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Neuro Block

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
Created by: duanea00