Mark P. Tyrrell
Lynn Pebole Shell
EXPECTED LEARNING OUTCOMES
After completing this chapter, the student will be able to:
1. Define neurocognitive disorders
2. Identify the major neurocognitive disorders
3. Describe the historical perspectives and epidemiology of neurocognitive disorders
4. Discuss current scientific theories related to the etiology and pathophysiology of neurocognitive disorders, specifically dementia of the Alzheimer’s type (DAT)
5. Identify the diagnostic criteria for neurocognitive disorders
6. Explain the pharmacological and non-pharmacological treatment options for persons with neurocognitive disorders
7. Describe common assessment strategies for individuals with neurocognitive disorders
8. Apply the nursing process from an interpersonal perspective to the care of patients with neurocognitive disorders, demonstrating an appreciation of the challenges that face family caregivers in caring for someone with dementia
Enriched model of dementia
Malignant social psychology
Positive person work
Progressively lowered stress threshold (PLST)
NEUROCOGNITIVE DISORDERS refer to a group of disorders in which a person experiences a disruption in areas of mental function. These areas include orientation, attention, logic, awareness, memory, intellect, language, abstract thinking, and reasoning. Two major neurocognitive disorders identified by the American Psychiatric Association (APA) are DELIRIUM and DEMENTIA. Delirium refers to an acute disruption in consciousness and cognitive function. Dementia refers to a group of conditions that involve multiple deficits in memory and cognition. With the exception of delirium, which tends to be sudden in onset and short-lived, neurodegenerative processes characterize many neurocognitive disorders. Those resulting from dementia are insidious, and usually present for a number of years by the time symptoms become apparent. Moreover, symptoms may be so insidious that they are ignored or misinterpreted by the individual, or by family members, or by health care professionals as being insignificant or representative of normal aging. Symptoms are typically present between 1 and 2 years before family members bring the person for medical attention (Wilkinson et al., 2005). The average length of time from onset of symptoms until diagnosis is 20 months; however, it can be up to 3 years before a firm diagnosis is made (Speechly, Bridges-Webb, & Passmore, 2008; Wilkinson et al., 2005). This often results in delay in reaching diagnosis. Subsequently, there is a lost opportunity to initiate an early treatment plan, one that might afford sufferers additional months of neurocognitive competence, preserve their quality of life longer, and afford them the opportunity to put their financial and personal affairs in order before significant neurocognitive decline takes hold (Giaquinto & Parnetti, 2006).
This chapter focuses on dementia and delirium because these are the two most common types of neurocognitive disorders found in clinical practice. Although both result in cognitive impairment and have profound implications for patients and their caregivers, the respective etiologies, treatments, and outcomes are distinctly different. Although delirium is commonplace, particularly among the hospitalized elderly, it usually arises from an underlying medical condition. Furthermore, in the majority of cases, the cause is readily identified and treatable, thus enabling the person to return to the community. For these reasons, delirium is addressed only briefly in this chapter.
This chapter covers the historical aspects and epidemiology of neurocognitive disorders and includes a detailed description of the major neurocognitive disorders as described according to discrete symptoms in the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; APA, 2013). Relevant scientific theories related to the etiology and pathophysiology of dementia are described along with common pharmacotherapy and nonpharmacotherapy strategies used in the treatment of dementia, specifically dementia of the Alzheimer’s type (DAT). Application of the nursing process from an interpersonal perspective is discussed, including a plan of care for a patient with dementia.
Delirium occurs suddenly and is the result of an underlying medical condition. Dementia occurs gradually and involves multiple problems of memory and cognition.
