CHAPTER 35

Treatment of Seniors

Dan G. Blazer, M.D., Ph.D.

David C. Steffens, M.D., M.H.S.

Psychiatrists who work with older adults encounter diagnostic and therapeutic problems that are more complex than those encountered in young adult and middle-aged patients. Most older patients with psychiatric disorders do not fit easily into the diagnostic categories of DSM-5 (American Psychiatric Association 2013) because they experience multiple symptoms that affect both physical and psychiatric functioning. This is especially true for the oldest members of this population (Blazer 2000). Once the problem is formulated by the clinician, usual treatment approaches must be modified both to manage the functional disability that results from the psychiatric problem and to reverse the underlying disorder.

In an era in which specific psychiatric disorders are emphasized, psychiatrists working with older adults can benefit from the syndromal approach to impairment (Halter et al. 2009). In this chapter, we follow this syndromal approach by identifying seven psychiatric syndromes that are most prevalent among older individuals—acute confusion, memory loss, insomnia, anxiety, suspiciousness and agitation, depression, and substance use (Table 35-1)—and describing them within the context of managing the resultant impairment. Because the psychiatric disorders that contribute to these syndromes are described elsewhere in this text, we focus on the aspects of the syndromes that are unique to late life and on the management of the older adult with these syndromes.

Acute Confusion

Acute confusion, or delirium, is a transient neurocognitive disorder characterized by acute onset and global impairment of cognitive function. The older person with acute confusion exhibits a decreased ability to maintain attention to environmental stimuli and has difficulty shifting attention from one set of stimuli to another (Table 35-2; see also Chapter 24 in this volume, "Neurocognitive Disorders," by Weiner). Thinking is disorganized, speech becomes rambling, and a decreased level of consciousness is exhibited. Emotional disturbances often, but not always, accompany acute confusion and may be the presenting problem in late life. These emotional disturbances include anxiety, fear, irritability, and anger. Some older persons, in contrast, are apathetic and withdrawn during an episode of delirium and thus are much more difficult to diagnose. Sleep disturbances are typical. Acute confusion, by definition, is brief, usually lasting a few hours but possibly lasting weeks, such as in the case of confusion secondary to medications, and merges into the much less common chronic state (Blazer and van Nieuwenhuizen 2012).

Frequency and Origins

The frequency of delirium in the older population is difficult to estimate because many episodes are undetected due to their brevity. Most estimates of incidence range from 15% to 25% among patients on medical and surgical wards (Inouye 2006). When delirium is diagnosed in a hospitalized older patient, the hospitalization is usually prolonged, and both in-hospital and post-hospital mortality rates are increased. Mortality at 2-year followup approaches 50%. Acute confusion is especially a risk for Alzheimer's patients, and half of those who are hospitalized become confused (Fong et al. 2012).

Acute confusion in late life is the common outcome of a cascade of biological, cognitive, and environmental contributors. Biological brain function declines with age, although functional capacity varies greatly within age groups. Degenerative changes, such as those characteristic of Alzheimer's disease (AD), render the older person more susceptible to physiological changes secondary to aging and disease. These physiological changes include drug intoxication, electrolyte disturbance, infection, dehydration, hypoalbuminemia, and hypoxia. Visual and hearing impairment may also contribute to delirium. For example, an older adult with an early but progressive neurocognitive disorder and congestive heart failure may be especially at risk for developing acute confusion. The vulnerable nervous system cannot adapt to the decreased delivery of oxygen and glucose during failure because of a decreased reserve capacity and acute confusion emerges. Common external biological stressors that precipitate acute confusion in older adults at risk are listed in Table 35-3.

Cognitive contributors to delirium include a predisposition to hallucinations and delusions, such as that in an aging patient with a history of schizophrenia. Environmental contributors include the unfamiliar surroundings of a hospital or long-term-care facility and social isolation. Therefore, the hospital, where the convergence of these contributors is likely, is a high-risk environment for delirium. Additional factors that may contribute to delirium in the hospital include physical restraint and bladder catheter (Inouye 2006).

Treatment

The treatment of acute confusion in the older adult begins with prevention. Activities that can help prevent acute confusion include the following: 1) early mobilization to avert immobilization; 2) nonpharmacological approaches to behavioral disturbances to minimize the use of psychoactive drugs; 3) interventions to prevent sleep deprivation; 4) communication methods to orient the patient; 5) adaptive equipment such as eyeglasses and hearing aids for vision and hearing impairment; and 6) early correction of volume depletion (Inouye et al. 1999).

General therapy for the confused older individual, to be administered in parallel with specific therapy for the underlying cause of the acute confusion, begins with medical support. Vital signs and level of consciousness should be closely monitored (Inouye et al. 1999). All medications that are not critical should be discontinued. Vasopressor agents may be needed to increase blood pressure, and excessive fever should be treated with ice baths and alcohol sponges. When the syndrome of acute confusion is recognized and the precipitant of the confusion is established through history physical examination, and laboratory studies, the clinician can begin therapy Laboratory tests should be ordered as indicated, including thyroid function tests, measurement of drug levels, toxicology screen, measurement of ammonia or cortisol levels, electrocardiogram, and neuroimaging (Inouye 2006). Acute confusion may present as a psychiatric emergency that threatens permanent brain damage. Severe hypoglycemia, hypoxia, and hyperthermia are examples of critical conditions that may present as acute confusion. Therefore, the initial treatment should include the establishment of an adequate airway to ensure that the patient is breathing. Level of attention should be monitored using brief bedside tests (e.g., serial 7s and digit span).

The clinician must also pay special attention to reducing the demands that excess and conflicting environmental stimuli make on the patient's cerebral function. Order and simplicity in the environment are critical to the management of the confused older patient, who should be maintained in a quiet, simply furnished, and well-lit room. Lights should be left on at night. Care can best be facilitated by constant attention from familiar persons such as family members, who should frequently orient the patient to time, place, and person. Physicians, nurses, and other hospital personnel should explain all procedures. Restraints should be kept to a minimum. Behavioral agitation generally can be managed by judicious use of antipsychotic medications, such as haloperidol (administered either intramuscularly or orally), olanzapine, or risperidone, in low dosages.

Memory Loss

Memory loss is a frequent concern of older adults and their families. The syndrome of memory loss spans a wide range of severity, including subjective memory complaints of little consequence, mild forms of neurocognitive impairment that may represent preclinical forms of AD, and more severe syndromes of clinically diagnosable dementia (see Chapter 24 in this volume, "Neurocognitive Disorders," by Weiner). Patients with objectively measured memory loss may experience impairment in other areas of cognition, particularly if the memory impairment is moderate or severe (Table 35-4). Late-life memory loss is usually accompanied by a more or less sustained decline in cognitive function from a previously obtained intellectual level, usually with an insidious onset. Other cognitive capacities that decline with memory include language (e.g., aphasia), spatial or temporal orientation, judgment, executive function, and abstract thought. State of consciousness is usually not altered until very late in the memory loss syndrome, which is in contrast with acute confusion. However, individuals with vascular dementia may experience a fluctuating course of cognitive impairment.

