Neuro Flashcards

Question

TB Meningitis defintion and phases

Answer 1

*Hematogenous spread of infection from lungs or LN to brain parenchyma, forming small tubercules that rupture into the subarachnoid space/ventricles in the initial weeks following airborne acquisition *Subacute onset MC Complications: stroke, seizures, hydrocephalus, hyponatremia, vision loss, transverse myelitis Early Prodromal Phase, 1-3wks: insidious onset of malaise, fatigue, HA, low-grade fever, & personality change Meningitic Phase: typical meningitis sxs + protracted HA, vomiting, lethargy, confusion, varying degrees of cranial nerve palsies & long-tract signs (spasticity, ↑ reflexes, +Babinski) Paralytic Phase: occurs later as pace of illness rapidly quickens *confusion leads to stupor, coma, seizures, & often hemiparesis

Answer 2

DX: CSF NAAT, AFB smear/culture, LAM antigen CT/MRI: +/- hydrocephalus, basilar exudates, periventricular infarcts, parenchymal tuberculomas tx Intensive Phase: RIP + 4th agent x2mo *Rifampin *Isoniazid *Pyrazinamide Options for 4th agent: ethambutol, streptomycin, levofloxacin, ethionamide Continuation Phase: *Rifampin + Isoniazid x7-10mo

Answer 3

MCC: Cryptococcus neoformans *Opportunistic infection in HIV pts, CD4+ <200 *Insidious onset *Meningoencephalitis (brain parenchyma involved) sx MC: HA (develops over 1-2wks), almost always present *Meningeal signs, fever, & AMS may be minimal or absent Other s/sxs: cough, dyspnea, skin rash, visual/hearing loss dx DX: CSF culture, antigen (CrAg) India ink stain: round encapsulated yeast MRI/CT: hydrocephalus common tx Induction Therapy: *Amphotericin B + Flucytosine x2wks Consolidation Therapy: *Fluconazole 400-800mg QD x8wks Maintenance Therapy: *Fluconazole 200mg QD long-term

Answer 4

Focal (Partial): abnormal neuronal discharge from one discrete section of one hemisphere 1. w/ Retained Awareness (Simple) *no alteration in consciousness 2. w/ Loss of Awareness (Complex) *altered consciousness, automatisms (lip-smacking) *postictal state: confusion & loss of memory dx: EEG tx: supportive

Answer 5

Generalized: simultaneous neuronal discharge of both hemispheres (diffuse brain involvement) Type II: Generalized Seizures 1. Absence (Petit Mal) *brief lapse of consciousness, staring episodes w/ pauses *eyelid twitching, lip smacking; NO POSTICTAL 2. Atonic (Drop Attacks) *sudden loss of muscle tone 3. Tonic *extreme rigidity 🡪 LOC 4. Clonic *repetitive rhythmic jerking; often associated w/ postictal state 5. Myoclonic *no LOC *sudden, brief, sporadic involuntary twitching 6. Tonic Clonic (Grand Mal): LOC 🡪 tonic 🡪 clonic 🡪 postictal *Tonic Phase: LOC 🡪 rigidity (usually <60sec) 🡪 clonic phase *Clonic Phase: repetitive, rhythmic jerking (lasts <2-3min) *Postictal Phase: flaccid coma/sleep; variable duration dx: EEG tx: *absence (Petit Mal): Ethosuximide 1st line; valproic acid 2nd line *Grand Mal: valproic acid, phenytoin, carbamazepine, lamotrigine *Myoclonic: valproic acid, clonazepam *Febrile: phenobarbital

Answer 6

Status Epilepticus: seizure lasting ≥5min or >1 seizure within a 5min period w/o recovery between episodes Auras: sensory/autonomic/motor sxs of which the pt is aware of; may precede/accompany or follow seizures Automatisms: lip smacking, manual picking, patting, coordinated motor movements Diagnostics: neuroimaging once stabilized Management: *place pt in left lateral decubitus position *BDZs first line (lorazepam) *second line: phenytoin or fosphenytoin *third line: phenobarbital (refractory)

