Neurology Flashcards

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1
Q

syncope

A
  • loss of consciousness/postural tone 2ary to acute dec in cerebral blood flow; 20% pts have 1ary dx of anxiety, mood, or substance abuse
  • Ddx:
    • seizure
    • cardiat et: arrhythmias (sick sinus, v-tach, AV block, rapid SVT), obstruction of blood flow (aortic sten, HCM, mitral valve prolapse), massive MI
    • vasovagal: ↑parasymp, ↓symp stim, MCC, emotional stress, fear, etc.; premonitory sxs = pallor, sweat, light-headed, N, dec vision, roaring in ears; Tilt table study to reproduce sxs; tx = supine, elevate legs, BB
    • orthostatic HoTN: caused by ganglionic blocking agents, DM, old, defect in vasomotor reflexes; posture is main cause, + tilt table, tx with inc sodium and fluids, fludrocortisone
    • TIA, hypoglyc, hypervent, hypersensitivity, mech reduction of venous return (valsalva, postmicturition), meds
  • EKG FOR ALL PTS
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2
Q

Seizure

A
  • synchronoous dc of electrical activity or chonic disorder or recurrent, idiopathic seizures not reporduced by 2ary cause
  • causes: 4Ms and 4Is
    • Metabolic (hyponatremia, H2O tox, hypoglycemia, hyperglyc, hypocalc, uremia, thyroid storm, hypertherm
    • Mass lesions (brain met, 1ary brain tumor, hemorrhage)
    • Missing drugs (noncompliance w/ anticonvusants, withdrawal from ETOH, benzos, barbituates)
    • Miscellaneous: pseudosiezures (psych), eclampsia, HTN enceph, febrile
    • Intox (cocaine, lithium)
    • Infxn (septic shock, bact, viral meningitis, brain abscess)
    • Ischemia (embolic stroke, TIA, syncope)
    • Increased ICP (dt trauma)
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3
Q

epilepsy

A
  • chronic, reccurent seizures not produced by 2ary cause
  • Triggers: sleep dep, emotional stress, meds, infxn, alc
  • Causes: childhood and age
  • sxs: dz requires 2+ separate seizures (unprovoked)
  • dx: if known epileptic → check anticonculsant levels, if 1st seizure → CBC, CMP, gluc, renal fn, urinalysis
    • EEG(abnormal pattern is NOT dx on its own), CT, MRI, LP, preg, PRL (serum levels rise abruptly in postictal state only in true epilepsy)
  • tx: ABCs, check for noncompliance, check drug levels, increase dose of first anticonvulsant if persistent, add second drug if szs still uncontrolled. if controlled on 2 drugs, continue for 2y and then taper
    • first seizure: EEG with neuro consult, if normal then recurrence is low.
    • dont tx most pts with only one seizure
    • start antiepileptics only if EEG abnl, MRI abnl or status epilepticus
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4
Q

simple partial seizure (focal), or aura

A
  • sxs: consciousness INTACT (not impaired)
    • seizure is localized but may evolve - can be described as a sensation (N, epigastric sensation), abnl thought (fear, deja vu), or involuntary mvmt
    • pt can interact normally w/ enviro except for limitations imposed by seizure itself on local brain fns
    • may involve transient unilateral clonic-tonic mvmt
    • 60% of pts with partial epilepsy
  • dx: EEG
  • tx: phenytoin and carbamazepine (alternatives = phenobarb, depakote, primidone)
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5
Q

Complex partial seizure

A
  • consciousness IMPAIRED (spans from minimal to complete unresponsiveness), preceding aura, ictal manifestations (1-3 mins), eyes usually open during ictus, automatisms (purposeless, involuntary, repetitive mvmts), epigastric sensation or vague cephalic sensation, olfactory or gustatory hallucinations, deja vu, micropsia, macropsia, fear, pleasure, anger, voices, music, speech arrest, absence-like sxs
    • contralateral: eye dev, arm extens, fencing posture, clonic mvmts of face, fingers, hand, foot
    • postictal confusion (fatigue, ipsilateral HA, mins to hours)
  • dx: EEG
  • tx: trileptal, lamictal, phenytoin and carbamazepine
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6
Q

Generalized tonic clonic (grand mal) seizure

A
  • eyes open and “roll to back of head”, begins with sudden LOC, apnea, urinary incontinence, vomiting
  • Tonic phase: extensor posturing for 20-60s (rigid trunk, limb extension, bilaterally symmetrical)
  • clonic phase: progressively longer periods of inhibition → lasting up to 60s
  • postictal phase: transient deep stupor → 15-30min of lethargy, confusion → hours to days of HA, muscle soreness, mental dulling, mood changes
  • signs: cyanosis, foaming at mouth, tongue biting, hypoxemia
  • dx: lactic acidosis, elevated catecholamines, increased CK, PRL, corticotropin, cort
    • EEG: generalized high amp rapid spiking
  • tx: roll pt onto side, levetiracetam, topiramate, zonisamide, phenytoin and carbamazepine, phenobarb, depakote, primidone
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7
Q

absence (petitmal) seizures

A
  • school aged children, resolves with age
  • sxs: disengage from current activity, “stare into space”, minor clonic activity (eye blinks, head nodding), brief (lasts a few seconds), but quite frequent (up to 100x/d), impairment of consciousness, no loss of postural tone and no postictal confusion
  • dx: EEG shows 3/s spike and slow wave activity
  • tx: ethosuximide, depakote, zonisamide
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8
Q

myoclonic seizures

A
  • rapid recurrent, brief muscle jerks of face or hands → massive bilat spasms simultaneously affecting head, limbs, trunk
  • occurs bilaterally, synchronously or asynchronously, may occur shortly after waking up, but can occur at any time
  • dx: EEG
  • tx: keppra (levatiracetam), depakote (valproic acid)
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9
Q

