Neuro review 3
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| ALS: Dx | UMN & LMN sx in 3 regions; UMN: clinical; LMN: EMG; CK nml or high
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| ALS Tx | Riluzole; cough assist device, chest PT, BiPAP; PEG feeding tube;
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| PLS: path | degeneration of lateral corticospinal tract
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| PLS clin findings | usu legs before arms; leg weak/stiff; spasticity; ave duration >8 yrs; many pts develop LMN sx & transition to ALS
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| PLS: dx | EMG, MRI (br & spcord), LP, evoked potls; B12, Lyme, RPR, long chain fatty acids
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| PMA | pure LMN dz; slower progress than ALS; often spares bulbar mx; CK very high
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| Kennedy dz | X-linked rec, TNR; mutation in androgen receptor; sx onset (wide age range); facial fasciculations, weakness mouth/tongue; dysphagia, limb weakness; gynecomastia, DM, oligospermia
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| Disorders of neuromx transmission (NMJ): | MG, LEMS, botulism
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| MG: path | Acquired autoimmune: Ach receptor insufficiency
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| MG S/S | fluctuating mx weakness (worse w/reps); asymmetric ptosis; tired face, difficulty chewing/swallowing; SOB
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| MG Dx | Tensilon test; Ach receptor & MuSK Abs; Repetitive nerve stim; Single fiber EMG; CT Chest to exclude thymoma
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| MG Tx | Symptomatic (Cholinesterase inhibitors); Firstline: steroids (alt immunosupp: CellCept, Cyclosporine); thymectomy
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| MG exacerbations | d/t infxn, PG, meds; may worsen resp sx; tx w/ plasmapheresis or IVIg, supportive respiratory care
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| MG: drugs to avoid | NM blockers; quinine; macrolides, FQ; botox; beta/CCB; IV contrast
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| LEMS | usu paraneoplastic (autoimm rare); proximal weakness / autonomic sx (dry mouth); hypo/absent reflexes; voltage gated Ca channel Abs; facilitation w/ RNS
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| Botulism MOA | irreversible blockade of Ach release
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| Botulism S/S | Diplopia, ptosis, dilated pupils; facial / resp weakness; descending paralysis; Autonomic dysfunction
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| Botulism Tx | supportive; horse serum antitoxin? (months to recover)
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| MD classified by: | distribution, inheritance and clinical features
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| MD: labs/studies | ultrastructural protein abnormalities; mx bx: mx fiber necrosis
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| Duchenne | onset at 3-5 yrs; calf pseudohypertrophy; loss of ambulation by teens; cardiomyopathy; death in 20s
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| Duchenne/Becker: Dx | Mx bx; genetic testing (need complete sequencing); CK sometimes >10,000; FH
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| Duchenne/Becker Tx | Prednisone (age 5) for Duchenne; Supportive (orthotics, resp, cardiac, PT/OT); cardiac TP in Becker
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| FSHD | auto dominant; asymmetric; eye or mouth closure weakness: may sleep w/ eyes open; pectoral & biceps/triceps atrophy (but normal deltoid); also scap winging; no fx on life exp; orthotics & counseling
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| FSHD Dx | genetic testing (95%); FH; mx bx rarely helpful
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| Emery Dreifuss | Humeroperoneal / scapuloperoneal weakness w/ early contractures (ankle neck elbow); teen onset (very thin); scap winging/deltoid sparing; x linked or auto dom; cardiac conduction block/arrhythmia (need pacemaker)
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| Most common MD's | Duchenne/Becker; myotonic; FSHD
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| Myotonic dystrophy | auto dom; any age; TNR
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| Myotonic dystrophy S/S | tenting upper lip; distal weakness; frontal bald; cataracts; conduction block; DM, infertile; cognitive impairment; percussion myotonia
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| Allelic vs non-allelic heterogeneity | allelic: 1 gene causes >1 condition; non-allelic: clinical syndrome is d/t >1 gene
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| Autosomal dominant | 1:1 M:F; multi generations; M-to-M transmission seen; variable expression (important); late-onset neurodegenerative dz's
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| Autosomal dominant disorders | Huntington, NF1/NF2, spinocerebellar ataxias, familial Alz, CMT
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| NF1: other manifestations: | hydrocephalus, seizures, learning disabilities, short, lack of GH, precocious puberty, Renal Artery stenosis
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| Auto recessive | >1 affected each generation; M:F 1:1; consanguinity; carriers usu asx; inborn errors of metabolism
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| Auto recessive disorders | PKU, Tay-Sachs, MSUD, Friedreich's, Wilson, homocystinuria, sickle cell
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| Wilson Dz | hepatolenticular degen (impaired ceruloplasmin synth); presents in teen years (hepatitis)
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| Wilson S/S | tremor, dysarthria, slow, hoarse, chorea, psych
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| Wilson: dx | high ceruloplasmin & copper; low copper on liver bx; Kayser Fleischer rings
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| Wilson: tx | reduce copper intake; chelate; transplant /
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| X-linked recessive | F-toM trans; M=affected, F=carrier;
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| X-linked rec dz | Duchenne/Becker MD; Kennedy; adrenoleukodystrophy; Menkes (kinky hair); Lesch-Nyhan; Fragile X
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| Duchenne/Becker Dx/Tx | genetic testing, elevated CK, EMG; Tx: supportive, corticosteroids, PT, ortho, cardiopulmonology
