NEUROLOGIC COMPONENTS	CHANGES
Central Nervous System
Neurons	Shrinkage in neuron size and gradual decrease in neuron numbers Structural changes in dendrites Deposit of lipofuscin granules, neuritic plaque, and neurofibrillary bodies within cytoplasm and neurons Loss of myelin and decreased conduction in some nerves, especially peripheral nerves
Neurotransmitters	Changes in precursors necessary for neurotransmitter synthesis Change in receptor sites Alteration in enzymes that synthesize and degrade neurotransmitters Significant decreases in neurotransmitters, including ACh, glutamate, serotonin, dopamine, and gamma-aminobutyric acid
Peripheral Nervous System
Motor	Muscular atrophy—decrease in muscle bulk Decrease in electrical conduction system
Sensory	Decrease in electrical conduction Atrophy of taste buds Alteration in olfactory nerve fibers Alteration in nerve cells of vestibular system of inner ear, cerebellum, and proprioception
Reflexes	Altered electrical conduction of the nerve due to myelin loss Altered reflex responses (ankle, superficial reflexes)
Reticular formation	Physiologic changes in the RAS results in decrease in stages 3 and 4 of the sleep cycle
Autonomic Nervous System
Basal ganglia	Slowing of autonomic nervous system response as a result of structural changes in basal ganglia

Neuroglia and Schwann Cells

Neuroglia and Schwann cells are the supportive cells of the CNS, making up approximately half of the brain and spinal cord tissue. Their role is to protect the neurons. As individuals age, the number of these protective cells increases. Each of these cells serves a different function.

Neuroglia cells vary in size and shape and are divided into two main classes: the microglia and macroglia (Fig. 29–3). The microglias are phagocytic scavenger cells related to macrophages that respond to infection or trauma to the CNS. The macroglia cells include astrocytes, oligodendrocytes, and ependymal cells. Astrocytes (astroglia) are star-shaped cells that provide the physical support for the neurons. They also regulate the chemical environment and nourish the neurons. These cells respond to brain trauma by forming scar tissue.

FIG 29–3 Types of neuroglial cells. (From Thompson JM, McFarlane G, Hirsch J, & Tucker S: *Mosby’s clinical nursing*, ed 4, St Louis, 1997, Mosby.)

Oligodendrocytes and Schwann cells produce myelin within the CNS and peripheral neurons, respectively. Ependymal cells form the lining of the ventricles, choroid plexuses, and central canal of the spinal cord. These cells help in the regulation of the cerebrospinal fluid (CSF) and blood–brain barrier.

Balance and Motor Function

Reticular Formation and Sleep Patterns

The RF is a set of neurons that extends from the upper level of the spinal cord through the brainstem up to the cerebral cortex. The RF contains both motor and sensory tracts that are closely connected with the thalamus, basal ganglia, cerebellum, and cerebral cortex. This group of neural fibers has both excitatory and inhibitory capability. The RF contains a physiologic element, the RAS, which regulates sensory impulses that are transmitted to the cerebral cortex. The lower portion of the RAS in the brainstem assists in the regulation of the wake–sleep cycle and consciousness. Sleep disorders are common in aging individuals. Risk factors for sleep disturbances include physical illness, medications, changes in social patterns (e.g., retirement or death of a spouse or loved one), and changes in circadian rhythm. Some sleep disturbances may also be part of the normal aging process resulting from neural changes in the RAS.

Normal sleep is organized into different stages that cycle throughout the night. The sleep stages are classified into the following categories (Brannon, 2008):

• Rapid eye movement (REM) sleep. This is the stage of sleep during which muscle tone decreases significantly. In advanced aging REM sleep is maintained without much decline.

• Non-REM sleep. This is subdivided into four stages. Stages 1 and 2 constitute light sleep, and stages 3 and 4 are deep sleep or slow-wave sleep. In aging there is an increase in the duration of stage 1 sleep and an increase in the number of shifts into stage 1 sleep. Stages 3 and 4 decrease significantly with age. Among the oldest old people (older than 90 years), stages 3 and 4 may disappear completely. Some older women have normal or even increased stage 3 sleep, whereas men have normal or reduced stage 3 sleep.

As individuals age, they spend more time in bed to get the same amount of sleep they obtained when younger; however, the total sleep time is only slightly decreased, with an increase in nocturnal awakenings and daytime napping. Hence older persons often report having earlier bedtimes and an increased sleep latency (time to fall asleep).

Excessive daytime somnolence is not part of normal aging. Somnolence indicates the presence of a pathologic condition. In the aging process there is a decrease in hypothalamic function; as a result, older clients have been observed to be more easily aroused from sleep by auditory stimuli, which suggests increased sensitivity to environmental stimuli and altered neuroendocrine function (Brannon, 2008).