Status epilepticus

A
  • causes: noncompliance, ETOH widrawal, intracranial infxn, neoplasm, metabolic dz, drug overdose
  • sxs: prolonged, sustained unconsciousness w/ persistent convulsive activity lasting longer than 30 min OR 2 or more sequential seizures without full recovery of consciousness between them
  • dx: EEG, MRI
  • tx: ABCs, IV, O2, monitor, CMP, Ca, Mg, Phos, CBC, UTox, troponin, AED levels, gluc
    • if hypoglyc, give 100mg IV thiamine and 50ml 50% dextrose, 0.1 mg/kg IV lorazepam, repeat if persistent
    • IV fosphenytoin or IV phenytoin 20mg/kgIV, monitor HR and BP
    • Intubation, IV phenobar
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10
Q

Bell’s palsy

A
  • hemifacial weakness/paralysis of mm innervated by CN VII dt swelling of cranial nerve
  • uncertain cause, possibly viral
  • sxs: URI preceding event, acute onset unilateral facial weakness/paralysis, both upper and lower parts of face - mastoid pain, decreased tearing, cannot raise eyebrow on affected side, weak orbicularis oculis (unable to close eye), impairment or loss of taste
  • signs: check ext ear canal for rash or vesicles to r/o Ramsay Hunt, hyperacusis (tuning fork)
  • dx: clinical, consider Lyme dz (dont use steroids), EMG testing if paresis fails to resolve in 10d
  • tx: no tx required, short course of prednisone and acyclovir, wear eye patch to prevent abrasion, surg decompress of CN VII, prognosis good (80-90% full recovery in 6wk-3mo)
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11
Q

transient ischemic attack

A
  • brief episode of neurologic dysfn caused by focal brain or retinal ischemia, blockage in flow does not last long enough to cause permanent infarction, retinal artery (MCA) → amaurosis fugax
  • sxs: sudden onset neuro deficit, lasts minutes to <1h, reversal of sxs within 24h
  • dx: carotid doppler US, MRA of neck
  • tx: hospital admission for new onset and recurrent TIA, unless confident dx of cause of event can be made, antiplatelet tx (ASA +/- dipyridamole OR clopidogrel), if high risk → warfarin should be used, RF for recurrent stroke, average 5% risk per year
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12
Q

Lacunar stroke

A
  • internal capsule, pons, thalamus, causes 20% of all strokes; usually affects subcortical structures
  • Narrowing of large arterial lumen dt thickening of vessel wall (not by thrombosis)
  • RF: hx of chronic HTN and DM
  • affected arteries: MCA, circle of Willis, basilar and vertebral arteries
  • sxs: hemiparesis - weakness of entire left or right side
    • internal capsule: pure motor hemiparesis
    • pons: dysarthria, clumsy hand
    • thalamus: pure sensory deficit
  • dx: focal features and usually contralateral pure motor or pure sensory deficits
  • tx: prevention of lacunar strokes: control HTN
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13
Q

CHADS2 scoring

A
  • for stroke risk
  • C: cardiac failure
  • H: HTN
  • A: age >75y
  • D: diabetes
  • S: stroke or TIA (2 pnts)
  • each other is 1 pnt each
  • CHADS score 2 or greater is associated with annual risk of sstroke over 4%
  • 0: ASA
  • 1: ASA or warfarin
  • 2: anticoagulated unless specific CI
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14
Q

Migraines

A
  • W>M, MC + FHx, precipitating factors = emotional stress, hormones, not eating, weather, sleep disturbances, odors, neck pain, lights, ETOH, smoke, sleeping late, heat food, exercise, sex
  • Comorbidities: sleep disturbances
  • sxs: recurrent attacks
    • 4 phases:
      • Prodrome: euphoria, depression, irritability, cravings, C, neck stiffness, etc.
      • Aura (25%)
      • HA: unilateral, pulsatile, V, photophob, better w/ lying down, dark, quiet
      • Postdrome: pain w/ sudden mvmts, drained, exhausted
  • dx: clinical, neuroimaging indicated for first/worst HA, >50yo, head CT, MRI
  • complications: status migrainosus, persistant aura w/out infarction, migrainous infarciton, migraine aura-triggered seizure
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15
Q

Migraines with and without aura

A
  • w/aura: autosomal dominant with incomplete penetrance
  • w/out aura: most common type (75%)
  • causes: serotonin depletion
  • aura sxs: aura (doesnt always precede HA, gradual development but can be acute <5min, no longer than 1h, pos and neg features, completely reversible)
    • positive sxs: visual (bright lines, shapes, objects), auditory (tinnitus, etc.), somatosensory (burning, pain, paresthesia), or motor (jerking, repetitiv rhythmic movements)
    • Negative sxs: loss of vision, hearing, feeling, or ability to move a part of the body
  • non-aura sxs: sever unitaleral throbbing HA lasts 4-72hrs, N/V, photophobia, increased sens of smell
  • aura dx: at least 2 attacks, fully reversible aura
    • characteristics, at least 2: 1 aura spreads gradually over >5mins, and 2+ sxs occur in succession, each aura lasts 5-60mins, at least 1 aura is unilateral, aura followed by HA within 60mins
  • non-aura dx: at least 5 attacks, lat 4-72hrs, at least one of N or V or both
  • tx: NSIADs, tylenol, antiemetics (mild-mod), PO triptan or sumatriptan, naproxen, SQ suma, nasal suma and solmitriptan (mod-severe), DHE agonist, sumatriptan, DONT USE BB AS INITIAL TX IF >60 AND IN SMOKERS
    • emergent migraines: sumatriptan, metoclopramide, prochlorperazine, DHE, Ketorolac
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16
Q

