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Neuro Block
| Question | Answer |
|---|---|
| Head trauma, disoriented => lucid => coma | Epidural Hematoma |
| Lens shaped hemorrhage | Epidural Hematoma |
| Concave shped hemorrhage | Subdural Hematoma |
| Unilateral facial weakness w/ inability to close eye | Bell palsy (self-limiting) |
| Adolescent female w/ HA. +FHx. Severe HA, N/V, photphobia. +/- auras (usu contra to HA) | Migraine HA |
| Male, recurrent relapsing HA. Worsened w/ EtOH, Lacrimation, salivation, rhinorrhea | Cluster HA |
| Sudden onset thunderclap HA, "worse HA of my life" | Subarachnoid hemorrhage |
| >50 yo female w/ HA. Temporal artery tenderness or blindness | Temporal arteritis (Giant cell arteritis). Elevated ESR, get temporal artery biopsy |
| Recurrent episodes of vision change, diplopia, weakness & tingling in extremities that resolve | MS |
| HA worse in AM w/ focal neuro deficits | Brain Tumor (MC is glioma) |
| s/p Fall w/ bilateral LE weakness, urinary and rectal incontinence, decreased rectal tone | Cauda equine syndrome = neurosurgical consult |
| Ascending paralysis | GBS |
| Paralysis after Campylobacter enteritis | GBS |
| Young kid with difficulty standing from seated position. Calf muscle wasting | Muscular dystrophy (weakness begins at pelvic girdle) |
| Pediatric with fever or Hx URI with encephalopathy, emesis, hyperactive reflexes, hepatomegaly, elevated liver enzymes | Reye's syndrome from URI/post-flu or aspirin use |
| "Ash leaf" hypopigmentation of trunk & Ext, shagreen patch, sebaceous adenomas, seizures, mental retardation; assoc w/ PCK, renal hemartomas | Tuberous sclerosis (auto dominant) |
| Ortho BP defn | drop of 20 (SBP) or 10 (DBP) within 3 min of standing |
| fluctuating weakness/fatigability of voluntary mx (diplopia, blurry vision, ptosis, difficulty swallowing); resp difficulty, limb weakness (worsened w/activity); bulbar sxs (dysarthria, dysphagia, fatigable chewing) | Myasthenia gravis |
| Light touch: Side of Neck: | C2-3 |
| Light touch: Tip of Shoulder: | C4 |
| Light touch: Lateral Deltoid: | C5 |
| Light touch: Thumb: | C6 |
| Light touch: Middle Finger: | C7 |
| Light touch: Pinky Finger: | C8 |
| Light touch: Medial Forearm at elbow: | T1 |
| Light touch: 1st Dorsal web: | Radial nerve |
| Light touch: Palmar middle pad: | Median |
| Light touch: Palmar small pad: | Ulna |
| Light touch: Groin: | L1 |
| Light touch: Upper thigh: | L2 |
| Light touch: Outer thigh at knee: | L3 |
| Light touch: Medial ankle: | L4 |
| Light touch: Dorsal 1st web space: | L5 |
| Light touch: Lateral ankle: | S1 |
| Light touch: Buttock: | L2-3 |
| Light touch: Perianal: | L4 |
| DTR: Biceps: | C5 |
| DTR: Brachioradialis: | C6 |
| DTR: Triceps: | C7 |
| DTR: Knee: | L 3,4 |
| DTR: Ankle: | S1 |
| DTR: 0: | absent |
| DTR: 1: | diminished |
| DTR: 2: | average |
| DTR: 3: | exaggerated |
| DTR: 4: | clonus |
| Ischemic stroke pathophys | atheroembolic (50%); cardioembolic (30%); OR 2/3 thrombotic & 1/3 embolic |
| Stroke pathophys | 80% ischemic, 20% hemorrhagic |
| Hemorrhagic stroke pathophys | parenchymal ICH (10-15%); subarachnoid (5-10%) |
| Most common parenchymal ICH: | Hpertensive intracerebral hemorrhage |
| Primary ICH presentation | HA, N/V; progressive hemiparesis & hemisensory def; HTN (on hx and on PE) |
| Primary hypertensive ICH: typical locations | Thalamus; Basal Ganglia; Pons; Cerebellum |
| ICH presentation: Thalamus/ Basal Ganglia | Contralateral Motor/ Sensory Deficit; Aphasia, Neglect; Depressed LOC with mass effect, IVC extension |
| ICH presentation: Cerebellum | Ipsilateral Ataxia; Depressed LOC |
| ICH presentation: Pons | Vertigo, Diplopia; Crossed signs; Depressed LOC |
