-110 mmHg systolic) Hematomas/hemorrhages o Note: hemorrhages appear as hyperdense areas on CT scan, whereas infarcts are hypodense parenchymal areas o Subarachnoid hemorrhage d/t rupture of an aneurysm (usually anterior circle of Willis) RFs of aneurysm: polycystic kidney diseases, smoking, HTN, hyperlipemia, high alcohol consumption Sx: “worst headache of my life”; su dden onset severe headache, meningeal irritation (stiff neck, photophobia), photophobia), fever, loss of consciousness (sudden increase in ICP), focal neurological complications Dx: CT w/o contrast, LP (blood, xanthochromic xanthochromic CSF; may have elevated WBC) WBC) WBC count should not exceed the normal ratio of 1 WBC for every 500-1000 RBCs; if elevated above this, consider meningitis EKG: may have large or inverted T waves (d/t excessive sympathetic activity) activity) Angiography to determine the site of aneurysm (CT angiography, catheter angiography, or MRA) Tx: nimodipine (calcium channel blocker; prevents future ischemic stroke), e mbolization (coiling)> surgical clipping, ventriculoperitoneal ventriculoperitoneal shunt if hydrocephalus occurs, seizure prophylaxis with phenytoin Syncope o Transient LOC and postural tone w/ spontaneous recovery d/t transient global decrease in cerebral perfusion (not regional hypoperfusion like TIA) o causes: vasovagal: fainting d/t excessive vagal tone hypotension w/o reflex increase in HR or vasomotor tone; #1 cause of syncope prodromal sx: nausea, yawning, diaphoresis triggers: micturition, defecation, coughing, emotion (stress or fear), pain tx: if young pt w/no PMhx then just reassurance & D/C home carotid sinus hypersensitivity hypersensitivity occurs in old men; triggers (pressure on carotic sinus)= turning head, tight collar, shaving neck over area dx: carotid massage to massage to reproduce sx (auscultate 1 st to ensure no bruits) orthostatic hypotension: hypotension: decrease >20mm Hg with postural changes causes: diabetic neuropathy neuropathy (autonomic insufficiency), other peripheral neuropathy (alcoholic, nutritional, amyloid), parkinsonism, idiopathic dysautonomia, dysautonomia, hypovolemia, anti-HTN/ vasodilator drugs, neuro disorder (ShyDrager syndrome) physical deconditioning, sympathectomy, acute dysautonomia (guillain-barre syndrome variant) cardiac disease: arrhythmias or outflow obstruction (aortic stenosis, hypertrophic hypertrophic obstructive cardiomyopathy) cardiomyopathy) arrhythmias #1 cause of cardiac induced syncope (usually bradycardia) bradyarrhythmias: bradyarrhythmias: sinus bradycardia, sinoatrial block, s inus arrest, sinus syndrome, AV block
tachyarrhythmias: tachyarrhythmias: supraventricular tachycardia, with structural cardiac disease, atrial fibrillation a/w the wolf Parkinson-white syndrome, syndrome, atrial flutter with 1:1 AV conduction cardiopulmonary cardiopulmonary disease: PE, pulmonary HTN, atrial myxoma, myocardial disease (massive MI), LV myocardial restriction or constriction, pericardial constriction/tamponade, constriction/tamponade, aortic outflow tract obstruction (aortic valve ste nosis, hypertrophic obstructive cardiomyopathy) cardiomyopathy) vascular disease (TIA, carotid stenosis): r/o with carotid artery U/S or duplex scanning neurologic disorder (seizures, (seizures, intracranial lesions); consider EEG or CT/MRI is hx suggest seizures or intracranial lesions
seizures o o
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o
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Tremors Physiologic Causes: fear, anxiety, fatigue, metabolic (hypoglycemia, hyperthyroid, pheochromocytoma), pheochromocytoma), toxic (alcohol withdrawal, valproic acid, lithium, methylxanthines=caffeine or theophylline) o Essential tremor Autosomal dominant (~1/3 of cases) Tremor occurs at rest and with intention Exacerbated by intentional activity and caffeine, decreased by alcohol use Tx: propanolol o Neurologic diseases: Parkinson’s, cerebellar disease, Wilson’s disease Meningitis o Causes: infectious, medications, SLE, sarcoidosis, sarcoidosis, carcinomatosis o Sx: headache, fever, N/V, stiff painful neck, malaise, photophobia, altered mental status (confusion, lethargy, coma), myalgias, seizures Increased ICP, kerning’s sign (unable to extend knees wit h hips flexed), brudzinski’s sign (passive flexion of neck causes thigh/leg flexion) N. meningitidis: Maculopapular rash w/ petechiae or purpura Varicella or HSV: vesicular lesions Complications: Complications: seizures, coma, brain abscess, subdural empyema, DIC, respiratory arrest; deafness, brain damage, hydrocephalus o Acute: onset w/in hrs-days Bacterial Neonates (<3mo): GBS> E.coli >listeria monocytogenes; klebsiella spp. Kids (3mo-18yrs): Neisseria meningitidis > strep pneumoniae >H. influenzae Adults (18-50): Strep pneumo > N. meningitidis > H. influenzae Elderly (>50 yo): Strep pneumo > N. meningitidis > listeria monocytogenes Immunocompromised: Immunocompromised: L. monocytogenes > gram (-) bacilli > strep pneumo Aseptic meningitis Enterovirus, HSV, certain bacteria, parasites, fungi o chronic: onset w/in wks-months mycobacteria, fungi, lyme dz, parasites o differential diagnosis: meningitis, brain or epidural abscess, subarachnoid hemorrhage hemorrhage bugs that cause meningitis: strep pneumo (#1), N. meningitidis (#2), GBS/strep agalactiae, listeria monocytogenes, H. influenzae; staph aureus or staph epidermidis following neuro procedures; enteroviruses, HSV 1 or 2, cryptococcus (HIV pts), TB, rocky mountain spotted fever o dx: CSF exam (lumbar puncture), blood cultures CT scan before lumbar puncture if focal neurologic signs or abnormal level of consciousness, papilledema Normal LP: WBC <5 (all lymphocytes or monocytes), glucose 50-75, protein <60 bacterial: elevated bacterial: elevated opening pressure, elevated WBC (PMNs) & protein, low glucose, glucose , gram stain usually positive aseptic/viral meningitis: increased lymphocytes, protein normal, glucose normal HSV: normal/increased opening pressure, elevated WBC (lymphocytes), (lymphocytes), normal/ normal/elevated elevated protein, protein , normal glucose, high RBC count o If HSV meningitis is suspected MRI (enhancement of the temporal lobes), HSV polymerase chain reaction analysis o
epilepsy: seizure of unclear etiology partial seizures: focal to one part of the body simple=intact consciousness, complex= loss of consciousness absence (petit-mal) seizures occurs in children consciousness only briefly impaired; appears as if the person is staring into space tx: ethosuximide ethosuximide generalized tonic-clonic seizures causes: electrolyte disturbances (hypo/hypernatremia, hypomagnesemia, hypocalcemia), uremia, hypoxia, hypoglycemia, CNS infection (encephalitis, meningitis, abscess), CNS anatomic abnormalities (trauma, stroke, tumor), hepatic failure, drug withdrawal (alcohol, barbiturate, benzodiazepine), cocaine toxicity sx: phases of muscular rigidity (tonic) followed by muscle jerking (clonic) dx: BMP (r/o metabolic disturbance), toxin screen, CT or MRI of head (r/o anatomic defect), electroencephalogram (EEG) EEG is only done if there is no other clear etiology of the seizure Status epilepticus Tx: IV benzodiazepine (Lorazepam, diazepam) diazepam) fosphenytoin> phenytoin phenobarbital neuromuscular blocking agent (succinylcholine, vecuronium, vecuronium, or pancuronium) pancuronium) + intubation+ general anesthesia (midazolam or propafol) Phenytoin SE: hypotension & AV block (b/c also a class Ib antiarrhythmic) Treatment Treatment is not always necessary following a single seizures Treatment indications: status epilepticus, abnormal EEG, family hx of seizures 1st choice= phenytoin, valproic acid, or carbamazepine; alternatives= gabapentin, topiramate, lamotrigine, oxcarbazepine, levetiracetam if single agent not effective, try an alternative drug; if still not effective 2 drugs; if still not effective surgical correction of a seizure focus treat until pt is seizure-free for 2 yrs, then test if discontinuation can be done via a sleep deprivation EEG driving restrictions: recommend that the patient find an alternate means of transportation
