Late life and neurocognitive disorders - summary of chapter 14 of Abnormal Psychology by Kring, Davison, Neale & Johnson (12th edition)

Clinical psychology
Chapter 14
Late life and neurocognitive disorders

Aging: issues and methods

As we age, physiological changes are inevitable, and there may be emotional and mental changes as well.
Many of these influence social interactions.

The problems experienced in late life

Mental health is tied to the physical and social problems in a person’s life.
No other have more of these problems than the elderly.

As people age, the quality of depth of sleep declines.
Sleep apnea: a disorder in which a person stops breathing for seconds to minutes during the night. Increase with old age.

Several problems are evident in the medical treatment available during late life.

  • The chronic health problems of older people seldom diminish.
  • Time pressure of the health care system.
    Polyharmacy: the prescribing of multiple drugs to a person. Can result.
  • Most psychoactive drugs are tested on younger people.

Research methods in the study of aging

Three kinds of effects:

  • Age effects:
    The consequences of being a certain chronological age
  • Cohort effects:
    The consequences of growing up during a particular time period with its unique challenges and opportunities.
  • Time-of-measure effects:
    Confounds that arise because events at a particular point in time can have a specific effect on a variable that is being studied.

Two major research designs

  • Cross-sectional
    The investigator compares different age groups at the same moment in time on the variable of interest.
  • Longitudinal studies
    The researcher periodically retests one group of people using the same measure over a number of years or decades.
    Selective mortality: when people are no longer available for follow-up because of death.

Psychological disorders in late life

The DSM criteria are the same for older and younger adults.
The process of diagnoses must be considered with care. DSM criteria specify that a psychological disorder should not be diagnosed if the symptoms can be accounted for by a medical condition or medication side effects.
Clinicians must be extremely careful to consider the interactions between physical and psychological health.

Estimating the prevalence of psychological disorders in late life

Persons over age 65 have the lowest overall prevalence of mental disorders of all age groups.

Mot people with psychological disorders in late life are experiencing a continuation of symptoms that began earlier.

Why so low?

  • Methodological issues
  • Might be some processes related to aging that promote better mental health

Methodological issues in estimating the prevalence of psychopathology

  • Methodologically, older adults may be more uncomfortable acknowledging and discussing mental health or drug use problems compared to younger people.
  • There may be cohort effects.
  • People with mental illness are at risk for dying earlier.

Enhanced coping abilities developed across the life course may help protect people from mental illness during late life.

Neurocognitive disorders in late life

Dementia

Dementia: a descriptive term for the deterioration of cognitive abilities to the point the functioning is impaired.
Difficulty remembering things is the most common symptom of dementia.
Los of control of impulses.
Delusions and hallucinations may occur.
Language disturbances.
Delirium: a state of mental confusion.

The course of dementia may be progressive, static, or remitting, depending on the cause.

DSM-5 provides parallel diagnoses like those for mild cognitive impairment as well as for dementia.

Not all people with mild cognitive symptoms develop dementia.

Prevalence of dementia is 0,4 percent. Increases with age.

DSM-5 criteria for Mild neurocognitive disorder

  • Modest cognitive decline form previous levels in one or more domains based on both of the following:
    • Concerns of the patient, a close other, or a clinician
    • Modest neurocognitive decline on formal testing or equivalent clinical evaluation
  • The cognitive deficits do not interfere with independence in everyday tasks, 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 delirium and are not due to another psychological disorder.

DSM-5 criteria for Major neurocognitive disorder

  • Significant cognitive decline from previous levels in one or more domains based on both of the following:
    • Concerns of the patient, a close other, or a clinician
    • Substantial neurocognitive impairment, or equivalent clinical evaluation
  • The cognitive deficits interfere with independence in everyday activities
  • The cognitive deficits do not occur exclusively in the context of delirium and are not due to another psychological disorder.