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| X-linked dom | F-to-F transmission (lethal to males); Rett; Aicardi; Lissencephaly 2
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| Rett dz | 6-18 mos; live to 40s; autism; cardiac & scoliosis
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| Mitochondrial dz | multi generations; trans by F only; 1:1 M:F affected; MERRF, MELAS, LHAN, Kearns-Sayre
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| MELAS | d/t pt mutation of transfer DNA from leucine; <40 yo; lactic acidosis; HA, stroke, seizure, short; progressive dementia; Dx high serum pyruvate & lactate, stroke lesions; no tx
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| TNR: mode of inheritance | can be multiple modes of inheritance
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| TNR dz | Huntington, Fragile X, myotonic dys; Kennedy; spinocerebellar ataxia; Friedreich
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| Alz dx/tx: | dx of exclusion (neuropsych eval); MRI/CT: hippocampal atrophy; amyloid on PET (Pittsburgh B); LP: inc tau, dec amyloid-beta 42; tx: cholinesterase inhib
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| Alz: APOE gene | E2: protective vs Alz; E4: inc risk of dev Alz
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| Alz dz: main reason for genetic counseling is: | info only
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| Parkinson dz | usu unilateral onset; resting tremor, slow, cogwheel rigidity, festinating gait, masked facies, postural instability
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| Parkinson: TRAP = | Tremor, Rigidity, Akinesia, Postural instability
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| Pathological hallmark of Parkinson: | Lewy body (alpha-synuclein is main component)
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| Most common genetic form of Parkinson: | PARK8
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| Ulnar neuropathy | stretch / compress ulnar n.; cubital tunnel or Guyon canal (FCU mx may be spared); d/t pressure, bone spurs, cysts; sensory precede motor sx
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| Ulnar neuropathy: provoking factors | Elbow Flexion (Cubital), Wrist Extension (Guyon's); Nighttime
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| Ulnar neuropathy: Dx | Hx; EMG/NCS can help find site of lesion
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| Ulnar neuropathy: Tx | modify activity; extensor splint at night; NSAIDs; surgery (nerve transposition or ligament release); No C'steroids
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| Radial neuropathy: etiology | axilla (crutches); Saturday night palsy; handcuffs; humerus fx
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| Radial neuropathy: Dx | Motor>sensory; weakness in extension & arm ext rotation; forearm atrophy; xray shoulder/humerus
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| Meralgia paresthetica: patho | stretch/compress lat fem cutaneous n.
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| Meralgia paresthetica: RF | obesity; DM; PG; hip hyperextension; lumbar lordosis
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| Meralgia paresthetica: Dx | pain, paresthesia, numb; outer thigh; usu unilateral (relieved by sitting); no motor sx
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| Meralgia paresthetica: Tx | often self-ltg; hydrocortisone injxn; nerve transposition
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| Fem neuropathy: RF | lithotomy posn (inguinal lig); DM; retroperitoneal neoplasm/hematoma; pelvic fx; fem art cath (n. trauma)
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| Fem neuropathy: Dx | Quads atrophy/weakness; sensory impairment anteromedian thigh; decreased patellar DTR; EMG/NCS; CT/MRI
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| Fem neuropathy: Tx | Tx etiology; splints/braces; PT
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| Sciatic n. palsy: Dx | 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)
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| Sciatic n. palsy: Dx tests | EMG/NCS (distinguish from peroneal neuropathy); xray
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| Sciatic n. palsy: Tx | Tx etiology; behave change; anti-inflam; PT; surg
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| Peroneal n. palsy: Dx | weak dorsiflexion (foot drop) & eversion; sensory loss/ paresthesia: anterolateral calf & foot dorsum; EMG/NCS? Tx sim to sciatic n. palsy
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| CN VII palsy (Bell): etiology | idio; HIV, sarcoid, Lyme, tumor; HSV infxn? RF = PG, DM
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| CN VII palsy: Dx | abrupt; facial paralysis (some upper sparing); drooping corner of mouth; ptosis/ forehead smooths out; ear pain; dysgeusia; hyperacusis
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| CN VII palsy: to distinguish btw peripheral & central lesion: | peripheral: complete paralysis forehead mx; central: partial sparing forehead mx
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| 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
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| CN VII palsy: Tx | prednisone; artificial tears/eye patch; No Surg
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| CMT: genetics | usually auto dom
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| CMT: patho | Type I: demyelinating; II: axonal; Motor>Sensory; Lower > Upper; childhood/young; slow progression
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| CMT I vs CMT II: Dx | CMT II: less mx wasting/ secondary weakness; less common postural tremor/arm involvement; NO peripheral n. hypertrophy
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| CMT Dx: | H&P; DNA testing; Nerve/mx bx (confirmatory); EMG/NCS
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| CMT: EMG/NCS | CMT I: segmental demyelination; reduced motor & sensory conduction velocity; CMT II: axonal loss; normal/sl dec motor conduction, dec SNAPs; chronic partial denervation in affected mx
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| Dejerine-Sottas Dz (CMT III): patho | phytanic acid disturbance; prog demyelinating neuropathy; infancy/kids
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| Dejerine-Sottas Dz: Dx | weakness, ataxia; sensory loss; DTR: global hyporeflexia; high CSF pro; EMG/NCS: dec motor velocity, sensory conduction
