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Neurology Flashcards

1
Q

What are the 4 D’s of posterior circulation strokes?

A

Diplopia
Dizziness
Dysphagia
Dysarthria

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2
Q

Ischemic strokes take how long to show up on CT?

A

6 hours

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3
Q

What is the function of the lateral corticospinal tract? What is the clinical presentation of a lesion here?

A

Movement of ipsilateral limbs and body

Ipsilateral paresis at and below level of lesion

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4
Q

What is the function of the dorsal columns? What is the clinical presentation of a lesion here?

A

Fine touch, vibration, proprioception

Ipsilateral loss at and below lesion

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5
Q

What is the function of the spinothalamic tract? What is the clinical presentation of a lesion here?

A

Pain, temperature

Contralateral loss of pain and temp at and below level of lesion

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6
Q

What areas of the spinal cord does polio affect? Symptoms?

A

Anterior horns

LMN symptoms

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7
Q

What areas of the spinal cord does MS affect? Symptoms?

A

random areas of the dorsal columns and anterior corticospinal tracts

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8
Q

What areas of the spinal cord does ALS affect? Symptoms?

A

Anterior horns and lateral corticospinal tracts

UMN and LMN s/sx

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9
Q

What treatment for MS ALS?

A

Riluzole (riLOUzole for LOU Gehrig’s disease)

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10
Q

What areas of the spinal cord does complete occlusion of the anterior spinal artery affect? Symptoms?

A

Everything but dorsal columns

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11
Q

What areas of the spinal cord does tabes dorsalis affect? Symptoms?

A

Dorsal columns and nerve roots

Sensory ataxia and poor coordination

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12
Q

What areas of the spinal cord does syringomyelia affect? Symptoms?

A

Anterior white commissure of spinothalamic tract

cape like, bilateral loss of pain and temperature in upper extremities.

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13
Q

What areas of the spinal cord does Vit B12 affect? Symptoms?

A

-Dorsal columns, lateral corticospinal tract, and spinocerebellar tracts

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14
Q

What is the presentation of an UMN lesion to the facial nerve?

A

Contralateral deficits of the LOWER face only

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15
Q

What is the presentation of an LMN lesion to the facial nerve?

A

Ipsilateral facial paralysis

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16
Q

What are the disease that Bell’s palsy is commonly seen in? (5)

A 
AIDS
Lyme disease
Sarcoidosis
Tumors
DM
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17
Q

What are the components of the CHANGes mnemonic for s/sx that occur with MCA stroke?

A 
Contralateral paresis / sensory loss
Hemiparesis
Aphasia (dominant side)
Neglect (nondominant side)
Gaze preference toward side of lesion
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18
Q

tPA is indicated if a stroke has occurred within what timeframe?

A

Less than 3 hours

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19
Q

What is the max BP that is allowable prior to the use of tPA?

A

185/110

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20
Q

When is ASA indicated in the treatment of a stroke?

A

If it has been more than 3 hours since onset, and not hemorrhagic

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21
Q

What is the role of treating fever/hyperglycemia in an acute stroke?

A

Better prognosis if treated

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22
Q

What is the treatment for increased ICP in the setting of ischemic stroke?

A

Mannitol and hyperventilation

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23
Q

What spinal level does the biceps reflex test?

A

C5

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24
Q

What spinal level does the triceps reflex test?

A

C7

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25
Q

What spinal level does the patellar reflex test?

A

L4

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26
Q

What spinal level does the achilles reflex test?

A

S1

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27
Q

What is the single greatest risk factor for stroke?

A

HTN

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28
Q

What are the components of the SAMPLE STAGES contraindications for tPA administration?

A
  • Stroke / head trauma in the last 3 months
  • Anticoagulation with INR more than 1.7
  • MI in the past 3 months
  • Prior intracrainial bleed
  • Low platelets
  • Elevated BP
  • Surgery in past 14 days
  • TIA within 6 months
  • GI or urinary bleeding past 21 days
  • Elevated BG
  • Seizures at onset of stroke
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29
Q

A stroke or head trauma within what timeframe is a contraindication to tPA?