| Anterior circulation consists of: | Ant choroidal, ant cerebral, MCA |
| Anterior circulation supplies: | Cortex, subcortical white matter, basal ganglia, internal capsule |
| Anterior circulation stroke | Hemispheric s/s: aphasia, apraxia, hemiparesis, hemisensory loss, visual field defects |
| Posterior circulation consists of: | Verterbral & basilar arteries |
| Posterior circulation supplies: | Brain stem, cerebellum, thalamus, parts of temporal & occipital lobes |
| Posterior circulation stroke | Sxs of brainstem dysfn: coma, drop attacks, vertigo, N/V, ataxia |
| Thrombotic vs embolic stroke sx progression | Thrombotic: stepwise progression, often preceded by TIA; Embolic: abrupt & without warning |
| Amyloid angiopathy stroke: patho | Blood vessel degeneration; Dementia; Lobar hemorrhage |
| Amyloid angiopathy: presentation | Dementia; Episodic worsening; No h/ o HTN; poss acute limb weakness; BP less severe than in ICH; stroke d/t cerebral microhemorrhages |
| Venous infarction presentation | h/o OCP/SMK; HA; aphasia, weakness |
| Most common cause of subarachnoid bleed | aneurysm |
| Subarachnoid bleed: RF | HTN; SMK; heavy EtOH; genetics (polycystic kidney dz; Ehlers-Danlos; 1st-degree relative) |
| SAH stroke presentation | Abrupt severe HA; meningismus; depressed LOC; nonfocal neuro exam; BP rises precipitously; poss temp to 39C |
| Atheroembolic stroke characterized by: | Single vascular territory; Warning signs; Stepwise progression |
| Atheroembolic stroke presentation | Hx HTN, CAD; transient language disturbance; transient weakness |
| Ant cerebral art infarct: likely fx: | contralateral leg (motor > sensory) |
| MCA infarct: likely fx: | face/arm more than leg/vision; poss aphasia |
| Vertebrobasilar art infarct: fx: | Midbrain: 3d nerve nuclei; ipsilateral ptosis; eye deviated outward (bc CN VI is fine, but III is affected); crossed signs: pt has CNIII probs on one side and sensory probs on opp side of body |
| Subcortical infarct effects by body area: | face = arms = legs |
| Cortical infarct fx by body area: | gradation btw face, arms, & legs |
| Lacunar syndromes | Pure Motor Stroke; Pure Sensory Stroke; Ataxic Hemiparesis; Clumsy Hand Dysarthria |
| Cardioembolic stroke presentation | h/o A fib; aphasia; hemiparesis/hemisensory deficit affecting face and arm |
| Cardioembolic: dx | Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface) |
| Cardioembolic: possible etiology | A fib; Cardiomyopathy; Acute MI; Valvular heart dz |
| TIA S/S | Acute focal neuro def; S/S resolve within 24 hr; No rad evidence of infarction; Ischemic etiology, usu carotid or vertebral vascular distn |
| TIA: risk of subsequent stroke: | 11% risk of stroke within 3 mo; 1/3 of TIAs have stroke within 5 yrs; 63% of strokes occur within the first wk, 85% within first month |
| Modifiable RF for first stroke | *HTN*; A fib; carotid stenosis; DM; hyperlipidemia; prior stroke/TIA |
| Prevention of A fib RF: | Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin |
| Stroke prevention DM pts | glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins |
| TIA carotid: S/S | contralat hand-arm weak & sensory def; ipsilateral visual sx & aphasia or amaurosis fugax; poss carotid bruit (absent in high grade stenosis) |
| TIA vertebrobasilar S/S | diplopia, ataxia, vertigo, dysarthria, CN palsies, LE weak, blurred vision, perioral numbness, poss drop attacks |
| TIA DDx | Sz, migraine, syncope, hypoglycemia, mass lesion |
| SAH etio: aneurysm | nontraumatic: 75% saccular (berry) aneurysm, 50% mort; 5th-6th decade, M=F |
| aneurysm RFs | SMK, HTN, high chol; PKD, coarct |
| complex partial sz | may have aura, then impaired consciousness |
| simple partial sz has no: | impairment of consciousness |