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| Dejerine-Sottas Dz: Tx | Supportive; plasmapheresis; dietary restriction
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| Refsum dz: patho | Progressive Demyelinating Neuropathy; Early Childhood
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| Refsum dz: Dx | weakness, ataxia; sensory loss; DTR: global hyporeflexia; retinitis pigmentosa; CSF protein normal; nerve bx; EMG/NCS: dec motor velocity, sensory conduction; Tx supportive
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| Systemic-metabolic neuropathies include: | DM; uremia; alcoholic & nutrition def; paraproteinemias
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| DM neuropathy | sensory precedes motor; lower ext precedes upper; Hx: autonomic sx?; NCS nml / mildly slow
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| Charcot Arthropathy is a complication of: | DM peripheral neuropathy
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| Charcot Arthropathy | d/t Joint Subluxation, Periarticular fx; rocker bottom foot; pain, swelling, ulceration
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| Uremia: Dx | Symmetric sensory-motor; lower ext > upper; distal > proximal; severity correlates with degree of renal insufficiency
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| EtOH/Nutritional deficiency | cobalamin (B12) def; axonal > myelin; slow progression
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| EtOH/Nutritional deficiency: Dx | 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
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| AIDP (GBS): patho | Progressive Demyelinating; prob immune-mediated; Axonal Subtypes (AMAN; AMSAN)
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| AIDP (GBS): Dx: | H&P; high CSF pro (2-3 wks post onset); EMG/NCS: demyelination with delayed conduction (3-4 wks)
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| AIDP (GBS): Dx: MOTOR | Weakness; Symmetric; Proximal before Distal; Lower ext before Upper; Advanced: Resp mx Compromise, CN Involvement
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| AIDP (GBS): Dx: SENSORY | Paresthesias; Loss of Sensation; Distal before Proximal; DTR: Global hyporeflexia or areflexia; ANS: tachycardia, cardiac irreg; BP changes, pulmonary dysfn, loss of rectal tone
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| AIDP (GBS): Tx | Anti-inflam; plasmapheresis; IVIg; mech ventilation
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| Leprosy: 2 Types: | tuberculoid (multifocal) & lepromatous (symmetrical)
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| Most common causative of meningitis in adults | S. pneumo
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| When do LP? | suspect meningitis; not if suspect abscess
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| Glucose depressed: usually: | bac mening, or TB or fungal
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| Meningitis general S/S | HA, fever, neck / back stiffness, neuro impairment
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| Meningitis presentation | acute (hrs - days), usu w/ fever, HA, stiff neck, lethargy; usu without focal sx
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| Typical purulent meningitis orgs | N. meningitidis, S. pneumoniae, or H. influenzae
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| Chronic meningitis: orgs | TB; fungal
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| Encephalitis presentation | diffuse infxn; confusion, lethargy, often seizures; CSF may be nml
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| Increased WBC in CSF indicates: | inflammation (not necessarily infection)
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| Pneumococcal meningitis Tx | ceftriaxone (if GP diplococci seen, add Vanc, pending cx)
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| N. meningitidis | petechial rash; GN diplococci; often assoc w/DIC
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| Meningococcal meningitis: nasal carriage eliminated with: | Rifampin (alt: cipro or ceftriaxone)
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| Meningococcal meningitis: DOC | Acqueous Pen G
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| H flu meningitis | less common in adults; in setting of otitis or sinusitis; DOC ceftriaxone
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| Tuberculous meningitis | usu gradual onset; listlessness & irritability; CN palsies; active TB elsewhere; CSF inc WBC (100-150), mostly lymphs; abnml CXR; acid-fast normal
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| Abscess: common orgs | streptococcus, staphylococcus or anaerobes
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| Ring enhancing lesion is usually: | abscess or tumor
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| Abscess tx | prolonged IV Abx, surg drainage; monitor tx w/ serial scans; if <2 cm poss medical tx only
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| Rabies S/S | (> 10 days) delirium, painful swallowing, rage alternating with calm
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| Rabies incubation period | >10 days (usu 3-7 wks) (infected animal dies within 5-7 days)
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| Herpes encephalitis | more common in elderly; often medial temporal lobes; tx most pts w/ clin syndrome of viral encephalitis empirically for HSE
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| CJD Sx | usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG
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| MS epidemiology | F>M; 350K in US (1M world); onset 20-40 yo; most present w/relapsing form; prevalence increases with distance from equator
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| MS S/S | Optic neuritis; Transverse myelitis; Paresthesias; Ataxia; Weakness or incoordination; Spasticity; Cognitive impairment
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| MS: MRI findings | multiple characteristic lesions or plaques: periventricular or subcortical U-fibers, corpus callosum lesions
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| MS: CSF findings | evidence of oligoclonal bands or increased IgG index
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| MS: types of dx criteria | Schumacher; Poser: Macdonald
