Behavior, Cortical Function, and Dementia Flashcards

1
Q

what is memory?

A

the ability to learn and then recall information

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2
Q

what bilateral circuits or pathways does memory function depend on?

A

b/l circuits or pathways involving the TEMPORAL LOBE and THALAMUS.
specifically the hippocampus–> fornix –> mammillary body–> anterior thalamic nucleus

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3
Q

Wernicke-Korsakoff syndrome

a. what is it caused by
b. what is it

A

a. amnesia 2/2 b/l thalamic and mammillary body lesions

b. state of thiamine (B1) deficiency seen in malnourished alcoholics

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4
Q

Anoxia (cardiac arrest survivors) and Herpes simplex encephalitis sequelae

A

b/l hippocampal lesions cause amnesia

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5
Q

apraxia

A

inability to conceptualize and perform a skilled, learned, motor act on command, but may spontaneously carry them out at another time

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6
Q

gait apraxia

A

feet stuck in the mud/glued to the floor; 2/2 prefrontal lobe lesion

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7
Q

constructional apraxia

A

2/2 posterior cortical lesions, especially involving the parietal lobe; cant draw house or copy simple drawing

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8
Q

dressing apraxia

A

cannot put on and button a shirt; 2/2 posterior cortical lesions, especially involving the parietal lobe

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9
Q

agnosia

A

impaired recognition of perceived stimuli caused by lesions of the sensory association cortex

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10
Q

visual agnosia

A

pt cant id a bell by seeing it, but can recognize it by hearing it rung or touching it

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11
Q

tactile agnosia

A

inability to recognize objects solely fe feel or with eyes closed. severe degree of astereogenesis (lesion of parietal lobe or dorsal column-inability to id an object by touch sans sight)

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12
Q

prefrontal or frontal lobe syndrome

A
  • listless, apathetic, unconcerned
  • poor hygiene, incontinence
  • poor judgement, disinhibition (=impolite outbursts, rude humor, inappropriate sexual jokes)
  • exec function impaired=poor planning, cant do multistep tasks, aimless repetition of simple motor acts
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13
Q

may be noted on examination of someone with prefrontal or frontal lobe syndrome

A
  • gegenhalten or paratonia: increased limb tone or resistance
  • frontal lobe release sign: suck, snout and root; palmar and plantar grasp responses (all previously nml findings d/r infancy)
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14
Q

syndromes of temporal lobes may include:

A
  • amnesia (b/l hippocampal lesions)
  • cortical deafness (b/l auditory cortex lesions)
  • KLuver-Bucy syndrome
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15
Q

What type of lesion causes Wernicke’s aphasia?

A

a unilateral lesion of the superior-posterior dominant TEMPORAL lobe

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16
Q

Parietal lobe syndromes

A

-affect sensory cortex=astereognosis, agraphesthesia, and extinction on dbl simultaneous stimulation

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17
Q

what do lesions of the nondominant parietal lobe cause?

A

impairment of spatial relationships between the body and its surroundings.

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18
Q

describe a pt with anosognosia

A

unaware of her hemiparesis, which in extreme form consists of denial of that half of the body=hemispatial neglect

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19
Q

Gerstmann’s syndrome

A
  • 2/2 lesion of supramarginal or angular gyrus of the dominant parietal lobe
  • consists of: agraphia, R-L disorientation, dyscalculia, and finger agnosia
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20
Q

occipital lobe syndromes

A

-may involved b/l visual cortex and cause cortical blindness

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21
Q

Anton’s syndrome

A

denial or unawareness of visual loss

22
Q

b/l temporal occipital lesions may produce…

A

visual agnosia, a subtype of which is prosopagnosia=inability to recognize previously known faces

23
Q

dominant temporo-occipital lobe lesion may cause

A

color anomia

24
Q

define Delirium

A

=acute confusional state

  • fluctuating levels of attn and motor activity
  • moods, emotions may vary, hallucinations common
  • also: tremulousness, asterixis, myoclonus, ataxia, dysarthria
25
Q

causes of delirium

A
  • viral encephalitis (brain directly involved)
  • post-ictal state after a sz (brain directly involved)
  • systemic illness: kidney failure, metabolic abnormalities, meds/illicit rx
26
Q

define dementia

A

-general term for a diffuse impairment of cortical function which usually evolves less abruptly over a longer period of months to years and impedes the daily function of a pt

27
Q

first deficit noticed in dementia

A

memory loss then personality change: suspicious, mistrust, paranoia

28
Q

as dementia progresses what happens to the pt

A
  • pt gets disoriented to time and place
  • fails to recognize family and friends
  • becomes unable to perform basic tasks
29
Q

how is dementia diagnosed

A

depends heavily on family and friends observations

**always screen for depression

30
Q

what should evaluation of dementia include?

