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Boards and Wards Complete > Neurology (p373-388) > Flashcards

Neurology (p373-388) Flashcards

1
Q

A sudden, nonconvulsive focal neurologic deficit

A

Stroke

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2
Q

What is the most common source of emboli for a stroke?

A

carotid artheroma

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3
Q

Small infarct in the deep white matter, strongly associated with HTN and atherosclerosis

A

lacunar infarct

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4
Q

Pt is receptive and speaks fluently but words do not make sense. Dx? lesion?

A

Wenickie’s is “wordy”- temporal lobe lesion

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5
Q

Carotid emboli affects opthalmic artery. Dx?

A

Amaurosis fugax

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6
Q

Vertebrobasilar artery stroke affects brainstem. Dx?

A

Drop attach, vertigo, CN palsy and coma

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7
Q

Middle cerebral artery stroke affects dominant/frontal/temporal lobe. Dx?

A

aphasia

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8
Q

Middle cerebral artery stroke affects nondominant frontal or temporal. Dx?

A

Sensory neglect and apraxia

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9
Q

Middle or anterior cerebral artery affects parietal lobe on opposite side. Dx?

A

Hemiplegia

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10
Q

Middle or anterior cerebral artery stroke affects frontal lobe. Dx?

A

urinary incontinence and grasp reflex

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11
Q

Middle or posterior cerebral artery affects temporal or occipital lobe

A

homonymous hemianopsia

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12
Q

Expressive frontal lobe lesion where pt is unable to verbalize. Dx?

A

Broca’s aphasia

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13
Q

How many days post-infarct does edema in brain occur?

A

2-4 days

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14
Q

What is decorticate posturing indicate? What’s it look like?

A

cortical lesion, flexion of the arms

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15
Q

What is decerebrate posturing indicate? what’s it look like?

A

Midbrain or lower lesion, arm extension

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16
Q

What is the best Dx method for stroke? Gold standard?

A

Dx - CT but if negative, still need MRI head to rule out

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17
Q

How quickly after onset can tPA be initiated?

A

after 3-6 hours of onset, only for occlusive disease, not hemorrhagic

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18
Q

What is an absolute contraindication to tPA use?

A

intracranial bleed

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19
Q

What fraction of patients achieve full recovery of lifestyle after a stroke?

A

less than 1/3

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20
Q

What are the top 3 organisms that cause meningitis in adults

A

S. pneumo (50%)
N. meningitidis (25%)
H. influenzae (rare bc vaccine)

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21
Q

What populations is listeria seen?

A

Neonates, pregnant women, elderly and immunocompromised pts

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22
Q

What are the top 2 organisms that cause neonatal meningitis?

A

Group B strep (s. agalactiae)

E. Coli

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23
Q

Sign when pt cannot touch chin to chest

A

Meningismus

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24
Q

What is kernig’s sign?

A

pt is supine with hip and knees flexed at 90 degrees, examiner cannot extend knee

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25
Q

What is Brudzinski’s sign?

A

Pt is supine, when examiner flexes neck, pt involuntarily flexes hips and knees

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26
Q

What could be the causes of subacute/chronic meningitis?

A

fungal, mycobacterial, syphillis, non infectious disease like lymphoma/leukemia spreading to CSF or rarely carcinomatosis, SLE vasculitis, sarcoid

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27
Q

What are some causes of fungal meningits?

A

Cryptococcus and Coccidioides

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28
Q

What is the CSF findings in bacterial meningitis?
___ Cells?
___ Protein
___ Glucose

A

___ Cells? increased neutrophils
___ Protein elevated
___ Glucose low

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29
Q

What is the CSF findings in viral meningitis?
___ Cells?
___ Protein
___ Glucose

A

___ Cells? lymphocytes
___ Protein elevated/nml
___ Glucose normal

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30
Q

What is the CSF findings in fungal meningitis?
___ Cells?
___ Protein
___ Glucose

A

___ Cells? lymphocytes
___ Protein VERY elevated
___ Glucose low

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31
Q

What is the emperic therapy for community acquired meningitis by age?
Neonates?
Children-65 yrs?
>65 yrs?

A

Neonates 65 = ceftriaxone +vancomycin + penicillin

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32
Q

What fungal organism is seen in AIDS pts and causes meningitis?

A

Cryptococcus

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33
Q

What is the treatment for cryptococcal meningitis?

