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BioPsych PSYC20006 Theme 2 > Memory 4 > Flashcards

Memory 4 Flashcards

1
Q

What are some properties of AD?

A
  • Most common dementing illness
    • 50% of all primary dementing illnesses are AD
  • Age biggest risk factor
    • 65-70: 2%
    • 80: 20%
      • Problems of ageing population
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2
Q

Diagnosis of Alzheimer’s Disease?

A
  • Definite AD: Pathology
  • Can only diagnose Dementia of the Alzheimer Type (DAT)
    • DAT: Typical pattern of symptoms of Alzheimers
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3
Q

When does AD rise? What are some genetic markers of early onset?

A

Onset

  • Majority arise Sporadically
  • Age major risk factor

Early onset (Genetic)

  • Autosomal dominant:
    • Amyloid precursor protein (APP)
    • Presinilin 1 (PSEN1)
    • Presenilin 2 (PSEN2)
      • Alters production of amyloid β (Aβ) peptide
        • Principal component of senile plaques
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4
Q

Other than genetic marks, what are some groups of people who are more vulnerable? What are the factors?

A
  • Down syndrome
    • Occurs earlier 40s
  • No precipitating/cause factors known
    • Head injury has some evidence
  • Can have sudden decompensation
    • Other event (like a stroke) triggers AD
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5
Q

Clinical Features of DAT: Onset and Course?

A

Onset

  • Insidious (1-2 years prior to diagnosis)

Course

  • Slow deterioration over years (M = 8.5 years to death)
  • Occasional plateaus in deterioration
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6
Q

Clinical Features of DAT: Phases?

A

Phase 1

  • 2-3 years

Phase 2

  • Rapid deterioration

Phase 3

  • Terminal Stage
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7
Q

Clinical Features of DAT: Phase 1?

A
  • Failing memory
    • Amnestic presentation
    • Most Common
      • MTL
  • Muddled inefficiency in daily activites
  • Spatial disorientation
    • Don’t know how to get home
  • Mood disturbance
    • Agitated or apathetic
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8
Q

Clinical Features of DAT: Phase 2?

A
  • Intellect and personality deteriorate
  • Focal symptoms
    • Dysphasia, dyspraxia, agnosia and acalculia, wernicke
      • Temporal
  • Disturbance of posture and gait, increased muscle tone
  • Delusions/hallucinations can occur
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9
Q

Clinical Features of DAT: Phase 3?

A
  • Profound apathy
  • Bed ridden
  • Eventually lose neurological function
  • Bodily wasting occurs
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10
Q

What is Probable AD?

A
  • Deficits in 2 or more areas of cognition
    • Amnestic presentation
      • Most common
    • Nonamnestic presentations
      • Language, Visuospatial, Executive dysfunction
  • Progressive worsening of memory/cognitive functions
  • No disturbance of consciousness
  • Onset between 40 and 90
  • Absence of other causes
  • Biomarkers
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11
Q

What is Possible AD?

A
  • Made on the basis of dementia syndrome, however…
    • Variation in onset, presentation, or clinical course
    • Presence of another disorder, not considered causing dementia
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12
Q

What is Definite AD?

A

Histopathological evidence of AD obtainedfrom biopsy or autopsy

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13
Q

What is the pathology of AD?

A
  • Intensity of these features correlate closely with dementia severity
  • Grossly atrophied brain - whole brain shrunken
    • Frontal and temporal lobes > parieto-occipital regions
      • Note: This a different pattern
  • Extensive degeneration of neurons
    • Gilal cell proliferation
  • Extensive senile plaques and neurofibrillary tangles
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14
Q

What is the Course of neuropathological changes? What is the key criteria for getting a dementia diagnosis?

A
  1. Commence in MTL
  2. Spread to Temporal
  3. Spread to Parietal
  4. Spread to Frontal

(MTL > Temporal > Parietal > Frontal)

Note: Must see functional impact for dementia diagnosis

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15
Q

Clinical pattern of cognitive impairment in DAT: Amnesia?

Intially what happens, when MTL impairs?

A
  • Anterograde memory:
    • Impaired new learning
    • Impaired delayed recall
    • Impaired recognition memory
  • Retrograde memory
    • Intact for remote memories
    • Reduced for recent retrograde memories
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16
Q

Clinical pattern of cognitive impairment in DAT – Amnesia?

What happens when spread posteriorly to posterior temporal cortex and parietal cortex?

A

Temporal

  • Wernicke-type aphasia (Word salad. Gramatical/Fluent but content-less)

Parietal

  • Visuospatial deficits and topographical disorientation
    • Dyspraxia, agnosia and acalculia
17
Q

Clinical pattern of cognitive impairment in DAT – Amnesia. What happens when spread to frontal lobe?

A
  • Executive Dysfunction
  • Apathy (most common)
  • Agitation
18
Q

How do we treat AD? What cannot be done in AD?

A
  • Work by trying to re-balance the action of acetylcholine
    • This only helps in maintain AD
      • Improve quality of life, not length of life
  • No treatment to stop disease
  • No clear evidence that anything prevents AD (Diet, Exercise, etc)
19
Q

AD vs Normal Ageing?

A
  • Pathological changes are considerably greater in AD
  • Cognitive function in DAT is significantly impaired relative to same-aged peers
20
Q

Case study of AD: MK. What does she have initially (Not the assessment)?

A
  • Increasingly forgetful in last 2-3 years
  • Diabetes and hypertension,
  • Depression (anti-depressent had no effect)
  • Low average premorbid intellect

Could be: DAT, Depression, or just worried

21
Q

Case study of AD: MK. Initial Assessment?

A

Mild Cognitive Impairment. No Progression

Frontal: ok

  • Intact frontal lobe function (spread to frontal)
    • Attention and speed of information processing

Parietal: ok

  • Intact visuospatial skills (No spread to parietal)
  • No language deficits (No spread to temporal)

Memory: no

  • Memory impairment
    • Impaired relational learning (Amnesia type)
    • Impaired recall and recognition (No encoding)
22
Q

Case study of AD: MK. Assessment 2?

A

DAT. Shows progression and functional impact.

Frontal: ok

  • Intact frontal lobe function (spread to frontal)
    • Attention and intellect

Parietal: no (Change from intial assessment)

  • Subtle visuospatial deficit (spread to parietal)
  • Deficit in language (spread to temporal)
    • Wenicke-type aphasia

Memory: no

  • Memory impairment (Unchanged from initial assessment)
    • Impaired relational learning (Amnesia type)
    • Impaired recall and recognition (No encoding)

BioPsych PSYC20006 Theme 2 (4 decks)

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