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Neurology Flashcards

0
Q

Cluster headaches

  • male>female
  • freq: 1-2/day during cluster period
  • duration: 30-120 minutes
  • location: unilateral-orbital
A
  • non-pulsating
  • assoc: unilateral lacrimation, rhinorrhea or blockage, ipsilateral horners
  • tx: 100% O2, sumatriptan, intra-nasal lidocaine
  • prophylaxis: prednisone 60mg/d x 1 wk, ergotamine
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1
Q

Migraine Headaches

  • female > males
  • severity: moderate to severe
  • freq: every few weeks
  • duration: 1-2 days
A
  • location: unilateral -temporal or frontal
  • assoc: N/V,photophobia, aura, phonophobia
  • tx: analgesics, isomethepten, ergotamine, sumatriptan
  • prophylaxis:ASA, BB, TCA,CCB, divalproex sodium
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2
Q

Tension headaches

  • female>male
  • freq: variable
  • duration:30”-7days
  • location: bilateral, diffuse
A
  • type: non pulsating
  • assoc: none
  • tx: analgesics
  • prophylaxis: TCA, B blockers
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3
Q

Aura of migraine HA

*transient focal neuro dysfunction that deveops over few minutes and lasts no more than 60”. may preceed or accompany HA

A
  • visual-unformed flashes of light or zig zag lines in vision -#1
  • aphasia or speech disorder, or visual field defects
  • unilateral paresthesia or numbness
  • unilateral weakness
  • homonymous visual field defect
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4
Q

Rare manifestations of migraine headaches:

  • prolonged sensory or motor deficit, diploplia
  • altered consciousness
A
  • ischemic stroke
  • incr risk in migraine w aura
  • incr risk in smokers, or on OCP
  • incr risk of CV dz and MI
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5
Q

acute tx of migraines

  • ASA, acetaminophen
  • excedrin- above plus caffeine
  • midrin
A
  • triptan-drug of choice for moderate to severe migraine
  • contraindicated: uncontrolled HTN, severe hepatic/renal fxn, basilar or hemiplegic migraine, CAD or multiple risks for CAD
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6
Q

Prophylaxis of migraine headaches

  • indicated if >2 migraines/wk or severe disabling migraines
  • B blockers-only FDA approved: propranolol, timolol
  • TCA: amitriptyline best
A
  • verapamil
  • antiepileptics: valproate, topiramate
  • botulinum toxin
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7
Q

thunderclap headache

A

*severe HA that reaches maximum intensity in 60 seconds

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8
Q

Causes of thunderclap headache

  • subarachnoid hemorrhage
  • sentinal bleed from unruptured aneurysm
  • cerebral arterial, venous, or sinus thrombosis
  • dissection carotid or vertebral arteries
A
  • reversible cerebral vasoconstriction syndrome:
  • recurrent thunderclap HAs
  • acute infarct can occur
  • transient segmental can be seen on MRA, resolve by 12 weeks
  • may see in pregnancy or postpartum
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9
Q

treatment of thunderclap HA

A
  • CCB-verapamil or nimodipine
  • short term high dose steroids
  • IV Mg if induced by eclampia/preeclampsia in pregnancy
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10
Q

Dx thunderclap HA

A

CT head without contrast, if negative, do lumbar puncture

  • presence of xanthochromia on LP-ver suggestive of subarachnoid hemorrhage
  • MRA or CT angiogram if above tests negative
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11
Q

clinical features of subarachnoid hemorrhage

*severe diffuse HA of sudden onset without aura
“thunderclap” HA
*may have brief LOC

A
  • vomiting
  • retinal hemorrhage
  • ptosis + dilated pupil on one side =>posterior communicating aneurysm
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12
Q

DX of subarachnoid hemorrhage

A

CT head without contrast- if negative-do LP

*if CT & LP are negative-MRA or CT angio (catheter angiograpy preferred)

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13
Q

Tx subarachnoid hemorrhage

A
  • endovascular coiling or craniotomy + clip ligation
  • oral nimodipine X 21 days
  • pt in coma=> place ventricular drain
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14
Q

Complications of subarachnoid hemorrhage

  • rebleeding
  • hydrocephalus
A
  • vasospasm-focal ischemia and possible stroke
  • hyponatremia-cerebral salt wasting
  • ST depression and T wave inversion on EKG
  • reversible cardiomyopathy
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15
Q

clinical features Pseudotumor cerebri

*most are young, female, obese

A
  • headache, pulsatile tinnitus
  • transient visual abscurations
  • papilledema, blurred vision, diploplia, visual field loss
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16
Q

secondary causes pseudotumor cerebri

  • cerebral venous sinus thrombosis
  • focal neur findings, mental status change, seizures
  • increased risk w congenital or acquired thrombophilias, pregnancy and OCP’s
A
  • obesity, sleep apnea
  • renal failure
  • hypervit. A, tetracycline, glucocorticoids
  • OCP, amiodarone, retinoid
  • growth hormone
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17
Q

diagnosis of pseudotumor cerebri

A
  • MRI - if negative=> spinal tap=>CSF pressure >250mm

* visual field testing

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18
Q

Tx pseudotumor cerebri

A
  • acetazolamide, topiramate
  • repeated LPs, lumboperitoneal shunt,optic nerve sheath fenestration
  • weight loss
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19
Q

high grade or malignant astrocytoma brain tumors

A

most common

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20
Q

meningioma

A

dural based brain tumor

dense and uniform contrast enhancement

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21
Q

vestibular schwannoma

A

brain tumor
unilateral hearing loss
uniform enhancing lesion at cerebellopontine angle

