Neuro Flashcards

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1
Q

Bells Palsy defintion, sx, dx, tx

A

causes: Idiopathic, unilateral CN VII/facial nerve palsy leading to hemifacial weakness & paralysis due to inflammation or compression – LMN disorder

May be related to HSV reactivation

Risk Factors: DM, pregnancy (esp. 3rd TM), post URI, dental nerve block

Sx:
Sudden onset ipsilateral hyperacusis (ear pain) 24-48hrs followed by unilateral facial weakness or paralysis involving the forehead
*unable to life the affected eyebrow
*wrinkled forehead, loss of the nasolabial fold
*drooping of the corner of the mouth
*taste disturbances (anterior 2/3)
*biting the inner cheek
*eye irritation (d/t ↓ lacrimation & inability to fully close)

Bell phenomenon: eye on the affected side moves laterally & superiorly when eye closure is attempted

Weakness/paralysis ONLY affected the face

Dx: dx of exclusion

tx: No treatment required (>85% resolve in 1mo)

Supportive: artificial tears

Prednisone (esp. if started within 72hrs of sxs onset) reduces the time to full recovery and increases the likelihood of complete recuperation

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2
Q

Concussion definition, sx, dx tx

A

defintion:
Mild traumatic brain injury leading to alteration in mental status, w/ or w/o LOC

May result after blunt force or an acceleration/deceleration head injury

Sx:
HA, dizziness, psychosocial sxs, cognitive impairment

Confusion: confused or blank expression, blunted affect
Amnesia: pretraumatic (retrograde) or posttraumatic (anterograde); visual disturbances: blurred or double vision

Delayed response/emotional changes: emotional instability
Signs of ↑ ICP: persistent vomiting, worsening HA, increasing disorientation, changing levels of consciousness

dx: CT w/o contrast

tx: Cognitive & physical rest

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3
Q

Encephalitis defintion, sx, dx, tx

A

Infection of the brain parenchyma

Etiologies:
*HSV1 MCC
*VZV, EBV, measles, mumps, rubella, HIV

Meningeal sxs:
*HA, neck stiffness
*photosensitivity
*fever, chills, N/V
*seizures

*AMS, changes in personality, speech, & movement

PE: focal neurologic deficits
*hemiparesis
*sensory deficits
*cranial nerve palsies

dx:
FIRST CT scan
THEN LP
*normal glucose, increased lymphocytes

tx:
IV acyclovir if HSV related otherwise supportive

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4
Q

Epidural hematoma cause/location, sx, dx, tx

A

Location: arterial bleed MC between skull & dura

Mechanism: MC after temporal bone fracture 🡪 middle meningeal arterial disruption

sx:
Brief LOC 🡪 lucid interval 🡪 coma

HA, N/V, focal neuro sxs, rhinorrhea (CSF fluid)

CN III palsy if tentorial herniation

dx: CT: convex (lens-shaped) bleed
*does NOT cross suture lines

tx:
+/- herniate if not evacuated early

Observation if small

If ↑ ICP: mannitol, hyperventilation, head elevation, +/- shunt

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5
Q

Subdural Hematoma cause/location, sx, dx, tx

A

Location: venous bleed MC
- between dura & arachnoid d/t tearing of cortical bridging veins

MC in elderly

Mechanism: MC blunt trauma (“contre-coup”), venous bleed

sx:
Varies, may have focal neuro sxs

Chronic:
*insidious onset of HA
*cognitive impairment
*somnolence
*occasional seizures
CT 🡪 HYPOdense

dx:
CT: concave (crescent-shaped) bleed
*bleeding CAN cross suture lines

tx:
Hematoma evacuation vs. supportive
Evacuation if massive or ≥5mm midline shift

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6
Q

Intracerebral Hemorrhage defintion/causes, sx, dx, tx

A

*bleeding within the brain parenchyma
*may compress the brain, ventricles, & sulci