Sensorimotor Function

The nervous system depends on specialized sensory receptors to gather information about the internal and external environment. These receptors include those needed for vision, hearing, smell, touch, equilibrium, and pain sensation. Gradual changes occur in these sensory receptor sites as the aging process take place.

Vision changes that occur with aging are significant. The lens of the eye thickens, becoming yellow, cloudy, and less elastic. The thickening of the lens reduces the amount of light passing through the lens. As the lens becomes less elastic, it loses its ability to focus on close objects. The change in elasticity also narrows the visual field and diminishes depth perception. The yellowing of the lens and changes in size and thickening of the cornea make it difficult to see at night. In aging the fluid of the eye also becomes cloudy, reducing light sensitivity. These changes in the eyes lead to a gradual decrease in color perception, potentially affecting the ability of older individuals to distinguish between blues, greens, and violets.

The ear consists of the outer ear, middle ear, and inner ear. Presbycusis is the hearing loss associated with the aging process. With presbycusis older persons are unable to hear high frequencies and are unable to clearly hear consonant sounds such as f, g, s, z, t, sh, and ch. Other age-related auditory changes involve the collapse and narrowing of the auditory canal and thickening of earwax, which increase hearing difficulty.

With aging, there is a decrease in the number of taste and smell receptors and slower nerve transmissions, although these losses are highly variable. The loss of taste and smell receptors means that food is not as appetizing to the older adult. Aging adults are also less likely to detect the bad taste or smell of spoiled food. Their reduced ability to smell also may make them unable to rapidly detect smoke, gas leaks, or other toxic fumes.

The somatic receptors respond to touch, pressure, cold, pain, and body position. These receptors also become less sensitive as aging occurs. Older individuals therefore experience a decreased ability to feel pain and cope with temperature changes. These and additional age-related changes are presented in Table 29–1.

Assessment of Cognitive Function

The assessment of neurocognitive function is an essential part of a comprehensive assessment in older adults. Neurocognitive function assessment includes several components and can be easily incorporated into the general assessment of older adults through history taking, physical examination, and the use of selected screening instruments. A complete mental status assessment should include attention, memory, orientation, perceptions, thought processes, thought content, insight, judgment, affect, mood, language, and higher cognitive functions (see Chapter 14 for the components of a cognitive or mental status assessment). Neurologic assessment includes the evaluation of cranial nerves, gait, balance, distal deep tendon reflexes, plantar responses, primary sensory modalities in the lower extremities, and cerebrovascular integrity. Complete neurocognitive examinations should be performed on all older adults to establish baseline function and to detect potentially reversible conditions causing mental and behavioral disturbances.

Few older adults recognize the symptoms of cognitive decline in themselves. It is often a friend or family member who reports these symptoms to the nurse or physician caring for the client. An interview with the friend or family member, physical assessment, and the use of structured mental status assessments assist the nurse in identifying cognitive decline in older adults (Elliott, Horgas, & Marsiske, 2008).

One of the early manifestations of cognitive decline may be observed in the functioning of older adults. It is important to include functional assessment as part of the assessment of older adults. Simple questions that may be asked in the history include their ability to perform activities of daily living (ADLs), such as bathing, dressing, toileting, and eating. Instrumental activities of daily living should also be addressed. These activities include the ability to clean house, shop, pay bills, and perform other functions that would allow clients to remain independent within their homes.

Selected Cognitive Function Screening Instruments

Functional Assessment

One screening tool that has been used to identify the presence and severity of dementia symptoms based on level of function and cognition in older adults is the Dementia Severity Rating Scale (DSRS) (Harvey, 2005). The DSRS is an 11-item instrument that can be easily and quickly administered and covers the areas of memory, orientation, judgment, community affairs, home activities, personal care, speech and language recognition, feeding, incontinence, and mobility or walking. A normal score on this instrument is four or less; the score increases as the older person’s cognition decreases.

Mental Status Examination

The MiniMental State Examination (MMSE) is one of the most widely used instruments in all settings and is useful for the assessment of orientation, immediate and recent memory, attention, calculation, and language and motor skills (Folstein, Folstein, & McHugh, 1975). Cognitive impairment is identified in individuals with scores of less than 24; however, educational level and age may have an impact on the results and must be taken into consideration when interpreting the results. The Mental State Questionnaire (MSQ) is a 10-item list, one of the shortest instruments used to assess cognitive function. This test is reliable in identifying clients with moderate to severe cognitive impairment. The MSQ is not beneficial for all client evaluations (Alexopoulos & Mattis, 1991). The Blessed Dementia Scale or Short Blessed Test (SBT) is another frequently used screening tool for the assessment of dementia; however, both aging and depression have an effect on Blessed Orientation-Memory-Concentration (BOMC) test performance (Jorm & Jacob, 1989). The BOMC test is a reduced version of the SBT and consists of six questions. This shortened version of the SBT is used by many disciplines.