DSM-5 (American Psychiatric Association 2013) introduced a new classification system for neurocognitive disorders (NCDs) that focuses on the constructs of mild neurocognitive disorder and major neurocognitive disorder (dementia). Once a delirium has been ruled out, the initial cognitive diagnostic task is to differentiate between normal neurocognitive function, mild NCD, and major NCD. The second step is to assign an etiological category, such as NCD due to Alzheimer's disease, vascular NCD, or frontotemporal NCD. Although neurocognitive dysfunction in older adults is usually analogous in the clinician's mind to learning and memory problems, DSM-5 also includes complex attention, executive function, language, perceptual motor problems, and social cognition among the neurocognitive domains that can be impaired by an NCD. Inclusion of mild NCD in DSM-5 has been justified on clinical grounds. Individuals with mild neurocognitive dysfunction may present with neurocognitive problems that do not meet criteria for a major NCD but are clearly disturbing them or their families. Although their symptoms and cognitive test results may not be severe enough to warrant a diagnosis of major NCD or dementia, these individuals may nonetheless experience difficulties with activities of daily living and express awareness of the problem. Mild NCD is currently a target for biomedical research, including studies of biomarkers and trials of treatment and dementia prevention interventions, and as these diagnostic and treatment approaches are developed, it is imperative that our diagnostic nomenclature keep pace (Blazer 2013).

Frequency and Origins

Subjective cognitive complaints are common, with one study finding that over 95% of adults ages 70-90 or their knowledgeable informants endorsed at least one cognitive complaint (Slavin et al. 2010). The investigators found that subjective memory complaints were associated with depression, anxiety, and a neurotic personality style.

Disabling memory loss may begin in midlife, but it is much more frequent in persons older than 75 years than in those ages 65-74. Prevalence estimates of memory impairment from community samples are generally 5%-15%, with most investigators estimating memory impairment in at least 10% of persons older than 65 years in the community and in 30%-50% of institutional residents (Evans et al. 1989). The syndrome of mild cognitive impairment (mild neurocognitive impairment in DSM-5), thought to be a transitional state between normal cognition and major neurocognitive impairment (dementia), particularly associated with AD, has been an intense area of study over the past decade. The incidence of mild cognitive impairment ranges from 1% to 6% per year while prevalence estimates range from 3% to 22% per year (Ganguli et al. 2004; Hänninen et al. 2002).

AD, the most common disorder contributing to memory loss, has been estimated to be prevalent in 6%-8% of community-dwelling persons older than age 65 years, and in more than 30% of persons ages 85 years and older. Prevalence estimates of AD include both mild and severe cases, so significant memory impairment may be found in only a proportion of persons identified as having the condition in community samples. Until age 75 years, the life expectancy of persons with AD or vascular dementia is reduced by one-half. After age 75 years, life expectancy is less affected by memory loss.

Potential causes of memory loss are listed in Table 35-5. Although the clinical presentation of memory loss does not always provide clear evidence for the etiology, there are some distinguishing characteristics, such as the increase in visual hallucinations in Lewy body disease and sudden declines in memory with vascular disease. Even those persons who have AD may experience significant decline over an interval, only to enter a plateau in functioning for a subsequent interval that may last for many months. Some neurocognitive disorders, however, do not lead to inevitable decline in function. For example, neurocognitive disorder associated with alcohol can be arrested if the person stops drinking and returns to a nutritional diet.

More than 50% of persons with chronic memory loss will, at autopsy, exhibit the changes of AD only. AD is characterized by neurofibrillary tangles, deposition of P-amyloid, and brain atrophy. The next most common contributor to the syndrome is vascular disease, characterized by multiple small infarcts of the brain. Clinically and pathophysiologically, it is difficult to disaggregate these disorders. Vascular neurocognitive disorder frequently is comorbid with AD. In contrast to AD, however, vascular neurocognitive disorder is more common in males than in females. Many patients with Parkinson's disease develop brain changes late in the course of the disease similar to those changes found in AD. Clinically, except for their parkinsonian symptoms, these patients cannot be distinguished from patients with AD. In addition, many patients with AD exhibit changes in the substantia nigra at autopsy. Approximately 5% of older persons experience memory loss as a result of chronic alcohol use. A variant of AD is Lewy body dementia, characterized by synaptophysin-containing cytoplasmic inclusions outside the substantia nigra. In addition to memory impairment, fluctuating cognitive function is characteristic of this disorder.

The primary risk factors for AD are age and family history, with the prevalence of AD, as mentioned previously, being an exponential function of age. Other risk factors for AD include Down syndrome, head trauma, and possibly lack of education. (Use of statins and/or nonsteroidal anti-inflammatory drugs [NSAIDs] may be protective [Breitner and Zandi 2001].) Genetic risk factors have received much attention in recent years, especially the relationship between the disease and the s4 allele of the apolipoprotein E gene (APOE; Roses 1994). Persons who carry at least one copy of the APOE s4 allele are at increased risk for AD. A proposed pathophysiological pathway for the e4 allele's role in the disease is that the e4 allele increases the deposition of p-amyloid, which in turn damages oligodendrocytes, the cells that produce myelin. Much less common forms of AD have been linked to chromosomes 14 and 1 (presenilin 1 and 2 genes). Most cases of AD, however, cannot be attributed to one etiological agent.

Male sex, hypertension, and possibly black race are risk factors for vascular dementia. Alcohol use regularly over many years is the primary cause of alcohol-induced amnestic disorder.

Diagnostic Workup

The diagnostic workup of the older adult with memory loss (Table 35-6) begins with a history the most important component of the evaluation. A history should be obtained from both family members and the patient. The nature and severity of memory loss should be assessed in conjunction with a chronological account of the onset of the older adult's problems and specific behavioral changes. The patient and family should be asked about common problems resulting from memory loss, such as becoming lost in a familiar place, having difficulties with driving, becoming repetitious, and losing objects. Medical history should include inquiries about relevant systemic diseases, trauma, surgery, psychiatric problems, diet, and alcohol and drug use. (A thorough documentation of prescription and over-the-counter drugs is essential.) Family history should include questions about relatives who have memory loss, Down syndrome, alcohol problems, and psychiatric disorders. The physical examination should include not only a thorough neurological examination but also a general physical workup to determine the health of the patient.

The nature and degree of the neuro-cognitive dysfunction should be assessed by both a thorough mental status examination and objective testing. Standardized mental status examinations, such as the Mini-Mental State Examination (Folstein et al. 1975) and Montreal Cognitive Assessment (Nasreddine et al. 2005), are available and are useful quantitative means of documenting memory loss at the initial evaluation.

The in-office or hospital-based initial assessment of memory and neurocognitive functioning is followed by a more in-depth evaluation of cognition with tests of specific functions such as executive functioning (Trail Making Test; Lezak et al. 2004), language (Boston Naming Test; Kaplan et al. 1983), memory (Wechsler Memory Scale; Wechsler 1987), and spatial ability (tests of constructional praxis). Performance on short screening and on more in-depth neuropsychological testing provides a baseline from which decline in function and/or response to therapeutic intervention can be determined (Welsh-Bohmer and Attix 2012).

Routine laboratory examination is essential, with special focus on findings that could contribute to memory loss, such as hypothyroidism, anemia, and (in rarer cases) vitamin deficiencies, such as deficiency of vitamin B₁₂. Magnetic resonance imaging (MRI) or computed tomography scans are now routine in the initial evaluation of memory loss. Much interesting research is emerging to explore the association of memory loss and functional imaging (e.g., positron emission tomography), but the utility of these functional scans is limited to clinical scenarios in which there is a high index of suspicion for frontotemporal neurocognitive disorder. Genotyping a patient with AD or a patient's family members cannot be justified at this time, despite the emerging evidence of a hereditary predisposition with certain genotypes such as APOE 4/4 (Roses 1997).

