Wk 8: Late life disorders

  1. Older adults
    • Older adults are usually defined as those over the age of 65
    • the young-old, those aged 65 to 74;
    • the old-old, those aged 75 to 84;
    • and the oldest-old, those over age 85.
    • People aged over 65 years represent the fastest growing demographic in the majority of countries
  2. Myths about late life
    • Severe cognitive problems do not occur for most people in late life, though a mild decline in cognitive functioning is common.
    • Older adults actually experience less negative emotion than do young people.
    • The elderly are actually more skilled at regulating their emotions.
    • Another myth, that older people are lonely- social selectivity.
    • Negative attitudes about the elderly learned early in life persist and become negative self-perceptions as people move into their later years.
    • Researchers have also shown that negative self-views about ageing can predict earlier death,
  3. Social selectivity
    As we age, our interests shift away from seeking new social interactions to cultivating a few social relationships that really matter to us, such as those with family and close friends.
  4. The problems experienced in late life
    • Older age is associated with physical decline, sensory acuity deficits, loss of loved ones, social stress of stigmatising attitudes towards the elderly and the cumulative effects of a lifetime of unfortunate experiences.
    • Eighty percent of elderly people have at least one major medical condition.
    • As people age, the quality and depth of sleep decline.
  5. Problems that complicate medical treatment for elderly people
    • One of the main difficulties is that the chronic health problems of older people seldom diminish; physicians focused on identifying cures can become frustrated when none are available.
    • Polypharmacy:  the prescribing of multiple drugs to a person due to not checking if person is taking other medications or seeing other health care providers.
    • This increases the risk of adverse drug reactions such as side effects and toxicity.
    • Most psychoactive drugs are tested on younger people. Gauging the appropriate dose for the less efficient metabolism of the kidneys and liver of the older person represents a challenge for the medical practitioner — side effects and toxicity are much more likely as people age
  6. Three kinds of effects important in ageing
    • Age effects: the consequences of being a certain chronological age.
    • Cohort effects: are the consequences of growing up during a particular time period with its unique challenges and opportunities.
    • Time-of-measurement effects: are confounds that arise because events at a particular point in time can have a specific effect on a variable that is being studied (eg. people tested right after experiencing the 2005 earthquake in Haiti might demonstrate elevated levels of anxiety)
  7. Research methods in the study of ageing
    • Cross-sectional:  the investigator compares different age groups at the same moment in time on the variable of interest.
    •  they do not provide clear information about how people change as they age.
    • Longitudinal: the researcher periodically retests one group of people using the same measure over a number of years or decades. 
    • Results can be biased by attrition, in which participants drop out of the study due to death, immobility or lack of interest.
    • Selective mortality: When people are no longer available for follow-up because of death.
    •  Selective mortality results in a particular form of bias, in that results obtained with the remaining sample are more relevant to drawing conclusions about relatively healthy people than about unhealthy people. 
    • Beyond attrition due to death, people with the most problems are likely to drop out from a study, whereas the people who remain are usually healthier than the general population.
  8. Psychological disorders in late life
    • The DSM criteria are the same for older and younger adults.
    • 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.
    • Because medical conditions are more common in the elderly, it is particularly important to rule out such explanations. 
    • eg. Age-related deterioration in the vestibular system (inner-ear control of one’s sense of balance) can account for panic symptoms such as severe dizziness.
  9. Estimating the prevalence of psychological disorders in late life
    • Findings indicate that persons over age 65 have the lowest prevalence of psychological disorders of all age groups.
    • Rates of schizophrenia are also low among the elderly.
    • Older adults are less likely to meet criteria for personality disorders compared to younger individuals.
    • Most people who have an episode of a psychological disorder late in life are experiencing a recurrence of a disorder that started earlier in life rather than an initial onset. 