A

3 months

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30
Q

An INR above what is a contraindication for tPA?

A

1.7

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31
Q

A MI within what timeframe is a contraindication to tPA?

A

3 months

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32
Q

A hemorrhagic stroke within what timeframe is a contraindication to tPA?

A

Ever

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33
Q

Major surgery within what timeframe is a contraindication to tPA?

A

14 days

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34
Q

Gi/GU bleeding within what timeframe is a contraindication to tPA?

A

21 days

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35
Q

What BG levels are a contraindication to tPA?

A

Below 50 or above 400

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36
Q

Name the artery likely affected: Contralateral paresis and sensory loss in the leg; cognitive or personality changes.

A

ACA

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37
Q

Name the artery likely affected: Contralateral paresis and sensory loss in the face and arm; gaze preference toward the side of the lesion.

A

MCA

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38
Q

Name the artery likely affected: vertigo, homonymous hemianopsia

A

PCA

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39
Q

Name the artery likely affected: Pure motor, pure sensory, ataxic hemiparesis, or dysarthria

A

Lacunar

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40
Q

What is the definition of a TIA?

A

Neurological deficit lasts less than 24 hours, and without findings on MRI

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41
Q

What are the indications for carotid endarterectomy in symptomatic and asymptomatic patients respectively?

A 
Symptomatic = 60%
Asymptomatic = 70%
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42
Q

What are the top three causes of subarachnoid hemorrhage?

A
  • Ruptured berry aneurysm
  • AV malformations
  • Trauma to the circle of Willis
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43
Q

What are the s/sx of a subarachnoid hemorrhage? (2)

A

Thunderclap HA

Neck stiffness

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44
Q

What is a “Sentinel bleed” in terms of patients with SAH?

A

Warning bleed that occurs a few days prior to presentation

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45
Q

If CT is negative, but there is a strong clinical suspicion of a SAH, what should be done?

A

LP to look for bleeding or xanthochromia

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46
Q

What imaging should be performed once SAH is confirmed? Why?

A

four vessel angiography to identify exact source of bleeding

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47
Q

What are the components of the “MAKE an SAH” more likely?

A

Marfan
Aortic coarctation
Kidney disease (AD polycystic)
Ehler-danlos

Sickle cell or smoking
Atherosclerosis
HTN

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48
Q

What are the treatment focuses after a SAH has been repaired? (3)

A
  • Maintaining BP below 150
  • prevent vasospasm
  • Decreased increased ICP
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49
Q

What is the drug of choice to prevent vasospasm in patients post SAH repair?

A

Nimodipine

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50
Q

What is the effect of vasospasm post SAH repair?

A

Major increase in morbidity and mortality

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51
Q

Where in the brain does intracerebral hemorrhage generally occur?

A

Deep brain regions (e.g. basal ganglia, pons, cerebellum, etc.)

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52
Q

What is the most common underlying cause of intracerebral hemorrhage?

A

HTN

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53
Q

What are the early symptoms of intracerebral hemorrhage? Late?

A
  • Focal motor or sensory deficits

- Features of increased ICP

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54
Q

What is the common cause of subdural hematoma?

A

Rupture of bridging veins

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55
Q

What is the common cause of epidural hematoma?

A

Middle meningeal artery tear

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56
Q

What are the s/sx of a subdural hematoma?

A

HA, changes in mental status, and/or focal neurological deficits

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57
Q

What are the s/sx of an epidural hematoma?

A

Immediate LOC, followed by lucid interval from minutes to hours

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58
Q

What are the CT findings of a subdural hematoma?

A

Crescent shaped, concave density

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59
Q

What are the CT findings of an epidural hematoma?