chronic migraine

A
  • HA occuring 15 or more days/mo, features of migraine on at least 8 d/mo
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17
Q

tension HA

A
  • unkown cause, W>M, precipitated by stress, depression, anxiety, most prevelent HA in general population and second most prevalent disorder in the world
  • sxs: bilateral, “vice like”, encircles entire head, nonthrobbing, lasts 30min to 7d
  • signs: increased pericranial m tenderness
  • dx: CT/MRI, blood work, spinal fluid analysis
    • at least 10 eps of HA, lasting 30min to 7d each, at least 2 of (bilateral, pressing or tightening, mild or mod, not aggravated by routine activity)
  • tx: NSIADs, triptans
    • emergent setting: metoclopramide + diphenhydramine, ketorolac, chlorpromazine
    • pregnancy: butalbital with tylenol
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18
Q

cluster HA

A
  • rare, middle aed men, chronic cig smokers, episodic (90%), last 2-3mo, chronic cluster last 1-2y, HA do not remit
  • sxs: unilateral, excruciating orbital, supraorbital, or temporal pain (behind the eye), deep, burning, searing or stabbing pain
    • associated: ipsilateral lacrimation, facial flushing, nasal stuffiness/dc, begins few hrs after pt goes to bed, awakens from sleep, occur nightly 2-3mo, then dissapear, worse with alcohol and sleep
  • signs: pallor, diaphoresis, horner syndrome, restlessness, agitation, focal neuro symptoms, sensitivity to alc
  • dx: at least 5 attacks, either or both - conjunctival injection or lacrimation, nasal congestion or rhinorrhea, eyelid edema, forehead or facial sweating or flushing, sensation of . fullness in ear, miosis or ptosis, restlessness or agitationattacks occur between qod and 8/d for more than half the time when disorder is active
  • tx: O2 inhalation via nonrebreather, SQ sumatriptan
  • prophylaxis: verapamil, ergotamine, methylsergide, lithium, steroids, resolution w/in 1 wk
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19
Q

bacterial meningitis etiology, RF, and sxs

A
  • acute = hours to days, chronic = within weeks to months, commonly caused by mycobacteria, fungi, Lyme dizease, or parasites
  • inflamm of meningeal membs, infxs agents colonize nasopharynx and resp tract, neonatal = listeria monocytogenes
  • MCC: strep pneumo, H flu, N meningitidis
  • sxs: TRIAD = fever, nuchal rigidity, change in mental status
    • HA (more severe lying down), N/V, stiff painful neck, malaise, photophob, AMS (confusion, lethargy, coma)
  • signs: ​Rash (maculopap rash with petechiae for N mening) or vesicular lesions (varicella/HSV), inc ICP and its manifestations (papilledema, szs)
    • cranial nerve palsies, +Kernig, +Brudzinski
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20
Q

bacterial meningitis dx and tx

A
  • dx: lumbar puncture - unless evidence of space-occupying lesion (neut predom, cell count >1000, low gluc, elevated prot)
    • CT scan of head - recommended before performing LP if focal neuro signs or evidence of space-occupying lesion with high ICP
    • blood cx - prior to abx
  • tx: empiric tx after LP, IV abx immediately if CSF cloudy or bact suspected, steroids if cerebral edema present
    • early onset (<7d) = amp
    • late onset (7d-3mo) = amp + cefotaxime
    • late late (>3mo) = cefotaxime (3rd gen) + vanco
  • health maint: vaccinate asplenic pts and immunocomp for meningococcus
  • prophylax: rifampin or ceftriaxone for close contacts of meningococcal
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21
Q

aseptic (viral) meningitis

A
  • caused by a variety of non-bact pathogens, frequently viruses (enterovirus 70 or 71, coxsackievirus A7 or A9 and HSV), MC in summer and fall temps
  • sxs: acute onset of subacute fever, chills, HA, photophob, pain on eye mvmt, N/V/D, myalgias, rash, pleurodynia, myocarditis, herpangina
  • signs: meningismus without local neuro signs, drowsiness or irritability
  • dx: LP (pleocytosis - lymphocyte predom, cell count <1000, normal gluc, elevated prot)
  • tx: supportive, analgesics and fever reduction, better prog than acute bacterial meningitis
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22
Q

age or RF: associated etiology of bacterial meningitis and tx

A
  • infants <3mo: GBS, E. coli, Klebsiella, Listeria
    • tx: cefotaxime + vanc + amp
  • 3mo-50y: N mening, strep pneumo, H flu
    • tx: ceftriaxone or cefotaxime + vanc
  • >50y: strep pneumo, N mening, listeria
    • tx: ceftriaxone or cefotaxime + vanc + amp
  • impaired cellular immunity (i.e. HIV): strep pneumo, N mening, listeria, aerobic G- (pseudo)
    • tx: ceftazidime + vanc + amp
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23
Q