Answer 7

MOI: *MC after blowout vertebral body burst fractures (flexion) *anterior spinal artery injury or occlusion *direct anterior cord compression deficit: Motor deficit: *lower extremity > upper extremity* (corticospinal) Sensory deficit: *pain, temperature (spinothalamic tract) *light touch *may develop bladder dysfunction (retention, incontinence) preservation: *proprioception, vibration, pressure (dorsal column spared)

Answer 8

MOI: *hyperextension injuries (50% occur w/ MVA), falls in elderly, gunshot wounds, tumors, cervical spinal stenosis, syringomyelia *MC incomplete cord syndrome *it affects primarily the central gray matter (including the spinothalamic tracts) Motor deficit: *upper extremity > lower extremity*; the distal portion of the upper extremity more severe involvement (e.g., hands) from corticospinal involvement Sensory deficit: *pain/temp (spinothalamic tract) deficit greater in upper extremity; sometimes described as a “shawl” distribution preservation: proprioception, vibration, pressure (dorsal column spared)

Answer 9

*rare *damage to posterior cord or posterior spinal stenosis deficit: LOSS OF PROPRIOCEPTION/VIBRATORY SENSE ONLY preservation: *pain & light touch *NO motor deficits

Answer 10

MOI: *unilateral hemisection of the spinal cord *MC after penetrating trauma (tumors may cause it) *rare injury deficit: Ipsilateral deficits: *motor (lateral corticospinal tract) *vibration/proprioception (dorsal column) Contralateral deficits: *pain/temperature (lateral spinothalamic tract) usually 2 levels below the injury (where spinothalamic tract crosses at the spinal cord level) preservation: none

Answer 11

*autoimmune peripheral nerve disorder due to autoantibodies against the acetylcholine receptor on the muscles, leading to weakness *strong association w/ an abnormal thymus gland (e.g., hyperplasia or thymoma) 75%; HLA-B8 & DR3 PATHO: autoantibodies against acetylcholine postsynaptic receptor at the neuromuscular junction cause decreased skeletal muscle neuromuscular transmission w/ muscle recovery after a period of rest sx Ocular weakness Generalized weakness Weakness is worsened w/ repeated muscle use & throughout the day *diplopia & ptosis *bulbar muscle weakness *respiratory muscle weakness May lead to respiratory failure = myasthenic crisis dx *acetylcholine receptor antibodies initial test of choice *electrophysiology testing *chest imaging (CXR, CT, MRI) 🡪 thymus gland *Edrophonium (Tensilon) test: improvement after admin *ice pack test: improvement of ocular sxs after ice pack admin for 10min tx Long term 🡪 pyridostigmine or neostigmine first line Myasthenic crisis or severe: *plasmapheresis *IVIG Thymectomy

Answer 12

Transient episodes of neurologic deficits caused by focal brain, spinal cord, or retinal ischemia w/o acute infarction 3 main types: - embolic: AFIB, left ventricular thrombus - lacunar: penetrating small vessels - large artery: ischemia due to atherosclerosis sx Neurologic deficits lasting <24hrs – most last for a few minutes w/ complete resolution in 1hr Amaurosis fugax: transient monocular vision loss “temporary shade down on one eye” PE: carotid bruits may be heard dx Neuroimaging + neurovascular imaging + r/o cardioembolic source *neuroimaging: CT initial, MRI more sensitive *neurovascular: CT/MR angiography, carotid Doppler Conventional angiography: definitive (invasive) tx Place pt in supine position to increase cerebral perfusion, avoid lowering BP unless >220/120 - thrombolytics contraindicated Noncardiogenic TIA: - antiplatelet therapy: aspirin, clopidogrel ABCD2 score 0-3: aspirin alone ABCD2 score ≥4: aspirin + clopidogrel - carotid endarterectomy recommended if internal carotid artery stenosis 50-99% w/ a life expectancy of at least 5yrs - long term: reduce modifiable RF (DM, hyperlipidemia, HTN control), exercise

