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
clinical presentation of brain tumors
* headache-worse w laying down, cough, valsalva * seizure, papilledema, focal neuro deficits * impaired lateral gaze, dementia, personality changes * gait disorder
25
treatment of symptomatic brain tumor
dexamethasone
26
Upper motor neuron lesion
weakness, spasticity hyperactive tendon reflexes Babinski sign-extensor planter reflex
27
Lower motor neuron (anterior horn cells, motor roots, peripheral nerves)
weakness, hypotonia, atrophy loss of tendon reflexes fasciculations sensory symptoms if mixed nerve is involved
28
Muscle diseases
weakness- proximal >distal no sensory changes reflexes preserved, atrophy no fasciculations, eye and bulbar muscles spared
29
neuromuscular junction
``` weakness increases with activity no sensory symptoms eye and bulbar muscles involved reflexes normal no atrophy or fasciculations ```
30
Argyll Robertson pupil
no reaction to light reacts to accommodation **syphilis
31
Relative afferent pupillary defect (RAPD)
no response to direct light but constricts when light shown in the other eye **MS
32
3rd nerve palsy
ptosis = dilated pupil
33
Horners syndrome
ptosis + constricted pupil
34
pin point pupils
narcotic overdose pontine damage thalamic hemorrhage
35
unilateral enlarged pupil in comatose
midbrain lesion or compression of 3rd CN
36
bilateral dilated unreactive pupil in comatose pt
severe bilateral midbrain damage | anticholinergic overdose
37
paralysis of 6th CN
inability to move the eye outward | eye turns toward the nose when looking straight
38
paralysis of 3rd CN
eye displaced downward and outward ptosis eye can only move laterally and downward +/- dilated nonreactive pupil
39
diplopia
Monocular: does not correct by covering one eye Binocular: corrects by covering one eye
40
3rd CN paralysis *acute isolated 3rd nerve paralysis w pupillary involvement=>posterior communicating artery aneurysm
* acute isolated 3rd nerve paralysis without pupillary involvement - age 50: vascular, most common is diabetes-microinfarction of 3rd nerve
41
Trigeminal neuralgia
vascular compression of the trigeminal root
42
clinical features of trigeminal neuralgia
*episodes knife like pain lips,gums,cheeks, or chin, lasts seconds to 2 minutes
43
triggers for trigeminal neuralgia
* touching specific points on face * talking, chewing * exposure to breeze, bright light or loud noise
44
trigeminal neuralgia do MRI in all cases to r/o
structural compression of nerve
45
treatment of trigeminal neuralgia
* carbamazepine or oxcarbazepine * others: baclofen, gabapentin, lamotrigine * heat or gamma knife radiosurgery or surgical microvasc. decompression
46
Infranuclear facial nerve paralysis
``` Bell's palsy Ramsay Hunt Syndr Acoustic neuroma Pontine tumor or infarction Guillain Barre, sarcoid, lyme ```
47
Bell's palsy *assoc Herpes simplex virus type 1
*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
48
Ramsay Hunt syndrome
* herpes zoster involving geniculate ganglion | * vesicular lesions in pharynx or external auditory canal & freq involves the 8th CN
49
peripheral vertigo (vestibular nerve or inner ear) * severity: +++ * N/V: ++ * tinnitus/hearing loss: some cases
* nystagmus: unidirectional, horizontal (never vertical) * visual fixation: inhibits nystagmus and vertigo * assoc central abnl: none
50
causes of peripheral vertigo
``` vestibular neuritis labyrinthitis Menieres dz acoustic neuroma benign positional ```
51
Central vertigo (brain stem or cerebellum) * severity: + * N/V: +/- * tinnitus/hearing loss: none
* nystagmus: multidirectional, vertical * visual fixation: no inhibition of nystagmus or vertigo * assoc central abnl: dysarthria, diplopia, ataxia, weakness
52
causes of central vertigo
brain stem dysfunction due to demyelinating, vascular or neoplastic diseases
53
conductive hearing loss - external auditory canal or middle ear * air conduction-abnormal * bone conduction-normal
* 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
54
sensory-neural hearing loss (inner ear, 8th nerve, or central auditory pathway) * air conduction-abnormal * bone conduction- abnormal * Rinne test- abnormal in both locations
*weber test- hears only on the normal side
55
Unilateral lesion of the spinal cord * pain & temp sense lost below the lesion - OPPOSITE side * spastic paralysi on SAME side as the lesion
* loss of vibration and position sense SAME side below the lesion * *TOUCH sense is not lost**
56
Syringomyelia * progressive myelopathy characterized by cavitation of central spinal canal * usually starts from mid cervical cord
* wasting of muscles of neck, shoulder, arms * progressive spastic paraparesis * loss of pain & temperature sensation
57
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
