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Assessment, Personality and Psychopathology > Dementia > Flashcards

Dementia Flashcards

1
Q

Different Types of Onset Dementia

A

Young onset dementia - under 65

  • Genetic influence
  • Onset in 40s and 50s

Late onset - over 65

  • Genetic influence is not the biggest risk factor
  • 85 years average age of diagnosis
    95% of cases
  • Estimated to be above 1 million in 34 years in Australia
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2
Q

Mild Cognitive Impairment

A

(Mild Neurocognitive Disorder)

  • modest cognitive decline
  • no interference in complex activities of daily living
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3
Q

Dementia

A

(Major Neurocognitive Disorder)

  • severe versions of the former
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4
Q

Disease Pathways of Dementia

A
  • Alzheimer’s 60-80%
  • Lew body dementia 5-10%
  • Vascular
  • Frontotemporal
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5
Q

DSM-V Criteria For Mild Neurocognitive Disorder

A

A. Evidence of modest cognitive decline from a previous level of performance in one or more cognitive domains based on:

  1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a mild decline in cognitive function; and
  2. A modest impairment in cognitive performance, preferably documented by standardised neuropsychological testing or, in its absence, another quantified clinical assessment

B. The cognitive deficits do not interfere with capacity for independence in everyday activities

C. The cognitive deficits do not occur exclusively in the context of a delirium

D> The cognitive deficits are not better explained by another mental disorder

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6
Q

DSM-V Criteria for Major Neurocognitive Disorder

A

A. Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains based on:

  1. concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function
  2. a substantial impairment in cognitive performance, preferably documented by standardised neuropsychological testing or, in its absence, another quantified clinical assessment

B. The cognitive deficits interfere with independence in everday activities

C. and D. same as Minor

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7
Q

Testing Cognition

A

Screening Tools

  • Mini-mental state exam (MMSE)
  • Montreal cognitive assessment (MoCA)
  • Impacted by education, language fluency, sensory deficits
  • Must exclude medical history, blood tests, physical examination etc
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8
Q

Basic Idea of Alzheimer’s

A
  • 1906, treated person dying of symptoms of memory loss, language problems and unpredictable behaviour
  • Aggregation of proteins in abnormal fashion in Alzheimer’s, creation of amyloid plaques, neurofibrillary tangles
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9
Q

Criteria for Alzheimer’s

A
  • Insidious onset and gradual progression of impairment
  • Genetic mutation from family history
  • No evidence of mixed etiology (absence of other neurodegenerative disease)
  • Some may have the pathology but not the cognitive impairment, separating the disease from the dementia
  • Separating positive biomarkers from cognition, finding AD specific features
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10
Q

Drugs Associated with Alzheimer’s

A

Human monoclonal antibodies

  • Removes amyloid and shows statistically significant slowing in the decline in cognitive function
  • Downside of regular monitoring (brain imaging) due to risk of small bleeds in the brain

Acetyl-cholinesterase inhibitors and NMDA

  • No impact on the progression of the disease
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11
Q

Vascular Damage Leading to Dementia

A
  • Stroke
  • Damage to myelin sheath
  • Damage to the lining of the blood vessels
  • Impaired blood flow
  • Damage to the blood brain barrier
  • Managing changes in blood pressure
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12
Q

Highest Risk of Dementia

A

Highest risk is high blood pressure

  • Because it associated with age
  • Increases with age
  • Drives vascular risk factors
  • High blood pressure in mid life (40s etc) have higher risk of dementia in late life
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13
Q

Vascular Neurocognitive Disorder

A
  • Consistent with vascular etiology
  1. Temporally related to one or more cerebrovascular events
  2. Complex attention (including processing speed) and frontal-executive function
  • Evidence of the presence of cerebrovascular disease
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14
Q

Issues for Diagnosis of Dementia

A
  • Prodromal and presymptomatic phase may last 20-30 years
  • Maybe should be intervening 65 or younger to manage for 85 year mean
  • Pathology does not map directly onto symptoms
  • Most late onset dementia has mixed pathology
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15
Q

Lifestyle Risk Factors to Dementia

A
  • Smoking
  • Loss of hearing
  • Sleep
  • Alcohol
  • Physical Inactivity
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16
Q

Clinical Risk Factors to Dementia

A
  • High cholesterol
  • Diabetes mellitus
  • Blood pressure
17
Q

Dopamine Agonist Producing Symptoms Similar to the Psychotic Symptoms Characteristic of SZ

A
  • Gave 16 addicts large doses of methamphetamine
  • 12 patients developed paranoid psychosis - most common symptom was ideas of reference
18
Q

Antipsychotic Medications Blocking Dopamine Receptors

A
  • Therapeutic does is strongly related to drug’s binding affinity for D2 receptors
  • If you have psychosis, drugs taken reduces the psychosis
19
Q