| Most common cause of tonic-clonic in pts (onset < 30 yo): | idiopathic epilepsy |
| Clonic seizures: | usu in childhood; impaired consciousness, followed by asymmetric bilateral jerking |
| Most common seizure type: | complex partial |
| complex partial sz: | 10-30 yo; common post-head trauma; 50% abnml CT/MRI; 50% mesial temporal sclerosis; 20% hamartoma |
| complex partial sz: etio by age | 30-60 yo: poss brain tumor; >60 yo: more likely stroke |
| Status epilepticus dx does not apply to: | continuous simple partial seizures |
| EtOH withdrawal seizure: | onset 6-48 hr after last drink; often primary generalized, often have Todd paralysis |
| Sz remission: | usu within 3 yrs of first seizure; prolonged remission in 60% of such pts |
| Factors against sz remission | FH; psych comorbid; febrile seizure hx; more seizures; age |
| Todd paralysis = | post-ictal focal weakness in part of body, confined to L or R, usu arms/legs |
| Most common agent of meningitis in adults | S. pneumo |
| Meningitis general S/S | HA, fever, neck / back stiffness, neuro impairment |
| Meningitis presentation | acute (hrs - days), usu w/ fever, HA, stiff neck, lethargy; usu without focal sx |
| Typical purulent meningitis orgs | N. meningitidis, S. pneumoniae, or H. influenzae |
| Chronic meningitis: orgs | TB; fungal |
| Encephalitis presentation | diffuse infxn; confusion, lethargy, often seizures; CSF may be normal |
| N. meningitidis | petechial rash; GN diplococci; often assoc w/DIC |
| H flu meningitis: commonly found: | less common in adults; in setting of otitis or sinusitis |
| Tuberculous meningitis S/S | usu gradual onset; listlessness & irritability; CN palsies; |
| Abscess: common orgs | streptococcus, staphylococcus or anaerobes |
| Herpes encephalitis: commonly found: | more common in elderly; often medial temporal lobes |
| CJD S/S | usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG |
| MS S/S | Optic neuritis; Transverse myelitis; Paresthesias; focal neuralgia; Ataxia; Weakness/ incoordination; Spasticity; Cognitive impairment |
| Lhermitte's sign = | electrical sensation down body w/ neck flexion; seen in MS |
| MS pathophys | immuno d/o assoc w/CNS Ig prodn & T-lymph alteration; poss viral etio |
| MS pattern of sxs | affect multiple areas over time (if they don't, prob not MS) |
| Anti Epileptic Drugs: titration | Start low & gradually increase; initiate with 1/3-1/4 of anticipated maintenance dose & increase over 3-4 weeks |
| when Anti Epileptic Drugs may be dc'd: | If onset btw age 2-35 & normal EEG; seizure-free period 2-4 yrs; complete ctrl within 1 yr; very gradual taper over 6 mos; relapse usu within first few mos after withdrawal; f/u in 5 yrs if no probs |
| Lucid interval seen in what trauma? | epidural hematoma |
| subdural hematoma: blood source | usu venous (bridging veins in space) |
| subdural hematoma: etiology | Acceleration/ Deceleration injury; Veins transversing subdural space |
| 2/3 of all cerebral infarcts are: | MCA stroke |
| Lacunar stroke | 15-20% of strokes; small vessel ischemia; HTN; usually pure sensory OR motor |
| Argyll Robertson pupil = | pupil reacts to light but does not accommodate (seen in tertiary syphilia/tabes dorsalis) |
| NPH (chronic hydrocephalus) S/S: | Incontinence, gait abnormalities, dementia |
| Ulnar neuropathy | stretch / compress ulnar n.; cubital tunnel or Guyon canal; d/t pressure, bone spurs, cysts; sensory precede motor sx |
| Ulnar neuropathy: provoking factors | Elbow Flexion (Cubital), Wrist Extension (Guyon); Nighttime |
| Radial neuropathy: etiology | axilla (crutches); Saturday night palsy; handcuffs; humerus fx |
| Radial neuropathy: S/S | Motor>sensory; weakness in extension & arm ext rotation; forearm atrophy; xray shoulder/humerus |
