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Neuro review 3

ALS: Dx UMN & LMN sx in 3 regions; UMN: clinical; LMN: EMG; CK nml or high
ALS Tx Riluzole; cough assist device, chest PT, BiPAP; PEG feeding tube;
PLS: path degeneration of lateral corticospinal tract
PLS clin findings usu legs before arms; leg weak/stiff; spasticity; ave duration >8 yrs; many pts develop LMN sx & transition to ALS
PLS: dx EMG, MRI (br & spcord), LP, evoked potls; B12, Lyme, RPR, long chain fatty acids
PMA pure LMN dz; slower progress than ALS; often spares bulbar mx; CK very high
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
Disorders of neuromx transmission (NMJ): MG, LEMS, botulism
MG: path Acquired autoimmune: Ach receptor insufficiency
MG S/S fluctuating mx weakness (worse w/reps); asymmetric ptosis; tired face, difficulty chewing/swallowing; SOB
MG Dx Tensilon test; Ach receptor & MuSK Abs; Repetitive nerve stim; Single fiber EMG; CT Chest to exclude thymoma
MG Tx Symptomatic (Cholinesterase inhibitors); Firstline: steroids (alt immunosupp: CellCept, Cyclosporine); thymectomy
MG exacerbations d/t infxn, PG, meds; may worsen resp sx; tx w/ plasmapheresis or IVIg, supportive respiratory care
MG: drugs to avoid NM blockers; quinine; macrolides, FQ; botox; beta/CCB; IV contrast
LEMS usu paraneoplastic (autoimm rare); proximal weakness / autonomic sx (dry mouth); hypo/absent reflexes; voltage gated Ca channel Abs; facilitation w/ RNS
Botulism MOA irreversible blockade of Ach release
Botulism S/S Diplopia, ptosis, dilated pupils; facial / resp weakness; descending paralysis; Autonomic dysfunction
Botulism Tx supportive; horse serum antitoxin? (months to recover)
MD classified by: distribution, inheritance and clinical features
MD: labs/studies ultrastructural protein abnormalities; mx bx: mx fiber necrosis
Duchenne onset at 3-5 yrs; calf pseudohypertrophy; loss of ambulation by teens; cardiomyopathy; death in 20s
Duchenne/Becker: Dx Mx bx; genetic testing (need complete sequencing); CK sometimes >10,000; FH
Duchenne/Becker Tx Prednisone (age 5) for Duchenne; Supportive (orthotics, resp, cardiac, PT/OT); cardiac TP in Becker
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
FSHD Dx genetic testing (95%); FH; mx bx rarely helpful
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)
Most common MD's Duchenne/Becker; myotonic; FSHD
Myotonic dystrophy auto dom; any age; TNR
Myotonic dystrophy S/S tenting upper lip; distal weakness; frontal bald; cataracts; conduction block; DM, infertile; cognitive impairment; percussion myotonia
Allelic vs non-allelic heterogeneity allelic: 1 gene causes >1 condition; non-allelic: clinical syndrome is d/t >1 gene
Autosomal dominant 1:1 M:F; multi generations; M-to-M transmission seen; variable expression (important); late-onset neurodegenerative dz's
Autosomal dominant disorders Huntington, NF1/NF2, spinocerebellar ataxias, familial Alz, CMT
NF1: other manifestations: hydrocephalus, seizures, learning disabilities, short, lack of GH, precocious puberty, Renal Artery stenosis
Auto recessive >1 affected each generation; M:F 1:1; consanguinity; carriers usu asx; inborn errors of metabolism
Auto recessive disorders PKU, Tay-Sachs, MSUD, Friedreich's, Wilson, homocystinuria, sickle cell
Wilson Dz hepatolenticular degen (impaired ceruloplasmin synth); presents in teen years (hepatitis)
Wilson S/S tremor, dysarthria, slow, hoarse, chorea, psych
Wilson: dx high ceruloplasmin & copper; low copper on liver bx; Kayser Fleischer rings
Wilson: tx reduce copper intake; chelate; transplant /
X-linked recessive F-toM trans; M=affected, F=carrier;
X-linked rec dz Duchenne/Becker MD; Kennedy; adrenoleukodystrophy; Menkes (kinky hair); Lesch-Nyhan; Fragile X
Duchenne/Becker Dx/Tx genetic testing, elevated CK, EMG; Tx: supportive, corticosteroids, PT, ortho, cardiopulmonology
