A thorough history, physical examination, and basic laboratory studies are important to fully evaluate the patient and rule out medical and medication-related causes of insomnia and depression. Additionally, the selection of the appropriate antidepressant medication (selective serotonin reuptake inhibitors, tricyclic antidepressants [TCAs], monoamine oxidase inhibitors, or atypical antidepressants), adequate dosages, and a sufficient trial period are imperative in the treatment of depression in the elderly. In seniors, an adequate antidepressant trial is longer than that for younger adults, with a complete response often seen after six to 12 weeks. Nuances related to medication therapy in the geriatric population should be clearly expressed by pharmacists in recommendations and educational communications. The impact of aging and medical conditions associated with aging on the pharmacokinetic profile of a medication and the increased risk of associated side effects must be understood with regard to geriatric dosage guidelines, disease-drug contraindications (eg, TCAs and cardiac conduction defects), and drug interactions (eg, CYP450 inhibition and possible toxicities).

When sleep medication is deemed the best course of treatment after careful consideration of nonpharmacologic interventions (eg, sleep hygiene, stimulus-control therapy, and sleep-restriction therapy) in the elderly, short-acting nonbenzodiazepine hypnotics (zolpidem or zaleplon) are recommended. These medications reduce both sleep latency, due to their quick absorption and onset, and the risk of daytime sleepiness the following day, due to their short half-life. Caution should be exercised when a longer-acting hypnotic is prescribed in a geriatric patient since associated side effects may be particularly pronounced in seniors. Longer-acting hypnotic agents may be associated with changes in sleep architecture such as a reduction in delta or deep sleep, morning hangover with excessive daytime sleepiness, impaired motor coordination, and visuospatial problems that may contribute to an increased risk of injury. In an attempt to prevent rebound insomnia, a very gradual taper is recommended when termination of treatment is warranted.

Conclusion

When caring for older patients, it is important to make the distinction between pathological changes and normal aging. Remaining cognizant of this helps to avoid not only dismissing a treatable pathology as merely an accompaniment to old age but also treating a natural aging process as a disease while overlooking the possibility of iatrogenic effects.

Insomnia may be a symptom of medical and psychiatric conditions, changes in lifestyle, or medications, among other precipitating factors. When an elderly patient presents with complaints of insomnia, the clinician should assess for possible depression since many seniors do not seek help for or verbally express symptoms of this condition, which is common among them and is associated with morbidity and mortality. By raising awareness that insomnia, a symptom of depression for many people, may be reported more readily than depressive symptoms, pharmacists may become involved in identifying those at risk for depression and in facilitating the appropriate evaluation, intervention, and education of patients and their families and caregivers.

Information on the importance of sleep to overall health and well being is a good starting point in counseling an individual regarding treatment for insomnia. A discussion on lifestyle and an action plan for the implementation of both drug and non-drug interventions should occur. Lifestyle interventions include obvious but important advice regarding a regular sleep schedule, a comfortable, dark bedroom environment, and avoidance of factors that interfere with sleep onset like caffeine, vigorous exercise, large meals, and alcohol near bedtime. Goals of treatment, realistic expectations, and expected duration of therapy should be reviewed. Reviewing individual patient factors influencing the type of drug therapy recommended reassures the person how the hypnotic will relieve their specific sleep problem. For example, a discussion regarding the lack of daytime sleepiness with zaleplon and zolpidem is useful when a patient expresses concerns over falling asleep at work. A discussion of how a drug like temazepam requires dosing one to two hours prior to sleep for maximum sleep-inducing effects is necessary to prevent the patient from considering that drug ineffective. A better understanding of how a drug works can help patients appreciate the effect of the medication in their situation. Patients can benefit from being better educated regarding realistic expectations from their hypnotic drug. Patients should understand that hypnotic efficacy means a return to normal sleep patterns with its natural variation of occasional delayed sleep latency and nighttime awakenings. Patients should understand that success of hypnotic drug therapy is not measured by immediate unconsciousness that lasts eight hours every night.

