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neuro12 Flashcards

1
Q

classic pathology for alzheimer’s disease

A

neurofibrillary tangles (NFTs) and senile plaques in the cerebral neocortex and hippocampus; loss of neurons in the cerebral cortex and gliosis

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2
Q

factors assoc with increased risk of alzheimers

A

female, age, history of head trauma, and Down syndrome

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3
Q

gene assoc with alzheimers

A

ApoE4 on chrom 19 assoc with both early and late onset AD

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4
Q

pathogenesis of alzheimers

A

amyloid beta precursor protein mutations cause increased amyloid beta production with subsequent aggregation in neurons;

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5
Q

sundowning

A

seen in alzheimers; worsening psych manifestations during the evening and night; patient usually dies within 5-10 years

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6
Q

possible early diagnostic markers of alzheimers

A

elevated tau protein and low A-beta-42 in the CSF

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7
Q

MRI in alzheimers

A

may show up to 40% reduction in size of hippocampus, amygdala, and thalamus

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8
Q

what are NFTs

A

intracellular accum of phosphorylated tau protein

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9
Q

what are senile plaques

A

extracellular deposits of amyloid surrounded by dystrophic axons

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10
Q

treatment for alzheimers

A

acetylcholinesterase inhib like donepezil or rivastigmine, as well as memantine ,an NMDA receptor antag

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11
Q

prophylaxis for alzheimers?

A

use of vitamin E, NSAIDs, and estrogens has been proposed; no good data

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12
Q

average length of time from symptom onset to diagnosis for alzheimers

A

2 to 3 years

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13
Q

diagnosis of vascular dementia

A

presence of dementia and two or more of the following: focal neuro signs; onset that is abrupt, stepwise or stroke-related; or brain imaging showing multiple strokes, lacunes, or extensive deep white matter changes

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14
Q

vascular dementia is assoc with what

A

Binswanger disease (microvascular disease), a lacunar state, and large strokes

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15
Q

dementia with lewy bodies clinical picture

A

looks like parkisonism but with visual hallucinations;

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16
Q

dementia with lewy bodies has a marked worsening with what drug

A

haloperidol and other neuroleptics

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17
Q

patholgic hallmark of dementia with Lewy bodies

A

Lewy body (eosinophilic intracellular inclusion of alpha synuclein), but can also have NFTs and amyloid plaques like in AD

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18
Q

difference between Lewy body dementia and PD

A

both have Lewy bodies; in PD, they are in the substantia nigra; in Lewy body dementia they are in the cortical neurons

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19
Q

management of lewy body dementia

A

low dose of atypical neuroleptics like risperidone and quetiapine

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20
Q

three key distinguishing features of dementia with Lewy bodies

A

fluctuations of alerteness, visual hallucinations, and an extraordinary sensitiviey to neuroleptics

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21
Q

life span in dementia with Lewy bodies

A

usually in 10 to 15 years

22
Q

Steele-Richardson-Olszewski syndrome AKA

A

progressiv supranuclear palsy

23
Q

main features of progressive supranuc palsy

A

supranuc ocular palsys (failure of vertical gaze), dysarthria, dysphagia, extrapyramidal rigidity, gait ataxia, and dementia; falls and gait abnormalities;

24
Q

other feautres of progressive supranuclear palsy

A

dementia may occur early or develop later; frontal lobe abnormalities predominate. Patients may become apathetic

25
Q

diagnostic eval of progressive supranuc palsy

A

atrophy of the dorsal midbrain, globus pallidus, and subthal nuc

26
Q

characteristic path of progressive supranuc palsy

A

NFTs, neuronal loss, and gliosis in many subcortical structures

27
Q

Huntington disease- lesions where

A

basal ganglia

28
Q

symptoms of HD appear when

A

between ages of 35 and 45

29
Q

triad of huntington’s

A

chorea, behavioral changes or personality disorder (frequently OCD), and dementia

30
Q

diagnosis of HD

A

atrophy of the caudate on brain imaging and demonstration of more than 40 CAG repeats in the HD gene on chrom 4

31
Q

pathology of HD

A

severe destruction of the caudate and putamen (striatal GABA-ergic neurons) and loss of neurons in the cerebral cortex (layer 3)

32
Q

pathology of HD- next

A

; the HD gene leads to aberrant processing of cell rpoteins with formation of deposits in the nucleus and activation of intracellular mechanisms of death

33
Q

treatment for HD

A

pharmacologic management of dementia and chorea with dopaminergic antags, including neuroleptic drugs

34
Q

life expectancy in HD

A

10 to 20 years after onset

35
Q

can parkinsons disease have dementia

A

yes, can cause subcortical dementia; about 30% of patients with PD have dementia

36
Q

frontotemporal lobar dementia

A

significant alterations in personaluty, social behavior, and language

37
Q

how does FTLD present initially

A

cognitive and behavioral deficits other than memory loss

38
Q

types of FTLD

A

frontotemporal dementia; nonfluent aphasia, and semantic dementia

39
Q

molecular pathology of FTLD

A

abnormalities in tau protien or in a protein called TDP-43

40
Q

prion-related diseases that cause dementia

A

Creutzfeld-akob disease; Gerstmann-Straussler-Scheinker syndrome; and fatal familial insomnia

41
Q

pathology of prion diseases

A

spongy degeneration, neuronal loss, gliosis, and astrocytic proliferation resulting from accum in the brain of a mutated protease-resistant prion protein

42
Q

most common prion disease

A

Creutzfeld-jakob disease

43
Q

pyramidal sign vs extrapyramidal sign

A

pyramidal is voluntary motor; extrapyramidal is invol motor like basal gang and cerebellum; damage to extrapyramidal system results in dyskinesias

44
Q

characteristics of dementia of CJD

A

rapidly progressive dementia with pyramidal signs, myoclonus, cerebellar or extrapyramidal signs, and periodic sharp waves on EEG; focal neuro signs

45
Q

MRI in CJD

A

evolving cortical and basal gang abnormalities during the course of the disease

46
Q

CSF in CJD

A

typically normal, but the presence f protein 14-3-3 is relatively sens and specific for CJD

47
Q

prognosis for CJD

A

no treatment; most die within a year

48
Q

HIV-associated dementia complex

A

patients report memory problems, difficulty with concentration, and poor attention; MRI shows cortical and subcortical atrophy

49
Q

metabolic causes of dementia

A

Wilson disease, hypothyroidism, vit B12 def, hypercalcemia, Addison disease

50
Q

characteristics of B12 def

A

dementia, SC, and peripheral nervous system disfunction; neuropathy and memory loss; anemia and sore tongue

51
Q

treatments for alzheimers

A

cholinesterase inhib (donepezil or rivastigmine or galantamine) or NMDA receptor antag (memantine)

52
Q

REM sleep behavior disorder

A

clonazepam is treatment; often seen in dementia with lewy bodies

Neuro (43 decks)

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