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22
Q

metastatic brain tumor

A

breast
lung
melanoma
*solitary metastatic lesion=>surgical resection

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23
Q

CNS lymphoma

A
  • most occur in immunosuppressed, single or multiple mass lesions
  • non hodgkin B cell lymphoma
  • related to EB viral infection
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24
Q

clinical presentation of brain tumors

A
  • headache-worse w laying down, cough, valsalva
  • seizure, papilledema, focal neuro deficits
  • impaired lateral gaze, dementia, personality changes
  • gait disorder
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25
Q

treatment of symptomatic brain tumor

A

dexamethasone

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26
Q

Upper motor neuron lesion

A

weakness, spasticity
hyperactive tendon reflexes
Babinski sign-extensor planter reflex

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27
Q

Lower motor neuron (anterior horn cells, motor roots, peripheral nerves)

A

weakness, hypotonia, atrophy
loss of tendon reflexes
fasciculations
sensory symptoms if mixed nerve is involved

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28
Q

Muscle diseases

A

weakness- proximal >distal
no sensory changes
reflexes preserved, atrophy
no fasciculations, eye and bulbar muscles spared

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29
Q

neuromuscular junction

A 
weakness increases with activity
no sensory symptoms
eye and bulbar muscles involved
 reflexes normal
no atrophy or fasciculations
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30
Q

Argyll Robertson pupil

A

no reaction to light
reacts to accommodation

**syphilis

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31
Q

Relative afferent pupillary defect (RAPD)

A

no response to direct light but constricts when light shown in the other eye

**MS

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32
Q

3rd nerve palsy

A

ptosis = dilated pupil

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33
Q

Horners syndrome

A

ptosis + constricted pupil

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34
Q

pin point pupils

A

narcotic overdose
pontine damage
thalamic hemorrhage

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35
Q

unilateral enlarged pupil in comatose

A

midbrain lesion or compression of 3rd CN

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36
Q

bilateral dilated unreactive pupil in comatose pt

A

severe bilateral midbrain damage

anticholinergic overdose

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37
Q

paralysis of 6th CN

A

inability to move the eye outward

eye turns toward the nose when looking straight

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38
Q

paralysis of 3rd CN

A

eye displaced downward and outward
ptosis
eye can only move laterally and downward +/- dilated nonreactive pupil

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39
Q

diplopia

A

Monocular: does not correct by covering one eye

Binocular: corrects by covering one eye

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40
Q

3rd CN paralysis

*acute isolated 3rd nerve paralysis w pupillary involvement=>posterior communicating artery aneurysm

A
  • acute isolated 3rd nerve paralysis without pupillary involvement
  • age 50: vascular, most common is diabetes-microinfarction of 3rd nerve
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41
Q

Trigeminal neuralgia

A

vascular compression of the trigeminal root

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42
Q

clinical features of trigeminal neuralgia

A

*episodes knife like pain lips,gums,cheeks, or chin, lasts seconds to 2 minutes

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43
Q

triggers for trigeminal neuralgia

A
  • touching specific points on face
  • talking, chewing
  • exposure to breeze, bright light or loud noise
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44
Q

trigeminal neuralgia do MRI in all cases to r/o

A

structural compression of nerve

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45
Q

treatment of trigeminal neuralgia

A
  • carbamazepine or oxcarbazepine
  • others: baclofen, gabapentin, lamotrigine
  • heat or gamma knife radiosurgery or surgical microvasc. decompression
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46
Q

Infranuclear facial nerve paralysis

A 
Bell's palsy
Ramsay Hunt Syndr
Acoustic neuroma
Pontine tumor or infarction
Guillain Barre, sarcoid, lyme
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47
Q

Bell’s palsy

*assoc Herpes simplex virus type 1

A

*weakness evolves over 12-48hrs and may be preceded by retroaural pain +/- hyperacusis
Tx: prednisone 60-80mg/d x 7 days +/- valcyclovir 1gm TID x 7days

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48
Q

Ramsay Hunt syndrome

A
  • herpes zoster involving geniculate ganglion

* vesicular lesions in pharynx or external auditory canal & freq involves the 8th CN

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49
Q

peripheral vertigo (vestibular nerve or inner ear)

  • severity: +++
  • N/V: ++
  • tinnitus/hearing loss: some cases
A
  • nystagmus: unidirectional, horizontal (never vertical)
  • visual fixation: inhibits nystagmus and vertigo
  • assoc central abnl: none
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50
Q

causes of peripheral vertigo

A 
vestibular neuritis
labyrinthitis
Menieres dz
acoustic neuroma
benign positional
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51
Q

Central vertigo (brain stem or cerebellum)