X-linked dom F-to-F transmission (lethal to males); Rett; Aicardi; Lissencephaly 2
Rett dz 6-18 mos; live to 40s; autism; cardiac & scoliosis
Mitochondrial dz multi generations; trans by F only; 1:1 M:F affected; MERRF, MELAS, LHAN, Kearns-Sayre
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
TNR: mode of inheritance can be multiple modes of inheritance
TNR dz Huntington, Fragile X, myotonic dys; Kennedy; spinocerebellar ataxia; Friedreich
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
Alz: APOE gene E2: protective vs Alz; E4: inc risk of dev Alz
Alz dz: main reason for genetic counseling is: info only
Parkinson dz usu unilateral onset; resting tremor, slow, cogwheel rigidity, festinating gait, masked facies, postural instability
Parkinson: TRAP = Tremor, Rigidity, Akinesia, Postural instability
Pathological hallmark of Parkinson: Lewy body (alpha-synuclein is main component)
Most common genetic form of Parkinson: PARK8
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
Ulnar neuropathy: provoking factors Elbow Flexion (Cubital), Wrist Extension (Guyon's); Nighttime
Ulnar neuropathy: Dx Hx; EMG/NCS can help find site of lesion
Ulnar neuropathy: Tx modify activity; extensor splint at night; NSAIDs; surgery (nerve transposition or ligament release); No C'steroids
Radial neuropathy: etiology axilla (crutches); Saturday night palsy; handcuffs; humerus fx
Radial neuropathy: Dx Motor>sensory; weakness in extension & arm ext rotation; forearm atrophy; xray shoulder/humerus
Meralgia paresthetica: patho stretch/compress lat fem cutaneous n.
Meralgia paresthetica: RF obesity; DM; PG; hip hyperextension; lumbar lordosis
Meralgia paresthetica: Dx pain, paresthesia, numb; outer thigh; usu unilateral (relieved by sitting); no motor sx
Meralgia paresthetica: Tx often self-ltg; hydrocortisone injxn; nerve transposition
Fem neuropathy: RF lithotomy posn (inguinal lig); DM; retroperitoneal neoplasm/hematoma; pelvic fx; fem art cath (n. trauma)
Fem neuropathy: Dx Quads atrophy/weakness; sensory impairment anteromedian thigh; decreased patellar DTR; EMG/NCS; CT/MRI
Fem neuropathy: Tx Tx etiology; splints/braces; PT
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)
Sciatic n. palsy: Dx tests EMG/NCS (distinguish from peroneal neuropathy); xray
Sciatic n. palsy: Tx Tx etiology; behave change; anti-inflam; PT; surg
Peroneal n. palsy: Dx weak dorsiflexion (foot drop) & eversion; sensory loss/ paresthesia: anterolateral calf & foot dorsum; EMG/NCS? Tx sim to sciatic n. palsy
CN VII palsy (Bell): etiology idio; HIV, sarcoid, Lyme, tumor; HSV infxn? RF = PG, DM
CN VII palsy: Dx 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
CN VII palsy: Tx prednisone; artificial tears/eye patch; No Surg
CMT: genetics usually auto dom
CMT: patho Type I: demyelinating; II: axonal; Motor>Sensory; Lower > Upper; childhood/young; slow progression
CMT I vs CMT II: Dx CMT II: less mx wasting/ secondary weakness; less common postural tremor/arm involvement; NO peripheral n. hypertrophy
CMT Dx: H&P; DNA testing; Nerve/mx bx (confirmatory); EMG/NCS
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
Dejerine-Sottas Dz (CMT III): patho phytanic acid disturbance; prog demyelinating neuropathy; infancy/kids
Dejerine-Sottas Dz: Dx weakness, ataxia; sensory loss; DTR: global hyporeflexia; high CSF pro; EMG/NCS: dec motor velocity, sensory conduction
Dejerine-Sottas Dz: Tx Supportive; plasmapheresis; dietary restriction
Refsum dz: patho Progressive Demyelinating Neuropathy; Early Childhood
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
Systemic-metabolic neuropathies include: DM; uremia; alcoholic & nutrition def; paraproteinemias
DM neuropathy sensory precedes motor; lower ext precedes upper; Hx: autonomic sx?; NCS nml / mildly slow