Risk Factors:
*HTN MCC of spontaneous ICH
*cerebral amyloid angiopathy MCC of nontraumatic ICH in the elderly
*arteriovenous malformation MCC in children
*trauma, older age, high ETOH intake, coagulopathy

sx:
Neurologic sxs usually increase within min-hrs
*HA, N/V
*syncope
*focal neuro sxs (hemiplegia, hemiparesis, seizures)
*altered mental status

PE:
*may have focal motor & sensory defects

dx: CT w/o contrast

tx:
Supportive: gradual BP reduction

Prevention of increased intracranial pressure
*raising head of the bed 30 degrees
*limiting IV fluids
*BP management
*analgesia, sedation

Reduction of intracranial pressure: IV mannitol

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7
Q

Subarachnoid Hemorrhage defintion, causes, sx, dx, tx

A

Bleeding between the arachnoid membranes & the pia mater

Etiologies:
*MC due to a ruptured berry aneurysm at the anterior communicating artery
*AVM, stroke, trauma

sx:
*sudden, intense thunderclap HA (unilateral, occipital area)
“worse HA of my life”
*N/V, meningeal sxs (photophobia, neck stiffness, fever)
*LOC
PE:
*meningeal signs: nuchal rigidity, + Brudzinski, + Kernig
*CN III palsy – fixed, dilated, “blown” pupil
*Terson Syndrome: retinal hemorrhages

dx:
CT scan w/o contrast
LP 🡪 performed if CT (-)
*xanthochromia

tx:
Supportive: bed red, stool softeners, lower intracranial pressure
*Nimodipine reduces cerebral vasospasms, improving neurologic outcomes

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8
Q

Guillain Barre Syndrome defintion, sx, dx, tx

A

Acquired autoimmune demyelinating polyradiculopathy of the peripheral nervous system

PATHO: autoantibody attacks the myelin sheath of the peripheral nerves after an infection

sx:
*symmetric ascending weakness & sensory changes (paresthesias, pain) – distal lower extremities first
*may develop weakness of the respiratory muscles & bulbar muscles (swallowing difficulties)

PE:
*LMN signs: ↓ DTRs, flaccid paralysis, weakness
*sensory deficits; cranial nerve palsies (CN VII)
*autonomic dysfunction: tachycardia, arrhythmias, hypotension or HTN, breathing difficulties

dx:
Electrophysiologic studies
*decreased motor nerve conduction velocities & amplitude

CSF analysis
*high protein w/ a normal WBC count

tx:
*plasmapheresis, IVIG first line
*mechanical ventilation

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9
Q

Tension HA sx, dx, tx

A

MC overall cause of primary HA – mean age of onset ~30yrs

Risk Factors: mental stress, sleep deprivation, eye strain

sx:
Bilateral: pressing, tightening “band-like,” nonthrobbing (nonpulsatile) steady or aching HA (often worsens throughout the day)
*worsened w/ stress, fatigue, noise, or glare
*not worsened w/ routine activity (as in migraines)
*usually not pulsatile & not associated w/ N/V, photophobia, phonophobia, or focal neuro sxs (auras)
PE: usually normal but may have pericranial muscle tenderness (head, neck, or shoulders)

dx: clinical

tx:
First line: NSAIDs & other analgesics (acetaminophen or aspirin); local heat
Anti-migraine medications

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10
Q

Trigeminal neuralgia causes, sx, dx, tx

A

PATHO: compression of the trigeminal nerve (CN V) root by the superior cerebellar artery or vein (90%); idiopathic (!0%)

MC in middle-aged women
In younger pts, suspect multiple sclerosis

sx:
HA: paroxysmal, brief, episodic, stabbing, lancinating or shock-like pain in the 2nd/3rd division of the trigeminal nerve, lasting sec-mins
*worse w/ touch, chewing, brushing teeth, drafts of wind, & movements (often unilateral)

Pain starts near mouth & shoots to eye, ear, & nostril on the ipsilateral side & often occurs many times throughout the day