Treatment

Most pharmacological therapies are based on the cholinergic hypotheses of memory and include primarily cholinesterase inhibitors, tacrine, donepezil, rivastigmine, and galantamine, which are available to physicians in office-based practice. (Tacrine is rarely used due to side effects, specifically liver dysfunction.) These drugs have proven moderately effective in reducing decline in memory up to 6 months after administration, but their long-term ability to retard memory loss is questioned. Studies are now emerging to suggest that cognitive function among subjects using these agents is indistinguishable from that among control subjects after 1-2 years. Memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has been approved for the treatment of moderate to severe AD (based on the theory that glutamatergic overstimulation may cause excitotoxic neuronal changes). Other strategies used frequently with less objective evidence of efficacy include the use of NSAIDs in low dosages, estrogen replacement therapy, and antioxidants such as vitamin E. Patients in late life who have memory loss may be referred to specialized centers (memory disorder clinics) where they can be evaluated and, if they meet criteria, enrolled in a clinical trial where they may receive a number of experimental agents, including estrogens.

Ancillary treatments for memory impairment include diet, exercise, and cognitive stimulation, as well as careful control of blood pressure, cholesterol, blood glucose, and other conditions associated with increased stroke risk.

Psychotropic medications are used extensively in patients with memory loss, primarily because of neuropsychiatric symptoms such as verbal or physical aggression, anxiety, depression, psychoses, and severe agitation or regressive behavior (see "Suspiciousness and Agitation" section later in the chapter) (Katz et al. 1999). Other secondary behaviors, however, such as wandering, inappropriate verbalization, repetitive activities (touching), obstinacy in following suggestions or commands, hoarding of materials, stealing, and inappropriate voiding, are not as amenable to medication. Therefore, the first step for the clinician treating the patient with memory loss is to assess what symptoms might be responsive to a medication.

After determining that the emerging behavioral problem cannot be handled through nonpharmacological means and is ongoing, medication can be prescribed with caution. Decision making around pharmacological treatment has become very challenging in the past few years, with reports linking atypical antipsychotics to increased cardiovascular mortality risk, leading to the black box warning by the U.S. Food and Drug Administration (FDA) in 2005. More recently, the FDA issued a safety announcement about citalopram, an antidepressant frequently prescribed for elderly patients, linking daily doses above 40 mg to abnormal cardiac rhythms, including torsades de pointes (U.S. Food and Drug Administration 2012). Although the FDA highlights the recommendation that patients should not be prescribed citalopram at daily doses above 40 mg, in subsequent information for health care professionals, the FDA recommends that for individuals ages 60 years and older, the maximum daily dose of citalopram should be 20 mg.

Agitation and anxiety can be treated with antianxiety agents (e.g., short-acting benzodiazepines), anticonvulsants (e.g., carbamazepine), β-blockers, lithium, and occasionally low doses of antidepressant agents (e.g., trazodone) at night. Clonazepam may be of benefit in agitated patients with vascular dementia; however, the episodic mood swings and acute confusion that often accompany such dementia are not as responsive to medications.

Despite the FDA warning, most clinicians recognize that antipsychotics are effective psychotropic agents for controlling severe agitation, aggressive behavior, and psychoses. If atypical antipsychotics are being considered for management of severe agitation, consultation with the family to explain the FDA warning, as well as the benefits and risks of treatment versus no treatment, and careful documentation of prior treatment attempts and assent of the family is warranted. Most neuroleptics are effective but produce side effects, and therefore the selection of a drug is usually determined by the side-effect profile least adverse for a given patient. The atypical antipsychotic agents, such as olanzapine, quetiapine, and risperidone, are the preferred drugs at present primarily because of the lower immediate side-effect profile. The most troublesome side effects that result from using antipsychotic agents are postural hypotension (and the risk of falling) and tardive dyskinesia, both of which are less frequent among users of the atypical antipsychotics.

Because depression (even the syndrome of major depression) is frequent among patients with chronic memory loss, the use of an antidepressant agent is often indicated (Reifler et al. 1989). In general, the antidepressant agent will not lead to an improvement in memory. Postural hypotension and anticholinergic side effects are the major concerns for patients taking the antidepressant medications. For this reason, selective serotonin reuptake inhibitors (SSRIs) with the fewest potential side effects (e.g., sertraline, escitalopram) are preferred (Lyketsos et al. 2003).

Whatever medication is prescribed to the older adult with memory loss, it should be tapered slowly on a periodic basis to determine whether the medication continues to be required. If the drug is not required, then an unnecessary and potentially dangerous drug can be eliminated from the medication regimen. Careful documentation of the target symptoms for the medication and monitoring of the effectiveness of the medication in reversing these symptoms assist the physicians and nursing staff in identifying drugs that can be discontinued.

Behavioral management of the patient with memory loss not only is useful to the patient but also provides the patient's family with a sense of accomplishment in the presence of an illness that tends to leave a family feeling helpless and bewildered. The family and the physician should develop behaviors such as familiar routines and consistent repetition of instructions that promote both patient and family security. The family, as much as possible, should provide moments of fun with the patient, even when these brief moments of relief are quickly forgotten by the patient. Families can substitute for the patient's lost abilities by performing tasks for the patient, such as putting out clothes in the morning. Family members should not hesitate to "do for" these patients, because patients with memory loss are truly more dependent than other elderly persons. Families must also compensate for the loss of impulse control that accompanies memory loss. One means is distraction; the patient who is about to remove his or her clothes or masturbate in public can be distracted by being engaged in conversation or by being asked to walk with a family member. Patients with memory loss can usually assist in household tasks, even when the disorder is moderately severe. Although the older adult with memory loss cannot prepare a meal alone, he or she can work with the spouse or other family members in routine tasks.

Management of memory loss must include a review of the patient's environment for safety. Typical safety problems include behaviors such as becoming lost or wandering into busy traffic, using medicines erratically or accidentally, falling (secondary to poor lighting or slippery surfaces), having accidents while driving, and leaving things unattended (e.g., leaving appliances turned on). Home visits by geriatric nurse specialists are most hopeful in reviewing the household for potential problems.

Perhaps the most important long-term component for managing the older adult with memory loss is support of the family. Families are the primary caregivers of elderly persons with memory loss until the memory loss becomes severe enough to lead to institutionalization. With proper support, the older person can remain at home for a longer period of time, and the family can function more effectively in the midst of the devastation of the severe memory loss. Education of the family about the expected progression of memory loss, as well as the many behaviors that accompany such loss but that may not be intuitively recognized as resulting from the illness, is key to family support. Excellent educational materials are available and support groups are located throughout the world to assist the family of the patient with memory loss. In addition, families must be monitored for caregiver stress. If the clinician is not sensitive to the potential for stress in caregivers, then family members may exceed their limits and experience burnout, which could lead to neglect and/or abuse of the older adult. Respite for the caregiver, education, and therapy are essential in keeping the care system operative.