Cognitive impairment has been documented as a health concern for many centuries. Indeed, there are apparent references to such conditions in the literature of ancient Greece and Rome. For example, Juvenal (AD 60–130) wrote:
But worse than all bodily failing is the weakening mind which cannot remember names of slaves nor the face of a friend he dined with last evening, cannot remember the names of offspring begotten and reared. (Juvenal, cited in Gilliard, 1993)
Up until the 20th century, older adults with organic brain disease were generally diagnosed as having SENILE DEMENTIA. This was a term that categorized memory loss as part of normal aging. In the early part of the 20th century, neuropathologists began to recognize that a number of conditions could lead to senile dementia including Alzheimer’s disease (now referred to as DAT), arteriosclerotic brain disease, and neurosyphilis. In 1903, a young German physician, Alois Alzheimer, established a laboratory for brain research at the Munich Medical School. Three years later, Alzheimer presented a case study of a 55-year-old woman in which he described an unusual disease of the cerebral cortex characterized by memory loss, disorientation, and hallucinations. The woman in question died shortly afterward and Alzheimer carried out a postmortem examination that showed various anomalies in her brain, including a thinning of the cerebral cortex, senile plaques, and neurofibrillary tangles. The disease that Alzheimer first described more than a century ago bears his name to this day. In 1968, the link between the neuropathological features of DAT and the cognitive disorder of DAT were established by Blessed, Tomlinson, and Roth (1968). In the following decade, the biochemistry of DAT became more clearly understood, initially with the discovery of the cholinergic deficit, and later with the identification of beta-amyloid peptide.
Subsequent work throughout the 20th century revealed that a number of different types of dementia exist and that a myriad of other conditions could result in neurocognitive impairment such as that seen in senile dementia. The symptoms presented may be similar; however, the neurocognitive disorders differ in their etiology.
The increase in life expectancy in industrialized countries over the past few decades has resulted in a greater incidence of neurocognitive disorders, particularly those resulting from neurodegenerative conditions such as dementia. One reason for the increased incidence is that dementias are age related; hence, the longer one lives, the greater the chance of being diagnosed with a dementia. Indeed, dementias account for the majority of neurocognitive disorders seen in mental health care, and DAT is by far the most common dementia in the Western world, accounting for between 55% and 65% of all cases.
Current statistics reveal that delirium is a common neurocognitive disorder in debilitated and elderly patients, including those with dementia (Sousa-Ferreira, Ferreira, Ferreira, Amaral, & Cabral, 2015). It is estimated that about 50% of people with delirium have an overt psychosis (Boyle & Hands, 2009).
In both developed and developing countries, the number of people older than 65 years of age is rising steeply, and as dementia is age related this will inevitably lead to a rise in the number of people who have dementia. Indeed, recent estimates suggest that this number will double every 20 years and that by 2040, this number will amount to more than 115.4 million people globally who have some form of dementia (Prince et al., 2013).
DAT accounts for between 60% and 80% of all dementias and is found in all human populations worldwide (Alzheimer’s Association, 2014). In the United States, it is estimated that one in nine people aged 65 years and older has DAT. By age 85 years, approximately one third of individuals have the disease. In 2050, the total number of individuals diagnosed with DAT in the United States is projected to be 13.8 million (Alzheimer’s Association, 2014). More women than men are diagnosed with the disease, probably due to the greater longevity of females. Although DAT is primarily a disease of old age, occasionally people in their 40s or 50s are diagnosed with the condition.
Delirium is the most commonly occurring neurocognitive disorder. DAT accounts for more than half of all dementias globally.
Dementia of the vascular type affects men more often than women. Because the symptoms are similar to Alzheimer’s, definitive diagnosis can be difficult. To complicate matters, dementia of the vascular type and DAT can coexist in the same person.
Neurocognitive disorders include delirium and dementia. Although several types of dementia have been identified, four major types are presented here: DAT, dementia of the vascular type, dementia with Lewy bodies, and frontotemporal dementia.
Although each type of dementia has its own distinctive set of clinical features, a number of common features exist. It is not unusual for some individuals to have more than one dementia at the same time; for example, someone may have both DAT and dementia of the vascular type and will present with some of the features of both conditions. In this regard, Smith and Buckwalter (2005) describe four groups of symptoms that are commonly seen in dementia. These are summarized in Table 16-1.