A

IV amphotericin +/- flourocytosine followed by fluconazole

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34
Q

What kind of stain will show Cryptococcus in the CSF?

A

India ink

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35
Q

What kind of fungal meningitis is seen in Arizona/ California?

A

Coccidioides

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36
Q

What is the treatment for TB meningitis when seen in the elderly?

A

RIPE

Rifampin, Isoniazid, Pyrazinamide and Ethambutol

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37
Q

What is the treatment for brain abscesses?

A

surgical drainage and antibiotics

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38
Q

What is the disease with unknown etiology, but causes relapsing limb weakness, increased deep tendon reflexes, nystagmus, tremor, sccanning speech, paresthesias, optic neuritis and +Babinski sign?

A

Multiple sclerosis

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39
Q

Where is MS common

A

Northern latitiudes

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40
Q

What is seen on lumbar puncture in patients with MS?

A

increased CSF immunoglobulines manifested as multiple oligoclonal bands on electrophoresis

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41
Q

What is the treatment for MS?

A

interferon B or glatiramer acetate –> may induce prolonged remission in some patients

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42
Q

Disease that’s an acute autoimmune demyelinating dz involving peripheral nerves. Ascending weakness/paralysis, bilateral facial nerve palsy, may be preceded by gastroenteritis

A

Guillain-Barre Syndrome

43
Q

What are some causes to Guillain Barre syndrome?

A

Campylobacter
Mycoplasma
viral infection
immunization

44
Q

What is seen on CSF to Dx guillain barre?

A

albumin-cytologic dissociation (CSF protein very high, without increase in cells seen)

45
Q

What is the treatment for Guillain barre?

A

Plasmapharesis, IVIG, intubation for respiratory failure

46
Q

What kind of demyelination occurs in central pontine myelinolysis?

A

diamond shaped region of demyelination in the basis pontis

47
Q

Pt with bilateral pallidal necrosis, headache, nausea, cherry red color of lips

A

Carbon monoxide poisoning

48
Q

Lesion related to mammilary bodies

A

Thiamine deficiency which causes Wernickie’s encephalopathy

49
Q

Where is the degeneration neurologically for B12 deficiency?

A

posterior columns and lateral corticospinal tract

50
Q

What labs do you do for B12 deficiency that are more sensitive than than B12?

A

Methylmalonic acid and homocysteine levels

51
Q

What is another name of Hepatolenticular degeneration?

A

Wilson’s disease

52
Q

Where is the brain lesion in Wilson’s disease?

A

basal ganglia

53
Q

How do you diagnose Wilson’s disease?

A

decreased serum ceruloplasmin

54
Q

What is the treatment for Wilson’s disease?

A

penicillamine or liver transplant if drug fails

55
Q

Why does hepatic encephalopathy occur?

A

brain toxicity secondary to excess ammonia and other toxins not degraded by malfunctioning liver

56
Q

What are some findings seen in hepatic encephalopathy?

A

hyperreflexia, asterixis, dementia, obtundation/coma

57
Q

What is the treatment for hepatic encephalopathy?

A

lactulose, neomycin and protein restriction to decrease the ammonia related toxins

58
Q

What is the protein defect in Tay Sachs disease? What does it lead to a build up of?

A

Hexosaminidase A defect leads to build up of ganglioside GM2

59
Q

What is seen on the macula of a Tay Sach’s pt?

A

Cherry red spot

60
Q

How do you diagnose Tay Sachs?

A

biopsy of rectum or enzymatic assay, no Tx

61
Q

What is a complex seizure?

A

Loss of consciousness

62
Q

What is a simple seizure?

A

No loss of consciousness

63
Q

What is a generalized seizure?

A

Entire brain involved

64
Q

What is a partial seizure?

A

Focal area of brain involved

65
Q

What is a tonic sz?

A

prolonged contraction

66
Q

What is a clonic sz?

A

twiches

67
Q

What kind of sz is an absence sz?

A

complex generalized sz = brief LOC

68
Q

What kind of sz is a grand mal sz?

A

Complex generalized tonic-clonic sz

69
Q

What is one blood test you must always do in a pt who has a hx of seizure?

A

check blood level of medication

70
Q

What is a side effect of phenytoin?

A

gingival hyperplasia and hirsuitism

71
Q

What is a side effect of carbamazepine?

A

leukopenia/aplastic anemia and hepatotoxicity

72
Q

What is a side effect of Valproate?