Insomnia

Insomnia is more frequent in the elderly population than in any other age group; 28% of adults ages 65 years and older report insomnia, and 48% report difficulty both falling asleep and staying asleep and use of sedative-hypnotic medications (Foley et al. 1995). Both the lack of sleep and the subsequent medication use frequently lead to deterioration in daytime alertness and functioning. The most common causes of sleep disturbances in older adults are listed in Table 35-7.

Sleep changes characteristic in late life include decreased total sleep time, frequent arousals, increased percentages of Stage 1 and Stage 2 sleep, decreased percentages of Stage 3 and Stage 4 sleep, decreased rapid eye movement (REM) latency, decreased absolute amounts of REM sleep, and a tendency to exhibit a redistribution of sleep across the 24-hour day (e.g., napping during the day). Many of these sleep changes are similar to those that occur in depression and dementing disorders, although not as severe. Older persons are also more likely to phase-advance in the sleep-wake cycle, with a phase tendency toward "morningness" (see Chapter 19 in this volume, "Sleep-Wake Disorders," by Reite and Weiss-berg).

Frequency

Approximately 5% of all elderly persons who initially report no sleep problems report new symptoms each year (Ancoli-Israel 2000). The proportion of older persons living in long-term care facilities who have sleep problems and take sedative-hypnotic agents is much higher than in the community. Obstructive sleep apnea is more prevalent in elderly men than women, with the apnea index (i.e., the number of apneic episodes per hour of sleep) being 5 or greater in 25%-35% of elderly persons in the community. The prevalence of periodic leg movements in sleep (experienced most commonly as leg kicks and cold feet along with insomnia) probably ranges from 30% to 50% among healthy elderly persons in the community; polysomnography is generally required to confirm the diagnosis. Restless legs syndrome occurs in about 28% of older adults but does not require polysomnography to diagnose. Circadian rhythm sleep-wake disorders are frequently reported by elderly persons, especially in long-term care facilities.

Diagnostic Workup

The diagnostic workup of an older person with insomnia (Table 35-8) begins with assessment of the severity of the sleep disturbance. Screening questions during the interview should include an assessment of the patient's satisfaction with his or her sleep, daytime napping, fatigue during usual daily activities, and complaint by a bed partner or other observer of unusual behavior during sleep (e.g., snoring, pauses in breathing, periodic myoclonic movements). A careful medical and psychiatric history is necessary to identify or rule out serious diseases that contribute to the sleep problem.

A medication history is essential in determining the etiology of insomnia. Prescribed medications, especially sedative-hypnotics and anxiolytics, as well as alcohol use, have significant effects on sleep and also may impair cardiopulmonary function. Symptoms of the major psychiatric disorders affecting older persons, such as dementia, depression, or severe anxiety, may also lead to insomnia. If a sleep-wake cycle dysfunction is suspected, patients may be asked to keep a log of napping, going to sleep, and awakening. Physical and neurological examinations are necessary, especially when sleep apnea is suspected. Heavy snoring requires a thorough examination of the nose and throat, usually by an otolaryngologist.

Referral to a psychiatrist or neurologist with special interest in sleep disorders is indicated when the sleep problem persists. Upon referral, most patients, after a thorough history and physical examination and withdrawal from medication, are evaluated by polysomnography. Polysomnographic techniques have been improved in recent years; patients can now be fitted with a portable recording instrument and returned home to sleep for 2 evenings. Polysomnography, followed by a multiple sleep latency test, can be used to quantify daytime sleepiness as well as to document sleep apnea.

Treatment

The cornerstones of effective treatment of insomnia in late life are management of the underlying causes of the sleep disturbance and improved sleep hygiene. For example, a significant proportion of older adults with chronic insomnia also have psychiatric disorders, especially depression and alcohol problems. Both of these conditions are responsive to therapy. Physical problems such as hypothyroidism or arthritis may not be reversible, but the symptoms can be relieved with medications or other therapeutic interventions. Nocturnal myoclonus or restless legs syndrome may respond to medications such as dopamine agonists (e.g., pergolide), anticonvulsants (e.g., carbamazepine), benzodiazepines (e.g., clonazepam), or opiates in severe and otherwise treatment-resistant cases. Obstructive sleep apnea that does not respond to conservative management (e.g., the use of continuous positive airway pressure) may require surgery to improve flow in the nasopharyngeal region.

Institution of good sleep hygiene is the next step in managing insomnia among elderly patients (Table 35-9). First, the patient should be encouraged to initiate sleep at the same time every night, preferably at a later rather than an earlier time (to prevent early-morning wakefulness). The bedroom should be used primarily for sleeping and not for napping. Therefore, if the elderly patient has difficulty sleeping at night, the bed should be made up in the morning and the patient should be encouraged not to nap in the bed and to spend as little time as possible in the bedroom during the day. Exercising can facilitate sleep, but exercise should not be initiated after late afternoon. Alcohol and caffeine should be avoided in the evenings, and the evening meal should be moderate and at least 2-3 hours before bedtime. Fluid intake should also be limited during the 2-3 hours before bedtime (to prevent nocturia).

Bedrooms should generally be maintained at a temperature between 65° and 72°F. To maintain a cool bedroom, many elderly persons who cannot afford air conditioning are forced to leave their windows open at night, possibly exposing themselves to noises that are likely to disturb sleep. One means for decreasing the potential of noise to disrupt sleep is to provide white noise (e.g., a waterfall or rain sounds) using specially built devices or to run a fan during the night. If the elderly person still cannot sleep at night, he or she is encouraged to get up, go to another room, and engage in some nonstimulating activity (e.g., reading, listening to music). When the elderly person again becomes drowsy, he or she should return to the bedroom and attempt to initiate sleep once again. If the individual experiences a difficult night of sleep, he or she should make extra efforts the next day to avoid napping.

A number of medications can be used to facilitate sleep in elderly individuals (Table 35-10), although these medications should be used with care. If the elderly patient is taking medications that adversely affect sleep (e.g., long-term use of a sedative-hypnotic agent), the pharmacological approach to treatment is to discontinue that medication (usually over about 10 days for a sedative-hypnotic). If the sleep problem is secondary to a medical problem, then optimal management of the medical problem with medications can assist the patient with sleep. For example, adequate treatment of arthritis with analgesics can improve sleep.

The antidepressant agents not only are useful in managing the older adult with insomnia secondary to depression but also can be used as sedative agents, especially if prescribed at low dosages. For example, trazodone (25-50 mg) or doxepin (25 mg) may be preferable to using a long-term benzodiazepine if chronic use of a sedative is indicated. These drugs, however, have not been proven efficacious in clinical trials, and withdrawal may lead to rebound insomnia (in addition, they reduce time spent in REM sleep). In general, short- to medium-acting benzodiazepines are preferred over those that are more extended in length of action. Therefore, shorter-acting agents such as zolpidem (5 mg) and temazepam (15 mg) are preferred as a sedative-hypnotic. Zaleplon (5 mg) has the shortest half-life among these agents and does not appear to cause rebound insomnia or adversely affect psychomotor function (Ancoli-Israel 2000). Zaleplon may be used for individuals who wake up during the night. Eszopiclone (1-2 mg), although approved for long-term use to improve sleep, should be used with the same caution as other agents. Each of the newer agents has been proven to be safe and effective in older adults (Ancoli-Israel and Ayalon 2006).