Guillain-barre syndrome

A
  • autoimmune rxn against periph nerves, inflamm demyelination, Abs against postsynaptic nicotinic acetylcholine receptors at NMJ of skeletal mm cells
  • hx: previous viral infxn, surg, HIV, CMV, etc.
  • sxs: rapidly progressive bilat and flaccid weakness, usually symmetric, distal to central, sphincter control and micturition SPARED, absence of fever or other systemic sxs
  • signs: dec or absent DTRs in weak limbs
  • dx: BRIGHTON CRITERIA (LP - inc prot, nl glucose and pressure, WBC <50 cells; electrodx - dec motor nerve conduction velocity)
  • tx: admit and monitor for resp failure, HIGH DOSE IVIG, plasmapheresis for severe resp comp or weakness, DO NOT GIVE STEROIDS!!!
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24
Q

encephalitis etiology and sxs

A
  • diffuse inflamm of brain parenchyma and seen simultaneously with meningitis, usually viral in origin (HSV-1, arbovirus, enterovirus), toxoplasmosis, cerebral aspergillosis
  • RF: AIDS, immunosuppressed, travel to underdeveloped countries, mosquito exposure, exposure to wild animals (bats)
  • sxs: prodromal (HA, malaise, myalgia), within hrs-days, acutely ill, HA, fever, photophobia, nuchal rigidity, confusion, delirium, disorientation, behavior abnlities, focal neuro findings (hemiparesis, aphasia, CN lesions, and seizures)
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25
Q

encephalitis dx and tx

A
  • dx: CXR, urine and blood cx, UTox, chem, LP (lymphocytosis, normal glucose - viral), CSF cx neg, CSF PCR most sensitive and specific for HSV, CMV, EBV, and VZV, MRI brain, EEG, brain bx indicated in acutely ill pt with focal enhancing lesion on MRI w/o clear dx
  • tx: supportive, antivirals (acyclovir for HSV, ganciclovir or foscarnet for CMV), manage szs and cerebral edema
  • 10% mortality
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26
Q

concussion

A
  • falls (28%), MC (20%), struck by heavy object, assault
  • sxs: minor head injury (GCS >13), asxatic ~2hr, normal mental status, no evidence of skull fx, normal physical exam +/- LOC, sz activity, V, irritability, lethargy, HA, confusion, gait problems
  • dx: scalp hematoma, palpable crepitus, fundoscopic exam, neuro exam, SCAT2 (MMSE + physical), imaging usually normal and NOT required, CT if <48h, MRI if >48h, especially image if: severe HA/worsening, prolonged recovery, focal def, szs, slurred speech, unsteady gait, weakness, persitent vomiting, behavior changes, evidence of skull fx
  • tx: observe in ER x4h, rest until asxatic, light aerobic exercise, sport-specific training, noncontact training drills, full contact after medical clearance, return to play 24h for each stage
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27
Q

peripheral neruopathy (polyneuropathy)

A
  • refers to generalized relatively homogenous process affecting many peripheral nerves, with the distal nerves affected most prominently
  • causes: DM, alcohol abuse, HIV
  • sxs: symmetric distal sensory loss, burning or weakness, paresthesias (numbness or tingling), burning or pain in feet, gait abnlity, autonomic disturbances most commonly ikn hands and feet, weakness of lower legs and hand resulting in “stocking glove distribution” of sensory loss
  • signs: decreased DTRs, decreased vibration and two-point discrimination, Semmel-Weinstein (monofilament gauge)
  • dx: EMG and/or nerve conduction study (initial) if no clear etiology or when sxs rapidly progressive; labs = blood gluc, serum B12 with MMA (+/- homocysteine) and serum protein electrophoresis; m or nerve bx, skin bx, autonomic testing, quant sensory testing
  • tx: if DM, need tight control; if painful diabetic polyneruopathy - gabapentin, amitriptyline (TCA), alpha-lipoic acid
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28
Q

carpal tunnel syndrome etiology and sxs

A
  • numbness and tingling and/or pain in median nerve distribution, F>M
  • RF: obesity, female, comorbidity (DM, preg 3rd trim, RA, hypothyroid, genetics, aromatase inhib use
  • severe cases: clumsiness “difficulty holding objects, turning keys or doorknobs, buttoning clothing, or opening jar lids”
  • sxs: pain (involvement of first 3 digits, radial half of 4th digit, worse at night and awaken pt from sleep, better by shaking or wringing hands or blacing them under warm water), paresthesias (may radiate proximally into forearm or above elbow to shoulder, provo
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29
Q

carpal tunnel dx and tx

A
  • dx: phalen maneuver (flex wrist with elbow in full extension - backs of hands against one another - positive if pain and/or paresthesia in median innervated fingers within one minute of wrist flexion)
    • tinel test (percussion over prox portion of carpal tunnel - positive if pain and/or paresthesia, less sensitive than phalen sign - 50%)
    • nerve conduction study (NCS) with EMG (excludes polyneuropathy, plexopathy, and radiculopathy, delayed distal latencies and slowed conduction velocity
  • tx: mild = nocturnal wrist spint in neutral position x1mo, steroid injxns methylprednisolone, no more than 1/wrist q6mo, oral steroids prednisone daily 10-14d, PT/OT or yoga
    • moderate to severe = electrodiagnostic studies (first), surgical decompression
  • should resolve postpartum in pregnancy
30
Q