Depression Assessment

The Geriatric Depression Scale is widely used to identify depression in older adults (Yesavage et al, 1983). Patients answer 30 statements on this screening tool with either “yes” or “no.” A score of 11 or greater indicates possible depression and the need for more in-depth evaluation. See Chapter 14 for an in-depth discussion on the evaluation of depression in older adults.

Cognitive Function and Memory in Typical Aging

Forgetfulness as an inevitable consequence of aging is a myth that has had significant influence on society’s views of aging. Forgetfulness may affect both the young and old but should not be confused with true cognitive impairment. In reality, memory and delayed recall are not substantially decreased in older persons. If allowed time to learn new material, older persons experience no more memory loss than younger persons. Cognitive impairment involves mental status changes in addition to higher level cognitive functional changes such as failure to correctly spell common words, compute simple sums, balance a checkbook, drive a car safely, plan a meal, or follow grammatical conventions. A decline in cognitive function is an effect of disease, not an effect of the normal aging process.

Cognitive Disorders Associated with Altered Thought Processes

Several cognitive disorders are associated with altered thought processes in older adults. These include the three Ds of depression, delirium, and dementia, as well as cranial tumors, subdural hematomas, and normal pressure hydrocephalus. It is often difficult to accurately diagnose the underlying cause of altered thought processes in older adults because of the similarity in their presentations. Nevertheless, accurate assessment and diagnosis are essential for ensuring appropriate treatment to improve or potentially reverse the underlying pathophysiologic condition contributing to the individual’s impaired cognition.

Depression

The rate of depression among older adults has remained relatively stable over the past decade with approximately 12% of individuals older than the age of 65 reporting depressive symptoms (Federal Interagency Forum on Aging-Related Statistics, 2008). However, as one ages the rate of depression increases. The percentage of men older than the age of 85 reporting depressive symptoms is almost double that of men aged 65 to 74 (Federal Interagency Forum on Aging-Related Statistics, 2008). In older age, depression is associated with higher suicide rates than in the younger depressed population. Although older Americans make up 13% of the U.S. population, they account for 16% of all suicide deaths (National Institute of Mental Health, 2009). White men older than 50 years of age have the highest rate of suicide at approximately 50 suicide deaths per 100,000 men (National Institute of Mental Health, 2009). Dombrovski and Szanto (2005) report that older adults in the United States, especially the depressed elderly, are more likely to commit suicide than any other age group, although it is difficult to estimate the true incidence of suicide.

Clinical Manifestations

Depression may manifest itself through signs such as fatigue; constipation; psychomotor retardation; depressed mood; loss of interest, energy, libido, or pleasure; changes in appetite, weight, and sleep patterns; and agitation; anxiety; or crying (American Psychiatric Association [APA], 2004). Depression often is first seen in older adults as cognitive impairment, particularly in the areas of attention and concentration. Depressed older adults may neglect eating or caring for a chronic medical condition, predisposing them to the development of delirium.

Depression is also a common response to serious illness of any kind, particularly multiple sclerosis, hypothyroidism, lupus, hepatitis, acquired immunodeficiency syndrome (AIDS), vitamin deficiencies, and anemia. These conditions may produce depression in a more direct biologic sense. Drugs can also contribute to depressive symptoms (Box 29-1). Older adults require a careful medical history and physical examination before the diagnosis of depression can be made.

BOX 29–1 MEDICATIONS THAT MAY CONTRIBUTE TO DEPRESSION

• Amphetamines

• Analgesics, narcotics

• Antihypertensives

• Antimicrobials

• Antineoplastic agents

• Antiparkinsonian agents

• Barbiturates

• Benzodiazepines

• Digoxin

• Hypoglycemic agents (by causing hypoglycemia)

• Phenothiazides

• Steroids

• Sulfonamides

Late-life depression is often similar in presentation or may be concomitant to cognitive impairment and dementia caused by neurochemical changes and awareness of the loss of physical or intellectual functioning. Symptoms common to both depression and dementia include irritability, inability to concentrate or feel pleasure, loss of interest in life, and lack of energy and initiative. The term pseudodementia has been used to describe depression masquerading as dementia. Pseudodelirium is the term used when an older adult is seen with an acute confusion found to be due to depression. With a careful assessment, it is possible to make the appropriate diagnosis. Individuals with dementia are more likely to show signs of disorientation and loss of short-term memory and are less likely to feel sadness or guilt or to complain about pain, insomnia, and poor appetite. Table 29–2 offers a comparison of selective features associated with dementia, delirium, and depression. Refer to Chapter 14 for a comprehensive discussion of depression among older persons.