Anxiety

Among older persons, anxiety frequently is a symptom secondary to physical illness such as hyperthyroidism, occurs comorbidly with other psychiatric disorders such as depression, or is the primary symptom of a disorder such as generalized anxiety disorder (Blazer 1997; see also Chapter 12 in this volume, "Anxiety Disorders," by Stein and Sareen). Many of the anxiety disorders, however, are relatively less prevalent in late life. Although phobia disorders can affect persons at all stages of the life cycle, the more severe phobias, such as agoraphobia and social phobia, begin early in life and are more common among children and young adults than among older persons. Generalized anxiety disorder is a frequent diagnosis regardless of age, yet generalized anxiety is often co-morbid with other psychiatric disorders such as major depression. Panic disorder is relatively frequent and severe among younger persons but much less so among older persons (although data documenting a lower prevalence among older persons are sparse). Generalized anxiety is therefore the focus of most therapy.

Frequency and Origins

Community surveys of individuals with anxiety symptoms estimate that approximately 5% of older persons experience such disorders (Blazer et al. 1991). Approximately 20% of older persons report some cognitive or somatic symptoms of anxiety in community surveys, with somatic symptoms being more prevalent than cognitive symptoms. In a survey in North Carolina, simple phobia was found in 10% of persons ages 65 years or older, compared with 13% of persons in middle age (Blazer et al. 1985); these phobias are generally not disabling, however, because the older adult usually finds convenient ways to avoid the phobic situation. Agoraphobia was found in 5% of individuals ages 65 years or older, compared with 7% of the middle-age persons (Blazer et al. 1991). Anxiety and depression are frequently comorbid, reaching nearly 50% in some studies (Beekman et al. 2000).

Anxiety results from a number of medical and psychiatric conditions. Many medications lead to symptoms of anxiety (Table 35-11).

Many psychiatric disorders are manifested, in part, by symptoms of anxiety. Moderate to severe acute confusion is usually associated with anxiety and agitation, especially when the older person is in an unfamiliar place. Anxiety is a common accompaniment of major depression; older patients who experience major depression also meet the criteria for generalized anxiety disorder in more than 50% of cases (Blazer et al. 1989). Hypochondriasis is associated with anxiety, especially when dependency needs are not met by family and health care professionals. Dementing disorders, especially in the early and middle stages, are associated with anxiety and agitation. Later in the dementing disorder, the agitation is episodic and the cognitive, subjective anxiety is less well documented. Late-life schizophrenia with acute paranoid ideation is usually accompanied by agitation and anxiety, especially in the evenings when the older person is home alone. In addition, some older persons experience acute panic attacks and meet the criteria for panic disorder, and some exhibit symptoms of generalized anxiety without apparent biological or psychosocial causation.

The clinician must not overlook the possibility that the anxiety symptoms may be secondary to appropriate fear. Many older persons must expose themselves daily to situations that threaten their security. Older adults living in inner cities often fear being attacked as they walk the streets. Those with memory loss who live alone may fear that they will get lost driving to the doctor's office. Individuals who have lost the acuteness of their reflexes fear driving on busy, crowded highways.

Treatment

The use of nonpharmacological therapies such as relaxation training, cognitive restructuring, and activity structuring for the treatment of anxiety in older adults has not been studied extensively. Nevertheless, the successful application of cognitive-behavioral therapies to other psychiatric disorders in late life (especially depression), as well as the danger of medication, suggests that nonpharmacological therapies may be appropriate for treating anxiety disorders. Older persons who do not have cognitive dysfunction may be good candidates for relaxation training and biofeedback. No evidence has been forthcoming to suggest that older persons are less capable of taking advantage of these therapies than are middle-aged persons. Cognitive restructuring, based on the cognitive therapy described originally for depression (Blazer 1997), has not been adapted for anxiety in older adults to date. However, there is little evidence that non-structured psychotherapy is of benefit in treating generalized anxiety or panic episodes in late life.

The benzodiazepines (e.g., alprazolam, oxazepam, lorazepam) are the cornerstone of pharmacological therapy for the anxiety disorders (Table 35-12). These drugs repeatedly have been demonstrated to be effective for the control of anxiety when compared with a placebo and are relatively free of side effects. They are generally well tolerated by persons of all ages but present unique problems when prescribed to older persons. For example, the half-life of the benzodiazepines may be increased dramatically in late life, with diazepam (2.5-5.0 mg) having a half-life nearing 4 days in persons in their 80s. Older persons are also more susceptible to benzodiazepines' potential side effects, such as fatigue, drowsiness, motor dysfunction, and memory impairment. Clinicians must be especially careful when prescribing benzodiazepines to older individuals who drive. Therefore, the shorter-acting benzodiazepines, such as alprazolam (0.25 mg), oxazepam (15 mg), and lorazepam (0.5 mg), given two to three times a day, have been preferred agents in late life. Nevertheless, short-acting drugs in some older patients may lead to brief withdrawal episodes during the day and a rebound of anxiety

Antidepressant medications may also have a role in treatment of anxiety. For example, escitalopram has been shown to be efficacious in the treatment of generalized anxiety disorder in older adults (Lenze et al. 2009). Other SSRIs and serotonin-norepinephrine reuptake inhibitors (SNRIs; e.g., venlafaxine, duloxetine) may be effective in the treatment.

Other agents are generally less effective in controlling late-life anxiety. The antidepressant agents are useful in treating anxiety mixed with depression. Nevertheless, in many older persons with a mixed anxiety-depression syndrome, the depressive symptoms improve while the antidepressant is being used, yet the anxiety symptoms persist. Therefore, a combination of a benzodiazepine and an antidepressant is sometimes used. Some have suggested that β-blockers such as propranolol (10 mg twice daily) are valuable in treating anxiety disorders. These drugs must be monitored carefully, given their propensity to slow the heart rate.

Suspiciousness and Agitation

A frequent symptom in older adults, especially older adults experiencing cognitive impairment, is suspiciousness, which may range from increased cautiousness and distrust of family and friends to overt paranoid delusions. Among suspicious or paranoid older persons, a unique group has been described, especially in the European literature, for many years. Late-life paraphrenia (or, as more recently labeled, very-late-onset schizophrenia) has been distinguished from both chronic schizophrenia and dementia and is characterized by marked paranoid delusions in older adults who nevertheless maintain function in the community for months or even years (Almeida et al. 1995). Persons experiencing paraphrenia are predominately women and often live alone. However, marked suspiciousness and overt psychosis in conjunction with cognitive impairment are a more common manifestation of the syndrome. There is sparse empirical justification for disaggregating late-life paraphrenia from other psychotic disorders.

The predominant delusions encountered in older persons are persecutory delusions and somatic delusions. Persecutory delusions often revolve around a single theme or a series of connected themes, such as family and neighbors conspiring against the older person or a delusion of sexual abuse. Somatic delusions often involve the gastrointestinal tract and frequently reflect the older person's fear that he or she is experiencing cancer. Regardless of the etiology of suspiciousness and paranoid delusions, when older persons believe they are threatened from the social environment, often because they do not understand what is happening in that environment, agitation becomes paramount. Decreased cognitive functioning is the most common cause of suspiciousness and agitation and may result from both a loss of ability to evaluate the environment and direct neuropathological changes. Agitation in the suspicious older person is an acute symptom that may require emergency management, as described later in this section (see "Treatment").