Delirium is a medical condition characterized by fluctuating levels of disorientation and clouded consciousness, accompanied by cognitive impairment, altered mood states, altered perception, altered self-awareness, and an inability to focus and maintain attention (APA, 2013). The person is often drowsy during the day; however, at night the person experiences sleeplessness, agitation, and restlessness. It is an acute state with a rapid onset. Some of the many causes of delirium are outlined in Box 16-1.
In extreme cases, delirium represents a medical emergency and carries a high morbidity and increased mortality. In some cases, it may result in a permanent cognitive impairment (Hsieh, Madahar, Hope, Zapata, & Gong, 2015). Therefore, a sudden onset of delirium in an otherwise healthy individual may indicate an underlying life-threatening condition.
Dementia is an umbrella term used to describe various conditions that cause brain cells to die, leading to a progressive deterioration in memory and the ability to carry out everyday activities such as washing, dressing, eating, and communicating. Dementia may also affect a person’s mood and personality.
Many diseases can result in dementia. Four of these account for almost 90% of cases, with the most common being DAT, accounting for more than half of all the cases of dementia encountered in clinical practice.
Loss of interest
Decreased control over one’s behavior
Apparent selfishness, with lack of ability to consider the needs of others
Memory loss of recent events
Confabulation to make up what is forgotten
Difficulty learning new things
Deterioration of written and verbal language skills
Loss of the concept of time
Decreased ability to carry out skills and activities of daily living
Inability to put steps in correct sequence to get job done despite knowing what he or she wants to do
Altered stress threshold
Decreased ability to tolerate stress
Prone to anger
Irritation or becoming overwhelmed with situations that were not a problem previously; becoming more problematic and evident as disease progresses
BOX 16-1: CAUSES OF DELIRIUM
• Sensory impairment
• Metabolic disorders
• Emotional distress
• Social isolation
• Electrolyte imbalance
• Sleep deprivation
• Neurological conditions
• Severe medical illness
• Diabetes mellitus
• Myocardial infarction
• Thyroid crisis
• Liver or renal failure
• Anesthetic exposure
• Drugs and medications
Dementia of the Alzheimer’s Type
DAT is a progressive neurological condition characterized by the buildup of proteins in the brain called “plaques” and “tangles.” These proteins gradually damage and eventually destroy the nerve cells. Subsequently, it becomes more and more difficult to remember and to perform higher neurocognitive functions such as reasoning and use of language. The loss of memory of recent events may be one of the first difficulties noticed. The person may also become disorientated, be at a loss for a word when speaking, and have increasing difficulty with simple daily tasks such as using the telephone, preparing meals, or managing money.
Although the early signs and symptoms of DAT may vary from person to person, increasing memory loss over time is often the first noticeable symptom. Other common signs include getting stuck for words or having language difficulties; forgetting things (names, dates, places, and people); loss of interest in things of interest previously; difficulty in solving problems or in performing everyday tasks; misplacing things; poor or decreased judgment; changes in mood, behavior, and overall personality; and becoming easily disorientated, even in familiar surroundings.
Although signs and symptoms may vary in patients with DAT, often progressive memory loss is noticed first.
Dementia With Lewy Bodies
Dementia with Lewy bodies, which accounts for approximately 20% of all causes of dementia, is characterized by: progressive decline in neurocognitive functioning, drowsiness, lethargy, lengthy periods of time spent staring into space, disorganized speech, visual hallucinations, delusions, and motor symptoms including muscle rigidity and the loss of spontaneous movement. These latter features may result in falls. Depression is also common. This type of dementia results from the buildup of Lewy bodies (accumulated bits of alpha-synuclein protein) inside the nuclei of neurons in areas of the brain that control particular aspects of memory and movement. Although the reasons for this buildup are unknown, what is known is that alpha-synuclein accumulation is also linked to Parkinson’s disease (another movement disorder). People with dementia with Lewy bodies usually have no known family history of the disease. Average survival after the time of diagnosis is about 8 years, with progressively increasing disability (National Institute of Neurological Disorders and Stroke [NINDS], 2010a).