PE: usually normal but light palpation of “trigger zones” may trigger attack

dx: clinical

tx:
Carbamazepine first line; oxcarbazepine

Gabapentin, baclofen, lamotrigine

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11
Q

Migraine types, sx, dx, tx

A

MC in women; family hx (80%)

Types:
Migraine w/o aura (MC)
Migraine w/ aura

sx:
Usually lateralized, pulsatile (throbbing) HA often associated w/ N/V, photophobia, phonophobia; 4-72hrs duration, mod-severe intensity
*worsened w/ routine physical activity, stress, lack or excessive sleep, ETOH, specific foods (chocolate, red wine), hormonal (OCPs, menstruation), dehydration

Auras: focal neurologic sxs that usually last <60min; accompany or follow the HA within 60min
*visual (MC)
*auditory
*somatosensory
*loss of function (aphasia, hearing)

dx: clinical

tx:
Symptomatic (abortive) management
- NSAIDs, acetaminophen, aspirin first line if mild; some meds have caffeine to improve sxs
- IV fluids, placing pt in dark/quiet room
- triptans or ergotamines if mod-severe or no response to analgesics
- antiemetics (metoclopramide, prochlorperazine)

Prophylactic (preventative)
- anti-HTN: BBs (propranolol), CCBs
- TCAs, antidepressants, anticonvulsants (valproate, topiramate), NSAIDs

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12
Q

Cluster HA MC population, sx, dx, tx

A

Predominantly young & middle-aged males (10x MC than women)

Associated w/ multiple frequent HA w/ high intensity & brief duration

sx:
Triggers: worse at night, ETOH, stress, specific foods

HA: severe, unilateral periorbital or temporal pain (sharp, lancinating); bouts last <2hrs w/ spontaneous remission – bouts occur several times a day; may have 1-2 cluster periods a year (each lasting wks-mos)

PE: ipsilateral findings – Horner’s syndrome (ptosis, miosis, anhidrosis), nasal congestion, rhinorrhea, conjunctivitis, lacrimation

dx: clinical

tx:Acute:
- 100% oxygen first line
- antimigraine meds help during attack: SQ sumatriptan or ergotamines

Prophylaxis: verapamil first line

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13
Q

Idiopathic Intracranial HTN (Pseudotumor Cerebri) causes, sx, PE, dx, tx

A

Idiopathic increased intracranial (CSF) pressure w/ no clear cause evident on neuroimaging (CT/MRI)

Pseudotumor Cerebri: mimics a brain tumor w/ N/V, visual disturbances

s/sxs of increased ICP:
*HA: pulsatile, worse w/ straining or changes in posture
*retrobulbar pain that may be worse w/ eye movements
*N/V, tinnitus
*visual changes – may lead to blindness if not treated

Ocular Exam:
*fundoscopy: papilledema (usually bilateral, symmetric)
*may have visual field loss
*may have diplopia due to a cranial nerve V1 (abducens) palsy

dx
CT scan: performed prior to LP to r/o intracranial mass

LP: ↑ CSF pressure (≥250mmH2O) + otherwise normal CSF

tx
Acetazolamide first line (decreases CSF production) & weight loss recommended
- furosemide may be adjunct

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14
Q

Triptans MOA

A

MOA: serotonin (5HT-1b/d) agonists causes vasoconstriction & block pain pathways in the brainstem

Indications: mod-severe migraines or no response to analgesics in mild dz; can be combined w/ analgesics

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15
Q

Ergotamines MOA and indications

A

MOA: serotonin (5HT-1b/d) agonists cause vasoconstriction & block pain pathways in the brainstem
Indications: reserved use d/t ADRs and contraindications

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16
Q

Antiemetics MOA and indications

A

MOA: dopamine receptor antagonists; may also help reduce HA pain intensity

Indications: N/V in pts w/ migraine

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17
Q

Delirium defintion and MCC

A

Acute, abrupt, transient confused state due to an identifiable cause (e.g., medications, infections, electrolyte abnormalities, CNS injury, uremia, organ failure, illicit drug intoxication or withdrawal, etc.)