Dizziness

A
  • includes vertigo, light-headedness, faintness, imbalance
  • vasc dz cause presyncopal dizziness dt cardiac dysrhythmia, ortho HyTN, medication
  • vestibular causes dt peripheral lesions affecting labyrinths or vestribular nerves
  • Ask the D’s: diplopia, dysarthria, dysphagia, dysphonia, dysmetria, dysesthesia, drop attacks
  • deafness (transient and bilateral hearing loss is bad; abrupt onset unilateral loss may be bad or benign)
  • dyspnea (SOB)
31
Q

vertigo

A
  • when dizziness describes a sense of spinning or other motion (specifically the illusion of self or enviromental motion)
  • can be physiologic (after sustained head rotation), pathologic (vestib dysfn)
  • central etiology: multiple sclerosis, brain tumor, head injury, meds
  • sxs:
    • periph: sudden, intermittent, N/V, tinnitus, hearing loss, horizontal/rotary nystagmus
    • central: gradual, continuous, N/V, vertical nystagmus, no auditory component, motor, sensory, or cerebellar deficits
  • dx: dix-hallpike maneuver (nonfatigable nystagmus = central)
  • tx: Periph = vestib suppressants for acute sxs (diazepam, meclizine), Epley maneuver; Central = tx source (deep head-hanging maneuver)
32
Q

length of dizziness ddx

A
  • seconds: BPPV, ortho HoTN
  • minutes: TIA, migraine
  • hours: vestibular migraine, Meniere dz
33
Q

peripheral vs central vertigo

A
  • peripheral: unilateral hearing loss and aural sxs
    • unidirectional horizontal nystagmus (use Frenzel eyeglasses to aid detection)
  • central: bilateral hearing loss, unless lesion lies near root entry zone of auditory nerve, double vision, numbness, limb ataxia (brainstem or cerebellar lesion)
34
Q

head impulse test, diz-hallpicke maneuver, ancillary testing

A
  • HIT: vestribuloocular reflex with 20 deg rapid head rotations - pt fixates on target, head rotated to right or left. If deficient, rotation followed by catch-up saccade in opposite direction
  • Dix-Hallpike: sitting position, head turned 45 deg, hold pack of head and lower pt into supine w/ head extened backward 20 deg while watching eyes (post. canal BPPV = upbeating torsional nystagmus). If no nystagmus after 15-20 secs raist pt to sitting, repeat other side
  • Ancillary testing (audiometry if vestib dz suspected)
35
Q

Vestibular neuritis

A
  • sudden asymetry of inputs from 2 labrynths or in central connections, stimulating continuous rotation of head
  • Central (cerebellar, brainstem infarct, hemorrhage); Peripheral (affects vestribular nerve or labrynth)
  • sxs: sudden, unilateral vertigo (persists even when head remains still), N/V, oscillopsia (motion of visual scene), imbalance, central sxs (diplopia, weakness, numbness, dysarthria)
  • dx: head impulse test
  • tx: spontaneously resolves (steroids w/in 3 d onset, antivirals NOT beneficial unless herpes zoster (Ramsay Hunt) suspected, vestribular suppresant meds for sxs, resume normal activity ASAP, vestricular rehab
36
Q

Benign paroxysmal positional vertigo

A
  • Common cause of recurrent vert, caused by dislodged otoconia (calcium carbonate crystals) from utricular macula and moved to semicirc canal
  • sxs: brief (<1 min), provoked by change in head position
    • Post canal BPPV: upward, torsional nystagmus
    • Horizontal canal: horizontal nystag when lying ear down
    • Sup canal: rare
  • dx: + Dix hallpike (produces delayed fatigable nystagmus), Epley maneuver (for posterior canal BPPV)
  • tx: dix-hallpike maneuver (quickly turn pts head 90 deg while supine), avoid using meclizine or similar meds
37
Q

psychosomatic dizziness or vertigo

A
  • phobic postural vert, psychophysiologic, or chonic subjective dizziness
  • sxs: somatic manifestation of psychiatric condition (major depression, anxiety, panic), chronic dizziness and disequilibrium, increased sensitivity to self-motion and visual motion, worse with complex visual environments
  • dx: neruo exam and vestibular testing: normal
  • tx: SSRIs and cognitive behavioral tx, vestribular rehab tx
  • comorbidity: anxiety, autonomic sxs
38
Q

Acoustic neuroma

A
  • intracranial benign tumor affecting CN VIII, bilateral acoustic neruomas associated with neurofibromatosis type II, progressive vertigo
  • sxs: unilateral, progressive hearing loss, unsteadiness, vertigo, tinnitus, impaired speech discrim, HA
  • signs: decreased corneal reflex, diplopia, facial weakness or numbness
  • dx: head impulse test: deficient respone, MRI (dense enhancing lesions, enlarged internal auditory canal), LP (elevated protein)
  • tx: asymptomatic = serial MRIs; larger lesions = surgery or SRS
  • complicaiton: loss of corneal reflex from trigem involvement
39
Q

ischemic stroke

A
  • 85%
  • etiology in young pts: OCP, hypercoagulable states (preg, malig, vWF, antiphospholipid Ab syndrome), vasoconstrictive druge use (cocaine, amphet, polycythemia vera, sickle cell)
  • RF: age and HTN, smoking, DM, HLD, afib, Fhx of stroke, previous stroke/TIA, carotid bruit, drugs
  • dx: CT noncon differentiates hem vs ischem, MRI, EKG, carotid duplex scan, MRA (definitive test for stenosis of vessels of ehad/neck and for aneurysms)
  • tx: acute (IV O2 monitor), GRADUAL BP control (IV labetalol, DONT GIVE ANTIHTN MEDS UNLESS SBP >200, DBP >120, or MAP >130)
  • prevention: control HTN, DM, smoking, HLD, obesity, ASA, carotid endarterectomy
  • Stable stroke: t-PA tx (unless >3 hrs after event, uncontrolled HTN, bleeding dz, hx of surg or trauma), ASA, anticoagulants
    • if w/in 3h give thrombolytics
    • if after 3h give aspirin
  • anticoags, assess pts ability to protect airway, keep NPO, elevate HOB
40
Q