| Meralgia paresthetica: S/S | pain, paresthesia, numb; outer thigh; usu unilateral (relieved by sitting); no motor sx |
| Fem neuropathy: RF | lithotomy posn (inguinal lig); DM; retroperitoneal neoplasm/hematoma; pelvic fx; fem art cath (n. trauma) |
| Fem neuropathy: S/S | Quads atrophy/weakness; sensory impairment anteromedian thigh; decreased patellar DTR; EMG/NCS; CT/MRI |
| Sciatic n. palsy: S/S | weakness w/ leg flexion, dorsiflexion & foot eversion (drop foot); hamstring & ankle DTR dec/absent; sensory loss posterior thigh/leg/foot; tingling/burning/lanceting pain (worse w/standing, cough) |
| Peroneal n. palsy: S/S | weak dorsiflexion (foot drop) & eversion; sensory loss/ paresthesia: anterolateral calf & foot dorsum |
| CN VII palsy (Bell): etiology | idio; HIV, sarcoid, Lyme, tumor; HSV infxn? RF = PG, DM |
| CN VII palsy: S/S | abrupt; facial paralysis (some upper sparing); drooping corner of mouth; ptosis/ forehead smooths out; ear pain; dysgeusia; hyperacusis |
| CN VII palsy: to distinguish btw peripheral & central lesion: | peripheral: complete paralysis forehead mx; central: partial sparing forehead mx |
| CN VII palsy: prognosis | 60% spont resolve; 10% perm disfigurement/dysfn; best indicator of severity = progress first 2-3 days; worst: complete palsy at onset, advanced age, hyperacusis, severe initial pain |
| Systemic-metabolic neuropathies include: | DM; uremia; alcoholic & nutrition def; paraproteinemias; CTD, amyloidosis |
| DM neuropathy | sensory precedes motor; lower ext precedes upper; Hx: autonomic sx?; NCS nml / mildly slow |
| Uremia: S/S | Symmetric sensory-motor; lower ext > upper; distal > proximal; severity correlates with degree of renal insufficiency |
| Neuropathy: EtOH/ Nutritional deficiency | cobalamin (B12) def; axonal > myelin; slow progression |
| EtOH/Nutritional deficiency: S/S | Distal symmetric Polyneuropathy; sensory precedes motor; Lower ext precedes upper; cramps, painful paresthesias, tenderness; CNS Sx often precede PNS; mental status change; myelopathy; optic neuropathy |
| AIDP (Guillain-BS): patho | Progressive Demyelinating; prob immune-mediated; Axonal Subtypes (AMAN; AMSAN) |
| AIDP (Guillain-BS): Motor S/S | Ascending weakness; Symmetric; Proximal > Distal mx; Lower ext before Upper; Advanced: Resp mx Compromise, CN Involvement |
| AIDP (Guillain-BS): Sensory S/S | Pain/paresthesias; Loss of Sensation; Distal before Proximal; DTR: Global hyporeflexia or areflexia; autonomic dysfn: tachycardia, cardiac irreg; BP changes, pulmonary dysfn, loss of rectal tone |
| MyaGrav pathophys | Abs vs acetylcholine receptors |
| LEMS pathophys: | defective release of Ach in response to nerve impulse; may be assoc with small cell ca |
| MG vs LEMS: S/S | LEMS: power increases w/sustained contraction; MG: fatigability |
| Ataxic (intention) tremor | Absent at rest/start of movement; dysmetria; Dz of cerebellum / connections (MS; tumors; infarct; ethanol-induced cerebellar degeneration) |
| Athetosis = | slow writhing purposeless movements usu involving hands, tongue & face; usu in kids w/ cerebral palsy or result of kernicterus or hypoxia |
| Chorea: Sx | Involuntary, irregular jerky movements; can cause continuous movements. |
| Chorea: may be due to: | untreated strep infxn (Sydenham chorea), PG (chorea gravidarum) or Huntington dz |
| Tics | onset 2-13 yo; tx Haldol/pimozide |
| Hemiballismus | Violent flinging movements; Unilateral hemiballismus usu d/t infarct in contralateral subthalamic nucleus of Luys |
| Dystonia: | Maintenance of a persistent extreme posture in one or more joints. |
| Focal dystonias: | torticollis, writer's cramp, blepharospasm; tx Botox / surg |