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| MS: Goals of tx | Tx whole dz; slow accumulation of disability; Reduce relapse rate & CNS inflam (lesions) & progression of brain atrophy (shrinkage); improve pt QOL (including cognitive)
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| MS Tx options | IFN; glatiramer; poss immunosupp adjuncts for aggressive/ breakthrough; corticosteroids (methylprednisolone) for relapse
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| Majority of malignant gliomas are: | grade IV tumors (GBM or gliosarcomas)
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| Gliomas include: | astro; oligo; ependymoma; glial cells: support
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| Grade 1 Glioma = | Pilocytic Astrocytomas
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| Grade 2 Glioma = | Astrocytomas, Oligodendrogliomas
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| Grade 3 Glioma = | Anaplastic Astrocytomas, Anaplastic Oligodendrogliomas
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| Grade 4 Glioma = | GBM; Gliosarcoma
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| Diffuse astrocytomas include: | Low-grade infiltrative Astro (WHO II); anaplastic astro (WHO III); Glioblastoma (WHO IV)
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| Circumscribed astrocytomas include: | Pilocytic Astro (WHO grade I); Pleomorphic xanthoastrocytoma (PXA); Subependymal giant cell Astro (SEGA)
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| Well-differentiated Astro: | 10-15% of Astros; 35 yo; 5-10 yr surviv; cerebral hemi / cortex; slow growing; often undergo malig progression to AA or GBM
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| High-grade gliomas (III/IV): | invade via white matter tracts, cross via corpus callosum;
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| Primary characteristic of a grade IV glioma = | necrosis with vascular proliferation
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| Anaplastic astro | High-Grade; 1/3 of Astros; 45 yo; 3 yr surviv; usu in cerebral white matter; relatively fast-growing; Frequent progression to GBM
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| GBM | 50% of Astros; >60 yo; rare <30; 1 yr surviv; usu in cerebral hemi white matter; spreads rapidly & diffusely; Ring of tissue around necrotic core; Highly vascular
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| Oligodendroglioma | Usu presents at low-grade (II) stage; young / middle-aged; grade II >10 yr surviv; Fried-egg cells
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| Most common primary brain neoplasm = | GBM
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| Untreated GBMs: growth | double in size in 14 days
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| Brain tumor: genl clin presentation | HA; seizures; Cognitive dysfn; Focal neuro deficits; N/V; Sx endocrine dysfn; Visual sx; Sx from plateau waves (ICP changes)
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| Headache in brain tumor | 20% of pts present w/HA (more w/ post fossa tumor); usu d/t inc ICP; Progressive increase in HA freq & severity; Classic HA on waking or HA that wakens one from sleep
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| Seizure in brain tumor | 35% of pts present with this; often the sx that precedes dx; focal or secondarily generalized
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| Probably most common problem in pts w/brain tumors = | cognitive dysfn
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| Cognitive dysfn in brain tumor: | Frontal personality; Memory problem; Depression
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| Cognitive dysfn: Left hemispheric tumors: | language dysfunction
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| Cognitive dysfn: Right hemispheric tumors: | problems with visual perception & scanning
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| Brain tumor: Focal neurologic deficits | Hemiplegia; Hemiparesis; Ataxia; Nystagmus; Can mimic stroke
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| N/V more common in: | post fossa tumors
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| Endocrine sx: | hypothyroid; dec libido
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| Visual symptoms include: | Contralateral flashing lights; Visual field loss; Diplopia
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| Symptoms from plateau waves | Transitory episodes of altered consciousness & visual disturbances
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| Brain tumor: eval & dx | H&P; CT +/- MRI; EEG; LP; PET
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| Factors of better prognosis: | Young; High KPS; Lower pathological grade
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| Less significant prognostic predictors: | Long duration of sx; Absence of mental status changes; Cerebellar location; Small preop tumor size; Completeness of surgical resection
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| BCNU AE | fatigue, low blood counts, pulmo fibrosis
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| Tx for high grade gliomas | Primary tx = surg resection, RTx, CTx; most sig prognostic factors: extent of surg resection, age, & performance status
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| First treatment modality for high grade glioma | Surgery
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| Goals of surgery: | Confirm patho dx; improve sx rapidly; reduce number of ca cells requiring tx (removes hypoxic core of the tumor; relatively resistant to radiation & inaccessible to CTx)
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| Std tx for WHO III &IV gliomas: | Radiation tx (role of RT in WHO II gliomas is controversial)
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| RTx Modalities: | Whole brain (ltd use now in gliomas); Focal RTx: Conventional high-dose (59.4 Gy x 42 days; 2 cm border around tumor area) or IMRT; Stereotactic (gamma-knife)
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| RTx injury | Acute (fever, neuro def) or delayed encephalopathy (edema, MRI enhance); tx w/c'steroids; focal cerebral necrosis (mos-yrs): tx w/steroids & hyperbaric
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| Most frequent delayed effect of RTx | Diffuse cerebral injury; cortical dysfunction, progressive dementia, gait disturbance; WM destruction; MRI: lg ventricles, wide sulci, basal ganglia calcifn, hyperintense T2