* 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
58
clinical features of transverse myelitis *develop over hours to days bilateral sensorimotor signs w a clear sensory level *hyperreflexia & Babinski present
* urinary incontinence or retention * bowel incontinence or constipation * sexual dysfunction * Lhermittes sign- paresthesias radiating down spine or limbs with neck flexion
59
Diagnosis of transverse myelitis
* MRI-do entire spine=>enhancing intramedullary cord lesion * CSF pleocytosis or high IgG index * MRI brain =>demyelination on brain MRI suggests MS
60
causes of transverse myelitis * post infection or post vaccine * acute infection * systemic autoimmune:SLE,sarcoid, sjogrens
* paraneoplastic * idiopathic * multiple sclerosis * neuromyelitis optica (myelitis + optic neuritis)
61
Tx transverse myelitis
* high dose steroids | * plasma exchange if no response to steroids
62
most common demyelinating dz of the nervous system
* 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
63
clinical presentation of MS | *sensory loss or paresthesias, optic neuritits, diplopia, weakness, ataxia, hyperreflexia spasticity, heat sensitivity
* 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
64
Patterns of MS
* relapsing remitting * secondary progressive * primary progressive-worst prognosis * progressive relapsing
65
diagnosis of MS
* 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
66
treatment of acute relapses of MS- that produce functional impairment or initial attacks of optic neuritis
Methylprednisolone IV 1 gram/day for 3-5 days then oral prednisone for 2 weeks
67
disease modifying drugs for MS *no effective tx for primary progressive MS**
* 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
68
Parkinson's disease
unknown etiology | degeneration of dopamine contained in neurons in the basal ganglion
69
clinical presentation of Parkinsons dz *tremor: asymmetrical, more pronounced at rest, handwriting is small and irregular (essential tremor its large & tremulous)
* 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
70
secondary causes of Parkinsons dz * drugs:phenothiazine, reserpine,metoclopramide, antipsychotics,lithium * toxins: CO poisoning, MPTP-methylphenyl tetrahydro., mercury
* head trauma * wilsons disease * post encephalitis * MRI brain to r/o hydrocephalus or vascular lesions
71
First line tx of Parkinsons
levodopa & carbidopa levodopa & carbidopa & entacapone dopamine agonist: ergot-bromocriptine, pramipexole,, ropinirole, rotigotine patch
72
second line tx of Parkinsons
* MAO-B inhibitor-selegiline * anticholinergics * NMDA antagonists: amantadine (Symmetrel)
73
surgical tx Parkinsons
deep brain stimulation w implanted electrodes
74
Complicaions of levodopa therapy *wearing-off phenomenon: incr dose and freq of levodopa, add dopamine agonist +/- COMT inhibitor
* N/V: increase carbidopa dose * dyskinesias (choreiform & dystonic movements): add dopamine agonist +/- amantadine * psychosis: add atypical antipsychotic drug Quetiapine
75
Myasthenia Gravis
autoimmune neuromuscular disorder due to antibodies against acetylcholine receptors symptoms are provoked by exertion
76
clinical features of myasthenia gravis
* ocular: blur vision, binocular diplopia, ptosis | * generalized: limb weakness, slurred speech, dysphagia, dyspnea
77
diagnosis of myasthenia gravis
* 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
78
tx of myasthenia gravis
* *acetylcholinesterase inhibitor: pryridostigmine * immunosuppress: steroids, azathioprine, mycophenolate, cyclosporin, rituximab * thymectomy if thymoma and if
79
Myasthenia crisis
*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
Lambert-Eaton syndrome
paraneoplastic syndrome *most common malignancy: small cell lung cancer
81
clinical features of Lambert-Eaton
* muscle weakness, strength improvs with activity * dry eyes and mouth * erectile dysfunction * constipation
82
diagnosis of Lambert-Eaton
*EMG with repetitive nerve stimulatioon *calcium channel antibodies in serum CXR-if negative, do CT chest, abdomen , pelvis **TX: pyridostigmine
83
CVA types
thrombotic embolic hemorrhagic
84
TIA
transient episode of neurological dysfunction d/t focal brain, spinal cord, or retinal ischemia, without acute infarction
85
Carotid TIA
* contralaterial hemiparesis or sensory loss * aphasia if dominant site * ipsilateral visual loss-lasts few minutes, and loss evolves in less than one minute
86
vertebrobasilar TIA
*episodes of dizziness, diplopia, dysarthria, facial or circumoral numbness +/- bilateral weakness +/- drop attacks due to sudden weakness of legs
87
Intracerebral hemorrhage - clinical features-rapidly evolve:
* headache * vomiting * seizures * impaired consciousness * neurological deficit