High Risk: post-op, esp. if heart disease or DM

MC presentation of AMS in the inpatient setting

MCC: alcohol abuse (delirium tremens)
*thyroid storm

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18
Q

Delirium sx, dx, tx

A

Rapid onset associated w/ fluctuating mental status changes & marked deficit in short-term memory

*Acute & rapid deterioration in mental status (hrs-days)
*Fluctuating level of awareness
*Disorientation

Visual hallucinations (MC)

dx: Mental status exam (MMSE)

Labs:
*chemistry
*B12/folate

Febrile + delirious 🡪 LP (cerebral edema)

tx:
Usually associated w/ full recovery within 1wk in most cases
Treat the cause (almost always reversible)
Supportive care

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19
Q

Alzheimer Dementia causes, sx, dx, tx

A

*MC age-related neurodegenerative disease

PATHO: plaques containing beta-amyloid peptide & neurofibrillary tangles containing tau protein occur throughout the cortex

sx
*short-term memory impairment early & most prominent feature
*variable deficits of executive function, visuospatial function, & language

dx:
MRI: diffuse cortical atrophy

tx
First line: cholinesterase inhibitors
*donepezil, rivastigmine, galantamine

*Memantine: NMDA antagonist

20
Q

Lewy Body Dementia causes, sx, dx, tx

A

PATHO: alpha-synuclein-containing Lewy bodies occur in the brainstem, midbrain, olfactory bulb, & neocortex +/- Alzheimer pathology

*histologically indistinguishable from Parkinson disease

sx
*cognitive dysfunction, w/ prominent visuospatial & executive deficits
*psychiatric disturbance w/ anxiety, visual hallucinations, & fluctuating delirium
*Parkinsonian motor deficits w/ or after other features

dx: Histology: cortical Lewy bodies

tx
*cholinesterase inhibitors first line (lessen delirium)

21
Q

Vascular dementia causes, sx, dx, tx

A

PATHO: multifocal ischemic change
RF: HTN most important

sx: stepwise accumulation of cognitive deficits in associated w/ repeated strokes; sxs depend on stroke location

dx: MRI: white matter lesions, cortical, subcortical, or lacunar infarcts

tx: HTN control

22
Q

Frontotemporal Dementia causes, sx, dx, tx

A

PATHO: neuropathology is variable & defined by the protein found in intraneuronal aggregates

*personality first, memory later

Behavioral Variant:
*deficits in empathy, social comportment, insight, abstract thought, & executive function; relative preservation of memory
*behavior disinhibited, impulsive, & ritualistic, w/ prominent apathy & ↓ interest in sex or sweet/fatty foods
*focal right frontal atrophy, associated w/ ALS

Semantic Variant Primary Progressive Aphasia:
*deficits in word-finding, single-word comprehension, object & category knowledge, & facial recognition; behaviors may be similar to behavioral variant FTD
*focal, asymmetric temporal pole atrophy

Nonfluent/Agrammatic Variant Primary Progressive Aphasia:
*speech is effortful w/ dysarthria, phonemic errors, sound distortions, & poor grammar
*focal EPS & apraxia of the right arm/leg common, overlaps w/ corticobasal degeneration
*focal left frontal atrophy

dx: MRI: frontal + temporal atrophy

Histology: pick bodies (round/oval aggregates of Tau protein seen on silver-staining of cortex)

tx: none

23
Q

Viral Meningitis defintion, sx, dx, tx

A

*Systemic viral infection within the CNS restricted to the meninges, ependyma, & subarachnoid space