Frequency and Origins

Suspiciousness and paranoid behavior were found in 17% of persons in one community survey (Lowenthal 1964), and a sense of persecution was reported in 4% in another survey (Christenson and Blazer 1984). Thus, the perception by older persons that they live in a hostile social environment is common and represents a much larger proportion of older individuals than those who would be diagnosed with schizophrenia or suspiciousness secondary to cognitive impairment. Some of these suspicions may be justified if the older person lives in an unsafe community or has been the victim of fraud. Among persons in the community, less than 1% have schizophrenia or a paranoid disorder.

Many different disorders may lead to suspiciousness, delusions, and agitation (Table 35-13). Chronic schizophrenic disorder, which has its onset earlier in life and persists into late life, is perhaps the most easily identified cause of late-life suspiciousness (Vahia et al. 2012). Because schizophrenia tends to be characterized by a decline in social function over the life cycle and a shorter life expectancy (although the prognosis of schizophrenia varies greatly from person to person), chronic schizophrenia that persists into late life and yet leaves the older person relatively free of other symptoms is uncommon. Nevertheless, persons may experience severe symptoms of schizophrenia in early life or midlife and then enter a period of remission from which they do not relapse with further schizophrenic behavior until late life. Schizophrenia-like illness also may have its first onset in late life. These patients are less likely to experience negative symptoms and neuropsychological impairment and often respond to lower dosages of antipsychotic medication. Usually, depression and organic mental disorders do not contribute to these late-onset schizophrenia-like states. In contrast, organic mental disorders and late-onset depression are frequently associated with some psychotic symptoms.

Late-onset delusional disorder, with mild to moderate symptoms, is a more frequent cause of suspiciousness in late life. Delusions, often of being persecuted by family and friends, usually center on a single theme or a connection of themes. For example, an older woman may become convinced that her daughter was instrumental in the death of her husband (or that the daughter neglected her father during a chronic illness). The mother then may not listen to reason regarding the daughter's behavior and may never forgive the daughter for the perceived abuse or neglect. These delusions may lead to a withdrawal of affection, financial support, and social contact with the daughter.

Suspiciousness and agitation in late life are also commonly caused by psychotic symptoms associated with neurocognitive disorders. These symptoms, in contrast to late-onset delusional disorder, wax and wane over time in severity and in content. In some cases, the older adult functions well and does not appear to be disturbed by the delusional thoughts, even though the thoughts are frequently expressed. Imagined infidelity by a marriage partner is a common example. If the delusion does not create subjective stress and/or problems in management, regular evaluation of the patient and family without the use of medications is the preferred intervention. Persecutory delusions are most common and often emerge when the older person's environment is changed. Suspiciousness and agitation may derive from medications or from localized brain damage (e.g., in alcohol abuse and Huntington's chorea). Suspiciousness, however, usually results from the neurocognitive disorders such as AD and vascular neurocognitive disorder. For some persons with AD, paranoid thoughts may dominate other symptoms of the dementing illness, especially in the early stages. Perhaps the most common encounter psychiatrists have with suspicious older persons is with patients with AD who have become a management problem because of suspiciousness and agitation. Suspiciousness and agitation are also frequent symptoms of acute confusion.

Despite the range of disorders that may lead to suspiciousness in older persons, some investigators have suggested common psychobiological contributors to the syndrome in late life. A family history of suspiciousness and delusional thought is uncommon among suspicious older persons, and therefore hereditary contributions are probably less important than at earlier stages of the life cycle. Degeneration of subcortical tissues with aging may disrupt neurotransmission and higher brain functions, which in turn contribute to a deficiency in maintaining attention and filtering information, symptoms that have been associated with psychotic thinking. That women are more likely to experience more severe syndromes of suspiciousness than men in late life (in contrast to the equal sex distribution of psychoses earlier in life) has led some investigators to suggest that menopause and the resultant decrease in estrogen binding to dopamine receptors may place women at risk who were previously protected from developing suspicious thinking. Sensory deprivation also has been identified as a potential risk factor for suspiciousness, regardless of the underlying disorder. Social isolation also may contribute to suspiciousness.

Diagnostic Workup

The key to the diagnostic workup of the suspicious older person is the psychiatric evaluation. Because delusional thinking and agitation usually render the patient's history inaccurate, family members should be interviewed to review the patient's behavior, especially any change in behavior. Previous psychotic or delusional episodes should be documented, as well as previous treatment. Clinicians evaluating the suspicious older person should remember that older adults are occasionally abused by family members and, therefore, the seemingly delusional description of family behavior by the older individual may contain some truth.

Treatment

The management of suspiciousness in older adults requires 1) ensuring a safe environment; 2) initiating a therapeutic alliance; 3) considering and, if appropriate, instituting pharmacological therapy (Table 35-14); and 4) managing acute behavioral crises. The clinician must first decide whether hospitalization is necessary. In general, paranoid older persons do not adapt well to the hospital. Change from familiar surroundings and interactions with strange persons tend to exacerbate the suspiciousness. Nevertheless, older patients often are so disabled in their behavior secondary to suspiciousness and agitation that hospitalization is necessary.

Once the older patient is hospitalized, the clinician must initiate a therapeutic alliance, which may be accomplished by taking a medical approach to the patient and expressing concern about all of the patient's physical and emotional concerns. Most suspicious older patients are quite accepting of medical care and are trusting of physicians. It is rarely necessary for clinicians to confront patients regarding suspicions or delusional thinking; therefore, older patients' responses to questions can be supported emotionally (e.g., "I understand your concern"), and clinicians do not need to agree with or challenge statements made by patients that are known to be untrue.

The cornerstone of managing the moderately to severely suspicious older patient is medication, especially antipsychotic agents (see Table 35-14). Medications most frequently used to treat older persons are risperidone, olanzapine, quetiapine, and haloperidol. Dosage of these agents is relatively small initially, and one-half of the dosage should be given during the evening. In a large controlled study, lower dosages of risperidone (1 mg/day) significantly improved symptoms of psychosis and aggressive behavior with fewer side effects compared with 2 mg/day (Katz et al. 1999). Dosages can be increased if necessary. Clinicians should be mindful of the FDA warning about atypical antipsychotics. Physicians who prescribe antipsychotic medications for the treatment of suspiciousness in an older adult should carefully monitor the success of these agents and should discuss the potential benefits and potential risks with the patient and family. If the drug is deemed not successful—for example, if the target symptoms do not change with the medication—then it should be discontinued, given the significant side effects that may result. Tardive dyskinesia is five to six times more prevalent in elderly than in younger patients (Jeste 2000).

Finally, the physician must be prepared to deal with severe agitation and violent behavior (Table 35-15). Medications alone will not control these behaviors. Physicians must work with the nursing staff to prevent such behavior in patients at risk while they are in the hospital and must instruct families on methods of prevention when these patients are at home.

Periods of severe agitation are usually brief and, if managed properly, are soon forgotten by the older patient. Then the physician once more can work toward establishing a sustained therapeutic relationship with the patient.