  • severity: +
  • N/V: +/-
  • tinnitus/hearing loss: none
A
  • nystagmus: multidirectional, vertical
  • visual fixation: no inhibition of nystagmus or vertigo
  • assoc central abnl: dysarthria, diplopia, ataxia, weakness
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52
Q

causes of central vertigo

A

brain stem dysfunction due to demyelinating, vascular or neoplastic diseases

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53
Q

conductive hearing loss - external auditory canal or middle ear

  • air conduction-abnormal
  • bone conduction-normal
A
  • Rinne test
  • tuning fork in front of the ear (air conduction)-abnormal
  • at mastoid process (bone)-normal
  • weber test-tuning fork over center of forehead
  • hear better on affected side
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54
Q

sensory-neural hearing loss (inner ear, 8th nerve, or central auditory pathway)

  • air conduction-abnormal
  • bone conduction- abnormal
  • Rinne test- abnormal in both locations
A

*weber test- hears only on the normal side

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55
Q

Unilateral lesion of the spinal cord

  • pain & temp sense lost below the lesion - OPPOSITE side
  • spastic paralysi on SAME side as the lesion
A
  • loss of vibration and position sense SAME side below the lesion
  • *TOUCH sense is not lost**
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56
Q

Syringomyelia

  • progressive myelopathy characterized by cavitation of central spinal canal
  • usually starts from mid cervical cord
A
  • wasting of muscles of neck, shoulder, arms
  • progressive spastic paraparesis
  • loss of pain & temperature sensation
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57
Q

ALS-amyotrophic lateral sclerosis

  • progressive loss of motor neurons in cerebral cortex & anterior horn of spinal cord
  • asymmetric weakness of both upper & lower motor signs
A
  • hyperreflexia,spasticity in a weak atrophic limb suggest ALS
  • MRI cervical cord to r/o cord compression
  • no pain, no sensory loss, normal bowel & bladder function
  • Tx: riluzole (anti glutamate), BIPAP if FVC and symptoms of nocturnal hypoventilation
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58
Q

clinical features of transverse myelitis
*develop over hours to days
bilateral sensorimotor signs w a clear sensory level
*hyperreflexia & Babinski present

A
  • urinary incontinence or retention
  • bowel incontinence or constipation
  • sexual dysfunction
  • Lhermittes sign- paresthesias radiating down spine or limbs with neck flexion
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59
Q

Diagnosis of transverse myelitis

A
  • MRI-do entire spine=>enhancing intramedullary cord lesion
  • CSF pleocytosis or high IgG index
  • MRI brain =>demyelination on brain MRI suggests MS
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60
Q

causes of transverse myelitis

  • post infection or post vaccine
  • acute infection
  • systemic autoimmune:SLE,sarcoid, sjogrens
A
  • paraneoplastic
  • idiopathic
  • multiple sclerosis
  • neuromyelitis optica (myelitis + optic neuritis)
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61
Q

Tx transverse myelitis

A
  • high dose steroids

* plasma exchange if no response to steroids

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62
Q

most common demyelinating dz of the nervous system

A
  • multiple sclerosis.
  • plaques are widely distr. in white matter of brain, sp cord and optic nerves.
  • 50 fold incr risk in child of a patient w MS
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63
Q

clinical presentation of MS

*sensory loss or paresthesias, optic neuritits, diplopia, weakness, ataxia, hyperreflexia spasticity, heat sensitivity

A
  • intranuclear opthalmoplegia-unable to adduct involved eye, other eye fully abducts which shows horizontal nystagmus
  • paroxymal symptoms: dysarthria, ataxia, tonic contractions
  • Lhermittes: shock like sensation radiating to back on neck flexion
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64
Q

Patterns of MS

A
  • relapsing remitting
  • secondary progressive
  • primary progressive-worst prognosis
  • progressive relapsing
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65
Q

diagnosis of MS

A
  • MRI brain & spinal cord:periventricular bright T2 lesions, contrast enhancement with active disease
  • CSF: oligoclonal band, incr IGG index & synthesis rate, lymphocytic pleocytosis
  • evoked response testing
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66
Q

treatment of acute relapses of MS- that produce functional impairment or initial attacks of optic neuritis

A

Methylprednisolone IV 1 gram/day for 3-5 days then oral prednisone for 2 weeks

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67
Q

disease modifying drugs for MS

*no effective tx for primary progressive MS**

A
  • interferon beta-1a & interferon beta-1b:decreases relapse and slows progression
  • glatiramer (copaxone)-reduces relapse by 1/3
  • mitoxantrone-for worsening MS-cardiotoxic, AML possible s/e
  • natalizumab-decr relapse and disabling progression
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68
Q

Parkinson’s disease

A

unknown etiology

degeneration of dopamine contained in neurons in the basal ganglion

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69
Q

clinical presentation of Parkinsons dz

*tremor: asymmetrical, more pronounced at rest, handwriting is small and irregular (essential tremor its large & tremulous)

A
  • bradykinesia: abnl finger & toe tapping, decreased arm swing,slow gait,drag of feet, shuffling gait,falls,fixed expressionless face
  • rigidity, freezing gait,postural instability, incr falls, dementia
  • normal motor, sensory and DTRs
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70
Q

secondary causes of Parkinsons dz

  • drugs:phenothiazine, reserpine,metoclopramide, antipsychotics,lithium
  • toxins: CO poisoning, MPTP-methylphenyl tetrahydro., mercury
A
  • head trauma
  • wilsons disease
  • post encephalitis
  • MRI brain to r/o hydrocephalus or vascular lesions
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71
Q