TB: normal/increased opening pressure, increased WBC (monocytes), low glucose, high protein Repeat LP in 48 hrs shows decreased glucose from last value; AFB culture takes 6-8 wks; MRI (enhancement of the basal region) o tx: empiric antibiotics, steroids if cerebral edema (glucocorticoids decreased inflammation), vaccination; prophylaxis for close contacts (rifampin or ceftriaxone) start antibiotics after LP &blood cx unless there are anticipated delays such as need for CT, then start immediately infants <3mo: cefotaxime + ampicillin + vancomycin (aminoglycoside if <4 wk old) 3mo-50 yo: (ceftriaxone or cefotaxime) + vancomycin >50 yo: (ceftriaxone or cefotazime) + vancomycin + ampicillin immunocompromised: ceftazidime + ampicillin+ vancomycin o cryptococcal meningitis tx: IV amphotericin B + flucytosine, followed by chronic suppression with oral fluconazole lumbar puncture is still diagnostic if done 30min-2hrs after antibiotics If neisseria meningitidis is suspected, start antibiotics immediately Pneumococcus or meningococcus: 3 rd gen cephalosporin + vancomycin Listeria (gram (+) rod): ampicillin HSV: acyclovir + bacterial coverage until cx results are back TB: 4 drug treatment (isoniazid+ rifampin + pyrazinamide + ethambutol or streptomycin) vaccines all pt >65 yo :strep pneumo Asplenic pt against encapsulated organisms: strep pneumo, n. meningitidis, H. influenzae meningococcus (n. meningitidis) vaccine: immunocompromised, dorm/military o household & close contacts: rifampin (2x/day for 2 days) or 1x ciprofloxacin Supportive tx (analgesics, fever reduction) for aseptic meningitis; self-limited Brain tumors o Cerebellar tumor Sx: ipsilateral ataxia (pt fall towards the side of the lesion), nystagmus, intention t remor, ipsilateral muscular hypotonia, marked difficulty in coordination and performing rapid alternating movements; obstruction of CSF flow ICP headaches, N/V, papilledema Brain abscess o Can be d/t distant infections (lung, teeth, heart, GI, bone) or d/t contiguous spread of infection (middle ear, mastoids, paranasal sinuses) o Agents: aerobic and anaerobic streptococci (69-70%) and bacteroides spp. 9anaerobes; 20-40%) are the most common; staph aureus (10-15%) o Sx: headaches, focal neurologic deficit o Dx: CT scan (solitary/isolated ring-enhancing lesions) Neurologic lesions o Upper motor neurons: weakness, spasticity/ clonus/ increased muscle tone, hyperreflexia, extensor plantar responses o Lower motor neurons: weakness, wasting, fasciculations o Front lobe damage: apathy, inattention, disinhibition, labile affect Dominant front lobe: Broca (motor) aphasia o Parietal lobe damage Dominant parietal lobe damage: inability to read, write, name, or do math Nondominant parietal lobe damage: ignoring one side of body, trouble with dressing o Temporal lobe damage: memory impairment, hyperaggression, hypersexuality Dominant temporal lobe damage: Wernicke (sensory) aphasia o Occipital lobe damage: visual hallucinations/ illusions o Signs of cerebellar dysfunction: intention tremor, ataxia, broad-based gait, dysmetria, difficulty with rapid alternating movements, nystagmus, dysarthria, scanning speech; muscle hypotonia can be seen pendular knee reflex Cranial nerves o Locations Midbrain: CN 3,4 Pons: CN 5,6,7,8 Medulla: 9,10,11,12 o Trigeminal neuralgia 5th cranial nerve dysfunction sx: severe pain in the face (stabbing) pain precipitated by: chewing, touching the face, speaking words where the tongue strikes the back of t he front teeth tx: carbamazepine or oxcarbazepine; baclofen, lamotrigine; surgical decompression if not controlled by meds postherpetic neuralgia o d/t singles (herpes zoster reactivation); pain syndrome after resolution of the vesicular lesions o tx: shingles prevention: zoster vaccine to all pt >60yo incidence prevention following shingles: antherpetic meds (acyclovir, famciclovir, valganciclovir) pain control: tricyclic antidepressants, gabapentin, pregabalin, carbamazepine, phenytoin, or antiepileptic meds; topical capsaicin disk herniation o sx: pain at the site of compression, signs of nerve compression (if radiculopathy) o dx: x-ray, MRI cervical fracture o sx: can compromise innervation to the diaphragm if phrenic nerve interrupted o dx: tender to palpation, x-ray syringomyelia o fluid filled dilated central canal in the spinal cord; d/t tumor or severe trauma o sx: capelike distribution of loss (across upper back a nd both arms); loss of pain/temp, reflexes; muscle atrophy o dx: MRI (most accurate) o tx: surgical removal of tumor if present; drainage of fluid from the cavity anterior spinal artery infarction