Alzheimer’s disease

In Alzheimer’s disease, the brain tissue irreversibly deteriorates, and death usually occurs within 12 years after the onset of symptoms.
The illness may begin with absentmindedness and difficulties in concentration an in memory for new material. These shortcomings may be overlooked for several years, but eventually interfere with daily living.
As the disease develops, problems with language skills and word finding intensify. Visual-spatial abilities decline, which can be manifested in disorientation and trouble copying figures.
People with the disorder are typically unaware of their cognitive problems initially.
Memory continues to deteriorate, and the person becomes increasingly disoriented and agitated.

People with Alzheimer's disease have more plaques (small, round beta-amyloid protein deposits that are outside the neurons) and neurofibrillary tangles (twisted protein filaments composed largely of the protein tau in the axons of neurons) than would be expected for the person’s age.
The beta-amyloid plaques are most densely present in the frontal cortex and they may be present for 10 to 20 years before the cognitive symptoms become noticeable.
Tangles are most densely present in the hippocampus. Over time, as the disease progresses, plaques and tangles spread trough more of the brain.

The plaques and tangles appear related to a host of brain changes over time.
At early stages, there seems to be a loss of synapses for acetylcholingeric and glutamatergic neurons. Neurons also begin to die.
As neurons die, the cerebral cortex, entorhinal cortex, and hippocampus shrink, and later the frontal, temporal, and parietal lobes shrink. As this happens, the ventricles become enlarged.
The cerebellum, spinal cord, and motor and sensory areas of the cortex are less affected.

Heritability of 79 percent in Alzheimer’s disease.
Having one E4 allele increases the risk of Alzheimer’s disease.
People with two E4 alleles show overproduction of beta-amyloid plaques, loss of neurons in the hippocampus, and low glucose metabolism in several regions of the cerebral cortex even before they develop symptoms of Alzheimer’s disease.

Lifestyle variables may play a role in Alzheimer’s.

  • Exercise may ward off memory problems
  • Engagement in intellectual activities
  • Cognitive activity
    Cognitive reserve: the idea that some people may be able to compensate for the disease by using alternative brain networks or cognitive strategies such that cognitive symptoms are less pronounced.
  • Depression predicts more decline in cognitive functioning.

Frontotemporal dementia

Frontotemporal dementia (FTD) is caused by a loss of neurons in frontal and temporal regions of the brain.
The neuronal deterioration of FTD occurs predominantly in the anterior temporal lobes and prefrontal cortex.
Typically begins in the mid- to late 50s, and it proceeds rapidly. Death usually occurs within 5-10 years of the diagnosis.

Memory is not severely impaired in FTD.
The diagnostic criteria for FTD include deterioration in at least three of the following areas at a level that leads to functional impairment

  • Empathy
  • Executive function
  • Ability to inhibit behavior
  • Compulsive or perseverative behavior
  • Hyperorality
  • Apathy

In early stages, significant others may notice changes in personality and judgment.

The disorder strikes emotional processes in a more profound manner than Alzheimer’s disease does. It can damage social relationships.
Particular deficits seem to emerge in the ability to regulate emotions. People with FTD may not realize they are violating social conventions.

FTD can be caused by many different molecular processes.
FTD has a strong genetic component, although there may be multiple genetic pathways involved.

Vascular dementia

Vascular dementia is diagnosed when dementia is a consequence of cerebrovascular disease.
Most commonly, the person has a series of strokes in which a clot formed, impairing circulation and causing cell death.
Risk for vascular dementia involves the same risk factors as those for cardiovascular disease in general.

Because strokes an cardiovascular disease can strike different regions of the brain, the symptoms of vascular dementia can vary a good deal.
The onset of symptoms is usually more rapid in vascular dementia than in other forms of dementia.

Vascular dementia can co-occur with Alzheimer’s disorder.

Dementia with Lewy bodies

Dementia with Lewy bodies (DLB) can be divided into two subtypes, depending on whether or not it occurs in the context of Parkinson’s disease.