TABLE 29–2

CLINICAL FEATURES OF DEPRESSION, DELIRIUM, AND DEMENTIA

CLINICAL FEATURE	DEPRESSION	DELIRIUM	DEMENTIA
Onset	Can be abrupt or associated with life events	Sudden onset	Months to years
Duration	Weeks to months	Hours to days	Long term or lifetime
Mood	Consistent; sadness, anxiety, irritability	Labile; suspicious, mood swings	Fluctuating; depressed, apathetic, uninterested
Behavior	Variable; may have psychomotor retardation or agitation	Variable; hypokinetic or hyperkinetic	Variable with psychomotor retardation or agitation
Cognition
Orientation	Selected disorientation	Impaired with variable severity	Slow decline over time
Alertness	Normal	Lethargic or hypervigilant	Generally normal
Memory	Selective impairment	Impairment of recent memory and attentiveness	Early recent and later remote memory impairment
Thought processes	Intact with themes of hopelessness, helplessness, and self-depreciation	Difficulty maintaining concentration; disorganized; fragmented	Impoverished; impaired abstract thinking; word-finding difficulties; impaired judgment
Perception	Normal	Possible visual, auditory, and tactile hallucinations or delusions	Misperceptions not generally present
Speech and language	Normal to slowed	Slurred, forced, or rambling	Disordered; word-finding difficulties
MiniMental State Examination	Performance fluctuates over time	Acute fluctuations	Moderately stable with decreasing scores over time

Delirium

Delirium is described in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR) (APA, 2000) as a transient, organic mental syndrome characterized by a reduced level of consciousness, reduced ability to maintain attention, perceptual disturbances, and memory impairment. The onset of delirium is short, generally ranging from hours to days. Delirium occurs in all settings, including homes, assisted living facilities, nursing facilities, and hospitals. Frequently, when an older adult becomes delirious in a community setting, it precipitates a hospital admission, in part because of the underlying illness causing the delirium. Delirium occurs in 7% to 61% of older hospitalized clients, with associated morbidity rates ranging from 6% to 18% within this group (Royal College of Psychiatrists, 2005).

Risk Factors

The risk factors for delirium include advanced age, CNS diseases, infection, polypharmacy, hypoalbuminemia, electrolyte imbalances, trauma history, gastrointestinal or genitourinary disorders, cardiopulmonary disorders, and sensory changes. These factors can lead to physiologic imbalances increasing the risk for confusion (Fick & Mion, 2008). Specific laboratory testing should be guided by clues in the history and physical examination so that the physiologic causes of delirium can be identified.

Clinical Manifestations

Symptoms of delirium fluctuate and may include difficulty maintaining concentration or attention to external stimuli and a language disturbance, including slurred, forced, or rambling speech. Disorganized thinking demonstrated by tangential reasoning and conversation is often the presenting symptom. Other common symptoms of delirium include

• Clouding of consciousness or fluctuation of awareness

• Misperceptions, illusions, or hallucinations

• Disorientation to persons, place, and time

• Memory problems

• Increased or decreased physical activity

• Impaired judgment

Management

Early delirium research focused on the timely identification of delirium in hospitalized older adults. Current research focuses on the identification of risk factors and prevention strategies. Multiple instruments have been developed to assess for delirium. The acute confusion assessment instruments for nursing include the Clinical Assessment of Confusion-A&B (Vermeersch, 1986; 1992), the VAS-AC (Nagley, 1986), and the NEECHAM Confusion Scale (Neelon et al, 1996). There are also several medical-model delirium assessment scales, including the Delirium Rating Scale (Trzepacz, Baker, & Greenhouse, 1988), Delirium Symptom Interview (Levkoff, Besdine, & Wetle, 1986), and Confusion Assessment Method (CAM) (Inouye et al, 1990). All these instruments have demonstrated sensitivity and specificity for use with hospitalized older adults.

In one study, a program was developed for the early detection and treatment of older persons who developed symptoms of delirium during hospitalization (Inouye et al, 2007). Among the study participants older than the age of 70, 11.8% had delirium on discharge as measured by the CAM. The predictive model used in this study found five risk factors for delirium: cognitive impairment, visual impairment, functional impairment, comorbidity, and the use of physical restraints. The study validated the previously studied predictive model, and the authors concluded that at least four of the five risk factors for delirium are amenable to intervention. Table 29–3 outlines the assessment and intervention protocols used in the care of patients with delirium.