    • Why are rates of psychopathology so low in late life? 
    • Ageing relates to more positive emotionality and more close-knit social circles. 
    • Some have argued that methodological issues might be leading us to underestimate the prevalence of psychological disorders in late life.
  10. Methodological issues in estimating the prevalence of psychopathology
    • Response bias: Methodologically, older adults may be more uncomfortable acknowledging and discussing mental health or drug use problems compared to younger people.
    • Cohort effects: many people who reached adulthood during the drug-oriented era of the 1960s continue to use drugs as they age. Their generation is more likely to have problems with substance abuse in late life than previous generations had.
    • Selective mortality: People with psychological disorders are at risk for dying earlier.
  11. Neurocognitive disorders in late life: Dementia
    • It is an ‘umbrella’ term used to describe a clinical syndrome characterised by progressive deterioration of cognitive abilities to the point that functioning becomes impaired.
    • There are many different types of dementia, including Alzheimer’s disease, frontotemporal dementia, vascular dementia and dementia with Lewy bodies.
    • Generally the symptoms have a gradual onset, and are progressive and irreversible.
    •  In Australia, the prevalence of dementia in people aged 65 to 74 is 3.2 percent and increases progressively to 29.5 percent in those aged over 85 years.
  12. Mild cognitive impairment (MCI)
    • A separate diagnostic category used to describe signs of cognitive decline before functional impairment is present.
    • It is sometimes described as a transitional state between the cognition of normal ageing and dementia and is separated into amnestic and non-amnestic mild cognitive impairment.
  13. DSM-5 neurocognitive disorders
    • Neurocognitive disorder: Specify mild or major
    • Neurocognitive disorder associated with:
    • Alzheimer’s disease
    • frontotemporal lobar degeneration
    • vascular disease
    • traumatic brain injury
    • Lewy body disease
    • Parkinson’s disease
    • HIV infection
    • substance/medication use
    • Huntington’s disease
    • prion disease.
    • Neurocognitive disorder due to:
    • another medical condition
    • multiple aetiologies.
  14. DSM 5 criteria for mild neurocognitive disorder
    • People with mild neurocognitive disorder experience modest cognitive decline from previous levels in one or more domains (e.g., complex attention, memory, language, executive function, social cognition) 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 activities (e.g., 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 delirium and are not due to another psychological disorder.
  15. Difference between dementia and MCI
    • There is some debate about where to draw the line between mild cognitive impairment and dementia, as well as how early to diagnose mild cognitive impairment.
    • The DSM-5 distinguishes between mild and major neurocognitive disorder based on whether symptoms interfere with the ability to live independently.
    • The DSM-5 criteria for mild neurocognitive disorder require a low score on only one cognitive test.
    • This may lead to an artificially high rate of diagnosis for mild neurocognitive disorder.

    • It is important to note that not all individuals diagnosed with mild cognitive impairment develop dementia.
    • Among adults with mild cognitive impairment, about 10 percent per year will develop dementia; in comparison to 1 percent per year for individuals without mild cognitive impairment.
  16. Alzheimer’s disease
    • It is the most common type of dementia accounting for approximately 60 to 80 percent of cases.
    • Death usually occurs within 12 years after the onset of symptoms.
    • The most common symptom of Alzheimer’s disease is memory loss.
    •  In the early stage of the disease, memory impairment for recent events is common whereas long-term memory remains intact.
    •  Apathy is common- about a third of people develop full-blown depression as the illness worsens.
    • As the disease develops, problems with language skills and word finding intensify.
    • Visual-spatial abilities decline, which can be manifested in disorientation (confusion with respect to time, place or identity).
    • The person may also have difficulties with reasoning, problem solving or poor judgement.
    • In the terminal phase of the illness, personality loses its sparkle and integrity.
    • Finally, the person is oblivious to his or her surroundings.
  17. Alzheimers biology
    • 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.
    • Some people produce excessive amounts of beta-amyloid, whereas others seem to have deficiencies in the mechanisms for clearing beta-amyloid from the brain.
    • The beta-amyloid plaques are most densely present in the frontal cortex.
    •  Plaques can be measured using a specialised type of PET scan. Tangles are most often measured in cerebrospinal fluid, although they can be measured using a PET scan as well.
    • Tangles are most densely present in the hippocampus, an area that is important for memory. Over time, as the disease progresses, plaques and tangles spread through more of the brain.
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    • Immune responses to plaques lead to inflammation which then triggers a series of brain changes over time.
    • At early stages, there seems to be a loss of synapses for acetylcholinergic (ACh) and glutamatergic neurons.
    • Neurons also begin to die.
    • Ventricles enlarge.
    •  the entorhinal cortex and then the hippocampus and other regions of the cerebral cortex shrink, and later the frontal, temporal and parietal lobes shrink.
    • The cerebellum, spinal cord and motor and sensory areas of the cortex are less affected, which is why people with Alzheimer’s do not appear to have anything physically wrong with them until late in the disease process.
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  18. Schematic illustration of the dissection of a normal brain compare to one with Alzheimer’s disease.
    • As demonstrated in the diagram, Alzheimer’s disease results in overall cortical shrinkage, enlarged ventricles and atrophy of the hippocampi.
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  19. Alzheimers risk factors- genes and medical
    The gene ApoE-4: lead to an increased deposition of beta-amyloid plaques.  the genetic polymorphism on chromosome 19 with the largest contribution to Alzheimer’s disease.