Charcot Arthropathy is a complication of: DM peripheral neuropathy
Charcot Arthropathy d/t Joint Subluxation, Periarticular fx; rocker bottom foot; pain, swelling, ulceration
Uremia: Dx Symmetric sensory-motor; lower ext > upper; distal > proximal; severity correlates with degree of renal insufficiency
EtOH/Nutritional deficiency cobalamin (B12) def; axonal > myelin; slow progression
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
AIDP (GBS): patho Progressive Demyelinating; prob immune-mediated; Axonal Subtypes (AMAN; AMSAN)
AIDP (GBS): Dx: H&P; high CSF pro (2-3 wks post onset); EMG/NCS: demyelination with delayed conduction (3-4 wks)
AIDP (GBS): Dx: MOTOR Weakness; Symmetric; Proximal before Distal; Lower ext before Upper; Advanced: Resp mx Compromise, CN Involvement
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
AIDP (GBS): Tx Anti-inflam; plasmapheresis; IVIg; mech ventilation
Leprosy: 2 Types: tuberculoid (multifocal) & lepromatous (symmetrical)
Most common causative of meningitis in adults S. pneumo
When do LP? suspect meningitis; not if suspect abscess
Glucose depressed: usually: bac mening, or TB or fungal
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 nml
Increased WBC in CSF indicates: inflammation (not necessarily infection)
Pneumococcal meningitis Tx ceftriaxone (if GP diplococci seen, add Vanc, pending cx)
N. meningitidis petechial rash; GN diplococci; often assoc w/DIC
Meningococcal meningitis: nasal carriage eliminated with: Rifampin (alt: cipro or ceftriaxone)
Meningococcal meningitis: DOC Acqueous Pen G
H flu meningitis less common in adults; in setting of otitis or sinusitis; DOC ceftriaxone
Tuberculous meningitis usu gradual onset; listlessness & irritability; CN palsies; active TB elsewhere; CSF inc WBC (100-150), mostly lymphs; abnml CXR; acid-fast normal
Abscess: common orgs streptococcus, staphylococcus or anaerobes
Ring enhancing lesion is usually: abscess or tumor
Abscess tx prolonged IV Abx, surg drainage; monitor tx w/ serial scans; if <2 cm poss medical tx only
Rabies S/S (> 10 days) delirium, painful swallowing, rage alternating with calm
Rabies incubation period >10 days (usu 3-7 wks) (infected animal dies within 5-7 days)
Herpes encephalitis more common in elderly; often medial temporal lobes; tx most pts w/ clin syndrome of viral encephalitis empirically for HSE
CJD Sx usu later in life; rapidly progressive dementia, myoclonus, ataxia & somnolence; epileptiform pattern on EEG
MS epidemiology F>M; 350K in US (1M world); onset 20-40 yo; most present w/relapsing form; prevalence increases with distance from equator
MS S/S Optic neuritis; Transverse myelitis; Paresthesias; Ataxia; Weakness or incoordination; Spasticity; Cognitive impairment
MS: MRI findings multiple characteristic lesions or plaques: periventricular or subcortical U-fibers, corpus callosum lesions
MS: CSF findings evidence of oligoclonal bands or increased IgG index
MS: types of dx criteria Schumacher; Poser: Macdonald
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)
MS Tx options IFN; glatiramer; poss immunosupp adjuncts for aggressive/ breakthrough; corticosteroids (methylprednisolone) for relapse
Majority of malignant gliomas are: grade IV tumors (GBM or gliosarcomas)
Gliomas include: astro; oligo; ependymoma; glial cells: support
Grade 1 Glioma = Pilocytic Astrocytomas
Grade 2 Glioma = Astrocytomas, Oligodendrogliomas
Grade 3 Glioma = Anaplastic Astrocytomas, Anaplastic Oligodendrogliomas
Grade 4 Glioma = GBM; Gliosarcoma
Diffuse astrocytomas include: Low-grade infiltrative Astro (WHO II); anaplastic astro (WHO III); Glioblastoma (WHO IV)
Circumscribed astrocytomas include: Pilocytic Astro (WHO grade I); Pleomorphic xanthoastrocytoma (PXA); Subependymal giant cell Astro (SEGA)