A

Lens-shaped biconvex density

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60
Q

How can you differentiate an acute vs chronic subdural hematoma?

A 
Isodense = acute
Hypodense = chronic
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61
Q

What does a blown pupil suggest?

A

Impending ipsilateral brainstem compression

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62
Q

What is the most common agent to cause septic cavernous sinus thrombosis?

A

Staph Aureus

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63
Q

What are the s/sx of cavernous sinus thrombosis?

A

HA
Fever
visual disturbances

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64
Q

What is the best imaging modality to diagnose cavernous sinus thrombosis?

A

MRI

65
Q

What is the treatment for cavernous sinus thrombosis?

A

Penicillinase-resistant penicillin + 3rd gen cephalosporin

66
Q

What is the treatment for cavernous sinus thrombosis if a oral source is suspected?

A

Metronidazole

67
Q

Name the type of HA: unilateral, pulsating HA tha lasts 4-72 hours

A

Migraine

68
Q

Who is classically affected by migraines?

A

Women in their 20’s

69
Q

What is the underlying pathophysiology of migraine HAs?

A

Vasospasm and serotonin release

70
Q

What is the abortive therapy for a migraine HA?

A

Triptans

71
Q

What is the prophylactic therapy for migraine HAs? (4)

A
  • Anticonvulsants (e.g. gabapentin, topiramate)
  • TCAs
  • Beta blockers
  • CCBs
72
Q

Who is classically affected with cluster HAs?

A

25 year old man

73
Q

Name the type of HA: excruciating, brief, unilateral periorbital HA that occur many times a day

A

Cluster HA

74
Q

What is the classic associated symptom of a cluster HA?

A

Ipsilateral lacrimation

75
Q

When is an extensive workup for cluster HAs indicated?

A

First onset to r/o more severe causes

76
Q

What is the acute and chronic therapy for cluster HAs?

A 
Acute = oxygen
Chronic = verapamil or anticonvulsants
77
Q

Name the type of HA: bilateral pain, not aggravated by physical activity

A

Tension

78
Q

What is the treatment for tension HAs?

A

NSAIDs

Avoid exacerbating factors

79
Q

Jaw claudication + HA in an older person should be worked up for what disorder?

A

Temporal arteritis

80
Q

Complex partial seizures classically affect what part of the brain?

A

Temporal lobe

81
Q

What are the classic EEG findings of a absence seizure?

A

3 Hz spike and wave discharges

82
Q

What is a common triggering factor of absence seizures?

A

Hyperventilation

83
Q

What are the EEG findings of a tonic-clonic seizure?

A

10Hz during the clonic phase, and slow waves during the clonic phase

84
Q

What hormone levels may be elevated in the postictal state?

A

Prolactin

85
Q

Focal seizures in an adult should alway prompt evaluation for what pathology?

A

Tumors

86
Q

What is the first line anticonvulsant in children?

A

Phenobarbital

87
Q

What are the first and second line agents for absence seizures?

A 
1 = Ethosuximide
2 = Valproic acid
88
Q

What is the treatment for intractable temporal lobe seizures?

A

Anterior temporal lobe lobectomy

89
Q

What are some of the first line agents, besides anticonvulsants or benzos, in the treatment of status epilepticus?

A

Thiamine, then glucose

Naloxone

90
Q

When evaluating suspected BPPV, Nystagmus lasting longer than how long is concerning for a central lesion?

A

1 minute

91
Q

What is the typical presentation of vestibular neuritis (labyrinthitis)?

A

Acute onset of severe vertigo, head motion intolerance, and gait unsteadiness

92
Q

What is the difference in presentation of vestibular neuritis vs labyrinthitis?

A

Labyrinthitis = Auditory or aural symptoms (tinnitus, ear fullness, hearing loss)

Vestibular neuritis = Lacks auditory or aural symptoms

93
Q

What are the three major findings of peripheral vestibulopathy that differentiates it from strokes?