    • Many of the genes that increase risk for Alzheimer’s disease are related to immune function and cholesterol metabolism.
    • Immune processes and excessively high cholesterol can trigger inflammation and accordingly, conditions that involve immune and inflammatory processes also appear related to a greater risk of Alzheimer’s disease. 
    • For example, type II diabetes, which has been tied to immune and inflammatory changes, is related to greater risk of developing Alzheimer’s disease.
    • Similarly, brain traumas from accidents or injuries can also increase the risk of Alzheimer’s disease later in life.
  20. Alzheimers risk factors- lifestyle variables
    • For example, smoking, being single, obesity, depression and low social support are related to a greater risk of Alzheimer’s disease, while a Mediterranean diet, exercise, education and engagement in cognitive activities are related to a lower risk.
    • Regular exercise predicts less decline in cognitive functions.
    • Engagement in intellectual activities also appears helpful, with some proposing a ‘use it or lose it’ model of Alzheimer’s.

    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.

    Plausible that those brain changes influence motivation to take part in exercise or cognitive activities.

    The opposite direction of effects seems to occur as well: a lifetime history of depression predicts more decline in cognitive functioning.
  21. Frontotemporal dementia (FTD)
    • Characterised by 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.
    • FTD typically begins in the mid- to late 50s and it progresses rapidly; death usually occurs within 5–10 years of the diagnosis.
    • FTD is rare, affecting less than 1 percent of the population.
    • There are multiple subtypes of FTD, separated into a behavioural variant (bvFTD) and language variants.
    • FTD strikes emotional processes more profoundly than Alzheimer’s disease does and in doing so, it can damage social relationships. Particular deficits seem to emerge in the ability to regulate emotions.
    •  Persons with FTD do not seem to notice that they have made a social mistake and so they do not experience embarrassment in contexts where others might.
  22. bvFTD symptoms
    • Unlike Alzheimer’s disease, memory is not severely impaired in FTD.
    • The most common variant, bvFTD, is characterised by a progressive deterioration of personality, social skills and cognition.
    • Hallmark features of bvFTD include early behavioural disinhibition, such as socially inappropriate behaviour (e.g., kissing strangers, verbal aggression), loss of manners or decorum (e.g., inappropriate laughing, offensive jokes, loss of respect for personal space) and impulsive or careless actions (e.g., reckless driving, new onset gambling). 
    • The most common initial symptoms include loss of motivation, reduced interest in previously enjoyed activities and decreased initiation of behaviour. Loss of sympathy or empathy, perseverative behaviour, hyperorality (e.g., putting inedible objects in mouth) and dietary changes (i.e., preference for sweet foods) may also occur.
    • Because a person affected by this disorder might suddenly start to overeat, chain smoke, drink alcohol or demonstrate other behavioural symptoms, FTD is often misdiagnosed as a midlife crisis or as a psychological disorder such as depression, bipolar disorder or schizophrenia.
  23. FTD causes
    • FTD can be caused by many different molecular processes.
    • One of these is Pick’s disease, characterised by the presence of Pick bodies (spherical inclusions) within neurons.
    • Some people with FTD show high levels of tau, the protein filaments that contribute to the neurofibrillary tangles observed in Alzheimer’s disease, but others do not.
    • FTD has a strong genetic component.
  24. Language variants of FTD
    • Some of the language variants of FTD include progressive non-fluent aphasia (PNFA) and semantic dementia.
    • These dementias are characterised by progressive language impairment.
    • The language dysfunction is the most salient feature and deteriorates most rapidly in the course of the disease.
    • PNFA is characterised by agrammaticism in language production and effortful speech.
    • Agrammaticism refers to inappropriate word order, misuse of endings, pronouns and verb tense.