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| Std of care: high grade gliomas | Resection; RTx & 42 days temozolomide; then (if stable dz), adjuvant CTx
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| Stupp study result: | temozolomide added to RTx improves survival
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| CTx MOA & AE | targets DNA replication; AE: Myelosuppression; N/V; Fatigue; Constipation or diarrhea; DI
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| CTx: passage across BB depends on: | Molecule Size; Lipid solubility; Ionization state
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| CTx DI: | Dex (closing BBB); phenobarbital (dec nitrosourea efficacy); anti-epileptics (affect CTx metabm)
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| Low grad glioma: Tx | Bx (confirm dx & r/o high grade); seizures only: defer tx til progresses; if progressive sx: resect +/- CTx (+ RTx only if refractory)
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| VEGF | higher the VEGF, worse the prognosis; anti-VEGF Ab's effective in xenografts
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| Tumor blood vessels | dept on growth factor; leaky & fragile; less supported by pericytes; disorganized, twisted, variable pressure; inconsistent nutrient delivery to tumor tissue
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| Second leading COD in brain tumor pts: | thromboembolic complications
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| Meningioma | slow growing, benign; attached to dura mater; 13-26% of primary IC tumors; RF: prior radiation; often Asx; visual complications; DDx: neurofibromatosis; Firstline tx: Surgery
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| Ependymoma: worse prognosis: | <3 yo
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| Ependymomas within brain: locations | Infratentorial > supratentorial (2x)
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| Ependymoma | Usu slow growing; kids & YA; young adults; 4% all BT; from walls of ventricles or spinal canal (obstructive hydrocephalus); 90% are in brain, 10% in spinal cord (often adults)
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| Medulloblastoma | Malig, invasive embryonal cerebellar tumor; kids & YA; 70-80% 5-yr survival; Most arise in vermis (4th ventricle involvement)
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| Medulloblastoma: metastases | Metastasize via CSF pathways (Drop Mets); Rare mets to bone, lymph nodes, other extracranial sites
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| Medulloblastoma: Sig LT toxicities of tx: | Cognitive decline; Psychomotor / growth retardation; Hormonal deficits
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| Primary CNS lymphomas | Usu present deep in brain parenchyma; usu multifocal (diffuse lg cell B-cell lymphoma); Survival w/o tx <1 yr; Steroid tx & Methotrexate CTx
🗑
|
||||
| Primary CNS lymphomas: incidence increased in: | Immunodef pts; AIDS; Organ TP; older pt
🗑
|
||||
| Std of care: Grade I | Surgery +/- RT
🗑
|
||||
| Std of care: Grade II | Surgery; Observe; If progression: CTx
🗑
|
||||
| Std of care: Grade III | Surgery; RT with temozolomide; 12 cycles of temozolomide
🗑
|
||||
| Std of care: Grade IV | Surgery; RT with temozolomide; 52 weeks rotational CTx
🗑
|
||||
| Emergent eval of stroke | CBC/plt; PT/ PTT; Lytes, glu, renal; ECG/ markers of cardiac ischemia; Brain CT or MRI
🗑
|
||||
| Ischemic stroke patho | atheroembolic (50%); cardioembolic (30%)
🗑
|
||||
| Hemorrhagic stroke patho | parenchymal ICH (10-15%); subarachnoid (5-10%)
🗑
|
||||
| Most common parenchymal ICH: | Hypertensive 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
🗑
|
||||
| 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 130/80 mmHg (less severe than in ICH); stroke d/t cerebral microhemorrhages
🗑
|
||||
| Venous infarction presentation | 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; if first-degree rel w/this stroke)
🗑
|
||||
| SAH stroke presentation | Abrupt severe HA; meningismus; depressed LOC; nonfocal neuro exam
🗑
|
||||
| Atheroembolic Stroke characterized by: | Single vascular territory; Warning signs; Stepwise progression
🗑
|
||||
| Atheroembolic presentation | Hx HTN, CAD; transient language disturbance; transient weakness; Normal head CT; Doppler US: high grade stenosis (e.g., L ICA)
🗑
|
||||
| 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 fx: | face = arms = legs
🗑
|
||||
| Cortical infarct fx: | gradation btw face, arms, & legs
🗑
|
||||
| Lacunar syndromes | Pure Motor Stroke; Pure Sensory Stroke; Ataxic Hemiparesis; Clumsy Hand Dysarthria
🗑
|
||||
| Atheroembolic stroke: additional eval | Neuroimaging; Carotid US; MRA; CTA; Catheter angiography
🗑
|
||||
| Cardioembolic stroke presentation | h/o A fib; aphasia; hemiparesis/hemisensory deficit affecting face and arm; Carotid US normal (no brain lg vessel prob)
🗑
|
||||
| Cardioembolic: dx | Maximal deficit at onset; Multiple vascular territories; Cardioembolic source; Hemorrhagic infarction (Wedge shaped infarct towards cortical surface)
🗑
|
||||
| Cardioembolic: poss sources | A fib; Cardiomyopathy; Acute MI; Valvular heart dz
🗑
|
||||
| Cardioembolic stroke: additional eval | pulse; EKG; 24-48 hr EKG; TTE (microcavitation); TEE
🗑
|
||||
| TIA | Acute focal neuro def; S/S resolve within 24 hr; No rad evidence of infarction; Ischemic etiology; 11% risk of stroke within 3 mo; 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
🗑
|
||||
| Lifestyle mods affecting BP | wt reduction; DASH diet; sodium reduction; exercise; moderate EtOH consumption
🗑
|
||||
| Stroke comorbid RF's | CHD, CHF, DM, stroke
🗑
|
||||
| Prevention of A fib RF: | Low risk (0-1) ASA; mod (2) ASA or warfarin (but AE/bleed risks); high risk (>2) warfarin
🗑
|
||||
| Asx carotid stenosis: eval | Carotid bruit; Doppler US; MRA, CTA
🗑
|
||||
| Stroke prevention DM pts | glucose ctrl: no fx on stroke/macrovascular comp; tight BP ctrl (<130/80) effective; statins
🗑
|
||||
| Stroke prevention: hyperlipidemia | chol reduction w/statins
🗑
|
||||
| ASA recommended for 10-yr stroke risk of: | 6-10%
🗑
|
||||
| Ischemic stroke: Tx | tPA (within 4.5 hrs of sx onset); head CT w/o evidence of hemorrhage/complicating lesion
🗑
|
||||
| tPA absolute CI (<3 hr) | CT: bleed/comp (AVM); BP >185 or >110; recent stroke/ICH; bleed elsewhere; anticoag use; plt <100K; h/o seizure preceding stroke
🗑
|
||||
| tPA CI (3-4.5 hr) | >85 yo; NIH-SS >25; h/o both stroke/DM
🗑
|
||||
| If pt not tPA candidate: Tx: | poss endovascular tx; MERCI clot retriever?