Conclusion

The availability of newer drugs with an extremely short duration of effect offers the potential to dramatically change how insomnia is treated pharmacologically. Historically, hypnotic drugs have been taken prior to bedtime in anticipation of sleep difficulty. Drugs such as zaleplon, with a duration of effect of only one hour, now allow the treatment of insomnia when it occurs — either at bedtime or after the patient experiences difficulty falling asleep during the night. Just as the history of hypnotic agents has unfolded over the last 30 years and caused dramatic changes in prescribing patterns, it is certain that the agents will continue to evolve and will yield better and better pharmacological treatment options for insomnia. Clinicians must take full clinical advantage of what hypnotic agents offer, become familiar with what newer agents may offer, and maximize benefits and minimize adverse consequences through appropriate drug selection, dosing, and patient education.

Zolpidem: Zolpidem was marketed in the United States in the early 1990s as the first nonbenzodiazepine hypnotic with a specific effect on the omega-1 receptor. Due to its specificity, zolpidem lacks anticonvulsant, muscle relaxant, and anxiolytic effects, and has been shown to have less effect on sleep architecture and next-day performance compared to benzodiazepines. Its hypnotic efficacy is the same as that of benzodiazepine hypnotics. Rebound insomnia, memory impairment, dependence and withdrawal are uncommon. A 10 mg dose of zolpidem is recommended and has demonstrated hypnotic efficacy for five weeks without affecting sleep stages or producing tolerance, rebound, or detrimental effects on psychomotor performance. Nightly doses greater than 10 mg do not provide additional hypnotic effect and are associated with greater adverse effects. In the elderly, the recommended initial dose of zolpidem is 5 mg.

Because much of the clinical literature on triazolam is based on higher doses of 0.25 to 0.5 mg, its greater reports of rebound insomnia, memory and psychomotor impairment compared to zolpidem may be due to differences in dosage rather than any inherent differences in the two drugs. A review comparing zolpidem and triazolam concludes that the two drugs have similar pharmacokinetic and pharmacodynamic effects in humans. When given in usually recommended, equipotent doses, the drugs do not differ in efficacy, tolerability, residual effects, memory impairment, rebound insomnia, abuse potential, or other adverse effects. An evaluation of acute behavioral and subject-rated effects of different doses of zolpidem, triazolam and temazepam found dose-dependent differences but not significant differences among the three drugs. Expected adverse effects of zolpidem include dizziness, headache and gastrointestinal distress in 3%–5% of patients. Case reports of dependence and tolerance usually involve higher than recommended doses. Amnesia involving no recollection of telephone conversations when awakened within one hour of taking 5 or 10 mg of zolpidem has been reported.

Zaleplon: Although zaleplon has a pharmacologic profile similar to that of zolpidem, zaleplon offers a rapid absorption and onset of effect, no active metabolites, and an elimination half-life of one hour. This pharmacokinetic profile of very rapid onset and offset suggests zaleplon will be most useful for patients with sleep-onset insomnia but not those with early morning awakening. Zaleplon is also useful for patients who need to take a hypnotic agent for rapid effect but who have limited time before they must awaken. To date, hypnotic agents have primarily been used at bedtime in anticipation of sleep difficulty. Zaleplon is useful for treating insomnia when it occurs, even during the night and early morning, and for promoting naps at circadian times of heightened alertness. Clinical trials available thus far suggest that zaleplon 10 mg is an effective rapidly acting hypnotic without evidence of next-day residual sedation, memory impairment or rebound effects. Zaleplon, like zolpidem, has been studied in doses that are effective yet low enough not to be associated with the rebound insomnia seen with higher dose triazolam.

Zaleplon is rapidly absorbed, with peak plasma levels achieved within 1.1 hours after a 10 mg dose. In comparison, a 10 mg dose of zolpidem achieves peak plasma levels after 1.7 hours. The mean elimination half-life of zaleplon is one hour with a range of 0.8 to 1.4 hours. The pharmacokinetics and safety data do not differ significantly in younger adults and the elderly when given a 10 mg dose.

In several dose response studies evaluating single doses of zaleplon from 1 to 60 mg, zaleplon was generally well tolerated in doses up to 30 mg. The most frequent adverse effects associated with zaleplon included dizziness and headache. Symptoms began to appear approximately 30 minutes after dosing, peaked at one to two hours, and were no longer evident after four hours. No psychomotor impairment was seen with doses up to 15 mg. At 60 mg (six times the therapeutic dose), zaleplon produced clinically significant drowsiness, dizziness, and impaired coordination, but no effect on short-term memory.