Dementia of the Vascular Type
Dementia of the vascular type, also called vascular dementia, is caused by multiple mini strokes that lead to a disruption in blood flow to the brain. This disruption results in damaged brain tissue and subsequent loss of function. Some of these strokes may occur without noticeable clinical symptoms and hence are often termed as “silent strokes.” The onset of dementia of the vascular type is insidious. Thus, the person experiencing these mini strokes is unlikely to know that anything is wrong initially. With time, and as more areas of the brain are damaged and more small blood vessels are blocked, the symptoms become apparent. In some instances, however, the onset of symptoms may be sudden and may progress in a stepwise fashion, unlike the downward linear progression of DAT. Common presenting symptoms include: confusion, short-term memory deficits; wandering, getting lost in familiar places; rapid, shuffling gait; loss of bladder or bowel control; laughing or crying inappropriately; difficulty following instructions; and problems counting money and making monetary transactions. Unfortunately, the prognosis for those who have dementia of the vascular type is generally poor, thus emphasizing the importance of early life prevention. Although some people may appear to improve for short periods, resulting in episodes of lucidity, this is often followed by further decline when the individual has another stroke, thus the stepwise nature of the disease progression (NINDS, 2010b). Typically, individuals die from one of these strokes or from an associated heart disease. Thus, life expectancy with this type of dementia is typically shorter than for other forms of dementia.
Frontotemporal dementia is characterized by changes in the frontal and temporal lobes of the brain that control reasoning, personality, social behavior, and speech. This type of dementia was originally known as Pick’s disease because of the intracytoplasmic inclusions (Pick bodies) that are found in the neurons of those with the disease. The term Pick’s disease is now more commonly used in discussing the specific pathology involved in the clinical syndrome now known as frontotemporal lobar degeneration. Typically, a person with this type of dementia presents with two groups of symptoms: behavioral changes and problems with language. The behaviors involved are often antisocial in nature, including loss of social tact, inappropriate sexual behavior, lack of empathy, or lack of insight. Language problems include difficulty in understanding speech or articulating what one wants to say. Frontotemporal dementia has a strong genetic component and runs in families (NINDS, 2010c). Unlike other major dementias, memory remains intact.
Frontotemporal dementia is manifested by changes in behavior and language.
The majority of research addressing delirium and dementia focuses on the neurobiological influences for the disease. As stated earlier, delirium almost always results from a physiological disturbance that is a direct result of an underlying general medical condition. The neurobiological influences for the development of DAT are presented here.
The progressive brain dysfunction that characterizes DAT occurs in a staged biological sequence beginning with neuronal injury, leading to synaptic failure, and, in time, neuronal death (Nelson et al., 2012; Silvestrelli, Lanari, Parnetti, Tomassoni, & Amenta, 2006). Initially, NEUROFIBRILLARY TANGLES occur at various parts of the cerebral cortex. These tangles are thick clots of protein that reside inside damaged neurons and are made from a protein called tau (τ). They spread in a sequential and generally predictable manner to other parts of the cortex.
The neurofibrils become entangled for as yet unknown reasons. In general, the denser these filaments are, the more severe the dementia is (Nelson et al., 2012).
The neurofibrillary tangle process typically begins in the limbic system, an area of the brain concerned with emotion and memory storage. The hippocampus, one part of the limbic system, is primarily involved in the storage of recent memories, which may explain why recent memory loss is a common feature of this type of dementia. Moreover, damage to the locus ceruleus and associated parts of the limbic system may help explain why depression is a common feature of the disease. Deterioration of long-term memory tends to be delayed, probably because these memories are stored in a number of areas of the brain (Garand, Buckwalter, & Hall, 2000; Serrano-Pozo, Frosch, Masliah, & Hyman, 2011).