sx: loss of all function except for posterior column (positional and vibratory sensation intact); flaccid paralysis be low lesion, loss of deep tendon reflexes at the level of lesion; spastic paraplegia several wks later, loss of pain & temp sensation, extensor plantar response subacute combined degeneration of the cord o d/t vit B12 deficiency or neurosyphilis o sx: loss of positional and vibratory sensation spinal trauma o sx: acute onset of limb weakness and/or sensory disturbance; sphincter function impaired; loss od DTRs at the level of injury, hyperreflexia below the level of injury o tx: glucocorticoids brown sequard syndrome o unilateral hemisection fothe spinal cord o sx: loss of pain & temp on the contralateral side; ipsilateral loss of motor function & positional/vibratory sensation cauda equina syndrome o sx: low back pain, saddle anesthesia, bowel or bladder dysfunction; possible lower extremity weakness & loss of reflexes d/t compression of multiple sacral nerve roots o tx: surgical emergency brain abscess o can spread from contiguous infection (sinuses, mastoid air cells, otitis media) or from any source of bacteremia o sx: headache, N/V, fever, seizures, focal neurological findings o dx: MRI or CT (best initial; ring, contrast enhancing lesion with surrounding edema and mass effect), brain biopsy (most accu rate) LP is contraindicated d/t risk of herniation o Tx: empiric tx with penicillin + metronidazole+ (ceftriaxone or cefepime); vancomycin can be used instead of penicillin if pt has recent neurosurgery (increased risk of staph) Treat 6-8 wks IV, followed by 2 -3 mo orally Toxoplasmosis o Most common CNS mass lesion in AIDs pt o Sx: headache, seizures, focal neurologic deficits o Dx: CT or MRI (multiple enhancing lesions often in basal ganglia) o Tx: sulfadiazine + pyrimethamine #1 causes of altered mental status in elderly= dehydration Normal pressure hydrocephalus o d/t decreased CSF absorption at the arachnoid villi or obstructive hydrocephalus o Sx: gait disturbance (broad-based shuffling gait, bradykinetic), dementia, urinary incontinence o Dx: CT or MRI (dilated ventricles) o Tx: if repeated spinal taps cause improvement ventriculo-peritoneal shunts for definitive treatment Frontotemporal dementia o Causes: Pick’s disease May have a family hx of frontotemporal dementia o Sx: prominent personality changes (euphoria, disinhibition, apathy), compulsive behaviors (peculiar eating habits, hyperorality) , impaired memory Intact visuospatial functions o Dx: MRI (symmetrical frontal or temporal lobe atrophy) Multi-infarct dementia o Sx: rapid onset dementia o Dx: MRI (multiple areas of increased T-2 weighted density in the periventricular areas) Alzheimer’s disease o Sx: visuospatial problems early (getting lost while driving), anterograde memory dysfunction personality and behavioral changes hallucinations, changes in alertness o Dx: MRI (normal or diffuse cerebral cortex atrophy) o Tx: donepezil (anticholinesterase inhibitor increases Ach) Dementia with lewy body o Sx: fluctuating cognitive impairment with pronounced variation in attention and alertness, and bizarre visual hallucinations; motor features of parkinsonism (with poor response to dopaminergic agonist therapy); prominent or persistent memory impairment; deficits in attention, frontal-subcortical skills, and visuospatial ability Progressive cognitive decline that interferes with normal social or occupational functions Other features: repeated falls, syncope, transient LOC, neuroleptic sensitivity, systematized delusions Creutzfeldt-jakob disease o Fatal neurodegenerative disease d/t prions Occurs on older pts (500-70 yo); most case sporadic, other familial or iatrogenic o Sx: rapidly progressive dementia, myoclonus o Dx: EEG (periodic high voltage complexes; periodic synchronous bi or triphasic sharp wave complexes), brain biopsy (cortical spongiform changes) o