Depression

Depression is one of the more common and the second most disabling of the geriatric psychiatry syndromes (after memory loss) (Blazer 2003). Late-life depression that is not comorbid with physical illness and/or a dementing disorder is characterized by symptoms similar to those experienced at earlier stages of the life cycle, with some significant differences. Depressed mood is usually apparent in the older adult but may not be a spontaneous complaint. Older persons are more likely to experience weight loss (as opposed to weight gain or no change in weight) during a major depressive episode and are less likely to report feelings of worthlessness or guilt. Although older persons experience more difficulty with cognitive performance tests during a depressive episode, they are no more likely than persons in midlife to report cognitive problems subjectively. Complaints of cognitive dysfunction are common in more severe depressive episodes regardless of the person's age. Persistent anhedonia associated with a lack of response to pleasurable stimuli is a common and central symptom of late-life depression. Older persons are also more likely than younger persons to exhibit psychotic symptoms during a depressive episode. Studies have suggested that executive function is impaired in older adults with depression and that this impairment may be associated with a higher likelihood of relapse and recurrence of symptoms (Alexopoulos et al. 2000). Memory impairment in the context of geriatric depression may persist after successful treatment of the depressive symptoms (Lee et al. 2007). Table 35-16 summarizes the characteristics of older adults with depression.

Frequency and Origins

In community surveys, older adults are less likely to be diagnosed as having major depression than are persons in young adulthood or middle age. Depressive symptoms, however, are about equally prevalent across the life cycle and increase in the oldest old. Standardized interviews reveal that l%-3% of persons in the community are diagnosed as having dysthymia (Blazer et al. 1987). Major depression is much more prevalent, however, among older persons in the hospital and in long-term care facilities, ranging from 10% to 20% (Koenig et al. 1988). In a population-representative study in the United States, overall depression prevalence was 11.19% (Steffens et al. 2009). Prevalence was similar for men (10.19%) and women (11.44%). Whites and His-panics had nearly three times the prevalence of depression found in African Americans.

Late-life depression fits well in the bio-psychosocial model of psychiatric disorders (Blazer and Hybels 2005). Although a hereditary predisposition to depression is less likely among persons in late life who are experiencing a first onset of depression, a number of biological factors are associated with late-life depression. Poor regulation of the hypothalamic-pituitary-adrenal axis, as well as disruption of the sleep cycle and other circadian rhythms, is more likely to be present among older persons than among younger persons. These problems also have been associated with major depression. In recent years, considerable attention has been focused on the association of depression with lesions in subcortical structures and their frontal projections in the brain (Alexopoulos et al. 1997; Krishnan et al. 1997). Most older persons are satisfied with their lives and are not psychologically predisposed to depression. Nevertheless, some experience a demoralization and a despair resulting not only from incapacities due to aging but also from a sense of not having fulfilled their life expectations. Older persons must adapt to many adverse life experiences, especially losses of relatives and friends, yet they are often more likely to respond to these losses without difficulty than are persons who are younger. Older persons, for example, expect that they will lose family and friends through death, and those family and friends whom they do lose often have suffered chronic illnesses for some time, thus allowing older persons to grieve the loss, in part, before the actual loss.

Although major depression is relatively infrequent among older persons, it can be a challenging disorder to manage. Older persons also may experience bipolar disorder, with a first-onset manic episode after age 65 years. Psychotic depressions are more common in late life than at other stages of the life cycle (Meyers 1992). Other common types of late-life depression include depression associated with a medical condition or medication, such as a depressed mood secondary to antihypertensive medications, and depression associated with common neuro-cognitive disorders, such as AD and vascular neurocognitive disorder. Medical illness, such as hypothyroidism, frequently leads to a mood disorder. An adjustment disorder with depressed mood secondary to physical disability and/or chronic illness is among the most frequent causes of depressed mood among older individuals.

Diagnostic Workup

The patient's history and a collateral history from a family member are the keys to making the diagnosis of depression in late life. Although older persons may exhibit some tendency to "mask" their depressive symptoms, a careful interview almost invariably reveals significant depression if it is present. The history should be complemented by a thorough mental status examination with attention to disturbances of motor behavior and perception, the presence or absence of hallucinations, disturbances of thinking, and thorough cognitive testing. Psychological testing may be implemented to distinguish depression from dementia but should not be performed in the midst of a severe depressive episode. The laboratory workup of the depressed older adult is presented in Table 35-17. Some tests, such as the blood count and measurement of vitamin B₁₂ and folate levels, are useful in screening for medical illnesses that may present with depressive symptoms. The thyroid panel is essential in the diagnosis of the depressed older patient, given that subclinical hypothyroid disorders are frequently uncovered in the workup.

Although the abnormalities in sleep associated with depression frequently parallel those associated with normal aging, experienced polysomnographers can distinguish them. MRI is optional despite the association of subcortical white matter hyperintensities with late-life depression. The physician ordering laboratory tests for a depressed older patient also must consider the potential adverse health consequences for an older adult experiencing a severe or chronic mood disorder. For example, major depression is associated with decreased bone mineral density, placing older women with depression at greater risk for osteoporosis (Michelson et al. 1996).

Treatment

Clinical management involves pharmacotherapy, electroconvulsive therapy (ECT), psychotherapy, and work with the family. The pharmacological treatment of choice at present is one of the new-generation antidepressant medications (Table 35-18). Despite the advent of these newer agents, some geriatric psychiatrists still prefer to first administer one of the secondary amines, such as nortriptyline or desipramine, in healthy older adults. Each has relatively low anticholinergic effects and is known to be an effective antidepressant. Postural hypotension is the most troublesome side effect that older adults usually encounter when treated with the tricyclic antidepressants. The SSRIs fluoxetine, sertraline, paroxetine, citalopram, and escitalopram can be used at somewhat lower dosages than are prescribed at earlier stages of the life cycle (e.g., 10 mg/day for paroxetine). The most common adverse effects that limit the use of SSRIs are agitation and persistent weight loss. Paroxetine has been shown to significantly (but not dramatically) improve the symptoms of minor depression and dysthymia at dosages between 10 and 40 mg/day (Williams et al. 2000). The use of antidepressant medications, primarily the SSRIs, has increased dramatically over the past 25 years, with more than 10% of elderly persons ages 75 years and older taking antidepressants at any given time (Blazer 2000). If treatment with an SSRI is not successful, then the second-choice medications are usually the SNRIs, such as venlafaxine (beginning at around 37.5 mg/day) or duloxetine (beginning with 20 mg/day) (Alexopoulos et al. 2001).

The older person who has previously responded to ECT, does not respond to antidepressant medications, or experiences significant side effects from the medications may be a candidate for ECT. Presence of psychotic depression is also an indication for ECT. With proper medical support, ECT is a safe and effective treatment for older adults. Despite a higher level of physical illness and cognitive impairment, even the oldest patient with severe major depression may tolerate ECT as well as younger patients do and may demonstrate similar or better acute response. Unilateral nondominant ECT is preferred. If the treatment is successful, then maintenance ECT at progressively extended intervals is a method of preventing relapse. Magnetic seizure therapy and repetitive transcranial magnetic stimulation may be used for treatment-resistant depression in elderly patients (George et al. 1999; Lisanby et al. 2001).

Note. ^a Total daily dose of citalopram should not exceed 20 mg due to risk of cardiac arrhythmia.

Several studies have demonstrated the effectiveness of cognitive and behavioral therapies (including interpersonal psychotherapy) in outpatient treatment of older persons who have major depression without melancholia (Lynch and Aspnes 2004). Cognitive therapy also may be an adjunct for severe melancholic depressions that are treated concomitantly with medications. In a large controlled trial of patients older than 59 years with major depression, maintenance therapy with interpersonal therapy and paroxetine was significant in preventing or delaying recurrence (Reynolds et al. 2006). For long-term (2-year) maintenance, medications were more effective than psychotherapy. Cognitive-behavioral therapy is well tolerated by older people because of its limited duration and educational orientation, as well as the active interchange between therapist and patient.