A comparison of pharmacodynamic effects of different doses of zaleplon and zolpidem found that on many measures of cognitive and psychomotor effects, 20 mg of zaleplon was comparable to 10 mg of zolpidem. The order of agonist potency was found to be as follows: placebo < zaleplon 10 mg < zaleplon 20 mg < zolpidem

10 mg < zolpidem 20 mg. No rebound insomnia was observed in 106 patients discontinued from zaleplon 2–20 mg after five consecutive nights of use, and adverse effects were as common with placebo as with active drug.

Although zaleplon and zolpidem are similar in duration of sleep, they differ in residual side effects. After 10 mg doses, zolpidem has residual effects on performance and memory tests for up to five hours. Zaleplon has no such effects after two hours.

For adults, a bedtime dose of 10 mg is recommended; for elderly patients, an initial dose of 5 mg is recommended. Zaleplon can be given like other hypnotic drugs before bedtime, or it can be given in the middle of the night after a patient experiences difficulty falling asleep or staying asleep. Zaleplon’s very rapid onset and short duration of effect allows it the unique indication to be given anytime during the night as long as at least four hours of sleep time remain after dosing. Until zaleplon became available, hypnotic drugs had always been given in anticipation of sleep difficulty prior to bedtime. Hypnotic drugs could not be given during the night or repeated during the night for fear of residual hangover effects. Zaleplon is the first drug whose labeling allows for dosing during the night once sleep difficulty occurs because its short half-life minimizes the risk of morning hangover effects.

Rebound Insomnia and Memory Impairment: In the late 1980s and early 1990s, clinicians became aware that the benefits of a shorter half-life drug on next-day performance were countered by the increased risk of rebound insomnia and new memory impairment (anterograde amnesia) that was not commonly seen with the longer half-life drugs. These effects are also dose-related and can be minimized by use of the minimum effective dose consistent with appropriate clinician and patient expectations. Comparison of five benzodiazepine hypnotic agents found only the shorter half-life drugs to cause significant rebound insomnia.Rebound insomnia was defined as worsening of sleep compared to baseline. Triazolam in nightly doses of 0.5 mg caused rebound insomnia in each of four studies, was greatest the first night after withdrawal, and lasted from two to four nights.

Benzodiazepines can produce an impaired ability to store new memory while short-term memory is spared. The ability to use and remember previously acquired knowledge remains intact. The impaired ability to consolidate new memory seems to be independent of sedation. Anterograde amnesia is dose-related, seen more frequently with the higher potency benzodiazepines (e.g., triazolam, alprazolam, clonazepam, lorazepam, midazolam), and not dependent on elimination half-life. In addition, the elderly are more sensitive to this effect than are younger patients. There is also evidence to suggest that some tolerance develops to the sedative and psychomotor effects of benzodiazepines, but no tolerance develops to the anxiolytic and amnestic effects.

Sedating antidepressants have been used to induce sleep in doses lower than those generally used for depression in an attempt to avoid the benzodiazepines’ liabilities of dependence, rebound insomnia, and withdrawal effects. Low-dose tricyclic antidepressants (TCAs), such as amitriptyline or doxepin, were once the most commonly used antidepressants for insomnia. Trazodone in doses of 50–200 mg at bedtime has more recently become the preferred antidepressant for insomnia. Trazodone’s hypnotic efficacy has not been directly compared to that of the benzodiazepines. It has been studied only in populations of depressed patients with insomnia, and usually the insomnia was secondary to SSRI use.Trazodone offers prominent sedation with little anticholinergic effect, but a slow onset and noticeable orthostatic hypotensive effect. There is no concern regarding dependence or withdrawal after as long as four months of use. Compared to TCAs, trazodone offers better safety in overdose. Priapism, a rare but serious adverse effect, can occur with daily doses of trazodone as low as 50–200 mg. Male patients must be counseled about the possibility of this adverse effect.