Lacunar stroke

A
  • internal capsule, pons, thalamus, causes 20% of all strokes; usually affects subcortical structures
  • Narrowing of large arterial lumen dt thickening of vessel wall (not by thrombosis)
  • RF: hx of chronic HTN and DM
  • affected arteries: MCA, circle of Willis, basilar and vertebral arteries
  • sxs: hemiparesis - weakness of entire left or right side
    • internal capsule: pure motor hemiparesis
    • pons: dysarthria, clumsy hand
    • thalamus: pure sensory deficit
  • dx: focal features and usually contralateral pure motor or pure sensory deficits
  • tx: prevention of lacunar strokes: control HTN
41
Q

acute epidural hematoma

A
  • classic: talk and die
  • collection of blood between dura and bones of the skull
  • MCC: trauma
  • MC affects temporoparietal region, 2/2 laceration of middle meningeal artery
  • progressive sxs: hx of trauma with overlying skull fx, brief LOC, return to alterness (lucid interval), HA, V, lethargy, hemiparesis (coma 20%)
  • signs: associated hematoma
  • dx: noncon CT (lens shaped extraaxial collection of blood that doesnt cross suture lines)
  • tx: urgent neurosurg consult, if evidence of herniation (pupil dilation or contralat hemiparesis) - burr hole ipsilateral to trauma, decrease ICP
  • complications: herniation
42
Q

acute subdural hematoma

A
43
Q
  • MCC: trauma
  • other RF: ETOHism, szs, coagulopathies
  • Collection of blood between dura and arachnoid mater; source is bridging veins
  • sxs: nonspecific nonlocalizing sxs or absent, stable, or rapidly progressive HA< confusion, dpressed LOC, +/- szs
  • signs: hemiparesis - contralateral to lesion; ipsilateral pupillary dilation (75%)
  • dx: CT scan - hyperdense crescent-shaped extraaxial collection of blood, rarely crosses falx or tentorium, subacute lesions (2-3wks) = isodense
  • tx: immediate hosp, emergent neurosurg consult, unstable pts with rapidly worsening neurologic deficits - treat for increased ICP
A
44
Q

subarachnoid hemorrhage

A
  • bleeding into the CSF; outside brian parenchyma
  • RF: smoking, HTN, cocaine, ETOH use, 1st deg relative with SAH< F, AA, CT disorders
  • sxs: thunderclap HA, sudden onset severe HA, sudden transient LOC, N/V, neck pain, nuchal rigidity, photophobia, visual changes, dec LOC, sz
  • signs: HTN, retinal hemorrhage
  • locations: saccular aneurysms at bifurcations of arteries of the circle of willis
  • dx: fundoscopic exam, noncon CT, LP (CI in elevated ICP, thrombocytopenia, suspected epidural abscess, xanthochromia, elevated RBCs)
    • blood in CSF, xanthochromia (yellow CSF) is gold standard for dx, CT angio
  • tx: supportive care, admit, stool softeners (avoid straining), analgesia for HA, IV fluids, lower BP using CCB, vraniotomy and clippin (definitive), treat BP aggressivelyhigh mortality, most repleed occurs within first 3d after rupture
  • complications: rerupture, vasospasm, hydrocephalus, SIADH, HTN
45
Q

upper motor neuron lesion

A
  • degen of frontal motor neurons located in the motor strip (Brodmann area 4) and their axons traversing the corona radiata, internal capsule, cerebral peduncles, pontine base, medullary pyramids, and the lateral corticospinal tracts of the spinal cord
  • sxs: weakness with slowness, incoordination, stiffness (poor dexterity), hyperreflexia (ankle clonus), spasticity (spastic gait with poor balance and leg flexor spasms
46
Q

lower motor neuron lesion

A
  • degeneration of lower motor neurons in the brainstem and spinal cord producing muscle denervation
  • sxs: weakness (hand - difficulty manipulating small objects; proximal arm - difficulty bathing, dressing, grooming, eating; foot/ankle - ttripping, slapping gait, falling; proximal leg - cannot arise from chair, climb stairs, or get up off floor; upper face - incomplete eye closure
47
Q

weakness and paralysis

A
  • objective muscle weakness
    • yes
      • generalized
        • cachexia, myasthenia gravis, periodic paralysis
      • localized
        • asymmetric
          • regional neuro disorders, cerebrovascular or spinal cord dz, demyelinating disorder, compression neuropathy, mononeuropathy/mononeuritis multiplex, disuse atrophy, myasthenia gravis
        • symmetric
          • specific pattern: muscular dystrophy, hereditary neuropathy, myasthenia gravis
          • proximal: myopathy, duchenne muscular dystrophy, myasthenia gravis
          • distal: peripheral neuropathy, motor neuron dz, myasthenia gravis
    • no
      • cardiopulm dz, anemia, chronic infxn, malig, depression, deconditioning, arthritis, fibromyalgia
48
Q

amyotrophic lateral sclerosis etiology, sxs

A
  • amyotrophy with pathologic finding of lateral sclerosis, 65-70yo M>F, sporadic, only 10% familial
  • sxs:
    • asymmetric limb weakness: (upper extremity onset - hand weakness, but may bgin in shoulder girdle, lower extremity - weakness of foot dorsiflexion (foot drop))
    • bulbar sxs: (dysarthria, dysphagia, coughing, choking, inc masseter tone and difficulty opening mouth (trismus), laryngospasm)
    • autonomic sxs: constipation, urgency without incont, excessive sweating, early satiety, bloating
    • parkinsonism and supranuclear gaze palsy (facial masking, tremor, bradykinesia, postural instability)
    • tingling, resp muscle weakness, generalized weakness, wt loss
49
Q