Later in the disease another major pathological feature appears. Cerebral beta-amyloid (Aβ) plaques form on the outside of dead and damaged neurons, initially in poorly myelinated areas of the cortex. The plaques consist of fragments of dying cells mixed with Aβ protein. It appears that Aβ plaque enters the mitochondria of affected neurons wherein it interacts with a number of enzymes resulting in cell death. Some evidence suggests that inflammation around these Aβ plaques spreads to other neurons in the vicinity, leading to their destruction (Cummings, 2004; Nelson et al., 2012). Aβ protein is made from amyloid precursor protein (APP), which is coded on chromosome 21. Individuals with Down’s syndrome have an extra copy of this chromosome, thus increasing their risk of developing dementia. Indeed, almost three quarters of people with this condition who are older than 60 years of age have dementia.
A second protein, apolipoprotein E (Apo-E), is also implicated in the pathology of DAT. Apo-E plays a role in the transportation of cholesterol in the brain. Among the effects of Apo-E is the deposition of cerebral amyloid in the brain. Certain subtypes of Apo-E, specifically Apo-E3 and Apo-E4, have been found to increase the risk of dementia. However, Apo-E2 has been shown to decrease the risk.
A further feature of the etiology of DAT involves a deficiency of the neurotransmitter, acetylcholine (ACh), first discovered in the 1970s. ACh is manufactured in the brain from choline and acetyl coenzyme A in the presence of the enzyme choline-acetyl transferase (ChAT). Another enzyme, cholinesterase (ChE), “mops up” excess ACh at the synapse after neurotransmission has occurred. Studies have shown a deficiency in both ACh and ChAT and an excess of ChE in people with DAT. This has become known as the “cholinergic hypothesis.” Essentially, the cholinergic hypothesis suggests that “cognitive, functional, and behavioral dysfunction associated with DAT may be caused by an inability to transmit nerve cell impulses across cholinergic synapses” (Silvestrelli et al., 2006, p. 150). ACh increases attention span and facilitates learning. Furthermore, depletion of ACh has also been shown to result in memory impairment.
Although other neurotransmitters are also implicated in the etiology of Alzheimer’s, the cholinergic hypothesis has been most prominent in this area of research. Other neurotransmitters have been studied. For example, serotonin (5-HT) is also decreased in patients with DAT, leading to anxiety, agitation, and depression. Low levels of dopamine have also been observed, which may result in problems with mobility, psychosis, and apathy (Garand et al., 2000; Strac, Muck-Seler, & Pivac, 2015). In time, the destructive processes involved in this type of dementia spread to all parts of the brain, resulting in a wide variety of symptoms. In later stages of the disease, gross anatomical changes such as brain atrophy, enlarged ventricles, and widened sulky become apparent using neuroimaging techniques.
Pathological changes involved with DAT include neurofibrillary tangles, Aβ plaques, and Apo-E. ACh deficiency, referred to as the cholinergic hypothesis, is also implicated in the etiology of DAT. Other neurotransmitters, such as a deficiency of serotonin and dopamine, also may be involved.
Various treatment options are available for patients with neurocognitive disorders, specifically dementia. These include but are not limited to: psychopharmacology, reality orientation, validation therapy, reminiscence therapy, person-centered care, the enriched model of dementia, and the progressively lowered stress threshold (PLST) model. The focus of the discussion here is on DAT. Table 16-2 summarizes the major treatment options for the other types of dementia.
Treatment for delirium differs somewhat from that for dementia. With delirium, the main approach to treatment is the rapid identification and elimination or management of the cause, as well as symptomatic treatment until the person’s condition stabilizes. In cases where the person’s behavior is very disturbed, a low-dose antipsychotic or a benzodiazepine is useful in the short-term management of psychosis associated with delirium (Boyle & Hands, 2009). In addition, management also involves a low-stimulus environment, adequate hydration, normalization of the sleep-wake cycle, and the use of reality orientation.
Currently, there is no known cure for DAT or other related dementias. However, some drugs have been developed that have been shown to slow the progression of the disease.