Tx: none; death usually occurs within 12 months Parkinson disease (paralysis agitans) o Progressive neurodegenerative disease; mean age 70.5yo (pt >50-60 yo) d/t dopamine depletion in the substantia nigra (basal ganglia) and in the nigrostriatal pathway to the caudate & putamen increased inhibition of the thalamus & reduced excitatory input to the motor cortex o Secondary parkinsonism: antipsychotics (metoclopramide, prochlorperazine, reserpine, thorazine) & antiemetics are most common causes; repeated head trauma, encephalitis o Sx: tremor (“pill rolling”, at rest & decreased with purposeful action, 5-7 Hz frequency, may be a sensation of internal tremulousness), bradykinesia, rigidity (asymmetric, increased resistance to passive movement; cogwheel rigidity d/t tremor superimposed on increased tone), postural instability (orthostatic hypotension d/t inability of pulse and B P to reset a ppropriately with movement), micrographia (small writing), limited facial expression (hypomimia) Shy-Drager syndrome (multiple system atrophy): parkinsonism predominantly with orthostasis o
Tx: intravascular volume expansion (fludrocortisone, salt supplementation, alpha-adrenergic agonists, application of constrictive garments to the lower body); note that anti-parkinson drugs are generally ineffective
Motor sx
Sx: parkinsonism, autonomic dysfunction (postural hypotension, abnormal sweating, dry mouth, dry skin, disturbance of bowel/bladder control, abnormal salivation or lacrimation, impotence, gastroparesis), widespread neuro signs (cerebella, pyramidal, or lower motor neuron)
Craniofacial: hypomimia (masked facial expression), decreased spontaneous eye blink rate, speech impairment (hypokinetic dysarthria, hypophonia, palilalia= involuntary repetition of syllables/words/phrases), dysphagia, sialorrhea= drooling Visual: blurred vision, impaired contrast sensitivity, hypometric saccades, impaired vestibuloocular reflex, impaired upward gaze & convergence, eyelid opening apraxia Musculoskeletal: micrographia (small handwriting), dystonia, myoclonus, stooped posture, camptocormia (severe anterior flexion of the thoracolumbar spine), kyphosis, scoliosis, difficulty turning in bed
Gait: shuffling, short stepped gait, freezing, festination (involuntary quickening of the gait) Nonmotor sx
Cognitive dysfunction and dementia, psychosis and hallucinations (paranoid psychosis; visual hallucinations most common), mood disorders (depression, anxiety, apathy/abulia), sleep disturbances (insomnia sleep initiation problems, frequent awakening, and early morning awakening), fatigue, autonomic dysfunction, olfactory dysfunction, pain and sensory disturbances, dermatologic findings (seborrheic dermatitis) o Ambulia= loss of impulse/will/motivation to think, speak, and act
Dementia: subcortical; psychomotor retardation, memory difficulty, altered personality, problems with exe cutive function (decision making or multi-tasking), memory retrieval, visuospatial misperception o Cortical neuronal Lewy inclusion bodies filled with alpha synuclein+ amyloid plaques & neurofibrillary tangles (more common to Alzheimer’s disease) Dx: Based on clinical impression Brain MRI to r/o structural lesions Striatal dopamine transporter imaging (DaTscan) may be useful for pts where clinical diagnosis is unclear Treatment
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Dopamine agonists (pramipexole, ropinirole): best initial tx for severe parkinsonism
Pergolide and cabergoline should NOT be used d/t risk of valvular heart disease Bromocriptine is also not frequently used d/t SE Levodopa + peripheral decarboxylase inhibitor (carbidopa) is most effective for symptomatic treatment
Carbidopa inhibits aromatic AA decarboxylation; inhibits metabolism of levodopa in the peripheral circulation SE: “on/off” phenomena (episodes of too much dopamine and insufficient dopamine) COMT inhibitor (Entacapone, tolcapone): extend the duration of levodopa/carbidopa by blocking the metabolism of dopamine MAO B inhibitors (Selegiline, rasagiline): block metabolism of dopamine ; only MAO-B inhibitors are a/w the possibility of retarding the progression of parkinsonism