🗑
|
||||
| Acute stroke mgmt | Temperature; Fluids/Glucose; BP; Antithrombotic agents
🗑
|
||||
| Acute ischemic stroke: tx BP? | No (drop in MAP can drop CBF, make things worse)
🗑
|
||||
| Secondary stroke prevention | Plt antiaggregants (ASA); Anticoagulants; BP; Lipid lowering; Endarterectomy
🗑
|
||||
| Antihypertensives & stroke risk | each 10 mmHg drop in BP = 28% decrease stroke risk
🗑
|
||||
| Action tremor: | Most common; arise when attempting to maintain a fixed position; frequency is 7-13 Hz; Essential or physiologic
🗑
|
||||
| Essential tremor = | resembles slower freq physio tremor; essential or familial; common in later life; extremities, head (titubation), or voice
🗑
|
||||
| Drug causes of physiologic tremor | Amphetamines, theophylline, lithium and valproate.
🗑
|
||||
| Essential tremor Tx | Firstline: Beta-blocker (CI in COPD; asthma; DM; bradycardia; AV conduction probs); Primidone: effective but sedating; Tranquilizers (benzo) for anxiety related; EtOH: temporary suppression
🗑
|
||||
| Ataxic (intention) tremor | Absent at rest/start of movement; dysmetria
🗑
|
||||
| Ataxic tremor: Causes: | Dz of cerebellum / connections (MS; tumors; infarct; ethanol-induced cerebellar degeneration)
🗑
|
||||
| Ataxic tremor: Tx: | Meds usu ineffective; Weights; surgical lesions of ventrolateral thalamus may be effective in severe cases
🗑
|
||||
| Athetosis: | slow writhing purposeless movements usu involving hands, tongue & face; usu in kids w/ cerebral palsy or result of kernicterus or hypoxia (poss later in life d/t 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 yrs; tx Haldol/pimozide
🗑
|
||||
| Hemiballismus | Violent flinging movements; Unilateral hemiballismus usu d/t infarct in contralateral subthalamic nucleus of Luys
🗑
|
||||
| Myoclonus = | Shock-like contraction of a group of mx; irreg in rhythm/amplitude; may involve restricted grp mx or be generalized.
🗑
|
||||
| Myoclonus may result from: | anoxic damage, spinal cord injury, uremia, hepatic encephalopathy or other rare neuro syndromes
🗑
|
||||
| Myoclonus Tx | Clonazepam, Valproate (Both have limited efficacy)
🗑
|
||||
| Dystonia: | Maintenance of a persistent extreme posture in one or more joints.
🗑
|
||||
| Generalized dystonia: | dystonia musculorum deformans; a rare hereditary dystonia
🗑
|
||||
| Focal dystonias: | torticollis (dystonia of the neck), writer's cramp & blepharospasm (dystonia of the mx's involving eye closure).
🗑
|
||||
| Dystonia: Tx | Botox injxn increasingly common & helpful; Surgical tx (torticollis) also available; Medical tx (benzos, anticholinergics, neuroleptics) generally unsatisfactory
🗑
|
||||
| Parkinson dz: epi | 500,000 in US; 58 yo
🗑
|
||||
| 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
🗑
|
||||
| L-DOPA | 80% of pts improve; Sinemet treats akinesia & is less effective in treating tremor.