TYPE OF DEMENTIA
Dementia of Lewy bodies
Management of psychiatric, behavioral, and motor symptoms
Acetylcholinesterase inhibitors (donepezil and rivastigmine) for cognitive symptoms; also helpful for psychiatric and motor symptoms
Antipsychotic agents for hallucinatory symptoms are avoided due to risk of neuroleptic sensitivity worsening motor symptoms
Dementia of the vascular type
Alleviation of symptoms
Prevention of future mini strokes through dietary and lifestyle measures:
• Smoking cessation
• Hypertension control
• Cholesterol lowering
• Diabetes management
• Regular exercise
• Maintenance of healthy body weight (Nazarko, 2006)
Behavior modification (some success)
Antidepressant agents to manage some behavioral symptoms
DAT, dementia of the Alzheimer’s type.
Most of the drugs that have been approved for clinical practice focus on the cholinergic hypothesis. They attempt to boost the remaining activity at cholinergic synapses. Although a number of agents have the ability to do this, only cholinesterase inhibitors are currently licensed for use. These drugs delay the degradation of ACh at the synapse, theoretically prolonging its effect at this site and thus augmenting neurotransmission. Three such drugs are currently in use: donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl). These drugs, listed in Drug Summary 16-1, are used mainly in patients with mild to moderate DAT. Donepezil has also been approved for use in moderate to severe DAT. Although these drugs may enhance neurocognitive functioning in some patients, they do not alter the overall course of the disease.
A fourth drug, memantine (Namenda), is an N-methyl D-aspartate (NMDA) antagonist. NMDA receptor antagonists are a class of drugs that work to inhibit the action of the NMDA receptor. This drug has been developed for the treatment of people with moderate to severe dementia. It acts with a novel mechanism of action that targets glutamate, the principal excitatory neurotransmitter in the brain. Excessive activity of this neurotransmitter (excitotoxicity) has been shown to result in neuronal damage, neuronal cell death, and cognitive dysfunction. The drug acts to reduce this glutamatergic excitotoxicity. Recent research also suggests that memantine diminishes the toxic effects of Aβ and that it may also inhibit its production (Annweiler, Brugg, Peyrin, Bartha, & Beauchet, 2014; Silvestrelli et al., 2006).
Given the different mechanism of action of memantine and cholinesterase inhibitors, trials are underway to determine the effect of coadministration of memantine and cholinesterase inhibitors. Early findings suggest greater improvement in behavior, cognition, and activities of daily living (ADLs) in individuals receiving memantine and a cholinesterase inhibitor than those receiving either one alone (Matsunaga, Kishi, & Iwata, 2015).
Cholinesterase inhibitors are used to treat DAT. These agents do not cure the disease; rather, they are believed to help slow the progression of cognitive decline.
Free radicals are known to play a role in the aging process and, in particular, have been implicated in the etiology of some forms of dementia, including DAT. Antioxidants act as free radical scavengers and, among other things, appear to protect neurons from the damaging effects of Aβ. Vitamin C (ascorbic acid) and melatonin are powerful natural antioxidants.
Hormone Replacement Therapy
The incidence of DAT is particularly low in postmenopausal women who take estrogen. Therefore, some authorities recommend estrogen therapy as a protective mechanism against this type of dementia.
DRUG SUMMARY 16-1:
DRUGS USED TO TREAT DEMENTIAS
Nonsteroidal Anti-Inflammatory Drugs
Epidemiological evidence suggests that people who are on long-term nonsteroidal anti-inflammatory drug (NSAID) treatment, such as ibuprofen and naproxen sodium, seem to be protected in some way from developing DAT. It may be that NSAIDs, particularly those that target cyclooxygenase-1, inhibit inflammation around Aβ plaques, thus preventing this inflammatory process from affecting other neurons in the vicinity (Kumar, Singh, & Ekavali, 2015).
Cholesterol has been implicated in the etiology of both DAT and vascular dementia for many years now. The understanding of the role of Apo-E further reinforces this belief. The Apo-E gene provides instructions for making a protein called apolipoprotein E. This protein combines with fats (lipids) in the body to form molecules called lipoproteins. As a result, drugs such as statins and other cholesterol-lowering agents have become a major component of therapy as they have been shown to decrease the risk of developing DAT.
