Neuro Flashcards
Bells Palsy defintion, sx, dx, tx
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
Concussion definition, sx, dx tx
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
Encephalitis defintion, sx, dx, tx
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
Epidural hematoma cause/location, sx, dx, tx
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
Subdural Hematoma cause/location, sx, dx, tx
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
Intracerebral Hemorrhage defintion/causes, sx, dx, tx
*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
Subarachnoid Hemorrhage defintion, causes, sx, dx, tx
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
Guillain Barre Syndrome defintion, sx, dx, tx
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
Tension HA sx, dx, tx
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
Trigeminal neuralgia causes, sx, dx, tx
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
Migraine types, sx, dx, tx
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
Cluster HA MC population, sx, dx, tx
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
Idiopathic Intracranial HTN (Pseudotumor Cerebri) causes, sx, PE, dx, tx
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
Triptans MOA
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
Ergotamines MOA and indications
MOA: serotonin (5HT-1b/d) agonists cause vasoconstriction & block pain pathways in the brainstem
Indications: reserved use d/t ADRs and contraindications
Antiemetics MOA and indications
MOA: dopamine receptor antagonists; may also help reduce HA pain intensity
Indications: N/V in pts w/ migraine
Delirium defintion and MCC
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
Delirium sx, dx, tx
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
Alzheimer Dementia causes, sx, dx, tx
*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
Lewy Body Dementia causes, sx, dx, tx
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)
Vascular dementia causes, sx, dx, tx
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
Frontotemporal Dementia causes, sx, dx, tx
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
Viral Meningitis defintion, sx, dx, tx
*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
Bacterial Meningitis MCC, sx, dx, tx
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)
TB Meningitis defintion and phases
*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
TB meningitis dx and tx
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
Fungal Meningitis MCC, causes, sx, dx, tx
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
Type 1: Focal seizures
dx and tx
Focal (Partial): abnormal neuronal discharge from one discrete section of one hemisphere
- w/ Retained Awareness (Simple)
*no alteration in consciousness - w/ Loss of Awareness (Complex)
*altered consciousness, automatisms (lip-smacking)
*postictal state: confusion & loss of memory
dx: EEG
tx: supportive
Type 2: generalized seizures
defintion, dx and tx
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
- Atonic (Drop Attacks)
*sudden loss of muscle tone - Tonic
*extreme rigidity 🡪 LOC - Clonic
*repetitive rhythmic jerking; often associated w/ postictal state - Myoclonic *no LOC
*sudden, brief, sporadic involuntary twitching - 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
Status epileptics defintion, sx, dx, tx
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)
Anterior cord injury: MOA, deficits, preservation
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)
Central cord injury: MOI, deficit, preservation
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)
Posterior cord injury: deficits, perservation
*rare
*damage to posterior cord or posterior spinal stenosis
deficit: LOSS OF PROPRIOCEPTION/VIBRATORY SENSE ONLY
preservation:
*pain & light touch
*NO motor deficits
Brown sequard MOI, deficit, preservation
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
Myasthenia Gravis defintion, sx, dx, tx
*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
Transient Ischemic Attack definition, sx, dx, tx
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
Lacunar Infarcts defintion, sx, dx, tx
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)
Ischemic Strokes: thrombotic vs embolic
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
Ischemic Strokes location sx: Carotid/Ophthalmic, MCA, ACA, PCA, basilar artery
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
Ischemic Strokes dx and tx
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)
Peripheral vertigo nerve effected and sx
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
Peripheral vertigo sx and tx
benign position vertigo
Meniere
vestibular neuritis
labyrinthitis
*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
Central vertigo area effected and sx
Brainstem or cerebellum
sx:
*vertical nystagmus, nonfatigable (continuous)
*gait issues more severe
*gradual onset
*positive CNS signs
Central vertigo causes
Etiology:
*cerebropontine tumors
*migraine
*cerebral vascular disease
*multiple sclerosis
*vestibular neuroma
tx = treat underlying cause
Multiple Sclerosis definition + 3 main types
*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
MS sx, dx, tx
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