mild symptomatic benefit; only used for early disease Avoid tyramine-containing foods (wine, cheese); they precipitate HTN Anticholinergic drugs (benztropine, trihexyphenidyl): used for young pts when tremor or rigidity is the predominant sx (mild disease)
SE: dry mouth, worsening prostatic hypertrophy, constipation Amantadine: used for early or mild PD or for problematic dyskinesia Increases release of dopamine & NE from nerve endings; weak NMDA receptor antagonist; anticholinergic Psychosis: quetiapine or clozapine (atypical neuroleptics); stop or reduce drugs causing psychosis in reverse order of potency (anticholinergic, amantadine, COMT inhibitors, and lastly dopamine agonists)
Note: clozapine requires weekly or bi-weekly blood counts d/t risk of granulocytopenia (risk exponentially decreased with time; almost nothing >6mo) Daytime sleepiness: sleep hygiene, modafinil, methylphenidate, or judicious use of coffee during the day Fatigue: amantadine, stimulants (methylphenidate, pemoline) Depression: SSRI (SE possibly aggravates motor sx, adverse interaction with selegiline causing serotonin syndrome) Deep brain stimulation (electrical stimulation) Dopamine agonist for pt <65, levodopa for pt >65
Multiple sclerosis
Choose antipsychotics with the l east extrapyramidal sx (antidopaminergic)
Multiple neurologic deficits of the CNS; presents in 20-40s; insidious onset of intermittent neurologic deficits Sx: scattered motor & sensory deficits (paresthesias and numbness, weakness, gait disturbance, visual disturbances); optic neuritis blurry vision or visual disturbances (most common), painless loss of vision; diplopia, internuclear ophthalmoplegia; b/l trigeminal neuralgia; cognitive defects, mental status changes, emotional lability, dementia; spasticity (painful contracted muscles), hyperreflexia, fatigue, cerebellar deficits; scanning speech Internuclear ophthalmoplegia: inability to adduct 1 eye with nystagmus in the other eye o Dx: MRI ( demyelination plaques= white matter lesions surrounding the ventricles, corpus callosum, basal ganglia); lumbar puncture of CSF (elevated protein, <50-100 WBCs, oligoclonal bands/ elevated IgG, elevated myelin basic protein) o Tx: high dose steroids (glucocorticoids) for acute exacerbation (shorten duration) prevent relapse & progression: 1 st choice glatiramer acetate (copolymer 1) or interferon-beta; natalizumab (alpha-4 integrin inhibitor), mitoxantrone, azathioprine, cyclophosphamide, cyclophosphamide, methotrexate glatiramer acetate: synthetic mixture of polypeptides containing random combinations of 4 AA found in myelin basic protein; induces suppressor T-cells to down regulate the T-cell mediated immune response to myelin antigens natalizumab SE: progressive multifocal leukoencephalopathy (PML; new multiple white matter hypodense lesions) interferon beta is best for the relapsing-remitting form of MS immunosuppressive agents (cyclosporine, methotrexate, mitoxantrone, etc) can be used for the progressive form of MS (downhill course w/o c lear-cut remissions) Spasticity: baclofen, dantrolene, or tizanidine (central acting alpha agonist) Amyotrophic lateral sclerosis (ALS) o Loss of upper and lower motor neurons o Onset age 20-40 o Sx: weakness starting distally & asymmetrically, difficulty chewing & swallowing, difficulty speaking, decrease in gag reflex; pooling of saliva in pharynx aspiration, weak cough, respiratory difficulties Upper motor neurons: weakness, spasticity, hyperreflexia, extensor plantar responses Lower motor neurons: weakness, wasting, fasciculations o Dx: electromyography (loss of neural innervation in multiple muscle groups), elevated CPK o Tx: riluzole (reduces glutamate buildup in neurons; may prevent progression) Spasticity: baclofen Respiratory distress/failure: CPAP, BiPAP, tracheostomy & ventilator maintenance Most common cause of death is respiratory failure Charcot-marie-tooth disease o Genetic; loss of motor and sensory innervation o Sx: distal weakness & sensory loss, wasting in the legs (legs look like inverted champagne bottles), decreased DTRs, tremor foot drop o Dx: electromyography (most accurate) Foot drop o d/t damage