In addition to the above, the benefits of omega-3 fish oil, lecithin for those taking niacin, selegiline, and dehydroepiandrosterone (DHEA), to name but a few, are now established and are recommended by some authorities as agents for the prevention and treatment of dementia. Some interesting research is underway on the potential benefits of anti-amyloid pharmacotherapies, immunotherapy, substances that target mitochondrial dysfunction, and anti-apoptosis compounds.
For millennia, traditional herbal medicine has offered many plant-based remedies to treat age-related conditions including dementias. Some of these have been used with varying levels of success. Although the pharmacology underpinning many of these compounds has yet to be established, some compounds have been researched and their pharmacology has been validated. However, little evidence is available at the present time about their clinical application and utility. Nevertheless, a few exceptions exist, including ginkgo biloba extracts, some species of the herb sage (salvia), and the plant extracts galantamine and huperzine A. Many of these extracts inhibit cholinesterase and are antioxidant in nature. Ginko biloba enhances cerebral circulation.
REALITY ORIENTATION is a technique used to improve the quality of life of confused older adults by assisting them to gain a more accurate understanding of their surroundings. In this approach, people who are confused are regularly presented with information about time, place, and person in an effort to orientate them to the here and now. It is based on the assumption that people who are disorientated can return to the present if given sufficient information. The technique often entails the use of signs on bathroom and bedroom doors, for example, or the use of a reality orientation board displaying large-faced clocks and notices indicating the day, date, year, and so on. In addition, staff using this approach consistently orient the confused individual to his or her surroundings. However, evidence supporting the benefits of this therapy for people with dementia is mixed. Some suggest that it contradicts the person’s “reality” and thus increases frustration, anxiety, and anger (Haberstroh, Hampel, & Pantel, 2010). Another view is that reality orientation works well with people who are temporarily confused, such as those who are suffering from delirium or concussion, or who are experiencing disorientation as a result of relocation. However, it is of limited utility in dementia except perhaps in the early stages of the disease (Smith & Buckwalter, 2005).
VALIDATION THERAPY is one of the most popular psychosocial interventions for people with dementia. It is based on a number of principles, including the affirmation of the person’s feelings and the adoption of a nonjudgmental approach on the part of the caregiver. It was developed by Feil in the 1960s (Feil, 1967) and four stages of cognitive impairment are featured in her work: malorientation, time confusion, repetitive motion, and vegetation (Feil, 1992). Feil proposes that the disorientation observed in many people with dementia is a defense mechanism that may be a solution to past conflicts in their lives. Essentially, according to the theory, the person with dementia retreats into the past to resolve painful emotions. Therefore, validating the person’s reality can assist him or her in resolving some of these past conflicts. Thus, the emphasis is on going with the person to his or her reality (Feil, 1992). This would mean allowing the person to express emotions such as anger or sadness and then validating that emotion.
Traditionally, many lay and professional caregivers have been taught to use principles of reality orientation. However, some, such as Woods (2014), suggest that validation therapy principles are more useful. The person with dementia has a deteriorating short-term memory. Thus, it is difficult, if not impossible, for that person to be in the here and now. Recent memories are not as firmly established in the brain. Once the dementia has started to progress, it becomes increasingly difficult for the person to remember what he or she has just been told or what has happened in the immediate past because the person no longer has the ability to retain this information. Long-term memories, on the other hand, appear to be stored in a number of places in the brain and are likely to survive longer after the dementia has been established. Hence, the person with dementia is often able to talk at length and in great detail about events that occurred in the distant past. If reality orientation principles are used, the person with dementia is likely to fail or be unsuccessful because the brain no longer has the capacity to allow him or her to remember enough about the present. It cannot adequately store memories of the present and recent events. This may lead to anxiety and frustration and, consequently may result in deterioration of behavior. On the other hand, because people with dementia generally have a more intact long-term memory, they can remain competent and be successful if caregivers go with them to “their reality” through the use of reminiscence therapies, for example. Although the experience can be “validating,” reminiscence therapy is separate from validation therapy.