TABLE 29–3

RISK FACTORS FOR DELIRIUM AND INTERVENTION PROTOCOLS

TARGETED RISK FACTOR AND ELIGIBLE PATIENTS	STANDARDIZED INTERVENTION PROTOCOLS	TARGETED OUTCOME FOR REASSESSMENT
Cognitive Impairment^∗
All patients, protocol once daily; patients with baseline MMSE score of <20 or orientation score of <8, protocol 3 times daily	Orientation protocol: board with names of care team members and day’s schedule; communication to reorient to surroundings Therapeutic-activities protocol: cognitively stimulating activities three times daily (e.g., discussion of current events, structured reminiscence, or word games)	Change in orientation score
Sleep Deprivation
All patients: need for protocol assessed once daily	Nonpharmacologic sleep protocol: at bedtime, warm drink (milk or herbal tea), relaxation tapes or music, and back massage Sleep-enhancement protocol: unit-wide noise-reduction strategies (e.g., silent pill crushers, vibrating beepers, and quiet hallways) and schedule adjustments to allow sleep (e.g., rescheduling of medications and procedures)	Change in rate of use of sedative drugs for sleep^†
Immobility
All patients: ambulation whenever possible and range-of-motion exercises when patients chronically nonambulatory, bed or wheelchair bound, immobilized (e.g., because of extremity fracture or deep venous thrombosis), or prescribed bedrest	Early mobilization protocol: ambulation or active range-of-motion exercises three times daily; minimum use of immobilizing equipment (e.g., bladder catheters or physical restraints)	Change in ADL score
Visual Impairment
Patients with <20/70 visual acuity on binocular near-vision testing	Vision protocol: visual aids (e.g., glasses or magnifying lenses) and adaptive equipment (e.g., large illuminated telephone keypads, large-print books, and fluorescent tape on call bell), with daily reinforcement of their use	Early correction of vision, ≤48 hr after admission
Hearing Impairment
Patients hearing ≤6 of 12 whispers on Whisper Test	Hearing protocol: portable amplifying devices, earwax disimpaction, and special communication techniques, with daily reinforcement of these adaptations	Change in Whisper Test score
Dehydration
Patients with ratio of blood urea nitrogen to creatinine ≥18, screened for protocol by geriatric nurse-specialist	Dehydration protocol: early recognition of dehydration and volume repletion (i.e., encouragement of oral intake of fluids)	Change in ratio of blood urea nitrogen to creatinine

^∗Orientation score consisted of results on first 10 items on the MiniMental State Examination (MMSE).

^†Sedative drugs included standard hypnotic agents, benzodiazepines, and antihistamines, used as needed for sleep.

From Inouye SK: Risk factors for delirium and intervention protocols, N Engl J Med 340(9):669, 1999.

There are a number of interventions to prevent delirium in hospitalized clients. Assessment with the use of a validated instrument such as the CAM is the first line in preventing and treating delirium. Modifying risk and maintaining safety are key features of delirium care (Fick & Mion, 2008). An early study by Inouye (1999) resulted in the development of a broad spectrum of preventive interventions that may be modestly effective, including psychiatric or medical assessment, support, education, and reorientation. Inouye also found that interventions by nurses alone were as effective as interventions by physicians. Delirium management includes rapid diagnosis and treatment of the underlying cause, management of disruptive behaviors, and supportive care. As discussed in the Inouye et al study (2007), assessment of changes in older persons’ cognition is paramount. A thorough history and physical examination are essential for the identification of the onset, cause, direct physiologic manifestation of a general medical condition, or intoxication with or withdrawal from substances that may be contributing to the onset of delirium (American Psychiatric association, 2004).

The treatment of delirium entails the identification and treatment of the underlying cause. These treatment interventions may be categorized as pharmacologic and nonpharmacologic. Nonpharmacologic approaches include promoting activity, improving nutritional and fluid intake, decreasing sensory overstimulation or deprivation, and reassuring the older adult and his or her family members (Fick & Mion, 2008). Pharmacologic approaches may include antibiotics to treat underlying infections and the removal of potentially contributory medications. It may be necessary to use medications for the management of agitation and hallucinations (haloperidol) or alcohol withdrawal symptoms (benzodiazepines). The former can be used judiciously in the treatment of agitation and hallucinations, but polypharmacy should be avoided (see Evidence-Based Practice Box).