Benzodiazepines

Pharmacokinetic Differences: Flurazepam, the first benzodiazepine hypnotic drug, available in the United States since 1974, offers a rapid onset of effect but a long duration of effect. Flurazepam has an active metabolite with an elimination half-life of up to five days. Such a long elimination half-life minimizes the risk of rebound insomnia, but makes morning hangover, or daytime sedation, more likely. Doses of 15 mg of flurazepam or 20 mg of temazepam have been shown to impair coordination skills necessary for driving on the morning after use. Subsequently, benzodiazepines with shorter elimination half-lives were marketed as hypnotics. Temazepam has an elimination half-life of 8–20 hours, and triazolam 2–6 hours. Temazepam has the disadvantage of a slow onset of effect compared to flurazepam and triazolam. More recently, estazolam and quazepam were marketed in the United States. Estazolam is most similar to temazepam; it has a slow onset of effect of 1–2 hours and an elimination half-life of 8–24 hours. (The pharmacokinetic profiles of estazolam and other selected hypnotic agents are outlined in TABLE 2.) Quazepam is very similar to flurazepam in that it has a fast onset of effect, an intermediate to long elimination half-life, but overall, a long duration of effect due to an active metabolite whose half-life is 2–5 days. Quazepam was the first hypnotic drug to offer specificity for the omega-1 benzodiazepine receptor. However, this unique mechanism is quickly lost because the active metabolite of quazepam is N-desalkyl-flurazepam, the same active metabolite as flurazepam. Temazepam, estazolam, and triazolam do not have clinically important active metabolites.

Antihistamines: Most over-the-counter drug treatments for insomnia contain the antihistamines diphenhydramine, doxylamine or hydroxyzine. Individuals with insomnia report that these agents cause drowsiness and help them fall asleep. The most prominent disadvantage is the next-day “hang-over” effects of psychomotor impairment and anticholinergic side effects that can be intolerable. These agents are less effective for treating insomnia than are the benzodiazepines. Also, they typically are not effective for chronic insomnia because tolerance to the sleep-inducing effects often develops after one to two weeks of continuous use.

Melatonin: Melatonin is a naturally occurring hormone secreted by the pineal gland, which is located in the center of the brain. The pineal gland is connected to the retina via a nerve pathway that runs through the suprachiasmatic nucleus of the hypothalamus, the body’s circadian clock. The pineal gland produces melatonin (a byproduct of serotonin metabolism) only during the nocturnal phase of the circadian cycle and only in relative darkness. Exogenous melatonin has been promoted and studied as a treatment for insomnia, under the theory that rising melatonin levels “fool” the brain into sleep.

Melatonin currently has no established place in the treatment of insomnia, according to the International Consensus Conference on the Treatment of Insomnia. Melatonin has not demonstrated efficacy comparable to that of established hypnotics in relieving primary insomnia. Preliminary data suggest melatonin may be useful for treating abnormalities of the circadian clock, such as shift work, delayed-sleep phase syndrome (a persistent inability lasting more than six months to fall asleep and arise at conventional times — e.g., sleeping 1 AM to 9 AM instead of 11 PM to 7 AM), jet lag, and the recurring insomnia of the blind. (Loss of sight interferes with visual cues for natural circadian sleep regulation. People with blindness experience nocturnal sleep disruption and have a higher incidence of involuntary daytime naps and insomnia.) However, the only randomized double-blind trial of placebo and three regimens of melatonin (5 mg at bedtime, 0.5 mg at bedtime, and 0.5 mg taken on a shifting schedule) for jet lag found no difference in symptoms across all four groups.

Before pharmacists can recommend melatonin, important questions regarding its safety must be addressed. Emerging data regarding a vasoconstrictive effect on coronary arteries dictate a cautious approach. Depression and liver disease associated with melatonin have also been described in case reports. In addition, high doses of melatonin appear to have contraceptive effects in some women. Other alternative remedies, such as valerian and kava-kava, are used to treat insomnia even though evidence for efficacy, purity and safety is lacking.

Sleep experts universally recommend behavioral interventions, either alone or with adjunct medication, for the treatment of insomnia. When interventions such as keeping a regular sleep schedule; creating a dark, comfortable bedroom environment; and establishing a pre-bedtime ritual are effective, insomnia can be resolved without the expense of drugs or drug side effects. Specific interventions should be tailored to the type of sleep complaint. For example, eliminating alcohol for at least three to four hours before bedtime can alleviate fragmented sleep if alcohol is the cause. Avoiding exercise, heavy meals, or caffeine before bedtime can also benefit some patients. Light therapy is particularly beneficial for patients with circadian-rhythm sleep disorders, where an individual may delay sleep at night, then sleep in the next morning. Forcing the individual to awaken earlier, and exposing their face to 30–60 minutes of sunlight can “reset” the biologic clock so they naturally become sleepy earlier in the evening.

