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Clinical Neuroscience 2 > Clinical- 5 > Flashcards

Clinical- 5 Flashcards

1
Q

What is dementia?

A

acquire, generalized + usually progressive impairment of cognitive fxn

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2
Q

What is preserved in dementia, which goes away in coma or confusional states?

A

level of consciousness

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3
Q

What are the cognitive changes with age?

A

slower info processing, impaired learning, reduced word finding/fluency, increased reaction time

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4
Q

What are the neuro-opthalmologic changes with aging?

A

slow pupil, impaired upgaze, impaired convergence

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5
Q

What are the motor changes with aging?

A

atrophy of hand/foot muscles, increased msucle tone, flexion posture, small or board gait

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6
Q

What ar ethe sensory changes with aging?

A

reduced visual,auditory, gustatory, olfactory and vibration acuity

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7
Q

what are the reflex changes with aging?

A

primitive reflexes, absent abdominal and ankle reflexes

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8
Q

What are the 5 reversible causes of dementia?

A

normal pressure hydrocephalus, intracranial mass lesions, B12 deficiency, hypothyroidism, neurosyphilis

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9
Q

What are the 4 dementias with extrapyramidal symptoms?

A

THINGS WITH MOVEMENT PROBLEMS.

dementiawith Lewy bodies, corticobasal ganglionic degeneration, Huntingtions, progressive suprenuclear palsy

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10
Q

What are the 4 diseases withOUT extrapyrimidal symptoms?

A

Alz, Picks, Creutzfeldt-Jacob,normal pressure hydrocephalus

ALL THING WITHOUT MOVEMENT PROBLEMS

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11
Q

Alz- epidemiology

A

60-70% cause of dementia
15% of people >65
45% 85 and older
men = women

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12
Q

Alz- mutation

A

in APP, PS1 or PS2

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13
Q

Which trisomy has an icnreased risk of Alz?

A

Trisomy 21

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14
Q

Why do Downs have an increased risk of Alz?

A

the APP gene is on chromosome 21 –> more APP –> Alz!

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15
Q

Which apolipoprotein has an increased risk of Alz?

A

Apo E4

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16
Q

Which apolipoprotein is PROTECTIVE against Alz??(big board quesiton)

A

ApoE2

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17
Q

How do neuritic plaques form?

A

APP is cleaved by a-secretase or b-secretase incorrectly –> AB42 aggregates (normal is Ab40)

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18
Q

What is the fxn of tau?

A

stabilization of microtubules

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19
Q

What happens to tau in Alz?

A

it becomes hyperphosphorylated

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20
Q

What happens when tau gets phosphoprylated?

A

it dissociates from th microtubules –> aggregates form tangles

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21
Q

What happens if there is synaptic dysfxn?

A

memory loss

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22
Q

Why is the focal cerebral atrophy in Alz?

A

you lose glutamatergic and cholinergic neurons

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23
Q

What are the neurological manifestations of Alz?

A

progressive cognitive impairment, aphasia, anomia and acalculia, depression, apraxia

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24
Q

What are the motor manifestations of Alz?

A

gait disorders- short, slow,shuffling steps with flexedposture

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25
Q

Alz- Tx

A

no Tx to reverse existing deficits

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26
Q

What is the NMDA glutamate R antagonist to Tx Alz?

A

Mamantine

27
Q

What are the AchEi’s to Tx Alz?

A

Donepazil, tacrine, rivastigmine, galantamine

28
Q

Alz- imagining Dx

A

CT/MRI for cortical atrophy w/enlarged ventricles
PET for hypometabolsim/perfusion in temporal and parietal lobes. can use it wth Pittsburgh compound B which binds to amyloid plaques

29
Q

Alz- CSF Dx

A

increased CSF levels of AB42, tau, and P-tau

30
Q

Frontotemporal dementia (FD)- etiology

A

genetically inheirted but most are sporatic with unknown cause

31
Q

FTD- clinical findings

A

behavior cahnges, altered interpersonal interactions and conduct, semantic dementia (receptive aphasia), progressive nonfluent aphasia (expressive aphasia, brocas)

32
Q

FTD- Dx

A

MRI for frontal lobe atrophy, PET for hypometabolsim in regions, off Sx.

33
Q

Creutzeldt-Jacob Disease (CJD)- etiology

A

eating contaminated beef with prions. 85% are sporadic.

34
Q

CJD- Sx

A

cognitive abnormalities, memory loss, myoclonus, extrapyramidal signs, cerebellar signs

35
Q

CJD- Dx

A

EEG’s show sharp waves/spikes, elevated CSF protein, IMMUNODETECTION OF PRPsc in brain tissue or PRPc in lymphocytes

36
Q

Normal pressure hydrocephalus (NPH)- triad

A

dementia, gait apraxia + incontinence (wacky, wobble, wet)

37
Q

NPH- clinical findings

A

magnetic gait, dementia, incontinence

38
Q

NPH- Dx

A

CT/MRI show enlarged ventricles, normal opening pressure on LP, 30-50mL CSF removal IMPROVES Sx

39
Q

How long is the onset of dementia prior to the 1st motor Sx?

A

1 year

40
Q

What are the clinical findings to dementia with lewy bodies?

A

visaul hallucinations, parkinsonism, cognitive decline

41
Q

What are the lewy bodies?

A

round eosinophilic intracytoplasmic neuronal inclusions that contain a-synclein

42
Q

Vascular dementia- Hx

A

HTN, abrupt onset

43
Q

Vascular dementia- clinical findings

A

pseudobulbar palsy with dysarthria, dysphagia and pathological emotionality (woman period Sx)

44
Q

Vascular dementia- Dx

A

multiple large infarcts of MRI, low density in subcortical white matter

45
Q

What is the most common disorder mistaken for dementia?

A

depression

46
Q

What are the characteristics of both depression and dementia, which can be confusing to noob Dr.’s (MDs)?

A

mental slowness, apathy, self-neglect, withdrawal, irritability, difficulty with memory and concentration and changes in behavior + personality

47
Q

Now let’s play a quickfire game. I’ll say a characteristic and you tell me if it’s either depression or dementia. Ready?

Abrupt onset

A

depression

48
Q

Progressive deterioration

A

dementia

49
Q

Plateau of dysfxn

A

depression

50
Q

No Hx of depression

A

dementia

51
Q

Pt unaware of extent of deficits + doesnt complain of memory loss

A

dementia

52
Q

Somatic complaints or hypochondriases common

A

depression

53
Q

Variable affect

A

dementia

54
Q

Somatic complaints uncommon

A

dementia

55
Q

Insidious onset

A

dementia

56
Q

Prominent vegetative Sx

A

depression

57
Q

Impairment worse at night

A

dementia

58
Q

Neuro exam + labs abnormal

A

dementia

59
Q

Few vefetative Sx

A

dementia

60
Q

Impairment not worse at night

A

depression

61
Q

Neuro exam + labs normal

A

depression

62
Q

What are the etiologies to cause acute amnesia?

A

head trauma, ischemia, PCA occlusion, transiet global ischemia, alcoholic blackouts, wernickes encephalopathy, dissociatifve amensia

63
Q

What are the etiologies to cause chronic amnesia?

A

alcohol korsakoff syndrome, postencephalitic (HSV is big), tumor, paraneoplastic limbic encephalitis

Clinical Neuroscience 2 (16 decks)

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