A

Neutropenia, thrombocytopenia and hepatotoxicity

73
Q

At what point can you stop sz treatment?

A

If no seizure for 2 years and normal EEG

74
Q

Pt with breif period of unresponsiveness

A

Absence Seizure
1st line: ethosuximide/valproic acid
2nd line: lamotrigine

75
Q

Pt with dramatic convuslsions, LOC, incontinence and post-ictal confusion.Dx? Tx 1st line?

A

Tonic Clonic seizure (grand mal)

1st line: Valproic acid, carbamazepine, phenytoin

76
Q

Pt with sensory seizure or limited focal motor seizure. Dx? Tx?

A

Simple partial sz

Tx: Carbamazepine, phenytoin

77
Q

Pt with sz that starts as simple partial but then generalizes. Dx? Tx?

A

Complex partial sz

Tx: carbamazepine, phenytoin

78
Q

Pt with unremitting seizure –> respiratory compromise and rhabdomyolysis. Dx? Tx?

A

Status epilepticus

Tx: lorazepam/diazepam

79
Q

Continuous seizing lasting >5 minutes

A

status epilepticus

80
Q

How do you treat status epilepticus?

A

Maintain and protect airway, IV benzodiazepines for immediate control, followed by phenytoin loading and phenobarbital for refractory cases

81
Q

What age group does Alzheimer’s dementia primarily affect? In Down’s syndrome pts?

A

> 70 yrs

In Down’s 30-40 years

82
Q

Review Dementia vs Delirium table

A

p.386

83
Q

What is the efficacy of cholinesterase inhibitors on dementia?

A

slow early dementia, but no efficacy in late disease

84
Q

How is diagnosis of Alzheimer’s done? Difinitively?

A

Clinical dx, definitive is only possible at autopsy

85
Q

What is the only drug out there to treat moderate to severe Alzheimer’s

A

Memantine - protects brain cells from damage caused by the chemical messenger glutamate, but efficacy is uncertain.

86
Q

Pt presents with acute, stepwise decrease in neurologic function, multiple focal deficits on exam, HTN, old infarcts by CT or MRI. Dx?

A

Multiinfarct Dementia - make Dx by clinical and radiographic

87
Q

Pt presents clinically similar to alzheimer’s, more in women, onset at younder age . Predominates frontal (more personality changes seen) and temporal lobe

A

Pick’s Dz

88
Q

Pt presents with tremor, cog-wheel rigidity, bradykinesia, classic shuffling gait, mask-line facies +/- dementia

A

Parkinsonism

89
Q

What kind of neurons degenerate in Parkinsonianism?

A

Dopaminergic neurons in the substantia nigra

90
Q

What drug is the best for bradykinesia?

A

Levedopa-carbidopa (Sinemet)

91
Q

What is the best drug for tremor?

A

Anticholinergic like Benztropine

92
Q

What drug increases dopamine release and is good for mild Parkinson dz?

A

Amantadine

93
Q

What surgical options are available for Parkinsons?

A

Implanted deep brain stimulation, surgical pallidotomy for refractory cases

94
Q

Pt presents with progressive choreioform movements of all limbs, ataxic gait and grimacing. Dx?

A

Huntington’s chorea

95
Q

What is the gene defect in Huntington’s?

A

Autosomal CAG triplet expansion

96
Q

What part of the brain is atrophied in HD?

A

atrophy of striatum (especially caudate nucleus)

97
Q

How is dx of HD made?

A

MRI - looking for atrophy of the caudate

98
Q

Pt presents with upper and lower motor neuron disease causing weakness, fasciculations, progressing to denervation atrophy, hyperreflexia, spasticity and difficulty speaking/swallowing. Dx?

A

Amyotrophic Lateral Sclerosis (Lou Gehrig’s Dz, motor neuron dz)

99
Q

What are the 3 types of cerebral palsy

A

Spastic cerebral palsy
Athetoid or dyskinetic cerebral palsy
Ataxic cerebral palsy

100
Q

What is the most common form of CP?

A

individual’s’ muscles are stiff, making movement difficult

101
Q

What kind of CP can affect the entire body?

A

Athetoid/dyskinetic CP

102
Q

How do you treat CP?

A

Botox or baclofen to decrease spasticity

103
Q

What is the cause of CP?

A

70% of cases are events occurring before birth that impair normal brain development. In many cases, cause is unknown.

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