Mechanisms of Hypnotic Drugs

Benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) by increasing its affinity for its receptor. The benzodiazepine (BNZ) receptors also are known as omega-1, omega-2 and omega-3 receptors. The BNZ-1 receptors are located in areas of the brain that are involved in sedation, and BNZ-2 receptors are highly concentrated in areas responsible for cognition, memory, and psychomotor functioning. The BNZ-3 receptors are located in peripheral tissues and not involved in hypnotic efficacy. While benzodiazepines bind to at least these three omega receptor subtypes, zolpidem and zaleplon selectively bind to BNZ-1 receptors. Although hypnotic efficacy may not differ between benzodiazepines and the newer selective agents, the nonbenzodiazepine drugs theoretically should have less central adverse effects on cognition, memory, and psychomotor function. Compared to benzodiazepines, these agents have little effect on the normal stages of sleep, and few if any anxiolytic, anticonvulsant, or muscle relaxant properties.

Definition of Hypnotic Efficacy

Defining efficacy for a hypnotic drug is very difficult because efficacy is patient-dependent. Clinical trials evaluate hypnotic efficacy in a sleep laboratory, measuring time to sleep onset, frequency and duration of awakenings, total duration of sleep, and changes in sleep stages. None of these measurements can be accurately assessed in the usual treatment setting, so the clinician must rely exclusively on the patient’s self-report of his/her sleep before and after use of a hypnotic drug. Two pitfalls must be avoided in order to accurately evaluate hypnotic drug efficacy — inappropriate patient expectations and the patient reporting only his/her worst nights.

Clinicians must set an appropriate expectation for hypnotic effectiveness when a patient receives an initial prescription. Many patients believe the therapeutic endpoint of a hypnotic is a rapid onset of unconsciousness that is uninterrupted for eight hours. This expectation is unrealistic. A hypnotic is effective if it facilitates sleep that is both restful and restorative and allows usual functioning while awake. Normal sleep consists of some nights with occasional interruptions in sleep and some nights with six instead of eight hours of sleep. Counseling against unrealistic expectations may prevent patient-driven dose escalation, which increases the risk of adverse outcomes from hypnotic utilization.

In addition to setting appropriate expectations, the patient should be instructed to use a diary or journal to track sleep quality. This allows both patient and clinician to see averages over time. Without a diary, patients typically remember only their worst nights of sleep difficulty, which can lead to unnecessary increases in dosage.

In terms of dose-dependent hypnotic efficacy, the appropriate use of hypnotic agents has dramatically changed based upon lessons learned from triazolam. It was learned that 0.25 to 0.5 mg of triazolam was a significantly larger dose than was necessary to achieve optimal hypnotic effect, and withdrawal symptoms were significant. With doses of 0.125 to 0.25 mg, on the other hand, withdrawal effects are uncommon. A minimum effective dose for a hypnotic drug is usually not associated with significant rebound on withdrawal; rather, rebound insomnia upon withdrawal develops when doses are in excess of the therapeutic dose.

An understanding of normal sleep is essential in recognizing and effectively treating insomnia. Although individual sleep needs vary, between six and nine hours of total sleep are necessary to feel rested and refreshed and to have optimal daytime functioning. Polysomnography is not needed to evaluate typical insomnia in the clinical setting but provides valuable information on normal physiologic sleep.

Sleep is divided into five stages. Stage 1 is the initial stage, also known as “relaxed wakefulness.” Stage 2 is also relatively light yet makes up about 50% of total sleep time. Deep, restorative sleep takes place in stages 3 and 4. Rapid eye movement (REM) sleep occurs in cycles throughout the night. Some hypnotic agents affect the time spent in different stages of sleep.