A

MMSE-some standardized cognitive testing to be used as a baseline

31
Q

what type of imaging can be useful in dementia pts

A

brain scan, preferably MRI to determine if dementia is d/t chronic SDH, brain tumors or abscesses, multiple infarctions, or hemorrhages, or NPH

32
Q

what should you suspect in a younger pt with dementia

A

HIV

33
Q

what should be checked in all pts with memory or cognitive impairment?

A
  • CBC
  • chemistry profile
  • B12
  • thyroid
34
Q

Alzheimer’s Disease

A
  • m/c type of dementia in the US
  • diagnosis of exclusion
  • most cases are sporadic
35
Q

what is AD

A
  • degenerative dz

- earliest/most prominent deficit: MEMORY LOSS 2/2 pathological changes int he medial temporal lobes and hippocampi

36
Q

pathophys of AD

A
  • xs accumulation of protein BETA-AMYLOID in the form of extracellular amyloid OR senile cortical plaques.
  • BETA AMYLOID is a part of larger transmembrane BETA-APP (beta amyloid precursor protein) on chrom 21
  • BETA AMYLOID deposition=formation of intraneuronal neurofibrillary tangles
    • tangles consist of microtubule-associated TAU PROTEIN
37
Q

PET scans and AD

A

-PET scans utilizing Pittsburg Compound B (PIB), which selectively binds to beta amyloid, apparently show the typical AD uptake (in the prefrontal, temporal, and sensory association cortex)

38
Q

Slow down deteriorating course of AD by?

A
  • enhancing the cholinergic system with central acetylcholinesterase inhibiiors (AChE-I): DoNEpezil, Rivastigmine, or Galantamine
  • as dementia worsens, MEMANTINE can be added or used in place of AChE-I
  • MEMANTINE is an NMDA antagonist which opposed the excitotoxic effects of glutamate in the CNS
39
Q

Differential diagnosis of dementia subtypes

A
  • Alzheimer
  • vascular dementia
  • frontotemporal dementia
  • dementia with lewy bodies
  • NPH
  • Prion disease
40
Q

Alzheimer disease

A
  • early insidious short-term memory loss
  • language deficits and spatial disorientation
  • later personality changes
41
Q

Vascular dementia

A
  • stepwise decline
  • early executive dysfunction
  • cerebral infarction and or deep white matter changes on neuroimaging
42
Q

frontotemporal dementia

A
  • early personality changes
  • apathy, disinhibition and compulsive behavior
  • frontotemporal atrophy on neuroimaging
43
Q

dementia with Lewy bodies

A
  • visual hallucinations
  • spontaneous parkinsonism
  • fluctuating cognition
44
Q

NPH

A
  • ataxia early in dz
  • urinary incontinence
  • dilated ventricles on neuroimaging
45
Q

prion dz

A
  • behavioral changes
  • rapid progression
  • myoclonus and or seizures
46
Q

cholinesterase inhibitors (Rivastigmine, Galantamine, Donepezil)

A

may provide moderate symptomatic relief of cognitive symptoms and temporarily improve functioning in Alzheimers (but do not alter dz course)

47
Q

early findings in Alzheimers

A
  • anterograde memory loss (immediate recall affected, distant memories preserved)
  • visuospatial deficits (lost in own neighborhood)
  • language difficulties (difficulty finding words)
  • cognitive impairment with progressive decline
48
Q

late findings in Alzheimers

A
  • neuropsych (hallucinations, wandering)
  • dyspraxia (difficulty performing learned motor tasks)
  • lack of insight regarding deficits
  • noncognitive neurologic deficits (pyramidal and extrapyramidal motor, myoclonus, seizures)
  • urinary incontinence
49
Q

trihexyphenidyl

A

anticholinergic med sometimes used in tx of PD, generally in younger pts where tremor is the primary symptom

50
Q

pronator drift

A
  • sn and sp for UMN or pyramidal tract disease affecting the upper extremities
  • in pts with pyramidal lesions, the affected arm drifts downward and palm pronates toward the floor