  • DLB with Parkinson's disease
  • DLB without Parkinson’s disease.

The symptoms associated with this type of dementia are often hard to distinguish form the symptoms of Parkinson’s and Alzheimer’s disease.
DLB is more likely than Alzheimer’s disease to include prominent visual hallucinations and fluctuating cognitive symptoms.
People with DLB are often extremely sensitive to the physical side effects of anitpsychotic medications.
People with DLB often experience intense dreams accompanied by levels of movement and vocalizing that may make them seem as though they are ‘acting out their dreams’.

Dementias caused by disease and injury

A number of other medical conditions can produce dementia.

  • Encephalitis, a genetic term for any inflammation of brain tissue, is caused by viruses that enter the brain.
  • Meningitis, and inflammation of the membranes covering the outer brain, is usually caused by a bacterial infection.

Both can cause dementia.

The organism that produces the ventral disease syphilis can invade the brain and cause dementia.
Dementia can also be caused by

  • HIV
  • Head trauma
  • Brain tumors
  • Nutritional deficiencies
  • Kidney or liver failure
  • Endoctrine problems
  • Exposure to toxins
  • Chronic substance use

Prevention and treatment of dementia

A few drugs may provide modest protection against cognitive decline, but the effects are slim.
There is no cure for dementia.
Most efforts at presentation of Alzheimer’s disease have failed.

Medications

No medications have been shown to address the cognitive symptoms of FTD.
Medications may help slow decline, but they do not restore memory function to previous levels.

Medical treatments are commonly used to address psychological symptoms that commonly co-occur with dementia.

Although antipsychotic medications can provide modest relief for aggressive agitation, they also increase the risk of death among elderly people with dementia.

Psychological and lifestyle treatments

Supportive psychotherapy can help families and patients deal with the effects of the disease.
Generally, the therapists allows opportunities for the person with dementia and the family to discuss the illness.
The therapists also provides accurate information about the illness, helps family members care for the person in the home, and encourages a realistic rather than a catastrophic attitude in dealing with the many specific challenges that this cognitive disorder presents.

Exercise also appears to have modest benefits in improving cognitive function.

Behavioral approaches have been shown to help compensate for memory loss and to reduce depression and disruptive behavior among people with early stages of Alzheimer’s disease.

Delirium

DSM-5 criteria for Delirium

  • Disturbance in attention and awareness
  • A change in cognition, such as disturbance in orientation, language, memory, perception, or visuospatial ability, not better accounted for by a dementia
  • Rapid onset (usually within hours or days) and fluctuation during the course of a day
  • Symptoms are caused by a medical condition, substance, or toxin

Delirium: being off-track or deviating form the usual state. Typically described as a clouded state of consciousness.
The two most common symptoms are:

  • An extreme trouble focusing attention
  • Profound disturbances in the sleep/wake cycle

Vivid dreams and nightmares are common
Memory impairment, especially for recent events, is common

In the course of a 24-hours period, people with delirium have lucid intervals in which they become alert and coherent. They are usually worse during sleepless nights.
These daily fluctuations help distinguish delirium form other syndromes.

Perceptual disturbances are frequent in delirium.
Swings in activity and mood accompany these disordered thoughts and perceptions.

People of any age are subject to delirium, but it is more common among children and older adults.

Mortality rate for delirium is high.

Etiology of delirium

Delirium is caused by medical conditions.
Causes

  • Drug intoxications and drug-withdrawal reactions
  • Metabolic and nuritional imbalances
  • Infections or fevers
  • Neurological disorders
  • The stress of major surgery.

Delirium usually has more than one cause.

Treatment of delirium

Complete recovery form delirium is possible if the underlying cause is treated promptly and effectively.
Beyond treating the underlying medical conditions, the most common treatment is atypical antipsychotic medication.
It usually takes 1 to 4 weeks for the condition to clear, it takes longer in older people than in younger people.

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