Dementia

In 2002, roughly 2.5 million Americans were diagnosed with dementia. By 2030, Thurman reports in the State of Aging and Health in America that the number of Americans diagnosed with dementia will more than double to 5.2 million (Centers for Disease Control and Prevention [CDC], 2007). Not included in these statistics is the phenomenon of potentially reversible dementia. The primary types of dementia include Alzheimer’s disease (AD), vascular dementia (VaD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD).

Dementia is a syndrome of gradual and progressive cognitive decline. It has been defined as an alteration in memory in addition to acquired persistent alteration in intellectual function (e.g., orientation, calculation, attention, and motor skills) compromising multiple cognitive domains. In dementia, individuals are unable to do the things they used to do because of the mental changes associated with this disease process. Dementia may involve language deficits, apraxia (difficulty with the manipulation of objects), agnosia (inability to recognize familiar objects), agraphia (difficulty drawing objects), and impaired executive function (Alzheimer’s Association, 2007).

Although dementia is more common in older persons than in younger persons, it is not part of the normal aging process. Dementia is usually a condition occurring in later life because of changes in neurologic function caused by a disease process. Dementia has been linked to a variety of conditions. Research of the problem has been difficult because of the lack of a standard definition of mild dementia and difficulty in detecting symptoms of early dementia.

Reversible Dementia

Reversible dementia is a phenomenon that occurs when other pathologic conditions masquerade as dementia. Causes of potentially reversible dementia are presented in Box 29-2. It is important to identify and treat the underlying causes of dementia symptoms, but even if these disorders are identified and treated, not all individuals with dementia symptoms will improve (Koedam, 2008).

BOX 29–2 CAUSES OF POTENTIALLY REVERSIBLE DEMENTIA

Medications

Ethyl alcohol (ETOH) intoxication or withdrawal

Metabolic disorders

• Thyroid disease

• Vitamin B₁₂ deficiency

• Hyponatremia

• Hypercalcemia

• Hepatic dysfunction

Chronic subdural hematoma

Normal pressure hydrocephalus

Alzheimer’s Disease

AD is the most common form of dementia in older persons and accounts for 60% to 80% of individuals participating in research on dementia (Alzheimer’s Association, 2007). AD is a progressive, neurodegenerative disease characterized by the presence of neurofibrillary tangles composed of misplaced proteins within the brain, cortical amyloid plaques, and granulovascular degeneration of neurons in the pyramidal cell layer of the hippocampus. An estimated 5 million Americans have AD, and it is predicted that by 2050 the number of individuals with AD could rise to 13.4 million (Alzheimer’s Association, 2006). AD is the seventh leading cause of death in the United States (CDC, 2007). The personal and public price of AD is high. Medicare costs for beneficiaries with AD are expected to exceed the ability to absorb the cost (Alzheimer’s Association, 2007).

Risk Factors

Research has focused on genetic, nutritional, viral, environmental, and other causes of AD. Age is the single most important risk factor for the development of AD, as the number of people with the disease doubles every 5 years beyond age 65.

Genetic Factors

One risk factor for the development of AD is genetics, particularly in cases of presenile dementia, or dementia seen in individuals younger than the age of 65. Other genetic mutations causing excessive accumulations of amyloid protein are also associated with age-related (sporadic) AD (Waring & Rosenberg, 2008). AD may show autosomal dominant inheritance in families with presenile dementia. Chromosome 14 has been linked to early-onset familial AD in more than 70% of cases, and chromosome 19, closely associated with the gene responsible for the encoding of apolipoprotein E, has been linked to late-onset familial AD

EVIDENCE-BASED PRACTICE

Using Trained Volunteers with Delirium Patients

Background

Delirium is a common issue for hospitalized elderly patients. It is associated with an increased risk of mortality and overall poor patient outcomes. This study sought to examine the effectiveness and cost impact of a volunteer-mediated delirium prevention program by looking at two main components. In the first study patients were the focus of the data collection. The second study focused on how the nursing unit functioned as a result of the volunteer-mediated delirium program.

Sample/Setting

In the first study a total of 37 patients were enrolled over a 5-month period.

Methods

Both studies were conducted utilizing a before-and-after framework. Study 1 examined the impact of trained volunteers on patients’ therapeutic activities against a control group who received the standard nursing care practices without a volunteer. Study 2 looked at the program data to assess the impact on the nursing assistants usually employed to provide 1:1 care for delirious or demented patients.

Findings

The patients enrolled in the experimental group showed a lower incidence of delirium (6.3% versus 38.1%, P = 0.032), a reduction in the severity of the delirium, a decrease in the overall length of stay, and a decrease in the incidence of falls (control group 6.3% versus 19%, P = 0.26). The rudimentary cost analysis for Study 2 indicated that the savings related to a decrease in the length of stay would support the continuation of this pilot program to other geriatric acute care units.