    • Semantic dementia is characterised by impaired word comprehension and object naming.
    • It is a disorder of conceptual knowledge resulting in a loss of understanding of word meaning.
  25. Vascular dementia
    • By definition, vascular dementia is caused by cerebrovascular disease.
    • Most commonly, strokes cause a blood clot, which then impairs circulation and results in the death of neurons.
    • Risk for vascular dementia involves the same risk factors as those for cardiovascular disease in general — for example, high cholesterol, cigarette smoking and elevated blood pressure.
    • Because strokes and cardiovascular disease can strike different regions of the brain, the symptoms of vascular dementia vary.
    • The onset of symptoms is usually more rapid in vascular dementia than in other forms of dementia.
    •  Vascular dementia is the second largest cause of dementia accounting for 15 to 20 percent of cases and co-occurs with Alzheimer’s disorder in 50 percent of cases.
  26. Dementia with Lewy bodies (DLB)
    • In dementia with Lewy bodies (DLB), protein deposits called Lewy bodies form in the brain and cause the cognitive decline.
    • DLB is characterised by fluctuating cognition and alertness, visual hallucinations and spontaneous motor features of parkinsonism.
    • DLB is diagnosed when the cognitive symptoms occur before or concurrently with parkinsonian symptoms.
    • In contrast, Parkinson’s disease dementia is diagnosed when dementia occurs within the context of well-established Parkinson’s disease.
    • People with DLB are often extremely sensitive to the physical side effects of antipsychotic medications.
    • Another distinct symptom of DLB is that people often experience intense dreams accompanied by levels of movement and vocalising that may make them seem as though they are ‘acting out their dreams’.
  27. Dementias caused by disease and injury
    • A number of other medical conditions can produce dementia.
    • Encephalitis, a term for any inflammation of brain tissue, is caused by viruses that enter the brain.
    • Meningitis, an inflammation of the membranes covering the outer brain, is usually caused by a bacterial infection.
    • The organism that produces the venereal disease syphilis can invade the brain and cause dementia.
    • HIV, head traumas, brain tumours, nutritional deficiencies (especially of B-complex vitamins), kidney or liver failure and endocrine problems such as hyperthyroidism can result in dementia.
    • Exposure to toxins (such as lead or mercury) and chronic substance use are both additional causes.
  28. Medications for dementia
    • Despite intensive research in this area, there is no cure for dementia.
    • Because no medications have been shown to help address the cognitive symptoms of FTD, focus on interventions for other dementias.
    • Medications help slow decline, but they do not restore memory function to previous levels. 
    • The most commonly used medications for dementia are the cholinesterase inhibitors (drugs that interfere with the breakdown of acetylcholine).
    • Cholinesterase inhibitors have a slight effect in slowing memory decline compared to placebo.
    • Memantine (Namenda), a drug that affects glutamate receptors involved in memory, has shown small effects in placebo-controlled trials.
    • Medical treatments are commonly used to address psychological symptoms, such as depression and agitation that commonly co-occur with dementia. For example, antidepressants.
    • Treating depressive symptoms can often lead to improvements in cognitive symptoms.
    • Although antipsychotic medications can provide modest relief for aggressive agitation,  they also increase the risk of death among elderly people with dementia.
    • Surprisingly, when researchers developed a medication that removed beta-amyloid plaques, they found that cognitive deficits continued and even worsened after the plaques were removed, bc its already been there for 20 years.
    • Current thinking is that the best hope for future treatments may be treating the biological processes before symptoms (prevention)
  29. Dementia psychological and lifestyle treatments
    • Therapy can help families and patients cope with the diagnosis, discuss symptoms of dementia and provide support. 
    • Interventions to increase exercise also have modest benefits in improving cognitive function.
    • Cognitive training programs that focus on improving memory, reasoning or cognitive processing speed have shown modest benefits for older adults.

    • Behavioural approaches have been shown to help compensate for memory loss and to reduce depression and disruptive behaviour among people with early stages of dementia.
    • For example, external memory aids such as shopping lists, calendars, phone lists and labels can help when placed prominently as visual reminders.
    • Pleasant and engaging activities can be increased as a way of diminishing depression.
  30. Delirium
    • The term implies being off-track or deviating from the usual state.
    • delirium is Typically described as a clouded state of consciousness.