First line tx of Parkinsons

A

levodopa & carbidopa
levodopa & carbidopa & entacapone
dopamine agonist: ergot-bromocriptine, pramipexole,, ropinirole, rotigotine patch

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72
Q

second line tx of Parkinsons

A
  • MAO-B inhibitor-selegiline
  • anticholinergics
  • NMDA antagonists: amantadine (Symmetrel)
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73
Q

surgical tx Parkinsons

A

deep brain stimulation w implanted electrodes

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74
Q

Complicaions of levodopa therapy

*wearing-off phenomenon: incr dose and freq of levodopa, add dopamine agonist +/- COMT inhibitor

A
  • N/V: increase carbidopa dose
  • dyskinesias (choreiform & dystonic movements): add dopamine agonist +/- amantadine
  • psychosis: add atypical antipsychotic drug Quetiapine
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75
Q

Myasthenia Gravis

A

autoimmune neuromuscular disorder due to antibodies against acetylcholine receptors
symptoms are provoked by exertion

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76
Q

clinical features of myasthenia gravis

A
  • ocular: blur vision, binocular diplopia, ptosis

* generalized: limb weakness, slurred speech, dysphagia, dyspnea

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77
Q

diagnosis of myasthenia gravis

A
  • acetycholine antibodies, muscle specific kinase antibodies, TSH
  • EMG w repetitive nerve stimulation
  • edrophonium test=> rapid & transient impovement of strength
  • once dx confirmed: CT chest to exclude thymoma
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78
Q

tx of myasthenia gravis

A
  • *acetylcholinesterase inhibitor: pryridostigmine
  • immunosuppress: steroids, azathioprine, mycophenolate, cyclosporin, rituximab
  • thymectomy if thymoma and if <age 50 w generalized Mysathenia
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79
Q

Myasthenia crisis

A

*worsening of disease w weakness, difficulty swallowing and respiratory insufficiency
*best initial tx: plasmapheresis or IVIG
if no improvement immunosuppressive therapy. mechanical vent if VC <20ml/kg

80
Q

Lambert-Eaton syndrome

A

paraneoplastic syndrome

*most common malignancy: small cell lung cancer

81
Q

clinical features of Lambert-Eaton

A
  • muscle weakness, strength improvs with activity
  • dry eyes and mouth
  • erectile dysfunction
  • constipation
82
Q

diagnosis of Lambert-Eaton

A

*EMG with repetitive nerve stimulatioon
*calcium channel antibodies in serum
CXR-if negative, do CT chest, abdomen , pelvis
**TX: pyridostigmine

83
Q

CVA types

A

thrombotic
embolic
hemorrhagic

84
Q

TIA

A

transient episode of neurological dysfunction d/t focal brain, spinal cord, or retinal ischemia, without acute infarction

85
Q

Carotid TIA

A
  • contralaterial hemiparesis or sensory loss
  • aphasia if dominant site
  • ipsilateral visual loss-lasts few minutes, and loss evolves in less than one minute
86
Q

vertebrobasilar TIA

A

*episodes of dizziness, diplopia, dysarthria, facial or circumoral numbness +/- bilateral weakness +/- drop attacks due to sudden weakness of legs

87
Q

Intracerebral hemorrhage - clinical features-rapidly evolve:

A
  • headache
  • vomiting
  • seizures
  • impaired consciousness
  • neurological deficit
88
Q

causes of intracerebral hemorrhage

A

1: HTN

  • amyloid angiopathy-lobar hemorrhage in elderly
  • vascular malformations
  • anticoagulation/thrombolytics
  • cocaine, alcohol
89
Q

diagnosis of intracranial hemorrhage

A

CT head WITHOUT contrast

cerebral angiography if <age 45 or related to cocaine

90
Q

TX of intracerebral hemorrhage

A
  • SBP 140-160, mean pressure 70-130
  • surgery: cerebellar hemorrhage
  • mannitol, barbiturate coma, hyperventilation to decrease intracranial pressure
  • *NO role for steroids
91
Q

ischemic stroke

A

defined by presence of cerebral infarct on imaging

several types

92
Q

cardioembolic stroke

A
  • suspect when multiple infarcts seen on imaging

* most common cause ATRIAL FIB

93
Q

Large artery atherosclerosis as cause of ischemic stroke

A
  • may involve extracranial ICA or intracranial arteries
  • stroke occurs due to artery-to-artery emboli or decreased cerebral flow
  • greatest risk is stenosis >70%
  • no benefit of stenting intracranial blood vessels
94
Q

cryptogenic stroke as cause of ischemic stroke

A
  • **most common cause of ischemic stroke
  • imaging suggest embolic stroke
  • on evaluation, no cardioembolic or large vessel source is found
  • 25% may have paroxysmal A Fib so prolonged cardiac monitoring is advised
95
Q

Management of TIA

A
  • admit recommended for all seen within 72 hours of initial symptoms whose ABCD score is 3 or greater
  • risk of stroke is highest in first few days so eval. immediately
96
Q

Evaluation of TIA

A

ASA 81-325mg/d
clopidogrel, or asa + dipridamole
warfarin if due to A fib (add heparin until INR at target)
urgent endarterectomy if ICA stenosis 70-99%