Answer 13

Small vessel disease of the penetrating branches of cerebral arteries in the pons & basal ganglia Risk Factors: 80% have hx of HTN, DM sx 5 classic presentations: Pure Motor (MC): hemiparesis or hemiplegia in the absence of sensory or “cortical” signs (aphasia, agnosia, neglect, apraxia, hemianopsia) Ataxic Hemiparesis: ipsilateral weakness & clumsiness Pure Sensory Deficits: numbness, paresthesias of arm, face, leg on one side of the body in the absence of sensory or “cortical” signs Sensorimotor: weakness & numbness of the face, arm, leg on one side of the body in the absence of “cortical” signs Dysarthria (Clumsy Hand Syndrome): dysarthria, facial weakness, dysphagia, & slight weakness & clumsiness of one hand in the absence of “cortical” signs Dx: CT scan – small punched-out hypodense areas (lacunar infarcts) usually in central & noncortical areas (e.g., basal ganglia) tx: Aspirin, control RF (HTN, DM)

Answer 14

Acute onset of neurological deficits due to death of brain tissue from ischemia MC type of stroke Causes: *thrombotic: MC (2/3) *embolic: (1/3) commonly come from heart, aortic arch, or large cerebral arteries – sources: AFIB, valvular disease, patent foramen ovale Risk Factors: HTN most significant & modifiable RF

Answer 15

Carotid/Ophthalmic – amaurosis fugax (monocular blind) MCA – aphasia, neglect, hemiparesis, gaze preference, homonymous hemianopsia ACA – leg paresis, hemiplegia, urinary incontinence PCA – homonymous hemianopsia Basilary Artery – coma, cranial nerve palsies, apnea, drop attack, vertigo

Answer 16

dx: CT head w/o contrast – best initial to r/o hemorrhagic stroke; may be normal in first 6-24hrs tx: Immediate management: - within 3hrs of sxs onset: alteplase (thrombolytic) if no contraindications (BP >185/110, recent/bleeding d/o, recent trauma) - >3-4.5hrs: aspirin - BP control IF ≥185/110 Long-term management: - antiplatelet therapy: aspirin, clopidogrel, dipyridamole - anticoagulation ONLY if cardioembolic (AFIB) - statin (regardless of LDL level)

Answer 17

Labyrinth or vestibular nerve (part of CN 8) sx: *horizontal nystagmus (usually beats away from affected side), fatigable *sudden onset of tinnitus & hearing loss usually associated w/ peripheral compared to central causes

Answer 18

*benign position vertigo (MC): episodic vertigo + no hearing loss tx: Epley maneuver *Meniere: episodic vertigo + hearing loss tx: diet, antihistamines, HCTZ, etc *vestibular neuritis: continuous vertigo + no hearing loss tx: glucocorticoids, antihistamines *labyrinthitis: continuous vertigo + hearing loss tx: glucocorticoids, antihistamines

Answer 19

Brainstem or cerebellum sx: *vertical nystagmus, nonfatigable (continuous) *gait issues more severe *gradual onset *positive CNS signs

Answer 20

Etiology: *cerebropontine tumors *migraine *cerebral vascular disease *multiple sclerosis *vestibular neuroma tx = treat underlying cause

Answer 21

*autoimmune, inflammatory demyelinating disease of the CNS of idiopathic origin *associated w/ axon degeneration of white matter (brain & spinal cord) *MC in women & young adults 20-40yrs, colder climates; associated w/ HLA-DR2 3 MAIN TYPES: *Relapsing-Remitting (MC!): episodic exacerbations *Progressive Disease: progressive decline w/o acute exacerbations *Secondary Progressive: relapsing-remitting pattern that becomes progressive

Answer 22

Sensory disturbances: *pain, paresthesias Motor deficits: *weakness, gait & balance problems Visual disturbances: *diplopia, optic neuritis *trigeminal neuralgia Uhthoff’s Phenomenon 🡪 worsening of sxs w/ heat PE: Upper motor neuron signs *spasticity, upward Babinski, hyperreflexia, muscle rigidity Lhermitte’s sign 🡪 neck flexion causes lightening-shock type pain radiating from the spine down the leg Cerebellar: Charcot’s neurologic triad *nystagmus, staccato speech, intentional tremor Spinal cord sxs: bladder, bowel, or sexual dysfunction dx: Mainly clinical – at least 2 distinct episodes of CNS deficits MRI w/ gadolinium *hyperintense white matter plaques Lumbar puncture *↑ IgG & oligoclonal bands tx: Acute exacerbations: *IV glucocorticoids *plasmapheresis if unresponsive Prevention of relapse & progression: *Beta-interferon, Glatiramer