Sleep is divided into five stages. REM (rapid eye movement) sleep and NREM (non-rapid eye movement) sleep, which is further divided into 4 stages. The usual time it takes to fall asleep is between 15 and 30 minutes. Stage 1 of NREM, also known as “relaxed wakefulness,” initiates sleep. Approximately 50% of total sleep time is spent in Stage 2, a relatively light sleep also known as alpha rapid-wave sleep. Hypnotic drugs typically increase time spent in Stage 2 sleep. Fifteen to twenty percent of total sleep time is spent in Stages 3 and 4, or delta sleep. Delta sleep is the deep, restorative sleep time during which immune function is fortified and growth hormone is secreted. Time spent in delta sleep diminishes as patients age; at 75 years old, the stage is often nonexistent. NREM sleep is essential for rest, rejuvenation and the maintenance of overall health. The significance of REM sleep is not as well known. The body increases time spent in REM if deprivation occurs due to drugs, disease or fragmented sleep. Cycles of REM sleep occur throughout the night, approximately every 90 minutes. Time spent in REM increases toward the last three to four hours of sleep.

Patient Assessment

Individuals with insomnia are often seen by many different healthcare providers and are treated for a variety of concurrent health conditions. Thorough patient assessment includes taking inventory of all medications and medical problems to determine possible causes of insomnia. Ma huang (ephedrine), phenylpropanolamine (Dexatrim), caffeine, and nicotine gum are just a few examples of stimulating drugs known to interfere with sleep. Other possible drug causes of insomnia are listed in TABLE 1.

A discussion to determine the nature and duration of insomnia as well as any associated symptoms is the first step in managing the condition. Questions such as, “How long does it take you to fall asleep? How long are you able to maintain sleep? How do you feel the next day?” are all necessary in developing an individualized treatment plan. Awakening with sore limbs and overall less restful sleep can signify restless legs syndrome (RLS) or periodic limb movements during sleep (PLMS). Frequent awakenings accompanied by gasps for air may indicate sleep-disordered breathing or sleep apnea. These more serious primary sleep disorders require assessment and treatment by a sleep specialist. Empiric treatment of insomnia with hypnotics is dangerous for sleep apnea patients. Objective assessment of sleep by a family member or bed partner is optimal because individuals with chronic insomnia underestimate the amount of sleep they get and overestimate the time it takes them to fall asleep. Assessing functional ability associated with insomnia before and after treatment is essential in measuring the success of each therapeutic intervention.

Insomnia negatively affects as many as 10% of the U.S. population, and its impact on medical illnesses, work productivity, and quality of life is only recently being fully appreciated. The need to effectively treat insomnia means pharmacists must understand the relative role of nonpharmacologic and pharmacologic treatment options. Drug treatment options continue to evolve, with benzodiazepine hypnotics being challenged by the newer nonbenzodiazepine drugs zolpidem and zaleplon. In addition, many patients are increasingly turning to alternative treatments such as melatonin.

Diagnosis and Epidemiology

Insomnia is diagnosed when an individual has measurable difficulty initiating or maintaining sleep. There are many causes of insomnia, including stress, environmental changes (new surroundings, temperature, and noise), medical and psychiatric illness, medications, and substance use or abuse.

Two Gallup surveys of representative samples of the adult U.S. population asking if respondents “ever had difficulty sleeping” found prevalence rates of 36% and 49%, while 9% and 12% reported “regular” or “frequent” sleep difficulty.

A screening of nearly 2,000 primary care patients in a large health maintenance organization found that 10% reported current major insomnia, defined as taking at least two hours to fall asleep nearly every night.

By definition, transient insomnia lasts for a few days; short-term insomnia persists for up to three weeks, and chronic insomnia is diagnosed when insomnia continues for greater than three weeks. Investigating potential causes and duration of insomnia is necessary to develop an effective treatment plan, and to decide whether medication and/or behavioral interventions should be utilized.

Societal Impact

Insomnia has a profound impact on society and public health in many ways. Chronic insomnia can indicate untreated illness. Additionally, the condition contributes to injury and illness and may cause loss of productivity and diminished quality of life.

In a study of 10,778 men and women aged 35–59 years, poor sleepers were more than twice as likely as good sleepers to have ischemic heart disease in the following six years after onset of poor sleep. Insomnia is associated with gastrointestinal, renal, and musculoskeletal disorders, in addition to primary sleep disorders such as sleep apnea and periodic limb movements (PLMS) during sleep. Primary insomnia patients have been shown to have impaired immune system function due to reduced natural killer cell activity. Insomnia and excessive daytime sleepiness in the elderly is one of the leading predictors of institutionalization.

