Transcript Chapter 14

Abnormal Psychology, Twelfth Edition
by
Ann M. Kring,
Sheri L. Johnson,
Gerald C. Davison,
& John M. Neale
© 2012 John Wiley & Sons, Inc. All rights reserved.
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 Chapter
14: Late Life and Neurocognitive
Disorders
I. Aging: Issues and Methods
II. Psychological Disorders in Late Life
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 In
U.S., many people dread aging
• Elderly not revered as in other cultures
 When
are we old?
• Society arbitrarily sets old as over 65
• Young-old: 65-74 years, old-old: 75-84, oldest-old: 85+
 2001
census
• 12.4% or 35 million individuals were 65 or older
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
Aging involves inexorable cognitive decline
• Severe cognitive problems do not occur for most
 Mild declines are common

Late life is a sad time and most elderly are depressed
• Older individuals report less negative emotion than younger
people
 More brain activation in key areas when viewing positive images

Late life is a lonely time
• Some less likely to develop new friendships
• Social selectivity
 As we age, we focus on the interpersonal relationships that matter most
to us

Older people lose interest in sex
• Sexual activity does not decrease from mid-to late life for most
people
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
Problems multiply with age
• physical decline and disabilities
• sensory and neurological deficits
• loss of loved ones
• social stresses such as stigmatizing attitudes towards elderly
• Eighty percent of elderly people have at least one major medical condition

Sleep disturbances increase with age
• Insomnia
• Sleep apnea

Medical treatment
• Chronic problems instead of curable disorders
• Polypharmacy: Practice of prescribing multiple drugs to patients
• Psychoactive drugs usually tested on younger participants
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 Cross-sectional
studies
• Researcher tests different age groups at one point in
time
• Fails to provide information about how people change
over time
 Longitudinal
studies
• Researcher retests the same group of people with the
same measures at different points in time
 May extend over several years or decades
• Attrition a potential problem
 Selective mortality can lead to biased sample
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 Most
elderly do not have cognitive
disorders
• Prevalence has decreased over last 15 years
 Dementia
• A deterioration of cognitive function
 Delirium
• A state of mental confusion
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 Deterioration
of cognitive function
• Impaired social and occupational functioning
• Progresses over time
 Begins with difficulty remembering recent events
 Deficits
can be detected before impairment
becomes obvious
 Mild cognitive impairment develop slowly
 DSM-5 proposes two categories, differentiated by
ability to live independently:
• Mild neurocognitive disorder (mild cognitive impairment)
• Major neurocognitive disorder (dementia)
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
Minor cognitive decline from previous levels in one or more domains based on both of the
following:
o
Concerns of the patient, a close other, or a clinician
o
Neurocognitive performance below appropriate norms (i.e., between the 3rd and 16th
percentile) on formal testing, or equivalent clinical evaluation.

The cognitive deficits do not interfere with independence (i.e., tasks such as paying bills or
managing medications), even though greater effort, compensatory strategies, or
accommodation may be required to maintain independence.

The cognitive deficits do not occur exclusively in the context of a delirium and are not due
to another psychological disorder
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
Evidence of significant cognitive decline from previous levels in one or more domains
based on both of the following:
o
Concerns of the patient, a close other, or a clinician
o
Neurocognitive performance below the 3rd percentile on formal testing, or equivalent
clinical evaluation.

The cognitive deficits interfere with independence

The cognitive deficits do not occur exclusively in the context of a delirium and are not due
to another psychological disorder
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

Described by Alois Alzheimer in 1906
Irreversible brain tissue deterioration
• Death usually occurs within 12 years

Usually begins with
• Difficulty remembering recent events
• Learning new material
• Irritability

As disease progresses
• Language problems intensify, including word-finding
• Disorientation
 Time, place, and identity confusion
• Agitation
• Depression
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
Plaques
• β-amyloid protein deposits
• Primarily found in frontal cortex

Neurofibrillary tangles
• Protein filaments composed of tau in axons of neurons
• Primarily found in hippocampus



Measured using PET scans
Plaques most dense in frontal cortex; tangles most dense in
hippocampus
Loss of synapses for acetylcholinergic (Ach) and glutaminergic
neurons
• As neurons die, atrophy of cerebral and entorhinal cortices and hippocampus
• Enlargement of ventricles
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
Genetic factors
• Heritability 79%
• ApoE4 allele: Gene on chromosome 19
 Having one E4 allele increases risk by 20%
 Having two E4 alleles increases risk substantially more
 Related to over-production of beta-amyloid plaques, loss of neurons in the
hippocampus, and low glucose metabolism in cerebral cortex

Environmental factors
• Smoking, being single, low social support, and depression related to
greater risk of developing Alzheimer’s
• Mediterranean diet, exercise, education, and cognitive engagement
predict a lower risk
 e.g. solving crossword puzzles, reading the newspaper daily
• Cognitive reserve
 Use alternative brain networks to compensate for disease
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 Loss of neurons in frontal and temporal
• Memory not severely disrupted
 Impairment of executive functions
• Planning
• Problem solving
• Goal-directed behavior
 Difficulty recognizing and regulating
lobes
emotion
• Much more profound impact than Alzheimer’s
 Caused by multiple genetic
• Pick’s Disease
• High levels of tau proteins
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pathways
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 Typically
results from stroke (cardiovascular)
• Clot forms and impairs circulation
• Cells die
 Risk
factors
• Smoking, high LDL cholesterol, high BP
 Symptoms
can vary greatly, depending upon
location of strokes
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 Two subtypes
• With Parkinson’s
• No Parkinson’s
 Symptoms similar
to Parkinson’s and
Alzheimer’s diseases
• Shuffling gait
• Loss of memory
 Symptoms differ in that DLB patients have:
• Fluctuating cognitive symptoms
• Prominent visual hallucinations
• Intense dreams involving movement and vocalizing
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 Other
medical issues
• Encephalitis (inflammation of brain tissue by
•
•
•
•
•
viruses)
Meningitis (inflammation of covering membranes
by bacteria)
HIV
Head traumas
Brain tumors
Nutritional deficits (B-complex vitamins)
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
Medications
• No drug reverses Alzheimer’s disease
• Some drugs produce slightly less decline
 Cholinesterase inhibitors (drugs that prevent breakdown of
acetylcholine)
 Donepezil (Aricept)
 Galantamine (Reminyl)
Vitamin E, statins, and nonsteroidal antiinflammatory drugs have failed to find support
 Preventive work focuses on processes involved in the
creation of amyloid from its precursor protein
 Antidepressants for depression
 Antipsychotic medication for agitation

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 Psychological treatments
• Supportive psychotherapy for family and patient
• Education about disease and care
• Cognitive interventions when disease is in early
stages
 Labeling drawers, appliances
 Calendars, clocks, and strategically placed notes
• Exercise has been associated with cognitive
benefits
• Music appears to reduce agitation and disruptive
behavior
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
Clouded state of consciousness
• Extreme trouble focusing attention
• Disturbances in the sleep/wake cycle
• Fragmented thinking
• Speech is rambling and incoherent
• Disorientation
• Perceptual disturbances
• Memory impairments
• Mood swings


Secondary to underlying medical condition
Detection of delirium important but often missed
• Untreated, further cognitive decline and mortality may occur

Beyond treating the underlying medical conditions, the most
common treatment is atypical antipsychotic medication
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Copyright 2012 by John Wiley & Sons, Inc. All
rights reserved. No part of the material protected
by this copyright may be reproduced or utilized in
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