A

■ An abnormal vestibulo-ocular reflex as determined by a bedside head impulse test (ie, rapid head rotation from lateral to center while staring at the examiner’s nose).
■ A predominantly horizontal nystagmus that always beats in one direction, opposite the lesion.
■ No vertical eye misalignment by alternate cover testing.

94
Q

What is the treatment for labyrinthitis / vestibular neuritis? Prognosis?

A

Steroids and antivertigo agents

Resolves in two weeks

95
Q

What are the general s/sx of Meniere’s disease?

A

Vertigo with hearing loss, tinnitus, and ear fullness

96
Q

What is one of the first signs of Meniere’s disease?

A

Progressive, Low frequency hearing loss

97
Q

What are the diagnostic criteria for Meniere’s disease?

A

Two episodes lasting over 20 minutes with remission of s/sx between episodes

98
Q

What is the acute and chronic treatment for Meniere’s disease?

A 
Acute = Meclizine or benzos + antiemetics
Chronic = Avoid salt, diuretics
99
Q

Do cardiac etiologies of syncope typically have prodromal s/sx?

A

No

100
Q

Which heart valve disease is classically associated with syncope?

A

Aortic stenosis

101
Q

What is the general workup of new onset syncope?

A
  • Telemetry / holter for arrhythmias
  • ECG and cardiac enzymes to r/o MI
  • Echo to tilt-table test
102
Q

What, generally, is the pathophysiology behind Myasthenia gravis?

A

Antibodies directed against the postsynaptic acetylcholine receptors

103
Q

What is the best initial test for myasthenia gravis?

A

serology for the antibodies

104
Q

What is the role of a chest CT in the diagnosis of myasthenia gravis?

A

evaluate for a thymoma

105
Q

What is the treatment for myasthenia gravis?

A

Pyridostigmine or prednisone

106
Q

Why should patients with myasthenia gravis not be given beta blockers?

A

Due to its effects at the neuromuscular junction

107
Q

What are the abx that should be avoided in patients with myasthenia gravis?

A

Aminoglycosides

Fluoroquinolones

108
Q

What are the three muscles that are spared with Eaton-Lambert syndrome?

A

EOMs
Respiratory
Bulbar

109
Q

What is the treatment for eaton-lambert syndrome?

A

Corticosteroids

Azathioprine

110
Q

What are the cells that mediate MS?

A

T cells

111
Q

Which type of MS has the best prognosis?

A

The relapsing and remitting type

112
Q

What is charcot’s triad for MS?

A

Scanning speech
Internuclear ophthalmoplegia
(Intention tremor)
Nystagmus

(SIIN)

113
Q

Symptoms of MS classically worsen under what conditions?

A

Heat (how showers, hot summer, etc)

114
Q

Where are the white matter lesions classically located with MS?

A

Periventricular and in the corpus callosum

115
Q

What will CSF show with MS?

A

Increased IgG, or oligoclonal bands

116
Q

What is the treatment for MS?

A

Corticosteroids

Plasma exchange if not respond

117
Q

What are the ABCs of MS treatment?

A

Avonex (IFN-beta1a)
Betaseron (IFN-beta1b)
Copaxone

118
Q

What generally happens to the s/sx of MS with pregnancy?

A

Decrease

119
Q

What is the treatment for optic neuritis?

A

IV corticosteroids (Not oral)

120
Q

What are the 4 A’s of guillain-Barre syndrome?

A

Acute inflammatory demyelinating
Ascending paralysis
Autonomic neuropathy
Albuminocytological dissociation

121
Q

What are the CSF findings of Guillain-Barre syndrome?

A

Increased albumin in CSF (Albuminocytological dissociation)

-Protein more than 55 mg/dL

122
Q

What is the treatment for Guillain-barre syndrome?

A

IVIG

Plasmapheresis

123
Q

What is the role of corticosteroids in the treatment of Guillain-Barre syndrome?