88
causes of intracerebral hemorrhage
#1: HTN * amyloid angiopathy-lobar hemorrhage in elderly * vascular malformations * anticoagulation/thrombolytics * cocaine, alcohol
89
diagnosis of intracranial hemorrhage
CT head WITHOUT contrast | cerebral angiography if
90
TX of intracerebral hemorrhage
* SBP 140-160, mean pressure 70-130 * surgery: cerebellar hemorrhage * mannitol, barbiturate coma, hyperventilation to decrease intracranial pressure * *NO role for steroids
91
ischemic stroke
defined by presence of cerebral infarct on imaging | several types
92
cardioembolic stroke
* suspect when multiple infarcts seen on imaging | * most common cause ATRIAL FIB
93
Large artery atherosclerosis as cause of ischemic stroke
* 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
cryptogenic stroke as cause of ischemic stroke
* **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
Management of TIA
* 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
Evaluation of TIA
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
Risk factor management for TIA
BP< 120% of ideal body weight
98
ABCD scoring system in TIA AGE 60 or greater 1 BP 140/90 or greater 1
``` CLINICAL symptoms: *focal weakness w TIA 2 *speech impair w/o weakness 1 DURATION: 10-59" (1), 60" or longer (2) DIABETES 1 ```
99
significance of ABCD scoring **2 day risk of stroke** SCORE: 0-1 0% 2-3 1.3%
4-5 4.1% | 6-7 8.1%
100
anterior cerebral artery cva
* medial cerebral hemisphere * contralateral weakness and sensory loss in leg>arm * behavioral changes
101
Internal carotid artery cva
* ipsilateral vision loss * contralateral hemiparesis & sensory loss * homonymous heminopis * aphasia
102
Middle cerebral artery cva
* lateral cerebral hemisphere * contralateral hemiplegia & sensory loss * homonymous hemianopis * aphasia
103
Branch of middle cerebral artery cva
*contralateral hemiplegia without sensory loss or can have sensory loss without hemiplegia
104
Posterior cerebral artery
* ipsilateral 3rd nerve and contralateral hemiplegia or ataxia * homonymous hemianopia * cortical blindness if bilateral
105
basilar artery cva
* brainstem, pontomedullary junction * bilateral sensory & motor signs, CN 5-6-7, cerebellar signs * diminished pain & thermal sense over half of body * horners syndrome
106
vertebral artery
* brainstem, lateral medulla * vertigo, ataxia, nystagmus * Horners syndrome * diminished pain & thermal sense half of body
107
Posterior inferior cerebellar artery
* lateral medulla * ipsilateral facial sensory loss * contralateral body sensory loss * vertigo, ataxia, dysarthria
108
Prevention of stroke * Tx HTN * stop smoking * regular exercise * diet high fruit, veg, fiber, low in saturated fat
* anticoag if a fib * tx carotid disease if indicated * statin tx goal LDL< 100 * antiplatelet * glucose control w diabetes
109
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
* 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
Tx ischemic stroke continued: * possible intra-arterial thrombolytic tx in those w contraind. for IV thrombolysis * neurosurg eval for cerebellar infarct or bleed
* 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
no benefit of stenting a blocked intracranial vessel or extracranial-intracranial bypass of
of a completely occluded ICA compared to medical therapy
112
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
- select cases up to 4.5 hours onset of symptoms | * begin antiplatelet therapy w aspirin or plavix after 24 hours
113
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
* evidence active bleed, GI/GU bleeding in past 21 days | * platelet
114
for thrombolitic exceptions of 3-4.5 hours after onset of symptoms, additional contraindications for this later tx include:
* age >80 * combination of prior stroke + diabetes * NIH stroke scale >25 * oral anticoagulant use regardless of INR
115
Aphasia * disturbance in comprehension (sensory) or production (motor) of spoken or written language * several types: - global
- wernickes - conduction - pure word deafness - pure word blindness - isolation of speech area
116
Global aphasia
* 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
Wernicke's aphasia
* speech is fluent but does not make sense * parietal lobe involvement * MCA branch involvement
118
aphasia-conductive
* repetition is severely affected * parietal or frontal lobe * MCA branch
119
aphasia-pure word deafness
no auditory comprehension
120
aphasia-pure word blindness
inability to read, name colors dominant occipital lobe PCA involvement
121
aphasia-isolation of speech area
* caused by extensive brain damage from shock | * parrot like repetition of spoken words
122
Alzheimers Disease
* most freq cause of dementia * increased production and accumulation of beta-amyloid peptide which results in cell dysfunction =>deficiency of acetylcholine