| Parkinson dz: Sx | Rest tremor/3-6 hz; pill rolling; cogwheeling; rigidity; bradykinesia; difficulty initiating movement; masked facies; stooped posture, shuffling; disturbance of postural reflexes; diminished eye blinking rate |
| Parkinson dz: Patho | Degen nigrostriatal pathway, raphe nuclei, locus ceruleus & motor nucleus of vagus; dramatic loss of DA-containing neurons |
| Huntington Dz presentation | AD, varying age of onset; Sx often begin w/ psych disorder (immaturity, impulsivity, depression); later apathy & dementia; Chorea, Athetosis; butterfly ventricles (caudate atrophy) |
| Huntington chorea due to: | DA excess state |
| Tardive dyskinesia: Sx | Abnormal BLM (tongue thrusting & chewing); head movements (turning & bobbing); poss also abnormal limb movements; Sx can fluctuate & may take mos-yrs to resolve (sometimes permanent) |
| Tardive dyskinesia: most successful tx: | achieved with DA-depleting agents (tetrabenazine); also Vitamin E? |
| Action of acetylcholine & DA: | Act in opposite directions; adding DA is equivalent to blocking acetylcholine |
| Huntington dz genetics | Huntingtin gene is on short arm of chromosome 4; >35 CAG trinucleotide repeats = penetrance/affected/dz |
| Restless leg Syndrome can be primary, or secondary to: | periph neuropathy, uremia, PG, Fe def |
| Migraine dx criteria | ≥2 of: (Unilateral; Pulsating; Mod/ severe intensity; fx: avoidance of routine physical activity); 1 of: (N/V; Photophobia & phonophobia) |
| Severe episodic HA with cerebellar sx = | basilar migraine |
| Chronic migraine: dx | chronic daily HA ≥3 months; >8 d/mo x 3 mos |
| Sinus HA vs migraine | sinus usu continuous (not intermittent); TTP over sinuses; tx w/ Abx |
| chronic daily HA | ≥ 15 d/mo; primary or secondary (usu considered primary); ≥1 migraine/wk = RF for dev chronic daily HA |
| SUNCT = | Short-lasting; Unilateral; Neuralgiform HA, with Conjunctival injection & Tearing; rare; M>F (>50 yo) |
| SUNCT sx | burning, stabbing, throbbing; seconds to 4 min; 5-6 per hr; SBP may rise |
| Cluster HA = | M>F (older than migraine); severe, unilateral, nasal congestion, injected conjunctiva, ipsilateral sweating; at night (wakes pt) |
| HA red flags (SNOOP) | Systemic sx; secondary RF; neuro sx; onset sudden; older pt; Progression/prior HA hx; Pattern changes |
| Sumatriptan: indications | migraine (abortive tx); acute tx cluster HA; Fast onset, short duration; repeat dose in 1 hr if nec; Never give IV or IM |
| Migraine: prophylaxis | Beta (50-60% efficacy); TCA; SSRIs; bupropion; Valpro; verapamil; NSAIDs (ST for predictable) |
| Menstrual migraine: Tx | NSAIDs: begin 2-7 days prior to menses, continue through last day of flow; Hormonal therapy (OCP) |
| concomitant dysphasia, hemianopia, or focal epilepsy is a __ lesion | supratentorial |
| Subarachnoid hemorrhage may block __ causing hydrocephalus | arachnoid villi |
| T or F: diplopia, syncope, dizziness, vertigo, and paresthesia are symptoms of carotid disease | false |
| Cause of Amurosis Fugax | embolization of retinal arteries |
| a tumor in the supratentorial region may result in which pathologic disorder | epilepsy |
| Acute subdural hematoma: timeframe | Acute: 0-1 week |
| Chronic subdural hematoma: timeframe | >2 weeks |
| Most common cause of SAH | Trauma |
| Loss of consciousness requires: | Both cerebral hemispheres damaged OR brainstem lesion |
| Hollenhorst plaque | cholesterol emboli from carotid |
| Decorticate posturing: | hemispheric or diencephalic dysfn d/t destructive lesions or metabolic abnormality; hands come up (response to stimuli) but do not localize |
| Decerebrate posturing: | midbrain or upper pons dysfunction on a structural or metabolic basis; wrists flex (response to stimuli), not localizing |