    •  It is of an acute onset, usually hours to days, and is characterised by fluctuating consciousness, attention and cognition.
    • Occurs in the setting of a medical condition or substance intoxication or withdrawal.
    • Hyperactive delirium: may be restless, agitated, ­aggressive and hypervigilant. Psychotic symptoms such as hallucinations and delusions can also occur.
    • Hypoactive delirium: may be withdrawn, quiet, lethargic, drowsy and respond slowly to stimuli. This type of delirium is often missed or misdiagnosed as a depression or dementia.
    • When an individual demonstrates features of both hyper and hypoactive delirium, it is termed a mixed delirium.
  31. Delirium symptoms
    • Typical features include trouble focusing attention and profound disturbances in the sleep/wake cycle.
    • Patients, sometimes rather suddenly, have so much trouble focusing attention that they cannot maintain a coherent stream of thought.
    • They may have trouble answering questions and may not be able to engage in conversation because their mind wanders.
    • As the sleep/wake cycle becomes disturbed, patients become drowsy during the day, yet awake and agitated at night.
    • Vivid dreams and nightmares are common. 
    • Some people with delirium may become so disoriented that they are unclear about what day it is, where they are and even who they are.
    • Memory impairment, especially for recent events, is common.
    • Perceptual disturbances are frequent in delirium. People mistake the unfamiliar for the familiar; for example, they may state that they are at home instead of in a hospital.
    • People with delirium may shift rapidly from one emotion to another.
    • Fever, flushed face, dilated pupils, tremors, rapid heartbeat, elevated blood pressure and incontinence of urine and faeces are common.
    • In the course of a 24-hour period, people with delirium have lucid intervals in which they become alert and coherent. 
    • These daily fluctuations help distinguish delirium from other syndromes, especially Alzheimer’s disease.
  32. Delirium prevalence, risk factors
    • People of any age are subject to delirium, but it is more common among children and older adults. 
    • Among older adults, it is particularly common in nursing homes and hospitals.

    • One risk factor for delirium is a previous diagnosis of dementia, with two-thirds of all cases of delirium in older adults occurring in people diagnosed with dementia.
    • Other risk factors include older age, history of delirium, immobility, multiple comorbidities, chronic disease, sensory impairment, depression, certain medications and sustained sleep deprivation.
    • common risk factors for delirium within the hospital setting, such as sleep deprivation, immobility, dehydration, and visual and hearing impairment. 

    • Unfortunately, delirium is often misdiagnosed.
    • Physicians are particularly unlikely to detect delirium when lethargy is present.
    • Delirium is also often misdiagnosed when a person has dementia.
    • The clinical ‘feel’ of talking with a person with delirium is rather like talking to someone who is acutely intoxicated or in an acute psychotic episode.

    • Untreated, the mortality rate for delirium is high; more than one-third of people with the condition die within a year.
    • Beyond the risk of death, elderly adults who develop delirium in the hospital are at an increased risk of further cognitive decline.
  33. Aetiology of delirium
    • As noted in the diagnostic criteria, delirium is caused by medical conditions.
    • Several causes of delirium have been identified: drug intoxications and drug-withdrawal reactions, metabolic and nutritional imbalances (as in uncontrolled diabetes, thyroid dysfunction, kidney or liver failure, congestive heart failure or malnutrition), dehydration, infections or fevers (like pneumonia or urinary tract infections), neurological disorders (like dementia, head trauma or seizures) and the stress of major surgery.
    • One of the most common triggers of delirium is hip surgery.

    Why are older adults so vulnerable to delirium? Many explanations have been offered: notably, the physical declines of late life, the increased susceptibility to chronic diseases, the many medications prescribed for older people and the greater sensitivity to drugs.
  34. Treatment of delirium
    • Development of a delirium frequently depends on a combination of predisposing (e.g., dementia) and participating risk factors (e.g., medications, infections).
    • Complete recovery from delirium is possible if the underlying cause is treated promptly and effectively.
    • Preventative strategies are recommended to reduce the incidence of delirium.
    • It may help patients to stay oriented if clocks are placed within their field of vision, shades are open during the day and lights are turned off at night, and disruptions to sleep are minimised.
    • This intervention addressed common risk factors for delirium within the hospital setting, such as sleep deprivation, immobility, dehydration, and visual and hearing impairment.

    • If an individual is identified as having a delirium; non-pharmacological strategies are the first line of treatment. This includes normalising sleep patterns, avoiding restraints, reorientation and reassurance strategies, relaxation techniques, preventing complications, ensuring adequate hydration, providing clear instructions, minimising hearing or visual impairments (e.g., hearing aids/glasses), limiting room and staff changes, and ensuring pain relief is adequate, to name a few. 
    • Pharmacological treatments for delirium (e.g., antipsychotic medications) should only be considered if the individual’s behaviour or emotional disturbance is so severe that it threatens the person’s or others safety, will interfere with medical care and when non-pharmacological approaches failed.
Author
kirstenp
ID
348710
Card Set
Wk 8: Late life disorders
Description
Wk 8: Late life disorders 11.1 differentiate common misconceptions from established findings about age-related changes and discuss issues involved in conducting research on ageing 11.2 describe the prevalence of psychological disorders in the elderly and issues involved in estimating the prevalence 11.3 explain the symptoms, aetiology and treatment of cognitive disorders in the elderly.
Updated