123
Risk factors for alzheimers * age * family history * Downs syndrome
* rare mutatin in amyloid precursor protein:presenilin 1 & 2 mutation - early onset age 30-50 - autosomal dominant
124
clinical features of alzheimers
* predominant loss of short term memory * progressive impairment of ADL's * variety neuropsychiatric symptoms & behavior disturbance
125
Tx of alzheimers *best initial tx: donepezil, rivastigmine, galantamine (central acting cholinesterace inhibitors)
* N-methyl-D-aspartate receptor antagonist-memantine * vit E & C, ginkgo biloba * SSRI for depression, antipsychotic for agitatin, delusions and hallucinations
126
other causes of dementia: * multi-infarct :CT hypodense areas white&gray matter w no enhancement * B1 or B12 deficiency * hypothyroidism
* normal pressure hydrocephalus * CNS infections * creutzfeld-jakob disease * frontotemporal dementia
127
Normal-pressure hydrocephalus
* dementia, gait disturbance, urinary incontinence * CT shows dilated ventricles * Tx: ventriculoperitoneal shunt
128
CNS infectious causes of dementia
HIV syphilis cryptococcus
129
Creutzfeld-Jakob disease * cause:infectious prions * transmission: corneal transplant, contaminated growth hormone
* rapidly progressive:dementia, myoclonus, focal cortical signs & rigidity * EEG: markedly abnormal periodic discharges * MRI (diffusion weighted): cortical & basal ganglion abnormality
130
Frontotemporal dementia
* dementia, prominent personality & behavior changes, parkinsonism * MRI: prominent asymmetric frontal lobe atrophy
131
Guillain Barre syndrome
*rapidly progressive polyneuropathy
132
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
*weakness varies: mild difficulty walking to nearly complete paralysis of all extremities, facial, respiratory and bulbar muscles
133
Infectious agents assoc w Guillain Barre * #1: campylobacter jejuni * #2: CMV
* EBV * varicella zoster * mycoplasma pneumoniae
134
diagnosis of Guillain Barre
* nerve conduction study * CSF: increased protein, normal WBC (albuminocytologic dissociation) * anti-ganglioside antibodies
135
subtypes and variants of Guillain Barre *acute inflammatory demyelinating polyneuropathy-most common here
* Miller Fisher syndrome-ophalmoplegia w ataxia & areflexia-IgG antibodies to GQ1b * axonal forms: axonal neuropathy (japan & china), motor & sensory axonal neuropathy
136
Treatment of Gullain Barre * IVIG 2G/kg over 5 days * plasma exchanges * combo of 2 above is not better than either one alone
* NO role for steroids * DVT prophylaxis if pt cant walk * mechanical ventilation: if PCO2 >48, or PO2<15
137
Neurological complications of diabetes: * polyneuropathy * mononeuropathy * radiculopathy
* autonomic neuropathy | * diabetic amyotrophy
138
Polyneuropathy of diabetes
* numb, tingling, burinig pain of feet & hands | * then develop muscular atrophy, decreased reflexes and weakness
139
Mononeuropathy of diabetes
* wrist drop * foot drop * involvement of CN's 3-4-or 6th
140
diabetic radiculopathy
pain over distribution of one or more spinal nerves
141
diabetic autonomic neuropathy
diarrhea erectile dysfunction orthostatic hypotension
142
diabeetic amyotrophy
weakness of thigh muscles anorexia weight loss normal CPK
143
treatment of neurologic complications of diabetes
pregabalin or duloxetine or elavil or venlafaxine | ultram for pain relief
144
Partial (focal) seizures:
* simple * complex * secondarily generalized tonic-clonic seizures
145
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)
* symptoms can be: - sensory - motor - olfactory - visual or gustatory
146
Complex seizure disorder *alteration of consciousness lasting 1-2 minutes but may remain confused for 5-10 minutes after sz ends
* patient has blank stare and has automatisms (lip smacking, chewing, aimless walking, repetitive swallowing)
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Secondarily generalized tonic-clonic seizures
* begins as partial sz then get tonic clonic sz and resolves in 1-2 minutes * often urinary incontinence or tongue biting
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Generalized seizures *occur without warning
* tonic-clonic * absence seizure (petit mal) - sudden brief impairment of consciousness without loss of postural control and lasts 5-10 seconds
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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
* seizure meds usually started after a second seizure | * inpatient video EEG monitoring indicated in pt w seizures not responding to multiple medications
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AED: anti epileptic drugs * ALL seizure types: - lamotrigine, valproate, topiramate, levetiracetam, felbamate,..