Psychotic Symptoms Caused by Hyperactivity of the Dopaminergic System

A
  1. Antipsychotic drugs all block D2 receptors
  2. Dopamine agonists can cause schizophrenia like psychotic symptoms
  3. SZ patients show abnormally high levels of dopamine synthesis
  4. Also show high levels of dopamine receptors
20
Q

First-Rank Symptoms

A

Schneider

  • Audible thoughts (thought echo)
  • Voices arguing
  • Voices commenting on one’s actions
  • Delusions of control
  • Thought withdrawal, insertion, broadcast

FRS are actually diagnostic of SZ according to some criteria, empirical studies suggest FRS are not unique to SZ, but are far more common

21
Q

Primary Dopamine Pathways

A
  • 1 million of 100 billion neurons produce dopamine
  • Primarily located in substantia nigra and VTA (ventral tegmental area)
  • Involved in movement, reward and prediction error
22
Q

Dopamine Codes for Surprise - Schulz et al., 1997

A
  • Recorded from DA neurons in VTA
  • Monkeys learned that light flash preceded juice
  • Gave them reward 3 seconds after the light flash, the dopamine would only spike when the light was shining and not when they got the reward,
  • So it is not just reward that plays a role
  • Rather, dopamine is coding for surprise
23
Q

Dopamine Codes for Surprise

A

DA signals an error in predicted state of the world

  • Positive - better than expected
  • Negative - worse than expected
24
Q

Psychosis as a State of Aberrant Salience

A
  • Dopamine system is hyperactive, erratic
  • Leads to usually non-salient events grabbing attention and demanding explanation
  • Normally neutral events in the external world take on great significance to the patient
  • external vs internal
25
Q

Psychosis as a state of (external) aberrant salience

A

Prodromal symptoms

  • Everything meant something, a sense of greater awareness

Delusion of Reference

  • Innocuous events, actions become infused with salience due to erratic firing of dopamine neurons, attach ideas based on the expectations of these innocuous events
26
Q

Psychosis as a state of (internal) aberrant salience

A
  • Aberrant salience to self-generated actions
  • Self-generated sensations are normally perceived as less salient than externally-generated sensations in healthy people
  • Perhaps DA hyperactivity lead to self-generated actions being infused with abnormal salience
  • Delusion of control
  • Represent confusion between self-generated and externally-generated actions

Hearing yourself speak study

  • Brain activity evoked self-generated speech compared to identical speech when it is recorded and played back to the participant
  • Self-generated speech is typically suppressed compared to externally-generated speech in normal people
27
Q

Aberrant Salience to Thoughts

A
  • Perhaps self-generated thoughts are misperceived as externally-generated because they feel unusually salient
  • Delusions of thought insertion
  • Audible thoughts
28
Q

Limitations of Aberrant Salience Theory

A
  • Plausible, testable
  • Limited to psychotic symptoms – more difficulty accounting for negative symptoms
  • Doesn’t explain why dopamine is abnormal in SZ
  • Major strength: attempts to bride the explanatory gap between biological and psychological accounts for psychosis
29
Q

Pharmacological Treatments of SZ

A
  • Antipsychotic medications are currently most effective and widely-used treatments for SZ
  • Chlorpromazine was developed in 1952 as an anaesthetic
  • First of the ‘typical’ 1st gen antipsychotics
  • Effect related to dopamine antagonism
  • ‘Atypical’ or 2nd gen
  • Included clozapine
  • Block dopamine receptors and also act as a serotonin agonists
  • Both have unpleasant side-effects (low compliance rate)
  • After 19 months approx 75% have stopped taking them
30
Q

Side Effects of Pharmacological Treatments of SZ

A

Extrapyramidal symptoms

  • Tardive dyskinesia
  • Involuntary repetitive movements of face or mouth

Agranulocytosis

  • Loss of white blood cells
  • Very dangerous, requires regular blood tests
  • More common in typical drugs

Weight gain

Sedative and dysphoric effects

  • Worsen negative symptoms? E.g anhedonia, cognitive dysfunction, flat affect
31
Q

Psychotherapy for SZ

A
  • Medications, while relative effective against psychotic symptoms, are relatively ineffective against negative symptoms
  • Psychotherapy effective as an adjunct
  • Many SZ patients show residual psychotic and disorganised symptoms after medication
32
Q

CBT for negative symptoms

A
  • Compared to TAU
  • Found to be effective for negative symptoms
33
Q

CBT for psychotic symptoms

A
  • Involves teaching coping skills, increasing quality of life
  • Study challenged patients’ beliefs about command hallucinations
  • Found large reductions in compliance behaviour, lower levels of distress, lower levels of depression
  • Found it to be effective as an adjunct to pharmacotherapy

Assessment, Personality and Psychopathology (18 decks)

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