97
Q

Risk factor management for TIA

A

BP< 120% of ideal body weight

98
Q

ABCD scoring system in TIA

AGE 60 or greater 1
BP 140/90 or greater 1

A 
CLINICAL symptoms:
*focal weakness w TIA    2
*speech impair w/o weakness   1
DURATION: 10-59" (1), 60" or longer  (2)
DIABETES   1
99
Q

significance of ABCD scoring 2 day risk of stroke

SCORE:
0-1 0%
2-3 1.3%

A

4-5 4.1%

6-7 8.1%

100
Q

anterior cerebral artery cva

A
  • medial cerebral hemisphere
  • contralateral weakness and sensory loss in leg>arm
  • behavioral changes
101
Q

Internal carotid artery cva

A
  • ipsilateral vision loss
  • contralateral hemiparesis & sensory loss
  • homonymous heminopis
  • aphasia
102
Q

Middle cerebral artery cva

A
  • lateral cerebral hemisphere
  • contralateral hemiplegia & sensory loss
  • homonymous hemianopis
  • aphasia
103
Q

Branch of middle cerebral artery cva

A

*contralateral hemiplegia without sensory loss or can have sensory loss without hemiplegia

104
Q

Posterior cerebral artery

A
  • ipsilateral 3rd nerve and contralateral hemiplegia or ataxia
  • homonymous hemianopia
  • cortical blindness if bilateral
105
Q

basilar artery cva

A
  • brainstem, pontomedullary junction
  • bilateral sensory & motor signs, CN 5-6-7, cerebellar signs
  • diminished pain & thermal sense over half of body
  • horners syndrome
106
Q

vertebral artery

A
  • brainstem, lateral medulla
  • vertigo, ataxia, nystagmus
  • Horners syndrome
  • diminished pain & thermal sense half of body
107
Q

Posterior inferior cerebellar artery

A
  • lateral medulla
  • ipsilateral facial sensory loss
  • contralateral body sensory loss
  • vertigo, ataxia, dysarthria
108
Q

Prevention of stroke

  • Tx HTN
  • stop smoking
  • regular exercise
  • diet high fruit, veg, fiber, low in saturated fat
A
  • anticoag if a fib
  • tx carotid disease if indicated
  • statin tx goal LDL< 100
  • antiplatelet
  • glucose control w diabetes
109
Q

Tx ischemic stroke

  • Tx HTN only if >220/120
  • if eligible for thrombolytics, BP must be lowered & stabilized below 185/110 before thrombolytis started and maintained
A
  • antiplatelet tx: ASA 160-325mg=>after 2 wk change to asa 81mg + dipyridamole, plavix if asa contraindication
  • sq heparin 5000u BID for DVT prophy in immobile pt
  • tx of cerebral edema
  • IV thrombolytic tx
110
Q

Tx ischemic stroke continued:

  • possible intra-arterial thrombolytic tx in those w contraind. for IV thrombolysis
  • neurosurg eval for cerebellar infarct or bleed
A
  • cardioembolic stroke (AF + stroke , or other causes)
  • thrombolytics if present in 4.5 hours of onset of symptoms
  • do not use heparin (increase risk of intracranial hemorrhage)
  • start warfarin when neuro stable with small infarcts
  • delay warfarin for 2 weeks with large infarct
111
Q

no benefit of stenting a blocked intracranial vessel or extracranial-intracranial bypass of

A

of a completely occluded ICA compared to medical therapy

112
Q

Thrombolytic therapy in CVA

  • indicated for:
  • patients 18 or older presenting within 3 hours of onset of ischemic stroke that has measurable neurological deficit and CT shows no evid of bleed nor multilobar infarction
A
  • select cases up to 4.5 hours onset of symptoms

* begin antiplatelet therapy w aspirin or plavix after 24 hours

113
Q

Contraindications to thrombolytic therapy in CVA

  • previous stroke/serious head trauma within 3 months
  • BP>185/110 despite treatment
  • recent invasive surg inpast 2 weeks
  • INR>1.7 on warfarin,Incr PTT if heparin in past 48 hours
A
  • evidence active bleed, GI/GU bleeding in past 21 days

* platelet

114
Q

for thrombolitic exceptions of 3-4.5 hours after onset of symptoms, additional contraindications for this later tx include:

A
  • age >80
  • combination of prior stroke + diabetes
  • NIH stroke scale >25
  • oral anticoagulant use regardless of INR
115
Q

Aphasia

  • disturbance in comprehension (sensory) or production (motor) of spoken or written language
  • several types:
  • global
A
  • wernickes
  • conduction
  • pure word deafness
  • pure word blindness
  • isolation of speech area
116
Q

Global aphasia

A
  • both sensory & motor
  • due to large infarct involving DH, artery involved: MCA or ICA
  • Brocas-motor or nonfluent
  • difficulty in speech, involvement of dominant frontal lobe-MCA branch
117
Q

Wernicke’s aphasia

A
  • speech is fluent but does not make sense
  • parietal lobe involvement
  • MCA branch involvement
118
Q

aphasia-conductive

A
  • repetition is severely affected
  • parietal or frontal lobe
  • MCA branch
119
Q

aphasia-pure word deafness

A

no auditory comprehension

120
Q

aphasia-pure word blindness

A

inability to read, name colors
dominant occipital lobe
PCA involvement

121
Q

aphasia-isolation of speech area

A
  • caused by extensive brain damage from shock

* parrot like repetition of spoken words

122
Q

Alzheimers Disease

A
  • most freq cause of dementia
  • increased production and accumulation of beta-amyloid peptide which results in cell dysfunction =>deficiency of acetylcholine
123
Q