Implications

The economic crisis worldwide has placed acute care staffing on a razor edge with increased admissions of older adults. Utilization of volunteers trained to augment direct nursing care in those with delirium may be one method to decrease the morbidity of this condition.

From Caplan GA, Harper EL: Recruitment of volunteers to improve vitality in the elderly: the REVIVE study, Intern Med J 37:95, 2007.

(Waring & Rosenberg, 2008). Mutations in chromosome 21, the gene associated with Down syndrome (trisomy 21), have also been linked with development of the disease. All persons with Down syndrome who survive to the third or fourth decade develop the pathologic condition of AD (Jones et al, 2008). In spite of these data, AD is not an exclusively inherited disease.

Viral Factors

Viral illness such as herpes zoster, herpes simplex, or viral encephalitis is believed to be a possible risk factor for AD. Viral infection of the brain has become an important topic of study because of the association of dementia and AIDS. Researchers are studying the origin of the amyloid deposited in the senile plaques of brain cells of clients with AD. The amyloid precursor protein may have an important role in myeloid deposition in AD. Amyloid fibers become entangled around the cerebral blood vessels, and amyloid-laden neuritic plaques replace the degenerating nerve endings.

Environmental Factors

Environmental factors that are potentially associated with cognitive dysfunction include exposure to toxic substances or chemicals. The role of environmental factors in the expression of AD is supported not only by studies that reveal only a 40% concordance rate for AD in monozygotic twins but also by variations in age at the onset of dementia in monozygotic twin pairs. These findings suggest that nongenetic and potentially environmental factors may influence the development of AD. Head trauma occurring early in life with associated loss of consciousness has been associated with the development of AD in later years (Van Den Heuvel, Thornton, & Vink, 2007).

Nutritional Factors

Reports suggest an association between AD and vitamin B₁₂ deficiency because low serum vitamin B₁₂ concentrations are found in more than 10% of older people and the prevalence of low serum vitamin B₁₂ levels has been reported among people with AD. Hyperhomocysteinemia (plasma homocysteine of greater than 14 μmol/L) increases the risks for dementia and AD (Smith, 2008).

Clinical Manifestations

Symptoms of AD that may be identified by family members and nurses include the individual’s repeated questions and statements, forgetting to pay bills or take medications, increasing problems with orientation, and geographic disorientation. Other symptoms of AD include pervasive forgetfulness and memory loss, language deterioration, impaired ability to mentally manipulate visual information, poor judgment, confusion, restlessness, and mood swings. Personality changes may include apathy or loss of interest in previously enjoyed activities. Eventually AD destroys cognition, personality, and the ability to function.

Diagnostic Studies

Currently no validated test is available for the diagnosis of AD. Although autopsy remains the gold standard for the diagnosis of AD, clinical diagnosis has become increasingly accurate over the past several years (Alzheimer’s Association, 2007). Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans have been used to identify the hippocampal atrophy associated with the diagnosis AD. Because the costs are prohibitive and the findings are similar to those of clinical examination for the diagnosis of AD, these tests are not routinely recommended (Alzheimer’s Association, 2007).

Treatment

At this time there is no cure for AD. Several pharmacologic options have been introduced to slow the progression of the disease in its early stages. These new medications have transformed the care of AD clients. Tacrine (Cognex) was the first of the cholinesterase inhibitors, but because of the need to frequently monitor a client’s liver function, its use is limited. Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Reminyl), all cholinesterase inhibitors, were originally found to have fewer side effects and demonstrated greater cognitive and global functional improvement in early and midstage AD. These medications may keep some symptoms from becoming worse for a limited time. However, recently a study of 19,803 community-dwelling older adults with dementia receiving cholinesterase inhibitors had more frequent hospital visits for syncope and syncope-related events compared with 61,499 healthy control subjects (Gill et al, 2009). A fifth drug, memantine (Namenda), was approved for use in the United States. Combining memantine with other AD drugs promises to be more effective than any single therapy. Although cholinesterase inhibitors have been useful for older adults with AD, they have not been shown to have the same effects in older adults with other types of progressive dementia.

