Demantia Flashcards
DSM-5 strengths
DSM-5 weaknesses
Cognitive impairments (diagnosis: 7)
- Learning/memory: amnesia
- Attention/arousal
- Language: aphasia (fluent: comprehension (wernickes)), non-fluent (producing (brocas))
- Visual-perceptual functioning
- Motor skills: apraxia (routines but not on command)
- Executive functions
- Higher order intellectual functioning
Assessment:
- Difficult and lengthy
- Cognitive and behavioral tests, EEG, brain scams, blood tests, chemical analyses, behavioral observation etc.
WAIS-IV
Wisconsin card sorting task
Halstead-Reitan neuro-psychological test battery
Mini mental state examination
- Structured test that takes 10 mins and provides information on client’s overall levels of cognitive and mental functioning
DSM-5 categories: Delirium
- 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.
DSM-5 categories: Dementia (NCDs)
- Impairment of basic cognitive functions.
- May be associated with apraxia and agnosia
- Prevalence, age of onset etc vary depending on the NCD.
HIV infection
- 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.
Prion disease
- 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.
Vascular diseases
- 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.
Degenerative
- 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
Alzheimer’s characteristics
- 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.
Alzheimer’s etiology
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
Fronto-temporal
- 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.
Parkinson’s disease and lewy bodies
- 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
Huntington’s disease
- 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).
Biological treatment: drugs
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.
Biological treatments: Deep brain stimulation
- 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.
Cognitive rehabilitation: attention deficits
- Attention process training
- Time pressure management
Cognitive rehabilitation: visuospatial deficits
- Computer-assisted training
Cognitive rehabilitation: apraxia and coordinated self-help behaviors
- Gestural training (apraxia)
- Virtual computer-based training