🗑
|
||||
| L-DOPA MOA | precursor of DA (which cannot cross BBB; L-DOPA can)
🗑
|
||||
| Dopamine agonists MOA | Act like DA at DA receptor; may allow for reduction in dose of Sinemet required & may decrease on-off probs
🗑
|
||||
| Amantidine MOA | May increase DA release from nerve terminals; weakly effective
🗑
|
||||
| Anticholinergic drugs MOA: | May be more effective for tx of tremor; AE = confusion, constipation, dry mouth, urinary retention
🗑
|
||||
| Selegiline MOA | inhibits monoamine oxidase type B
🗑
|
||||
| Cabergoline MOA | inhibits COMT
🗑
|
||||
| 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
🗑
|
||||
| Huntington Tx | DA receptor blockers such as neuroleptics (haloperidol, chlorpromazine); DA reserve depleters (reserpine; no longer used); future: tetrabenazine? Tx often unsatisfactory
🗑
|
||||
| Wilson dz | Auto rec; onset 2nd-3rd decades; first sx: hepatic dysfn/cirrhosis; tremor/ bradykinesia, dysarthria, dysphagia; limbs rigid, facial mx fixed empty smile; arms: wing-beating tremor; Kayser-Fleischer (deep cornea)
🗑
|
||||
| Wilson: labs | Serum ceruloplasmin (Cu carrying pro) very low; urine Cu high
🗑
|
||||
| Wilson: patho | CNS changes: brownish discoloration of some basal ganglia; proliferation of protoplasmic astrocytes (Alzheimer Type II cells)
🗑
|
||||
| Wilson: Tx | Should begin before neuro Sx onset; early tx prevents neuro sequela devt; eat low Cu foods; sulfurated potash with meals (prevent Cu absorption); chelator (d-penicillamine) to remove absorbed Cu
🗑
|
||||
| Wilson dz: Tx: foods to avoid | liver; chocolate; mushrooms; shellfish; nuts
🗑
|
||||
| Tardive dyskinesia: cause | Iatrogenic d/t LT neuroleptic tx (esp Haldol; also atypicals, poss metoclopramide, amphetamines, L-dopa); may be result of DA receptor supersensitivity
🗑
|
||||
| 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: Tx | stop the offending drug; many tx tried w/ marginal success
🗑
|
||||
| Tardive dyskinesia: most successful tx: | achieved with DA-depleting agents (tetrabenazine); also Vitamin E?
🗑
|
||||
| Excess DA results in: | dyskinesia and chorea
🗑
|
||||
| Dopamine deficiencies cause: | Parkinsonian-like symptoms
🗑
|
||||
| Action of acetylcholine & DA: | Act in opposite directions; adding DA is equivalent to blocking acetylcholine
🗑
|
||||
| Migraine dx criteria | ≥2 of: (Unilateral; Pulsating; Mod/ severe intensity; fx: avoidance of routine physical activity); 1 of: (N/V; Photophobia an& phonophobia)
🗑
|
||||
| 5 phases of migraine | Prodrome; aura; HA; termination; postdrome
🗑
|
||||
| Severe episodic HA with cerebellar sx = | basilar migraine
🗑
|
||||
| Menstrual migraine tx | triptans given acutely; NSAIDs; OCP
🗑
|
||||
| Chronic migraine: dx | CDH ≥3 months; >8 d/mo x 3 mo;
🗑
|
||||
| Sinus HA vs migraine | sinus usu continuous (not intermittent); TTP over sinuses; tx w/ Abx
🗑
|
||||
| CDH | ≥ 15 d/mo; primary or secondary (usu considered primary); ≥1 migraine/wk = RF for dev CDH
🗑
|
||||
| CTTH: | CDH meeting TTH criteria
🗑
|
||||
| NDPH: | CDH dev within 3 days of sx onset, last ≥ 3 mo
🗑
|
||||
| MOH = | CDH assoc w/regular overuse for >3 month of one or more acute meds; try bridge tx; initiate preventive agent as analgesic is withdrawn
🗑
|
||||
| Med overuse indicators: | Simple analgesics: >3 d/wk; Triptans/ combo analgesics: >2 d/wk; Opioids/ergotamine: >2 d/wk
🗑
|
||||
| Hemicrania continua | Daily, continuous, strictly unilateral primary HA; assoc w/ cranial autonomic features (miosis, ptosis, eyelid edema, lacrimation, nasal congestion or rhinorrhea)
🗑
|
||||
| Hemicrania continua: dx & tx | dx: responds to indomethacin
🗑
|
||||
| Paroxysmal hemicrania | ≥ 20 frequent attacks (2-30 min); Pain severe & strictly unilateral, orbital, supraorbital, or temporal; Parasymp ipsilateral activation; Responds only to indomethacin
🗑
|
||||
| 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
🗑
|
||||
| Trigeminal autonomic cephalgias include: | SUNCT; cluster; trigeminal neuralgia
🗑
|
||||
| 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
🗑
|
||||
| Neuroimaging not needed when: | No focal neuro findings; Pt has stable pattern of recurrent HA; No h/o seizures
🗑
|
||||
| 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
🗑
|
||||
| Thunderclap HA (non-SAH) | dx after exclude SAH; peaks in 1 min, lasts 1 hr-10 days
🗑
|
||||
| Migraine tx considerations | Pt age; current health status; coexistent illnesses; migraine type
🗑
|
||||
| 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
🗑
|
||||
| Pt needs preventive med (as well as abortive) if: | >8 HA / month
🗑
|
||||
| Defn of trigger | causes HA more than 50% of the time within 24 hr
🗑
|
||||
| EEG 3/sec spike and wave = | Absence
🗑
|
||||
| Most common cause of tonic-clonic in pts (onset < 30 yo) is: | idiopathic epilepsy
🗑
|
||||
| Clonic seizures: | usu in childhood; impaired consciousness, followed by asymmetric bilateral jerking
🗑
|
||||
| Most common seizure type: | complex partial
🗑
|
||||
| complex partial: | 10-30 yo; common post-head trauma; 50% abnml CT/MRI; 50% mesial temporal sclerosis; 20% hamartoma
🗑
|
||||
| complex partial: 30-60 yo: | brain tumor?
🗑
|
||||
| complex partial: >60 yo: | stroke?