MC Etiologies: enteroviruses (esp. Coxsackievirus B & Echovirus), HSV-2, HIV

SXS: fever, HA, nuchal rigidity
*general malaise, myalgia, N/V, photophobia, diarrhea, rash
PE: absence of abnormal neurologic findings +/- transiently increased DTRs

dx:
CSF pattern: lymphocytic pleocytosis, mildly elevated protein, normal glucose

tx: Self-limited, only supportive tx
*analgesics, antiemetics, IVF

24
Q

Bacterial Meningitis MCC, sx, dx, tx

A

MCC: S. pneumoniae (gram+ diplococci), Neisseria meningitides (gram- diplococci), Haemophilus influenzae B (Hib)
*Acute onset

Classic SXS: severe HA, fever, stiff neck (nuchal rigidity), AMS
*Almost all pts will have 2/4 classic sxs
Other sxs: N/V, photophobia
Infants: fever, irritability, poor feeding, bulging fontanelles
*generally do not have stiff neck

+Kernig: inability/reluctance to allow full knee extension when hip flexed 90o
+Brudzinski: spontaneous hip flexion during passive neck flexion
N. meningitides: petechial rash on trunk, legs, & mucous membranes**

dx:
CT before LP if: immunocompromised, hx of CNS disease, new-onset seizure, papilledema, abnormal level of consciousness, focal neurological deficit
CSF pattern: neutrophilic pleocytosis, elevated protein, low glucose
Other: CSF gram stain & culture, PCR

tx:
Empiric ABX:
<1mo: ampicillin + gentamicin

> 50y: vancomycin + ampicillin + 3rd gen cephalosporin (ceftriaxone or cefotaxime)

Everyone else:
vancomycin + (ceftriaxone or cefotaxime)

25
Q

TB Meningitis defintion and phases

A

*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

26
Q

TB meningitis dx and tx

A

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

27
Q

Fungal Meningitis MCC, causes, sx, dx, tx

A

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

28
Q

Type 1: Focal seizures
dx and tx

A

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

29
Q

Type 2: generalized seizures
defintion, dx and tx

A

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

  1. Atonic (Drop Attacks)
    *sudden loss of muscle tone
  2. Tonic
    *extreme rigidity 🡪 LOC
  3. Clonic
    *repetitive rhythmic jerking; often associated w/ postictal state
  4. Myoclonic *no LOC
    *sudden, brief, sporadic involuntary twitching
  5. 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

30
Q

Status epileptics defintion, sx, dx, tx

A

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)

31
Q

Anterior cord injury: MOA, deficits, preservation

A

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)

32
Q

Central cord injury: MOI, deficit, preservation

A

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)

33
Q

Posterior cord injury: deficits, perservation

A

*rare
*damage to posterior cord or posterior spinal stenosis

deficit: LOSS OF PROPRIOCEPTION/VIBRATORY SENSE ONLY

preservation:
*pain & light touch
*NO motor deficits

34
Q

Brown sequard MOI, deficit, preservation

A

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

35
Q

Myasthenia Gravis defintion, sx, dx, tx

A

*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

36
Q

Transient Ischemic Attack definition, sx, dx, tx

A

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

37
Q

Lacunar Infarcts defintion, sx, dx, tx

A

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)

38
Q

Ischemic Strokes: thrombotic vs embolic

A

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

39
Q

Ischemic Strokes location sx: Carotid/Ophthalmic, MCA, ACA, PCA, basilar artery

A

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

40
Q

Ischemic Strokes dx and tx

A

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)

41
Q

Peripheral vertigo nerve effected and sx

A

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

42
Q

Peripheral vertigo sx and tx
benign position vertigo
Meniere
vestibular neuritis
labyrinthitis

A

*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

43
Q

Central vertigo area effected and sx

A

Brainstem or cerebellum

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

44
Q

Central vertigo causes

A

Etiology:
*cerebropontine tumors
*migraine
*cerebral vascular disease
*multiple sclerosis
*vestibular neuroma

tx = treat underlying cause

45
Q

Multiple Sclerosis definition + 3 main types

A

*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

46
Q

MS sx, dx, tx

A

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

47
Q
A