* Focal seizures: gabapentin, phenobarb, phenytoin, primidone, carbamazepine.. * absence seizures: ethosuximide
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status epilepticus *continuous seizure or repetitive discrete seizures w impaired consciousness in the interictal period
* if remains comatose after a seizure, do EEG to exclude ongoing status epilepticus * generalized convulsive status epilepticus * nonconvulsive status epil. - absence or partial seizures
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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
=> phenobarbital => more phenobarb => anesthesia w midazolam or propofol
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complications of status epilepticus
``` hyperpyrexia metabolic acidosis brain damage rhabdomyolysis CSF & peripheral leukocytosis ```
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causes of death in epilepsy
* trauma, drowning * status epilepticus * SUDEP-sudden unexpected death in epilepsy
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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
* postictal breathing problem or cardiac arrhythmia * inadequate therapy * inadequate tx or rapid withdrawal of therapy
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Mechanism of SUDEP
* resp arrest, laryngeal spasm, suffocation in prone position * pulm edema is #1 autopsy finding * hypercarbia & hypoxemia common after sz
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Prevention of SUDEP * sz control w appropriate medication * avoid sleep deprivation * avoid excess alcohol
* 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
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CT findings in infarct
hypodense area, no enhancement
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CT finding in multi infarct dementia
multiple hypodense areas | no enhancement
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CT findings in tumor or lymphoma
diffuse enhancing lesion or ring enhancement w central necrosis
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CT finding of brain abscess
ring enhancing lesion
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CT findings of toxoplasmosis
multiple ring enhancing lesions
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CT findings in cerebral atrophy
dilated ventricles & sulci
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CT findings in alzheimers
atrophy +/- non enhancing periventricular white matter lesions
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CT findings in AIDS dementia
atrophy +/- non enhancing white matter lesions
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CT findings in multiple sclerosis
periventricular & sub cortical white matter lesions | lesions enhance with active disease
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CT findings in NPH (normal pressure hydrocephalus)
dilated ventricles | normal sulci
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CT findings in multi-focal leucoencephalopathy
large non enhancing white matter lesions
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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?
Lumbar puncture
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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?
L 6th nerve paralysis due to infarction of the nerve
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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
aspirin alone
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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?
ALS-amyotrophic lateral sclerosis
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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?
leaking posterior communication aneurysm with compression of the 3rd nerve nucleus
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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?
vit B12 deficiency
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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?
EMG and nerve conduction studies ( Guillian barre)
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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
external auditory canal or middle ear
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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?
start high dose oral prednisone for one week- he has cluster HA
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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
cabamazepine
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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?
patching of L eye, prednisone, valacyclovir | Bells palsy
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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?
*Menieres disease
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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?
IVmethylprednisolone then oral prednisone
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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?
multiple sclerosis
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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?
MPTP intoxication-methyl-phenyl-tetrahydropyridine
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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:
L internal carotid artery
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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:
multiple hypodense lesions in white & gray matter
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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?
cocaine
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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?
propranolol- she has benign essential tremors
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72 y/o presents w R sided vision loss. exam: dense R homonymous hemianopsia. no other neuro abnormalities. likely lesion affecting the
L occipital lobe
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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?
normal pressure hydrocephalus
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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?
sed rate
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lesions that may be assoc with contrast enhancing CNS lesions in AIDS
toxoplasmosis CNS lymphoma brain abscess
192
alzheimers patients CT and PET scan show
CT: enlarged ventricles and sulci and non enhancing hypodense areas in white matter PET: hypometabolism in the parietal lobes
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True about MS *MRI in active disease: contrast enhanced white matter lesions in periventriccular and subcortical areas
* 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
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Presence of acetylcholine receptor antibodies confirms the dx of
myasthenia gravis
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major cause of death in pt with Duchenne muscular dystrophy is
respiratory failure
196
myotonic dystrophy may be complicated by
cardiac conduction defects
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complications of status epilepticus include
* hyperpyrexia * irreversible brain damage * CSF & peripheral leukocytosis * rhabdomyolysis * metabolic acidosis