Health screening surveys have shown that insomnia sufferers of all ages experience excessive daytime sleepiness, predisposing them to diminished cognitive ability, poor attention, lower productivity and decreased quality of life. One study assessing work and daily activities showed insomniacs reporting 10 times as many days absent from work than those without insomnia. Other U.S. surveys on insomnia describe difficulty completing simple tasks, coping with stress, making decisions, and functioning in family and social relationships.

Driver sleepiness is a causative factor in at least 2% of U.S. motor vehicle crashes. Peaks of driver sleepiness occur in the early morning and late afternoon, the natural circadian pattern for drowsiness. Long-haul truck drivers are perhaps the most extensively studied group of sleep-deprived drivers. In one study, 45 drivers had at least one six-minute interval of drowsiness while driving, as judged by analysis of video recordings of their faces. Eight drivers were objectively assessed as drowsy, and two drivers fell into the initial stage of sleep, as detected by polysomnography. Polysomnography is the measurement of physiologic sleep through EEG (electroencephalogram), EOG (electrooculogram) and EMG (electromyelogram).

Polysomnography objectively observes and measures sleep parameters in the laboratory; it is particularly useful in determining drug effects on sleep.

Absenteeism at work, higher rates of chronic illness, traffic accidents and overall diminished quality of life create significant indirect costs of insomnia, which are difficult to measure. Those aside, the direct cost of insomnia (including healthcare system utilization, prescription and nonprescription medication, and alcohol, which some patients use in an attempt to remedy insomnia) is estimated at $13.9 billion for 1995.

Why is it so important to assess the risk for depression in a senior with insomnia who may not feel comfortable with the subject or who feels stigmatized by self-reporting a depressed mood? As mentioned earlier, a depressive disorder is among the most common causes for sleep disturbances in the elderly. Furthermore, depression is one of the most common psychiatric disorders among the elderly, with clinically significant depressive symptoms appearing in 30% of institutionalized seniors and in 8% to 15% of community-dwelling elderly. It has been shown that patients with any medical diagnosis were twice as likely to develop depression than were patients without a medical diagnosis. Depression increases mortality in hospitalized patients, increases medical morbidity, worsens the outcomes of medical disorders, increases the perception of poor health and the use of medical services, and increases the economic burden on the health care system.

It must not be overlooked that depression is the psychiatric disorder most likely to raise the risk of successful suicide in the elderly (TABLE 3). Statistics reveal that suicide rates in the United States are highest in people 70 and older. Suicide in white men is 45% more common in those ages 65 to 69 than in those ages 15 to 19. It is about 85% more common in those ages 70 to 74 and greater than three and one half times more common in men older than 85 than in men in the 15-to-19 age group. While suicide attempts are rarer in older people than in younger people, they are more lethal as a result of more careful planning, more lethal self-destructive acts, and fewer indications of the intent. Younger patients are more likely to seek or respond to suicide interventions than are the elderly. Although mood disorders are more prevalent in women than men across the spectrum of age, successful suicide is disproportionately higher in males, especially in elderly men.

Diagnostic Questioning and the Geriatric Depression Scale (GDS)

Unless specific questions are asked, depression may go unrecognized, as it is well known that as many as 70% of seniors who commit suicide were seen by their primary care physicians within the last few weeks of their lives. Presentation of depression in the elderly varies as compared with that in the younger population. Rather than psychological complaints, somatic complaints often predominate in the clinical scenario. Although older patients often do not report a dysphoric mood, apathy and withdrawal are common. Loss of self-esteem is prominent, and guilt is less common. The inability to concentrate, with a resultant impairment of memory and other cognitive functions, is commonly seen. In addition to a review of systems, health care practitioners can question elderly patients regarding: sleep disturbance, appetite changes, trouble concentrating, lack of energy, and loss of interest. Whenever possible, in addition to ongoing primary care, referral for consultation with an experienced geriatric psychiatrist and/or psychologist is helpful in diagnosing and managing depressive disorders.

Senior care pharmacists may find the Geriatric Depression Scale (GDS) helpful in identifying depressed geriatric patients for referral for a full evaluation. The GDS may also be used subsequently by the pharmacist as an outcomes measure of antidepressant therapy in the management of depression.