amotrophic lateral sclerosis dx and tx

A
  • clinical dx: upper and lower MN signs and sxs, progressive spread, EMG (fibrillations, positive sharp waves), electrodiagnostics (dec motor conduction velocity), MRI (preferred to ro other causes), unilateral arm onset MC -> contralateral arm -> ipsilateral arm -> ipsilateral leg -> contralateral leg -> bulbar muscles
    • unilateral leg -> contralateral leg -> ipsilateral arm -> contralateral arm -> bulbar muscles
  • tx: riluzole bid
  • AE: astthenia, dizziness, GI upset, elevated LFTs
  • MCC death = progressive resp failure
  • complications: aspiration
  • median survival = 3-5y
50
Q

organophosphate and carbamate poisoning

A
  • bind to AchE and renders enzyme nonfunc - overabundance of Ach in synapses
  • insecticides, neuromuscular blockades (neostigmine, pyridostigmine), tx of glaucoma, myasthenia gravis, Alzheimers (pyridostigmine, tacrine, donepezil)
  • sxs: DUMBELS (D, urinarion, Miosis, bronchorrhea/bronchospasm/bradycardia, emesis, lacrimation, salivation/sweating)
  • dx: clinical, EKG (heart block, QTc prolongation, red blood cell AChE levels (measures degree of toxicity)
  • tx: atropine, pralidoxime (2PAM), 100% O2, endotracheal intubation, Ivf, activated charcoal, DO NOT DO GASTRIC LAVAGE
51
Q

Giant cell arteritis

A
  • age >50yo, F2x >M, inc risk of aortic aneurysm and dissection
  • sxs: malaise, fatigue, weight loss, low grade fever, new HA (severe), visual impairment (optic neuritis - blindness), jaw pain with chewing (intermittent claudication), tenderness over temporal artery, absent pulse, palpable nodules, polymyalgia rheumatica
  • dx: very elevated ESR, bx temporal artery (90% sensitive)
  • tx: high dose steroids to prevent blindness, start immediately, do not wait for bx results (treat 4wk, then taper and maintain 2-3y), follow ESR levels, if untreated, most self-limiting
52
Q

cerebellar ataxi

A
  • causes: stroke, trauma, tumor, multiple-system atrophy, fragile X
  • sxs: hx of difficulty maintaining balance when turning (wide base of support, lateral instability of the trunk, erratic foot placement, decompensation of balance when attempting to walk on a narrow base
  • signs: unable to tandem heel-to-toe, truncal sway in narrow based or tandem stance
  • dx: lab tests (utox, blood gluc, CMP, UA, CBC< lactate, pyruvate, ammonia, LP, CT head <<< MRI (especially if trauma or stroke suspected), EEG
  • tx: tx underlying cause
53
Q

sensory ataxia

A
  • causes: vitB12 def
  • sxs; stance destabilized with eye closure, look at feet when walking and do poorly in dark
  • tx: tx underlying cause
54
Q

spinocerebellar ataxia

A
  • only 60-75% pts have mutations in known loci, MC autosomal dominant ataxias, dt CAG repeats in dz-causing alleles
  • sxs: dysarthria, bulbar sxs, cerebellar ataxia
  • signs: hyperreflexia, inc tone, extensor platar responses, UMN findings (wasting and gen fasciculations), slow saccadic eye mvts, nystagmus (horiz or vert)
    • associated: hypotonia or rigidity, developmental delay, infantile spasms, autonomic dysfn, dysphagia, retinitis pigmentosa, dystonia, cognitive impairment, insomnia
  • dx: MRI (cerebellar atrophy)
  • tx: no effective tx
  • prognosis: most pts require a wheelchair by 10-15y after onset
55
Q

Friedreich ataxia

A
  • the only autosomal recessive ataxia, associated with DM, vit E def; mixed sensory and cerebellar ataxia, onset age <25
  • sxs: staggering gait, frequent falling, titubation (difficulty standing and running, clumsy hands, feet wide to maintain balance), dysarthria (presenting sx)
  • signs: scoliosis, pes cavus, pes equinovarus, truncal titubation (nodding mvmt of head), nystagmus, hammertoes, + Romberg sign, dysarthria, dysmetria, absence of DTRs, weakness (distal > proximal), loss of vibratory and proprioceptive sensation
  • complications: cardiomyopathy
  • dx: nerve conduction studies = nl, EKG and echo, MRI of spinal cord = cerebellar atrophy - small spinal cord
  • tx: oral 5-hydroxytryptophan, tx underlying heart failure, arrhythmias, and surg for scoliosis
  • prognosis: median age of death = 35yo, better prognosis if female
56
Q

intracerebral hemorrhage etiology, RF, sxs, signs

A
  • bleeding into brain parenchyma
  • causes: HTN (sudden inc) is the most common cause (ischemia stroke convert to hemorrhagic stroke), pt develops edema around lesion leading to herniation of brain tissues
  • location: putamen (40%), thalamus, lobar white matter, caudate, pons, cerebellum
  • RF: smoking, advanced age, antiocagulant use
  • sxs: abrupt onset of focal neuro def worse steadily over 30-90mins, dec LOC, HA, N/V, confusion, aphasia, hypersomnolence
    • pinpoint pupils = pons; poorly reactive pupils = thalamus; dilated pupils = putamen
  • signs: inc ICP, resp failure, HTN, hyperconvergence, absent vert gaze, horizontal gaze paresis, hemiparesis, hemisensory or hemimotor loss, quadriplegia, ataxia, stupor, coma
57
Q