Validation therapy focuses on the premise that past conflicts can be resolved by validating the person’s reality.
REMINISCENCE THERAPY involves the discussion of past activities, events, and experiences with another person or group of people. Aids such as videos, pictures, archives, and life story books often are used (Subramaniam & Woods, 2012). It can be formal or informal, using either an individual or group approach. Formal reminiscence is a structured activity. The caregiver schedules a reminiscence session in which the patient is prompted to recollect past events and memories. Informal reminiscence, on the other hand, is opportunistic. The caregiver engages the patient in discussion of past events or experiences, for example, after watching an old film or when the caregiver discovers the patient is perusing old family photographs (Hong & Song, 2009). A systematic review of studies on reminiscence therapy (Subramaniam & Woods, 2012) revealed an association among individual reminiscence work and psychosocial benefits, cognition, and well-being.
Reminiscence therapy can be formal, using a structured activity, or informal, using a specific event to stimulate discussion of past events.
The term person-centered care is used in many different contexts in health care and can mean different things to different people. Some people equate it to the individualization of care, whereas others see it as a philosophical approach with a particular value base. Still others see it as a set of techniques to assist those who work with people with dementia (Brooker & Surr, 2005). Regardless of the definition, person-centered care is seen as an approach to delivering high-quality care. However, it can only do so if the recipient of care is placed at the heart of the care agenda (Edvardsson, Winblad, & Sandman, 2008). The Bradford Dementia Group, established in 1992, is a multidisciplinary, multiprofessional group committed to making a difference to policy and practice in dementia care, through excellence in research, education, and training. They offer a comprehensive definition of person-centered care as it relates to caring for people with dementia. This definition emphasizes “respecting and valuing the individual as a full member of society” and recognizing that they have “all the rights of citizenship.” It focuses on rooting out discriminatory practices against people with dementia and their caregivers and on individualizing a plan of care that “is in tune with people’s changing needs giving increasing compensation and reassurance as cognitive disability increases.” The need to try to understand the perspective of the person with dementia and the importance of providing a supportive social psychology (explained in the following) are also enshrined in the definition, as these are key to ensuring that the person can “live a life where they can experience relative well-being” (Brooker & Surr, 2005, p. 13).
A number of models exist that help one understand key aspects of dementia from a psychodynamic perspective and help to ensure that the care of the person with dementia is person centered. In particular, these models help explain many of the behaviors in dementia, emphasizing that these behaviors are not just a result of the person’s neurological impairment. Two such models are Kitwood’s Enriched Model of Dementia and the PLST Model.
Kitwood’s Enriched Model of Dementia
Kitwood’s ENRICHED MODEL OF DEMENTIA acknowledges that the primary cause of problems for the person with dementia stems from the person’s neurological impairment. It also argues that other factors play a role in determining how the person with dementia lives with his or her illness. These factors include the person’s level of health and physical fitness, life history, personality, and social psychology. The model suggests that it is the complex interplay among these factors plus the person’s degree of neurological impairment that determines how dementia affects the way the person lives.
The inspiration for the model arose from Kitwood’s observation that some people with dementia who had considerable neurological impairment seemed to function better and have a better quality of life than others who had a lesser degree of neurological impairment. Kitwood hypothesized that the social and psychological environment in which the person with dementia lives could be supportive or damaging to his or her well-being. He used the term “MALIGNANT SOCIAL PSYCHOLOGY” to describe the damaging effects of the negative attitudes and prejudices of other people on someone’s personhood. He uses an opposite term, “POSITIVE PERSON WORK,” to describe how one could uphold the personhood of an individual with dementia. These are outlined in Table 16-3. The goal when working with this model is to maximize interventions that incorporate aspects of positive person work and minimize those that lead to malignant social psychology.