Any effective therapy for depression in older persons must include work with the family. Families are often the most important allies of the clinician working with depressed older patients. Families should be informed as to the danger signs, such as potential for suicide, in a severely depressed older family member. In addition, the family can provide structure for reengaging a withdrawn and depressed older person into social activities.

Substance Use

Substance use problems in later life are emerging public health concerns. Although all drugs can be abused, two categories of substance use are of particular concern: alcohol use and nonprescription use of prescription medications. Substance use in older adults is a hidden yet emerging epidemic. As the current baby boom generation enters later life, these problems will only increase in frequency due to the already greater burden of these problems among this cohort. Not only is the frequency of substance use increasing among older adults, but these elders bring complexities to their care that challenge the usual evidence-based practices and frustrate clinicians, patients, and families. Older adults rarely experience substance use problems in isolation. Physical health problems, comorbid mental health conditions such as depression and memory loss, and the medications prescribed to treat these problems complicate care.

Common signs and symptoms of substance use disorders are listed in Table 35-19 (Oslin and Mavandadi 2012). None may be initially associated by the clinician with a substance use problem, and therefore the underlying cause may be missed. Older persons who appear in emergency rooms with any of these signs and symptoms should always be evaluated for substance use. Both the patient and the family should be asked about use. Older persons are at increased risk because lean body mass and total body water volume decrease relative to body fat, leading to increased serum concentrations, absorption, and distribution of alcohol and drugs in the body.

Clinicians are not as likely routinely to screen elders for substance use, and older adults do not volunteer this information readily. Barriers to early identification or treatment may include insufficient knowledge, denial of substance problems by both the clinician and the patient, hurried office visits, stigma or shame about substance use, a general reluctance to seek professional help, lack of financial resources or transportation, comorbid conditions that complicate diagnosis or treatment (e.g., cognitive impairment), and a shrinking social support network (Center for Substance Abuse Treatment 1998). Compared with younger adults, older adults are less likely to report or perceive their alcohol or drug use as excessive or problematic.

Frequency and Causes

Alcohol use problems are by far the most frequent substance use problems in elderly individuals. In one large study, 66% of elderly male respondents and 55% of female respondents reported alcohol use during the past year, 13% of men and 8% of women reported at-risk use, and over 14% of men and 3% of women reported binge drinking (Blazer and Wu 2009). A small yet clinically important proportion of older adults (1.4%) reported nonprescription use of prescription pain relievers during the previous year (Wu and Blazer 2011). Combinations of acetaminophen and hydrocodone or propoxyphene were the most commonly used drugs. The use of illegal substances is rare in older adults but not absent. In a national survey of elders, 2.6% of subjects used marijuana, and 0.41% used cocaine (Wu and Blazer 2011). Marijuana use, however, is not a frequent cause of help seeking. The vast majority of these elders began use of illicit substances before age 30. Their referral in later life is often because of concomitant problems with the law (Wu and Blazer 2011).

Risk factors for substance use problems are presented in Table 35-20 (Oslin and Mavandadi 2012). In general, substance use decreases with age, but two caveats are critical. First, younger age cohorts today carry a significantly higher lifetime frequency of substance use than cohorts ages 65 years and older; therefore, these middle-aged persons will likely be more burdened with substance use problems in later life than current elders, placing increased pressure on an already inadequately trained and over-committed workforce serving older adults with substance use problems (Eden et al. 2012). Second, although substance use is less frequent among older adults, it is often more problematic given unique characteristics of the older adults. These include a greater likelihood to be taking multiple prescription medications and to have one or more comorbid physical and/or psychiatric problems. Older adults are often more isolated, which is a trigger for a number of risks, such as reduction in role obligations and absence of encouragement from family and friends.

Treatment

The first step in treating the older adult with a substance use problem involves detoxification and withdrawal. Symptoms of alcohol withdrawal include autonomic hyperactivity (increase in blood pressure and heart rate), restlessness, sleep problems, and, if severe, hallucinations, delirium, and even seizures. Older adults should be withdrawn gradually with a substitute for alcohol, such as diazepam.

Evidence-based studies have demonstrated that nonpharmacological treatment of both alcohol and substance use problems in later life is effective, although the studies have been sparse and small. The least intensive approaches to therapy should be employed initially in the office if serious withdrawal symptoms are absent (Center for Substance Abuse Treatment 1998; Wu and Blazer 2011). A brief intervention (such as a 10-to 15-minute discussion with the treating physician) is the recommended first step. If this is not successful, a variety of interventions may be employed, as listed in Table 35-21. Strategies that address age-specific psychological, social, and health concerns and contexts are recommended to incorporate into treatment plans for older substance abusers. The Center for Substance Abuse Treatment (2005) recommends the following components of any approach to treating substance use in older adults: 1) emphasis on age-specific treatment (e.g., mixed twelve-step programs may not be appropriate for the elderly); 2) use of supportive, nonconfrontational approaches that build self-esteem (in contrast to confrontational therapies often used with younger adults); 3) focus on cognitive-behavioral approaches (as opposed to more nondirective therapies); 4) development of skills for improving social support; 5) recruitment of counselors who are trained and motivated to work with older adults; and 6) use of age-appropriate pace and content. Compliance with treatment is usually improved if the setting for treatment remains in the primary care office.

For many years, disulfiram was the only medication available for long-term treatment of alcohol dependence, but it was seldom used because of adverse side effects. More recently, naltrexone and acamprosate have been demonstrated to be effective treatments.

Key Clinical Points

• Acute confusion is much more common in hospitalized older adults than usually recognized. Careful screening is necessary to identify these patients.
• Working with the family of a patient with memory loss is key to easing the suffering of the patient and preventing institutionalization prior to when absolutely necessary.
• Good sleep hygiene is more important than pharmacological management of insomnia in older adults.
• Generalized anxiety is usually comorbid with other conditions, such as depression or physical illness. Diagnosing comorbid conditions is the first step to managing anxiety in older adults.
• Suspiciousness and agitation are the most disruptive symptoms of dementing disorders.
• Uncomplicated depression in late life is as responsive to treatment as in midlife. Depression comorbid with physical illness or memory loss is much more difficult to treat.
• Substance use is increasing in frequency in older persons, which is particularly problematic given their often compromised health and use of prescribed medications.

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Suggested Readings

Alexopoulos GS, Katz IR, Reynolds CF III, et al: The Expert Consensus Guideline Series. Pharmacotherapy of depressive disorders in older patients. Postgrad Med Special Report, October 2001, pp 1-86

Blazer DG: Psychiatry and the oldest old. Am J Psychiatry 157:1915-1924, 2000

Blazer DG: Depression in late life: review and commentary. J Gerontol A Biol Sci Med Sci 58:249-265, 2003

Blazer DG, Steffens DC, Busse EW (eds): The American Psychiatric Publishing Textbook of Geriatric Psychiatry, 4th Edition. Washington, DC, American Psychiatric Publishing, 2009

Inouye SK: Delirium in older persons. N Engl J Med 354:1157-1165, 2006