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Clinical Psychology > Demantia > Flashcards

Demantia Flashcards

1
Q

DSM-5 strengths

A
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2
Q

DSM-5 weaknesses

A
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3
Q

Cognitive impairments (diagnosis: 7)

A
  1. Learning/memory: amnesia
  2. Attention/arousal
  3. Language: aphasia (fluent: comprehension (wernickes)), non-fluent (producing (brocas))
  4. Visual-perceptual functioning
  5. Motor skills: apraxia (routines but not on command)
  6. Executive functions
  7. Higher order intellectual functioning
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4
Q

Assessment:

A
  • Difficult and lengthy
  • Cognitive and behavioral tests, EEG, brain scams, blood tests, chemical analyses, behavioral observation etc.
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5
Q

WAIS-IV

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6
Q

Wisconsin card sorting task

A
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7
Q

Halstead-Reitan neuro-psychological test battery

A
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8
Q

Mini mental state examination

A
  • Structured test that takes 10 mins and provides information on client’s overall levels of cognitive and mental functioning
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9
Q

DSM-5 categories: Delirium

A
  • Confused and disorganized behavior
  • Short period (hours, weeks or months) of disturbance
  • Rapid and abrupt development after a specific traumatic event.
  • Results from disruption of the brain metabolism and neurotransmitter activity.
  • Common in elderly
  • 1-2% prevalence, increases with age, 14% for over 85y.
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10
Q

DSM-5 categories: Dementia (NCDs)

A
  • Impairment of basic cognitive functions.
  • May be associated with apraxia and agnosia
  • Prevalence, age of onset etc vary depending on the NCD.
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11
Q

HIV infection

A
  • Human immunodeficiency virus type 1.
  • Enters CNS early
  • Neurological difficulties develop in 60% of those infected.
  • MRIs: progressive cortical atrophy in the grey and white matter in the brain.
  • Weakened immune system, lack of concentration, short-term memory, slowed processing, motor deficits, mdd.
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12
Q

Prion disease

A
  • Fatal disease that attacks the brain and CNS.
  • Incubation period of 10-15 years, once symptoms appear, death within 4 months
  • Changes in mood, temperament and behavior, memory and concentration issues.
  • Deficits in verbal fluency, face recognition, executive functioning etc.
  • 1-2 cases per million people.
  • Prion: abnormal transmissible agent that induces abnormal folding of normal cellular proteins. Occurs at the cortical and subcortical level.
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13
Q

Vascular diseases

A
  • Damage to brain tissue causing a stroke.
  • Infarction: blood flow to the brain is impeded through embolism or thrombosis.
  • embolism: Blood clot in body > to brain > lodging > damage to cells > oxygen starvation
  • Thrombosis: blood clot > artery > blocks blood supply > brain cells starved of oxygen
  • Hemorrhage: Blood vessel ruptures and damage brain tissue. Result from hypertension or high blood pressure.
  • Very common over 65y
  • Symptoms: numbness, paralysis, slurred speech, loss of sight, aphasia, agnosia, apraxia, depression.
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14
Q

Degenerative

A
  • Slow, deterioration in cognitive, physical and emotions.
  • Gradually over years, frequent in elderly, 7% over 65y and 30% over 85y
  • Cortical areas: cognitive abilities
  • Subcortical areas: emotional and motor disturbances.
  • Diagnosis = hard
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15
Q

Alzheimer’s characteristics

A
  • May start at 20-30y
  • Progressive impairments in short-term memory, aphasia, agnosia, personality changes, physically weak, disorientation.
  • Duration: 8-10y
  • Risks: higher in women, 40% heritable if in family history, low educational status
  • Identification: thyroid functioning, blood, neuropsychological tests of cognition, genetics.
  • Neuro-imaging techniques exclude other alternative NCD.
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16
Q

Alzheimer’s etiology

A

Genetics:
- Faulty production of NT acetylcholine.
- High heritability (twins + family)
- APOE4 (19th chromosome) and GAB2.
Brain:
- Beta amyloid plaques: abnormal protein synthesis > clump > kills healthy neurons in limbic system.
- Neurofibrillary tangles: (TAO) abnormal collection of twisted nerve cells > errors in impulses > cell death.
- Gradual shrinkage of brain tissue
- Sulci widens and gyri shrinks
- Ventricles are enlarged

17
Q

Fronto-temporal

A
  • Loss of neurons that leads to behavioral, personality and language impairments and changes.
  • Main impact on emotional processes: apathy.
  • Lack of planning/organization, distractibility, poor judgement, social style, inability to regulate emotions etc.
  • 5% of all dementias, common in under 65y.
  • 50-60% genetic component.
18
Q

Parkinson’s disease and lewy bodies

A
  • Motor skills impaired, and psychological disturbances to 40-60%.
  • Tremor, motor difficulties, rigidity etc.
  • Damage to basal ganglia (substantia nigra): produces dopamine.
  • Symptoms appear age 50.
  • Memory and learning defitics, psychosis and depression.
  • Allostatic state (stress): accelerates process and causes atrophy in nerve cells of the brain.
  • Lewy bodies: abnormal protein deposit disrupting brain functioning and deplete dopamine.
  • 80% have lewy bodies.
  • 0.5% between 65-69y and 3% for over 85y.
  • Brain stem = apraxia, cortex = executive functioning
19
Q

Huntington’s disease

A
  • Inherited, disorder of CNS, dominant gene.
  • Symptoms after 35y.
  • Movement disorder (clumsiness, jerky movements etc)
  • Prevalence varies within cultures.
  • 4th chromosome - hunting-tin mHtt = cell death in basal ganglia (responsible for posture, muscle tone, motor skills).
20
Q

Biological treatment: drugs

A

Alzheimer’s: cholinesterase inhibitors = acetylcholine breakdown. Does not prevent dementia.
Fronto-temporal: no drugs
Parkinson’s: levodopa = counteracts decline in dopamine.
Vascular: thrombolytic therapy = breaks up blood clots.
HIV: antiretroviral reduces severity.

21
Q

Biological treatments: Deep brain stimulation

A
  • Parkinson’s
  • Surgically implanted device called neuro-stimulator. Electrical impulses to the ventral intermediate nucleus of the thalamus or basal ganglia.
  • Not significant effect on cognitive abilities.
22
Q

Cognitive rehabilitation: attention deficits

A
  1. Attention process training
  2. Time pressure management
23
Q

Cognitive rehabilitation: visuospatial deficits

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  1. Computer-assisted training
24
Q

Cognitive rehabilitation: apraxia and coordinated self-help behaviors

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  1. Gestural training (apraxia)
  2. Virtual computer-based training
25
Q

Cognitive rehabilitation: language and communication deficits

A
  1. Constraint-induced movement therapy
  2. Group communication treatment
26
Q

Cognitive rehabilitation: memory deficits

A
  1. Compensatory strategies
  2. Computer based procedures
  3. Teaching remembering strategies
  4. Errorless learning
27
Q

Cognitive rehabilitation: executive functioning deficits

A
  1. Goal management training
  2. CBT role playing
  3. Self-instructional training
28
Q

Cognitive rehabilitation: holistic rehabilitation

A
  • Targets several aspects at a time
29
Q

Caregiver support programmes

A
  • Tools to caregiver
  • Peer support groups

Clinical Psychology (7 decks)

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