in the common peroneal nerve or radiculopathy of any of the spinal roots that contribute to the peroneal nerve (L4-S2) o sx: high-stopping or “Steppage” gait d/t t he inability to dorsiflex the foot Restless leg syndrome o More common middle age-older pt; pt with chronic kidney disease and/or iron deficiency anemia o Sx: uncomfortable sensation or urge to move the legs (“creepy and crawly” sensation) worse at night or at rest; Worsened by caffeine relieved by moving the legs, massage, warming bed partner may complain of being kicked at night o Tx: dopamine agonists (pramipexole, ropinerole) Huntington disease o Autosomal dominant; Hereditary CAG trinucleotide repeat on Chr. 4; onset age 30-50 yo o Sx: choreaform movement disorder (dyskinesia), dementia, behavior changes (irritability, moodiness, antisocial behavior), mood disturbances (depression, apathy) Movement disorder progression: “fidgetiness” /restlessness, dystonic posturing, rigidity, akinesia Choreiform movements: facial grimacing, ataxia, dystonia, tongue protrusion, writhing movement of the extremities o Dx: clinical (movement, memory, mood changes); head CT or MRI (caudate nucleus atrophy enlargement of the lateral ventricles) o Tx: dyskinesia tetrabenazine; psychosis haloperidol or quetiapine Tourette disorder o Sx: vocal tics, grunts, coprolalia (involuntary swearing); motor tics (s niffing, blinking, frowning), obsessive-compulse behavior o Tx: neuroleptics (haloperidol, clonazepam, pimozide) Facial (7th CN) nerve palsy/ bell palsy o Causes: idiopathic, lyme disease, sarcoidosis, herpes zoster, tumors, stroke o Sx: paralysis of the entire side of the face (except stroke will only have lower face paralysis b/c upper face innervated from both hemispheres); difficulty eating, hyperacusis (sounds are extra loud d/t loss of stapedius muscle innervation), taste disturbances (CN7 detects taste in anterior 2/3 of tongue), difficulty closing the eye (especially at night) dryness corneal ulceration Central facial paresis will still have forehead furrowing; bell’s palsy (peripheral 7th nerve palsy) will have absence of forehead furrows o Dx: clinical; electromyography and nerve conduction studies (most accurate) o Tx: self-resolving (60%); prednisone; taping eye shut & lubricants at night to prevent corneal ulcers Peripheral neuropathies o Causes: diabetes mellitus (most common), uremia, alcoholism, paraproteinemia (monoclonal gammopathy of unknown significance=MGUS) o Sx: Ulnar: wasting of hypothenal eminence, pain in 4 th/5th fingers Radial: wrist drop Median n: thenar wasting, pain/numbness in first 3 fingers Lateral cutaneous nerve of thigh: pain/numbness of outer aspect of 1 thigh Occurs with pregnancy, obesity, sitting with c rossed legs Tarsal tunnel (tibial nerve): pain/numbness in ankle and sole of foot; worse with walking Peroneal: weak foot with decreased dorsiflexion and eversion o Tx: 1st choice=pregabalin or gabapentin; TCA antidepressants, seizure meds (phenytoin, carbamazepine, lamotrigine) Acute inflammatory polyneuropathy (Guillain-barre syndrome) o o
Autoimmune attack of myelin sheath in multiple peripheral nerves; no CNS involvement a/w infections, recent immunization, or pt with lymphoma, sarcoidosis, or SLE associated infections: campylobacter jejuni (#1), herpes viruses, mycoplasma, hemophilus influenzae, HIV o Sx: weakness/ parestheisas in the legs that ascends toward the chest (ascending paralysis), loss of DTRs; respiratory muscle weakness, autonomic dysfunction possible (hypo/hypertension, tachycardia) Note: sensation remains intact or is only slightly diminished o Dx: clinical diagnosis; nerve conduction studies/electromyography (decrease in propagation/velocity of electrical impulses d/t demyelination), CSF (increased protein, normal cell count) PFTs: decrease forced vital capacity and peak inspiratory pressure if diaphragm involved; earliest way to detect impending respiratory failure Serial measurement of bedside vital capacity is used to monitor respiratory function o Tx: self-resoling; IVIG (children) or plasmapheresis (adults) to reduce severity and length of disease Myasthenia gravis o Antibodies against Ach