| Most common reason for noting unreactive pupils: | an inadequate light source |
| Reactive pupils = | midbrain is intact |
| Intact pupillary responses in unresponsive pt w/ absent EOM & corneal responses: | metabolic (e.g., hypoglycemia) or drug ingestion (e.g., barbiturate) |
| Midposition (3-5mm) nonreactive pupils = | midbrain damage |
| Blown pupil = | unilaterally dilated, nonreactive pupil: sx of CN III (oculomotor nerve) compression (Aneurysm, Mass Lesion); dilated nonreactive pupil may also be 2/2 DM or drugs (atropine, scopolamine) |
| Small, reactive pupils: seen in: | pontine damage (infarct or hemorrhage) or with some drug use (opiates, pilocarpine). |
| Corneal sensation: | carried by CN V (Trigeminal); test with cotton swab pressed gently onto cornea; abnormal reponse suggests a pontine lesion |
| ALS: Dx criteria | UMN & LMN sx in 3 regions; UMN: clinical; LMN: EMG; CK nml or high |
| Primary lateral sclerosis: path | degeneration of lateral corticospinal tract |
| Primary lateral sclerosis clin findings | usu legs before arms; leg weak/stiff; spasticity; ave duration >8 yrs; many pts develop LMN sx & transition to ALS |
| progressive muscular atrophy | pure LMN dz; slower progress than ALS; often spares bulbar mx; CK very high |
| MyaGrav: pathophys | Acquired autoimmune: Ach receptor insufficiency |
| MyaGrav S/S | fluctuating mx weakness (worse w/reps); asymmetric ptosis; tired face, difficulty chewing/swallowing; SOB |
| Duchenne MD | onset at 3-5 yrs; calf pseudohypertrophy; loss of ambulation by teens; cardiomyopathy; death in 20s |
| Most common MD's | Duchenne/Becker; myotonic; Facioscapulohumeral dystrophy |
| Autosomal dominant disorders | Huntington, NF1/NF2, spinocerebellar ataxias, familial Alz, CMT |
| NF1: manifestations: | hydrocephalus, seizures, learning disabilities, short, lack of GH, precocious puberty, renal artery stenosis |
| X-linked recessive pattern | F-toM trans; M=affected, F=carrier |
| X-linked rec dz | Duchenne/Becker MD; Kennedy; adrenoleukodystrophy; Menkes (kinky hair); Lesch-Nyhan; Fragile X |
| X-linked dom dz | F-to-F transmission (lethal to males); Rett; Aicardi; Lissencephaly 2 |
| Mitochondrial dz | multi generations; trans by F only; 1:1 M:F affected; MERRF, MELAS, LHAN, Kearns-Sayre |
| Parkinson dz S/S | usu unilateral onset; resting tremor, slow, cogwheel rigidity, festinating gait, masked facies, postural instability |
| Parkinson: TRAP = | Tremor, Rigidity, Akinesia, Postural instability |
| Most common genetic form of Parkinson: | PARK8 |
| Central cord syndrome S/S | motor deficit in UE > LE; Varying degrees of sensory loss (pain/temp); most common of the incomplete spinal cord lesions (better prognosis) |
| Ligamentum flavum buckles into spinal cord => contusion to central regions of spinal cord = | Central cord syndrome |
| Anterior cord syndrome S/S | Paraplegia and dissociated sensory loss with loss of pain and temperature sensation; 2/2 infarction of the cord in the region supplied by the anterior spinal artery |
| Anterior cord syndrome: what fn is preserved: | Posterior column (position, vibration, deep pressure) preserved |
| Brown-Sequard syndrome: cause | Hemisection of the cord; From penetrating injuries; Rare |
| Brown-Sequard syndrome S/S | Ipsilateral motor loss w/loss of vibration, pressure, proprioception; contralateral loss of pinprick, pain, temperature sensations |
| Progressive demyelinating; brain, sp cord, optic n.; viral; F>M, peak 20-40yo | MS |
| Bell palsy sx | Abrupt onset upper & lower (ipsilateral) facial paresis/ paralysis, mastoid pain, hyperacusis, dry eyes, altered taste; ipsilat ear pain may precede |
| LP w/ decreased glucose, increased protein | Bacterial meningitis |