Risk factors for alzheimers

  • age
  • family history
  • Downs syndrome
A
  • rare mutatin in amyloid precursor protein:presenilin 1 & 2 mutation
  • early onset age 30-50
  • autosomal dominant
124
Q

clinical features of alzheimers

A
  • predominant loss of short term memory
  • progressive impairment of ADL’s
  • variety neuropsychiatric symptoms & behavior disturbance
125
Q

Tx of alzheimers

*best initial tx: donepezil, rivastigmine, galantamine (central acting cholinesterace inhibitors)

A
  • N-methyl-D-aspartate receptor antagonist-memantine
  • vit E & C, ginkgo biloba
  • SSRI for depression, antipsychotic for agitatin, delusions and hallucinations
126
Q

other causes of dementia:

  • multi-infarct :CT hypodense areas white&gray matter w no enhancement
  • B1 or B12 deficiency
  • hypothyroidism
A
  • normal pressure hydrocephalus
  • CNS infections
  • creutzfeld-jakob disease
  • frontotemporal dementia
127
Q

Normal-pressure hydrocephalus

A
  • dementia, gait disturbance, urinary incontinence
  • CT shows dilated ventricles
  • Tx: ventriculoperitoneal shunt
128
Q

CNS infectious causes of dementia

A

HIV
syphilis
cryptococcus

129
Q

Creutzfeld-Jakob disease

  • cause:infectious prions
  • transmission: corneal transplant, contaminated growth hormone
A
  • rapidly progressive:dementia, myoclonus, focal cortical signs & rigidity
  • EEG: markedly abnormal periodic discharges
  • MRI (diffusion weighted): cortical & basal ganglion abnormality
130
Q

Frontotemporal dementia

A
  • dementia, prominent personality & behavior changes, parkinsonism
  • MRI: prominent asymmetric frontal lobe atrophy
131
Q

Guillain Barre syndrome

A

*rapidly progressive polyneuropathy

132
Q

clinical features of Guillain Barre syndrome

  • numbness, paresthesia
  • symmetrical muscle weakness and absent tendon reflexes
  • weakness progresses over 12hours to 28 days
  • 2/3 cases preceeded by URI or diarrhea
A

*weakness varies: mild difficulty walking to nearly complete paralysis of all extremities, facial, respiratory and bulbar muscles

133
Q

Infectious agents assoc w Guillain Barre

  • # 1: campylobacter jejuni
  • # 2: CMV
A
  • EBV
  • varicella zoster
  • mycoplasma pneumoniae
134
Q

diagnosis of Guillain Barre

A
  • nerve conduction study
  • CSF: increased protein, normal WBC (albuminocytologic dissociation)
  • anti-ganglioside antibodies
135
Q

subtypes and variants of Guillain Barre

*acute inflammatory demyelinating polyneuropathy-most common here

A
  • Miller Fisher syndrome-ophalmoplegia w ataxia & areflexia-IgG antibodies to GQ1b
  • axonal forms: axonal neuropathy (japan & china), motor & sensory axonal neuropathy
136
Q

Treatment of Gullain Barre

  • IVIG 2G/kg over 5 days
  • plasma exchanges
  • combo of 2 above is not better than either one alone
A
  • NO role for steroids
  • DVT prophylaxis if pt cant walk
  • mechanical ventilation: if PCO2 >48, or PO2<15
137
Q

Neurological complications of diabetes:

  • polyneuropathy
  • mononeuropathy
  • radiculopathy
A
  • autonomic neuropathy

* diabetic amyotrophy

138
Q

Polyneuropathy of diabetes

A
  • numb, tingling, burinig pain of feet & hands

* then develop muscular atrophy, decreased reflexes and weakness

139
Q

Mononeuropathy of diabetes

A
  • wrist drop
  • foot drop
  • involvement of CN’s 3-4-or 6th
140
Q

diabetic radiculopathy

A

pain over distribution of one or more spinal nerves

141
Q

diabetic autonomic neuropathy

A

diarrhea
erectile dysfunction
orthostatic hypotension

142
Q

diabeetic amyotrophy

A

weakness of thigh muscles
anorexia
weight loss
normal CPK

143
Q

treatment of neurologic complications of diabetes

A

pregabalin or duloxetine or elavil or venlafaxine

ultram for pain relief

144
Q

Partial (focal) seizures:

A
  • simple
  • complex
  • secondarily generalized tonic-clonic seizures
145
Q

Simple seizure disorder

  • focal sz that does not impair consciousness
  • s/s may be localized to one area or spread to contiguous ipsilateral body parts (Jacksonian March)
A
  • symptoms can be:
  • sensory
  • motor
  • olfactory
  • visual or gustatory
146
Q

Complex seizure disorder

*alteration of consciousness lasting 1-2 minutes but may remain confused for 5-10 minutes after sz ends

A
  • patient has blank stare and has automatisms (lip smacking, chewing, aimless walking, repetitive swallowing)
147
Q