receptors at the neuromuscular junction muscle weakness o Sx: double vision, difficulty swallowing; ptosis, weakness with sustained activity, normal pupillary responses o Dx: acetylcholine rector antibodies (best initial), edrophonium test (short acting acetylcholinesterase inhibitor; improvement in motor function that lasts a few minutes), electromyography (most accurate; decreased strength with repetitive stimulation); CXR/CT/MRI (look for thymoma or thymic hyperplasia) o Tx: neostigmine or pyridostigmine (long acting acetylcholinesterase inhibitors) Acute exacerbation: IVIG or plasmapheresis If not controlled: <60 yo thymectomy, >60 yo prednisone Weaning off steroids: azathioprine, cyclophosphamide, or mycophenolate Schizophrenia o Sx: hallucinations (auditory) Mini mental status exam for dementia o <9 severe cognitive impairment, 10-20 moderate impairment, 21-24 mild impairment, 25-30= normal cognition o orientation to time (5), orientation to place (5), registration (3), attention and calculation (5), recall (3), language (2), repetition (10), complex commands (6) attention and calculation: serial sevens or sell “world” backwards language: naming a pencil and watch neurocutaneous diseases o tuberous sclerosis sx: neuro sx (seizures, progressive psychomotor retardation, slowly progressive mental deterioration), skin sx (adenoma sebaceum, shagreen patches, ash leaf patches), retinal lesions, cardiac rhabdomyomas adenoma sebaceum: reddened facial nodules shagreen patches: leathery plaques on the trunk ash lead patches: hypopigmented areas tx: seizure control o neurofibromatosis (von Recklinghausen disease) sx: neurofibromas, 8 th CN tumors, café au lait spots (cutaneous hyperpigmented lesions), meningioma and gliomas neurofibromas: soft, flesh colored lesions attached t o peripheral nerves tx: 8th CN lesions may need surgical decompression to help preserve hearing o sturg-weber syndrome sx: port-wine stain of face, seizures, CNS (homonymous hemianopsia, hemiparesis, mental subnormality) dx: skull x-ray (calcification of angiomas) tx: control seizures Lhermitte Test (barber chair phenomenon): electrical sensation that runs down the back and into the limbs; d/t lesion of the posterior column or caudal medulla o The patient is sitting or standing and the examiner is behind them and introduces lower cervical flexion A positive test results in production of an electrical “type” response or a “pins and needles” sensation near the end range of flexion o Diff dx: multiple sclerosis, vit B12 deficiency, behcet’s disease, transverse myelitis, radiation myelopathy, compression of the spinal cord (cervical spondylosis, disc herniation, tumor, Arnold-chiari malformation) Spurling’s test: assess nerve root pain ( radicular pain) in the neck o Downward pressure on the top of the patients head in the neutral position, in neck extension, and with neck extended and tipped to the affected side Lumbar puncture o Contraindications: acute head trauma, signs of elevated ICP, suspected subarachnoid hemorrhage Near a clear CT/MRI in these settings; risk of uncal herniation death o CSF analysis Condition Cells Glucose (mg/dL) Protein (mg/dL) Pressure (mmHg) Normal CSF 0-3 lymphocytes 50-100 20-45 100-200 Bacterial meningitis >1000 PMNs <50 ~100 >200 Viral/aseptic meningitis >100 lymphocytes Normal Normal/slightly increased Normal/ slightly increased Pseudotumor cerebri Normal Normal Normal >200 Guillain-barre syndrome 0-100 lymphocytes Normal >100 Normal Cerebral hemorrhage Blood (RBC) Normal >45 >200 Multiple sclerosis Normal/ slightly increased lymphocytes Normal Normal/slightly increased normal Sleep disorders o Circadian rhythm disorders Delayed sleep phase syndrome: inability to fall asleep at “normal” bedtimes such as 10pm-midnight; pt cannot fall asleep until 4-5am but have normal sleep if they are allowed to sleep until late morning; pt c/o insomnia and excessive daytime sleepiness Dx: sleep hx and sleep diary Advanced sleep phase disorder: inability to stay awake in the evening (usually after 7pm) making social functioning difficult; c/o early morning insomnia d/t early bedtime Head and neck Meniere’s disease o