| LP w/ decreased protein, very few neutrophils | syphilitic meningitis |
| 3 mHz spike-and-wave on EEG | Absence (petit-mal) seizures |
| Emergent eval of stroke | CBC/plt; PT/ PTT; Lytes, glu, renal; ECG/ markers of cardiac ischemia; Brain CT or MRI |
| Atheroembolic stroke dx studies | Normal head CT; Doppler US: high grade stenosis (e.g., L ICA) |
| Atheroembolic stroke: dx studies | Neuroimaging; Carotid US; MRA; CTA; Catheter angiography |
| Cardioembolic stroke imaging | Carotid US normal (no brain lg vessel prob) |
| Cardioembolic stroke: dx studies | pulse; EKG; 24-48 hr EKG; TTE (microcavitation); TEE |
| Asymptomatic carotid stenosis: dx studies | Carotid bruit; Doppler US; MRA, CTA |
| best modality to distinguish ischemic from hemorrhagic stroke: | CT |
| TIA definitive study: | arteriography; MRA more common (less invasive) |
| TIA dx studies | CT or MRI to r/o cerebral hemo; cardiac w/u; cbc, esr, coags, antiphospholipids; Poss echo, ecg, carotid doppler |
| SAH dx studies | CT (90%); CSF: hi opening P & bloody fluid; cerebral angiography, EEG |
| EEG: focal rhythmic discharge at onset, poss no ictal activity seen: | simple partial seizure |
| EEG: interictal spikes assoc w/slow waves in temporal/frontotemp | complex partial seizure |
| Seizure: labs | Glucose; lytes; AED levels; LP if poss meningitis; EtOH/tox if susp; ABG if susp hypoxia; poss CXR, CT, MRI |
| MS: MRI findings | multiple characteristic white matter lesions or plaques: periventricular or subcortical U-fibers, corpus callosum lesions |
| MS: CSF findings | oligoclonal bands, increased IgG index, myelin prodn/fragments |
| MS: types of dx criteria | Schumacher; Poser: Macdonald |
| When do LP? | suspect meningitis; not if suspect abscess |
| Glucose depressed: usually: | bac mening, or TB or fungal |
| Increased WBC in CSF indicates: | inflammation (not necessarily infection) |
| Tuberculous meningitis dx studies | active TB elsewhere in body; CSF inc WBC (100-150), mostly lymphs; abnormal CXR; acid-fast normal |
| Ring enhancing lesion is usually: | abscess or tumor |
| Brain tumor: eval & dx | H&P; CT +/- MRI; EEG; LP; PET |
| MRI: T1/T2 | T1: fat bright (water dark); T2: water bright |
| Trauma/Bleeds: imaging of choice | noncontrast CT |
| epidural hematoma: appearance on CT | lenticular (biconvex) |
| subdural hematoma: appearance on CT | Cross suture lines and extends over larger area; Crescent shaped |
| SAH: appearance on CT | Linear, within cisterns and sulci; bleed follows outlines of the gyri |
| Spinal cord lesion types: | Demyelination; Cysts; Infarction; Tumor |
| Edema on MRI | T1: dark; T2: bright |
| Purpose of CT in CVA | Not dx; only to r/o other conditions that would CI some tx (tumor, bleed) |
| CVA on CT | Hyperdense artery sign; loss of grey; CT normal up to 12 hours post; insula ribbon sign: blurring of gray-white junction |
| Brain neoplasm: imaging of choice | MRI |
| Ulnar neuropathy: Dx | Hx; EMG/NCS can help find site of lesion |
| Sciatic n. palsy: Dx tests | EMG/NCS (distinguish from peroneal neuropathy); xray |
| Guillain-Barre dx studies | NCS: slow S/M nerve conduction velocities; poss denervation/axonal loss; CSF high pro |
| MyaGrav dx studies | NCS: decrementing mx response; CXR to r/o thymoma; serum acetylcholine Ab |
| Huntington dz on CT | atrophy of cerebrum & caudate nucleus |
| Huntington dz on MRI/PET | decreased glucose metab |
| Neuroimaging not needed when: | No focal neuro findings; Pt has stable pattern of recurrent HA; No h/o seizures |
| HA: Consider neuroimaging when: | Neuro exam abnormal; progressively worsening HA; new persistent HA; new, rapid onset HA (thunderclap headache); HA does not respond to standard tx |