Secondarily generalized tonic-clonic seizures

A
  • begins as partial sz then get tonic clonic sz and resolves in 1-2 minutes
  • often urinary incontinence or tongue biting
148
Q

Generalized seizures

*occur without warning

A
  • tonic-clonic
  • absence seizure (petit mal)
  • sudden brief impairment of consciousness without loss of postural control and lasts 5-10 seconds
149
Q

Treatment of seizures

  • no rx if just a single unprovoked seizure with normal EEG & MRI
  • Tx after first seizure if high risk group (age>65, focal findings on EEG or MRI, hx of head trauma or focal seizure, postictal Todd paralysis
A
  • seizure meds usually started after a second seizure

* inpatient video EEG monitoring indicated in pt w seizures not responding to multiple medications

150
Q

AED: anti epileptic drugs

  • ALL seizure types:
  • lamotrigine, valproate, topiramate, levetiracetam, felbamate,..
A
  • Focal seizures: gabapentin, phenobarb, phenytoin, primidone, carbamazepine..
  • absence seizures: ethosuximide
151
Q

status epilepticus

*continuous seizure or repetitive discrete seizures w impaired consciousness in the interictal period

A
  • if remains comatose after a seizure, do EEG to exclude ongoing status epilepticus
  • generalized convulsive status epilepticus
  • nonconvulsive status epil. - absence or partial seizures
152
Q

treatment of status epilepticus

*IV lorazepam (Best initial tx) => repeat x 1 if no response in 5 minutes =>phenytoin or fosphenytoin =>more of the prior med given

A

=> phenobarbital => more phenobarb => anesthesia w midazolam or propofol

153
Q

complications of status epilepticus

A 
hyperpyrexia
metabolic acidosis
brain damage
rhabdomyolysis
CSF & peripheral leukocytosis
154
Q

causes of death in epilepsy

A
  • trauma, drowning
  • status epilepticus
  • SUDEP-sudden unexpected death in epilepsy
155
Q

risk factors for sudden unexpected death in epilepsy

  • gen tonic clonic sz
  • prone position after nocturnal seizure
  • frequent or recent sz
  • long post ictal EEG suppression
A
  • postictal breathing problem or cardiac arrhythmia
  • inadequate therapy
  • inadequate tx or rapid withdrawal of therapy
156
Q

Mechanism of SUDEP

A
  • resp arrest, laryngeal spasm, suffocation in prone position
  • pulm edema is #1 autopsy finding
  • hypercarbia & hypoxemia common after sz
157
Q

Prevention of SUDEP

  • sz control w appropriate medication
  • avoid sleep deprivation
  • avoid excess alcohol
A
  • in pt w nocturnal tonic clonic sz, increase HS dose of medication
  • after sz, reposition pt on side, stimulate pt for apnea or severe hypoventilation
158
Q

CT findings in infarct

A

hypodense area, no enhancement

159
Q

CT finding in multi infarct dementia

A

multiple hypodense areas

no enhancement

160
Q

CT findings in tumor or lymphoma

A

diffuse enhancing lesion or ring enhancement w central necrosis

161
Q

CT finding of brain abscess

A

ring enhancing lesion

162
Q

CT findings of toxoplasmosis

A

multiple ring enhancing lesions

163
Q

CT findings in cerebral atrophy

A

dilated ventricles & sulci

164
Q

CT findings in alzheimers

A

atrophy +/- non enhancing periventricular white matter lesions

165
Q

CT findings in AIDS dementia

A

atrophy +/- non enhancing white matter lesions

166
Q

CT findings in multiple sclerosis

A

periventricular & sub cortical white matter lesions

lesions enhance with active disease

167
Q

CT findings in NPH (normal pressure hydrocephalus)

A

dilated ventricles

normal sulci

168
Q

CT findings in multi-focal leucoencephalopathy

A

large non enhancing white matter lesions

169
Q

22 y/o male ER 2 hour hx severe diffuse HA. worst HA ever. had brief LOC prior to HA. +N/V, no vision chg.
hx HA in past but unilateral and throbbing and lasted 2 hours. neuro exam is normal, CT without contrast is negative. what is indicated next?

A

Lumbar puncture

170
Q

70 y/o w 20 yr hx diabetes presents w 2 day hx of diplopia. exam-inability to move L eye outward and diplopia on looking toward the left side. diplopia disappears with covering either eye. fundus exam-mild diabetic retinopathy, no papilledema. no other neuro findings, most likely cause of diplopia?

A

L 6th nerve paralysis due to infarction of the nerve

171
Q

76 y/o consults u w recurrent episodes L sided visual loss assoc w weakness of R arm and leg. about 4 episodes in 6 months, lasts approx 5-10”. exam: VSS, no focal neuro deficit. carotid duplex 45% narrowing of carotids, now recommend?a

A

aspirin alone

172
Q

60 y/o male w slow progressive weakness of arms, legs, and occ. difficulty swallowing. neuro : weakness, atrophy and fasciculations of upper extremities. lower extremities: weak, spasticity, hyperactive reflexes. no pain or paresthesia. CT head is negative.Most likely diagnosis?

A

ALS-amyotrophic lateral sclerosis

173
Q

32 y/o female to ER sudden onset of severe headache and diplopia. exam: R ptosis, R pupil is dilated and fixed. there is paralysis to adduction and elevatin of R eye. most likely Dx?