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
High-grade gliomas (III/IV): invade via white matter tracts, cross via corpus callosum;
Primary characteristic of a grade IV glioma = necrosis with vascular proliferation
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
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
Oligodendroglioma Usu presents at low-grade (II) stage; young / middle-aged; grade II >10 yr surviv; Fried-egg cells
Most common primary brain neoplasm = GBM
Untreated GBMs: growth double in size in 14 days
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)
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
Seizure in brain tumor 35% of pts present with this; often the sx that precedes dx; focal or secondarily generalized
Probably most common problem in pts w/brain tumors = cognitive dysfn
Cognitive dysfn in brain tumor: Frontal personality; Memory problem; Depression
Cognitive dysfn: Left hemispheric tumors: language dysfunction
Cognitive dysfn: Right hemispheric tumors: problems with visual perception & scanning
Brain tumor: Focal neurologic deficits Hemiplegia; Hemiparesis; Ataxia; Nystagmus; Can mimic stroke
N/V more common in: post fossa tumors
Endocrine sx: hypothyroid; dec libido
Visual symptoms include: Contralateral flashing lights; Visual field loss; Diplopia
Symptoms from plateau waves Transitory episodes of altered consciousness & visual disturbances
Brain tumor: eval & dx H&P; CT +/- MRI; EEG; LP; PET
Factors of better prognosis: Young; High KPS; Lower pathological grade
Less significant prognostic predictors: Long duration of sx; Absence of mental status changes; Cerebellar location; Small preop tumor size; Completeness of surgical resection
BCNU AE fatigue, low blood counts, pulmo fibrosis
Tx for high grade gliomas Primary tx = surg resection, RTx, CTx; most sig prognostic factors: extent of surg resection, age, & performance status
First treatment modality for high grade glioma Surgery
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)
Std tx for WHO III &IV gliomas: Radiation tx (role of RT in WHO II gliomas is controversial)
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)
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
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
Std of care: high grade gliomas Resection; RTx & 42 days temozolomide; then (if stable dz), adjuvant CTx
Stupp study result: temozolomide added to RTx improves survival
CTx MOA & AE targets DNA replication; AE: Myelosuppression; N/V; Fatigue; Constipation or diarrhea; DI
CTx: passage across BB depends on: Molecule Size; Lipid solubility; Ionization state
CTx DI: Dex (closing BBB); phenobarbital (dec nitrosourea efficacy); anti-epileptics (affect CTx metabm)
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)
VEGF higher the VEGF, worse the prognosis; anti-VEGF Ab's effective in xenografts
Tumor blood vessels dept on growth factor; leaky & fragile; less supported by pericytes; disorganized, twisted, variable pressure; inconsistent nutrient delivery to tumor tissue
Second leading COD in brain tumor pts: thromboembolic complications
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
Ependymoma: worse prognosis: <3 yo
Ependymomas within brain: locations Infratentorial > supratentorial (2x)
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)
Medulloblastoma Malig, invasive embryonal cerebellar tumor; kids & YA; 70-80% 5-yr survival; Most arise in vermis (4th ventricle involvement)
Medulloblastoma: metastases Metastasize via CSF pathways (Drop Mets); Rare mets to bone, lymph nodes, other extracranial sites
Medulloblastoma: Sig LT toxicities of tx: Cognitive decline; Psychomotor / growth retardation; Hormonal deficits
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
Created by: duanea00