| Use LP only after: | normal CT obtained & platelet count is normal |
| LP should be performed if: | Neuroimaging is normal or suggests dz that must be dx by measuring cerebrospinal fluid (CSF) pressure, cell count, and chem |
| Diagnostic LP: indications | CNS infxn (meningitis, encephalitis); HA (SAH); Pseudotumor cerebri (idiopathic ICH); MS; Support dx of NPH & predict response to surgical shunting |
| LP: CI | Suspected brain / epidural abscess; elevated ICP, esp if papilledema; suspect mass lesion; Ventricular obstn; |
| LP: insert needle into: | L3-L4 space (elderly: may need to do cisternal procedure) |
| Routine CSF analysis includes: | Opening pressure; Appearance/color; Consistency; Tendency to clot; Diff cell count; Protein; Glucose |
| CSF cloudy = | Inc WBC or protein |
| CSF: Xanthochromia (yellow tinge) = | hyperbilirubinemia, hypercarotenemia, melanoma |
| CSF: Red tinge = | Blood from bleeding into SA space or traumatic tap |
| CSF: Cells | Normal 0-5 small lymphs/ml; PMNs, lg monos & RBCs are never normal |
| CSF: RBCs & WBCs: | only present via ruptured blood vessels or by meningeal response to inflammation or irritation |
| WBC in CSF | Inc WBCs = inflam (>100, prob infxn); PMNs: bac infxn; Lymphs = viral or other (TB, fungal, ca); Eosinophils: shunt, parasitic infection & allergic rxn |
| CSF pressure | Normal 60-200 mm H2O (mean = 120); usu drops 5-10 mm for each ml CSF removed |
| CSF pressure: Marked elevation: | poss purulent meningitis or intracranial tumors |
| CSF pressure: Moderate elevation: | mild inflammation, encephalitis, neurosyphilis |
| CSF pressure: Elevated pressure with normal CSF: | confirms pseudotumor cerebri (benign ICH): one instance where LP is done despite presence of papilledema |
| CSF protein: increased in: | inc permeability of blood-CSF barrier (tumor, trauma, inflam), or increased intrathecal synthesis of Igs |
| CSF protein: decreased in: | CSF protein leak, hyperthyroidism, water intoxication |
| CSF glucose | Normal CSF glu 60-70% of plasma glu; Low levels assoc w/ bacterial or TB infection |
| CSF lactate: | usu parallels blood levels; if markedly different from blood level = biochem abnormality in CSF |
| Increased CSF lactate associated with: | CVA, IC bleed, bacterial meningitis; Not altered in viral meningitis; lactate may differentiate btw viral & bacterial |
| Organism conc required for detection on CSF smear: | 10,000/ /ml (Gram & AFB stains may be neg despite org presence in CSF; cx on several media; consider empiric tx) |
| CSF antigen serology: | More rapid, but less specific, than cx; cryptococcal Ag test very specific/accurate |
| Myasthenia gravis Dx studies | Tensilon test; Ach receptor & MuSK Abs; Repetitive nerve stim; Single fiber EMG; CT Chest to exclude thymoma |
| MD: labs/studies | ultrastructural protein abnormalities; mx bx: mx fiber necrosis |
| Duchenne/Becker: Dx studies | Mx bx; genetic testing (need complete sequencing); CK sometimes >10,000; FH |
| Duchenne/Becker Dx | genetic testing, elevated CK, EMG |
| Alz dx | dx of exclusion (neuropsych eval); MRI/CT: hippocampal atrophy; amyloid on PET (Pittsburgh B); LP: inc tau, dec amyloid-beta 42 |
| Pathological hallmark of Parkinson: | Lewy body (alpha-synuclein is main component) |
| Pseudoseizure | Clinically resembles seizure; does not have EEG evidence of seizure, or respond to epilepsy meds |
| NCS (nerve conduction) | uses electrodes; record response to shock (amp & timing) |
| EMG | uses needle; electrical activity observed during rest & activitation |
| NCS / EMG utility: | suspicion of peripheral nerve or mx injury; detect CTS; investigate polyneuropathy /poss etiology or radiculopathy |
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