intracerebral hemorrhage dx and tx

A
  • dx: noncon CT - hyperintense area with mass effect and (later) hyperintense surrounding edema, CT angio (coag panel and PLTs, ophthalmologic exam is mandatory to rule out papilledema
  • tx: admit, supportive care, control BP (IV labetalol, esmolol, or nicardipine - target = SBP <180 and MAP <130), reverse anticoagulants (FFP and vit K, protamine), mannitol and diuretics to reduce ICP, steroid harmful, rapid surg evacuation of hematomas, emergent neurosurg consult (high mortality rate (50% at 30d), surg if >3cm
  • complications: inc ICP, szs, rebleeding, vasospasm, hydrocephalus, SIADH
58
Q

locked-in syndrome

A
  • pts fully awake, yet quadriplegic and can communicate only by means of vertical eye mvmts and blinking
59
Q

coma

A
  • depressed level of consciousness to extent that pt is completely unresponsive to any stimuli
  • causes: structural brain lesions, global brain dysfn (met or systemic disorders), psychiatric causes
  • Glasgow coma scale
  • if breathing on own, brainstem is functioning
  • Eye opening (4; none, to pain, to voice, spont), verbal response (5; none, incomp, inappropriate, approp but confused, approp and oriented), motor response (6; none, decerebrate, decorticate, withraws from pain, localizes pain stim, obeys commands)
60
Q

criteria for brain death versus persistent veg state

A
  • irreversible absence of brainstem fn (brain death): unresponsive, panea despite adequate O2 and vent, no brainstem reflexes (pupils, caloric, gag, cornea, doll’s eyes)
  • persistent veg: completely unresponsive but eyes are open and appear awake, may have randome head or limb movements
61
Q

anterior cord syndrome

A
  • loss of pain and temp below level with preserved jnt position/vibration sense
62
Q

central cord syndrome

A
  • loss of pain and temp sensation at level of lesion, where spinothalamic fibers cross cord, with other modalities preserved (dissociated sensory loss)
63
Q

complete cord transection

A
  • rostral zone of spared sensory levels (reduced sensation caudally, no sensation in levels below injury); urinary retention and bladder distention
64
Q

brown-sequard syndrome

A
  • hemisection of the cord - loss of jnt position sense and vibration sense on same side as lesion and pain and temp on opposite side a few levels below the lesion
  • lesion of half-ipsilateral cervical cord lesion, contralateral sensory findings: pain and temp loss
65
Q

concussion

A
  • falls (28%), MC (20%), struck by heavy object, assault
  • sxs: minor head injury (GCS >13), asxatic ~2hr, normal mental status, no evidence of skull fx, normal physical exam +/- LOC, sz activity, V, irritability, lethargy, HA, confusion, gait problems
  • dx: scalp hematoma, palpable crepitus, fundoscopic exam, neuro exam, SCAT2 (MMSE + physical), imaging usually normal and NOT required, CT if <48h, MRI if >48h, especially image if: severe HA/worsening, prolonged recovery, focal def, szs, slurred speech, unsteady gait, weakness, persitent vomiting, behavior changes, evidence of skull fx
  • tx: observe in ER x4h, rest until asxatic, cervical spine immobilization if pt has paresthesias, numbness, or paralysis, minmum of 1-2d rest from physical activity
    • light aerobic exercise -> sport-specific training -> noncontact training drills -> full contact after medical clearance; return to play 24h for each stage
  • health maintenance: not necessary too awaken most children, if pt has concerning mech of inj or prolonged sxs awaken q4h
66
Q

Giant cell arteritis

A
  • age >50yo, F2x >M, inc risk of aortic aneurysm and dissection
  • sxs: malaise, fatigue, weight loss, low grade fever, new HA (severe), visual impairment (optic neuritis - blindness), jaw pain with chewing (intermittent claudication), tenderness over temporal artery, absent pulse, palpable nodules, polymyalgia rheumatica
  • dx: very elevated ESR, bx temporal artery (90% sensitive)
  • tx: high dose steroids to prevent blindness, start immediately, do not wait for bx results (treat 4wk, then taper and maintain 2-3y), follow ESR levels, if untreated, most self-limiting
67
Q

Dementia

A
  • RF: old age
  • sxs: insidious, progressive, preserved consciousness, rarely hallucinations, no tremor unless dt parkinson
  • tx: typically irreversible unless cause = hypothyroid, neurosyph, vitB12/folate/thiamine def, meds, hydroceph, depression, subdural hemotoma
    • pharm tx: vitE, tacrine, donepezil
68
Q

vascular dementia

A
  • multi-infarct, stepwise decline dt series of infarcts
  • M>W
  • sxs: forgetfulness in absence of depression and inattentiveness
    • cortical - speech difficulty, trouble performing routine tasks, sensory interpretation difficulty, confusion, amnesia, executive dysfn
    • subcortical - gait problems, urinary difficulties, motor deficits, personality changes
  • tx: control HTN and metabolic disorders, tx same as Alzheimer dz
69
Q

frontotemporal dementia

A
  • frontal lobe sxs: behavioral sx (euphoria, apathy, disinhibition) and compulsive disorders
  • primitive reflexes (frontal release signs): palmomental, palmar grasp, rooting reflexes
  • dx: MRI (frontal or ant temp lobe atrophy), PET (frontal and/or ant temp hypometabolism)
  • tx: supportive care, SSRIs for depression
70
Q

Lewy body dementia

A
  • Features of alzheimer and Parkinson dz but progression more rapid than in Alzheimer dz
  • sxs: visual hallucinations predominate, extrapyramidal features and fluctuating mental status, sensitive to adverse effects of neuroleptics (make worse)
  • tx: neuroleptics for hallucinations . and psychosis, cholinesterase inhibitors: donepezil, rivastigmine, galantamine, selegiline (slows progression)