An herbal plant extract from Ginkgo biloba has shown promise in stabilizing and occasionally improving cognitive performance and function in demented older adults for 6 months to a year (Birks & Grimley Evans, 2009). It has been used as a standardized form in Europe for many years but is sold in the United States as a nutritional supplement. Vitamin supplementation has been attempted and studied, but there is no consensus on the efficacy of this intervention. In a research review by Jia, McNeill, and Avenell (2008), there was insufficient evidence to support the efficacy of vitamin B₁₂ in improving the cognitive function of people with dementia and low serum B₁₂ levels. In another review, Malouf and Grimley Evans (2008) found no benefit from folic acid with or without vitamin B₁₂ in comparison with placebo on any measures of cognition or mood in the clinical trials they reviewed. The results of a 2004 metaanalysis of the role of vitamin E in the treatment of AD were inconclusive (Isaac, Quinn, & Tabet, 2008).

Although nonsteroidal antiinflammatory medications (NSAIDs) have been suggested in the treatment of AD, no evidence exists from randomized double-blind and placebo-controlled trials demonstrating their benefit (Vlad, Miller, Kowall, & Felson, 2008). Because ibuprofen and other NSAIDs have a significant side effect profile, including gastrointestinal bleeding, it needs to be demonstrated that the benefits of such a treatment outweigh the risk of side effects before ibuprofen can be recommended for AD treatment.

Nursing Management

Previously the management of clients with dementia consisted of helping patients and their families through progression of the disorder while allowing them as much dignity and independence as possible. This is clearly still true. However, the focus is now on maintaining cognitive and global function early in the disease process to postpone the need for institutional care.

Vascular Dementia

VaD is the second most frequently occurring type of dementia among older persons (Schneck, 2008). Often referred to as multiinfarct dementia, VaD is defined as a loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions resulting from cerebrovascular disease or cardiovascular pathologic conditions. VaD is associated with the progressive loss of brain tissue as a result of a series of small brain attacks (infarcts) caused by occlusions and blockages within the arteries to the brain. Individuals who have experienced a cerebrovascular accident (CVA) have an even greater risk of VaD.

Pathophysiologically, asymmetric regions of cerebral softening and hemorrhage are diffuse and irregular. If there is a series of brain attacks, the rate of decline in function increases. Some recovery of function may occur over time, but there is never full recovery. As the damage from the infarcts progresses and accumulates, more widespread evidence of diminished mental ability exists.

Risk Factors

Several medical problems place individuals at risk for the development of VaD. These include arteriosclerosis, blood dyscrasias, cardiac decompensation, hypertension, atrial fibrillation, cardiac valve replacements, systemic emboli for other reasons, diabetes mellitus, peripheral vascular disease, obesity, smoking, and vasospasms in segments of the brain (also referred to as transient ischemic attacks [TIAs]).

Clinical Manifestations

The onset of VaD may be gradual or abrupt. Gradual onset VaD occurs as a result of small lacunar infarcts that affect a very small area of the brain, causing memory, motor, or sensory perceptual function deficits. This phenomenon may not be obvious until several small infarcts have occurred. Abrupt onset VaD presents with immediate neurologic symptoms, such as one-sided weakness, gait abnormalities, or focal neurologic signs. Destruction of the brain tissue resulting from small emboli or brain attacks may be localized or diffuse. The usual progression of VaD follows a stepwise decline rather than the slow, steady decline associated with AD. Patients with VaD have an infarct, decline in function, and then experience a functional plateau before experiencing another insult and subsequent decline.

Symptoms of VaD depend on the location of the infarct and may include

• Impaired learning and impaired retention of new information

• Impaired handling of new tasks

• Impaired reasoning ability

• Impaired spatial ability and orientation

• Impaired language

These impairments generally interfere with work and social functioning. Other symptoms may include wandering, getting lost in familiar places, moving with rapid, shuffling steps, losing bladder or bowel control, inappropriately displaying emotions, and having difficulty following instructions. Not all brain attacks result in intellectual impairment; some affect movement, vision, or other functions.

Diagnostic Studies

Neuroimaging with either computed tomography (CT) or MRI usually reveals one or more areas of cerebral infarction. VaD is most often associated with diffuse or bilateral cortical or subcortical areas of infarction or microinfarction. Other than neuroimaging and clinical examination, no other diagnostic tests or biomarkers exist for the diagnosis of VaD.

Treatment

Research on the use of donepezil for improving cognitive function, clinical global impression, and ability to perform ADLs in patients with mild to moderate VaD has been promising (Dichgans et al, 2008). Nimodipine (Nimotop), a calcium channel blocker, has also demonstrated short-term benefit in the treatment of VaD; however, little evidence supports its efficacy with long-term use in VaD (Pantoni et al, 2005). There is insufficient evidence to support interventions for the tertiary prevention of VaD. Zekry (2009) supports the need for well-designed, rigorous clinical trials with better defined assessment criteria for VaD.