A

NOT indicated

124
Q

What is the prognosis for ALS?

A

Dead in 5 years

125
Q

What is the general history of ALS?

A

Asymmetric, slowly progressive weakness, with fasciculations,

126
Q

What is nerve functions are generally spared with ALS? (3)

A

Sensation
Eye movement
Sphincter tone

127
Q

Is pronator drift and UMN or LMN sign?

A

UMN

128
Q

Fasciculations are an UMN or LMN sign?

A

LMN

129
Q

Bulbar muscle weakness (CN XII, IX, X) excludes what neurological causes of ALS like symptoms?

A

Any pathology below the foramen magnum (cervical spondylosis, or compressive myelopathy)

130
Q

What are the pathological changes to the brain with alzheimer’s disease?

A

Neurofibrillary tangles and amyloid

131
Q

What will brain imaging show in a patient with vascular dementia?

A

Old infarction of extensive deep white matter changes 2/2 chronic ischemia

132
Q

True or false: there is no substantial motor involvement with AD

A

True

133
Q

What are the pathological brain findings in a patient with Pick’s disease (frontotemporal dementia)?

A

Pick bodies (round intraneuronal inclusions)

134
Q

What will imaging show in a patient with frontotemporal dementia?

A

Frontotemporal atrophy

135
Q

What is the time course of normal pressure hydrocephalus?

A

Gradual or abrupt in onset

136
Q

What is the time course of Creutzfeldt-Jakob disease?

A

Abrupt in onset

137
Q

What will an EEG show with CJD?

A

Periodic sharp wave complexes

138
Q

What are the pathological findings of lewy body dementia?

A

alpha-synuclein

139
Q

What are the two general treatments for AD?

A 
Cholinesterase inhibitors (donepezil)
NMDA receptor antagonists (memantine)
140
Q

How are the s/sx of vascular dementia different than other forms of dementia?

A

May be associated with motor or sensory deficits

141
Q

When is imaging indicated in the work up of vascular dementia?

A

Only if other etiology is suspected

142
Q

What is the treatment for vascular dementia?

A

Same as stroke prophylaxis

143
Q

What are the classic symptoms of frontotemporal dementia?

A

Disinhibition and significant behavior/personality changes early on

144
Q

What is the treatment for frontotemporal dementia?

A

Symptomatic

145
Q

What is the etiology of normal pressure hydrocephalus?

A

Inability to absorb CSF

146
Q

What are the three classic symptoms of normal pressure hydrocephalus?

A

Wet wacky and wobbly

147
Q

True or false: papilledema is uncommon in the setting of normal pressure hydrocephalus

A

True

148
Q

What is the treatment for normal pressure hydrocephalus?

A

LP of continuous lumbar CSF drainage for several days, followed by VP shunt

149
Q

What are the symptoms of CJD?

A

Dementia with myoclonic jerks

150
Q

What is the general progression of CJD?

A

Acute deterioration

151
Q

What are the CSF findings of CJD?

A

14-3-3 and tau proteins are seen

152
Q

What is the treatment for Lewy body dementia?

A

Symptomatic

153
Q

What is the nucleotide repeat found in HD?

A

CAD on chromosome 4

154
Q

What two areas of the brain are affected with HD?

A

Caudate nucleus and putamen

155
Q

What is the treatment for HD? (movement, psychosis, and depression)

A
  • Reserpine or tetrabenazine for movement
  • Atypical antipsychotics
  • SSRIs
156
Q

What is the deficiency seen in parkinson’s disease?

A

Idiopathic loss of dopamine in the substantia nigra

157
Q

What are the components of the parkinson tetrad?

A

Resting tremor
Rigidity
Bradykinesia
Postural instability

158
Q

What is the frequency of the pill rolling tremor of parkinson’s? What classically decreases the tremor?

A

4-6 Hz

Decreases with voluntary movement

A1 (32 decks)

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