🗑
|
||||
| Seizure: labs | Glucose; lytes; AED levels; LP if poss meningitis; EtOH/tox if susp; ABG if susp hypoxia; poss CXR, CT, MRI
🗑
|
||||
| Status epilepticus: does not apply to: | continuous simple partial seizures
🗑
|
||||
| EtOH withdrawal seizure: | onset 6-48 hr after last drink; often primary generalized, often have Todd's
🗑
|
||||
| Tx after single seizure: | If a structural lesion or recognized abnormal EEG
🗑
|
||||
| Remission: | usu within 3 yrs of first seizure; prolonged remission in 60% of such pts
🗑
|
||||
| Factors against remission | FH; psych comorbid; febrile seizure hx; more seizures; age
🗑
|
||||
| Awareness vs arousal | awareness: high level fn (resides diffusely in cerebral cortex); arousal: primitive (brainstem)
🗑
|
||||
| For LOC to occur: | Both cerebral hemispheres damaged OR brainstem lesion
🗑
|
||||
| Coma: causes | Cerebral infarction 10%; Cerebral hemorrhage 20%; Metabolic causes 50% (Drug ingestion >50%; Hypoglycemia 5-10%); Psych 2%
🗑
|
||||
| Coma: sudden onset d/t: | Cardiac arrest; SAH; 2nd to aneurysm; Brainstem infarct or hemorrhage; Bicerebral hemispheric infarction
🗑
|
||||
| Coma: onset over min-hrs d/t: | usually drug overdose; also hypoxia; hypoglycemia; SAH; hydrocephalus; AVM; meningitis; metab
🗑
|
||||
| Head trauma sx | Battle (mastoid); raccoon eyes (orbital) CSF rhinorrhea/ otorrhea (basilar)
🗑
|
||||
| Roth spots | sx of septic emboli; on funduscopic exam & btw toes
🗑
|
||||
| Hollenhorst plaque | chol emboli from carotid
🗑
|
||||
| Coma: sensation: may see: | Purposeful withdrawal bilaterally; absent response Unilaterally; facial Grimace; posturing
🗑
|
||||
| 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
🗑
|
||||
| Cheynes-Stokes: | Bilateral hemispheric lesions; most commonly seen in non-neurologic disorders (CHF); crescendo-decrescendo
🗑
|
||||
| Central neurogenic hyperventilation: | Commonly metabolic cause (Sepsis; DKA)
🗑
|
||||
| Apneustic: | Rare, but usually associated with pontine infarction; pt breathes in, holds breath 15-20 sec, breathes out
🗑
|
||||
| Ataxic breathing (Biot's respiration) | Damage to the medullary respiratory centers; breathing slows; long breathless pause; then inhales; this is often premorbid
🗑
|
||||
| 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 abnormality (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 caused by DM & some drugs (esp atropine, scopolamine)
🗑
|
||||
| Small, reactive pupils: seen in: | pontine damage (infarct or hemorrhage) or with some drug use (opiates, pilocarpine).
🗑
|
||||
| Bilateral midposition unreactive pupils: | hypothermia
🗑
|
||||
| Eye deviation occurs in what direction? | toward a unilateral hemispheric lesion and away from a unilateral brainstem lesion.
🗑
|
||||
| Functional testing of Eye Movements is done by: | oculo-cephalic reflex (Doll's head) or oculo-vestibular reflex (ice water calorics)
🗑
|
||||
| Oculo-cephalic reflex (Doll's head): CI | if there is a question of cervical spine injury
🗑
|
||||
| Oculo-cephalic reflex: Abnormal response = | absent or asymmetric eye movement: destructive lesion at midbrain or pontine level; poss also deep barbiturate poisoning
🗑
|
||||
| Oculo-vestibular reflex: Normal response (conscious pt): | Tonic (sustained) deviation of eyes toward stimulated side, w/ quick phase of nystagmus toward the opposite side
🗑
|
||||
| Oculo-vestibular reflex: Response in comatose pt w/ intact brainstem: | Tonic deviation of eyes, but no nystagmus
🗑
|
||||
| Oculo-vestibular reflex: Response in comatose pt w/ brainstem dysfn: | Loss of tonic deviation w/ stimulation of one, or both ears; if there is no tonic deviation there can be no fast response
🗑
|
||||
| Oculo-vestibular response does not: | distinguish between metabolic and structural causes of coma
🗑
|
||||
| Corneal sensation: | carried by CN V (Trigeminal); test with cotton swab pressed gently onto cornea; abnormal reponse suggests a pontine lesion
🗑
|
||||
| Coma: labs | GLUCOSE, lytes, renal, Ca, PO4, ABG, CBC, tox screen; CXR, imaging (after stabilization)
🗑
|
||||
| GCS: 3 tests | Eye, verbal, motor; range: 3-15; <8 means coma
🗑
|
||||
| GCS: eye | 1: no eye opening; 2: open in response to pain; 3: in response to voice; 4: open spontaneously
🗑
|
||||
| GCS: verbal | 1: None; 2: Incomprehensible sounds; 3: Inappropriate words; 4: confused; 5: oriented
🗑
|
||||
| GCS: Motor | 1: no response; 2: extension to pain; 3: flexion in response to pain; 4: withdraws from pain; 5: localizes to pain; 6: obeys commands
🗑
|
||||
| Brain death | no purposeful movements, pupil responses, EOM, corneal reflexes; spont resp / movements; DTRs may be present
🗑
|
||||
| Coma & sleep | Almost all coma pts will wake up to some degree; most develop a sleep-wake cycle
🗑
|
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