A

leaking posterior communication aneurysm with compression of the 3rd nerve nucleus

174
Q

56 y/o male w tingling hands and feet, poor memory and unsteady gait. exam: spasticity & weakness of legs, + ankle clonus, extensor plantar response, loss of vibratory sense in LE and + rhomberg sign. likely Dx?

A

vit B12 deficiency

175
Q

44 y/o female to ER w weakness and inability to walk. started 6 days ago w numb/weak of both hands and feet. gradually extended proximally of all extremities.. exam: quadriparesis, unable to close both eyes or move facial muscles, no DTRs. LP shows protein 100, normal glucose, no cells best test to confirm?

A

EMG and nerve conduction studies ( Guillian barre)

176
Q

36 y/o with hearing loss L ear. Rinnes test-best on L mastoid process, hears better L ear with tuning fork on center forehead. likely cause of disease affecting

A

external auditory canal or middle ear

177
Q

42 y/o male w episodes of severe HA for 3 days. Ha wakes him at night, always behind L eye, excruciating, lasts 2 hours. with the HA he has tearing of L eye, stuffiness of L nose and drooping of L eyelid. now recommend?

A

start high dose oral prednisone for one week- he has cluster HA

178
Q

60 y/o female w recurrent episodes intense pain lips, cheek and chin on L side several episodes a day and each lasts a few seconds . now recommend

A

cabamazepine

179
Q

54 y/o male with sudden onset of L facial weak, drooping of the saliva and inability to close L eye. exam: droop angle of mouth , unfurrowed forehead, unable to close L eye, and on opening mouth the face is pulled to R side. rest neuro exam normal. now recommend?

A

patching of L eye, prednisone, valacyclovir

Bells palsy

180
Q

26 y/o female w recur attacks of vertigo and tinnitus for 6 months. exam during episode: horizontal nystagmus that disappears on visual fixation on an object. audiogram: high freq hearing loss L ear. most likely dx?

A

*Menieres disease

181
Q

22 y/o female w pain & progressive visual loss R eye. 20/100R, 20/20 Leye. right pupil does not change in size when light shone in front of R eye but in front of L eye both pupils constrict. eye movements and fundus exam is normal. now recommend?

A

IVmethylprednisolone then oral prednisone

182
Q

28 y/o female w double vision. exam: unable to adduct L eye w nystagmus in the abducting R eye. exam otherwise normal. likely dx?

A

multiple sclerosis

183
Q

24 y/o to ER w generalized rigidity and inability to move quickly for past few days. exam: marked rigidity of muscles and severe bradykinesia. Likely Dx?

A

MPTP intoxication-methyl-phenyl-tetrahydropyridine

184
Q

55 y/o w long hx HTN presents w sudden onset weakness R arm & leg and aphasia. Hx of episodes of transcient vision loss of L eye in past 3 months, each lasting 5-10”. exam: complete loss vision L eye, aphagia, weakness R arm and leg . likely occlusion of:

A

L internal carotid artery

185
Q

72 y/o male w HTN, DM with progressive increasing memory loss. Hx of CVA 4 yr ago. exam: 170/100, poor memory, brisk tendon reflexes and extensor plantar response, CT would likely show:

A

multiple hypodense lesions in white & gray matter

186
Q

25 y/o male to ER with generalized sz. no hx of prior sz. acute intoxicaion with what drug may be responsible for his seizure?

A

cocaine

187
Q

50 y/o female w tremors both hands and difficulty writing due to tremors of hands. tremors disappear at rest and after drinking alcohol. now recommend?

A

propranolol- she has benign essential tremors

188
Q

72 y/o presents w R sided vision loss. exam: dense R homonymous hemianopsia. no other neuro abnormalities. likely lesion affecting the

A

L occipital lobe

189
Q

70 y/o female w poor memory, unsteady gait and urinary incontinence. exam: shuffling gait, broad based and unsteady. CT shows dilated ventricles and normal sulci. most likely dx?

A

normal pressure hydrocephalus

190
Q

76 y/o male with headache and intermittent blurring of vision for last 2 weeks. neuro exam is normal . most impt initial test in eval of this patient?

A

sed rate

191
Q

lesions that may be assoc with contrast enhancing CNS lesions in AIDS

A

toxoplasmosis
CNS lymphoma
brain abscess

192
Q

alzheimers patients CT and PET scan show

A

CT: enlarged ventricles and sulci and non enhancing hypodense areas in white matter
PET: hypometabolism in the parietal lobes

193
Q

True about MS

*MRI in active disease: contrast enhanced white matter lesions in periventriccular and subcortical areas

A
  • identical twins of patient w MS have an increased risk of developing active disease
  • chronic progressive disease has a poor prognosis
  • intranuclear opthalmoplegia in young pt is highly suggestive of MS
194
Q

Presence of acetylcholine receptor antibodies confirms the dx of

A

myasthenia gravis

195
Q

major cause of death in pt with Duchenne muscular dystrophy is

A

respiratory failure

196
Q

myotonic dystrophy may be complicated by

A

cardiac conduction defects

197
Q

complications of status epilepticus include

A
  • hyperpyrexia
  • irreversible brain damage
  • CSF & peripheral leukocytosis
  • rhabdomyolysis
  • metabolic acidosis

GI (10 decks)

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