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Chapter: Essentials of Psychiatry: Sleep and Sleep-Wake Disorders


The etiology of primary insomnia is unclear, but it may be dependent more on the factors that perpetuate it than on those that precipitated it.



Primary Insomnia


According to DSM-IV-TR criteria, primary insomnia is a subjec-tive complaint of poor, insufficient, or nonrestorative sleep last-ing more than a month; associated with significant distress or impairment; and without obvious relationships to another sleep, medical, or psychiatric disorder or physiological effects of a sub-stance. Primary insomnia is similar to some insomnia diagnoses in the International Classifi cation of Sleep Disorders, includ-ing psychophysiological insomnia, which is often ascribed toconditioned arousal factors; sleep state misperception, in which the magnitude of the subjective complaint often exceeds that of the objective abnormality; and idiopathic insomnia, with a child-hood onset and lifelong course.


The etiology of primary insomnia is unclear, but it may be dependent more on the factors that perpetuate it than on those that precipitated it. In general surveys of the prevalence of in-somnia in the population, about one in three people reported “in-somnia” during the previous year, about one in six described it as “serious”, and about one in 12 called it “chronic” (Ancoli-Israel and Roth, 1999). The rates of insomnia are higher in women than in men, in the elderly than in the young, and in the lower than in the higher socioeconomic classes. In a survey conducted by the Gallup Poll for the National Sleep Foundation (Ancoli-Israel and Roth, 1999), the most common complaint of insomniacs is waking up feeling drowsy rather than specific complaints about sleep, implying that the sleepiness insomniacs experience could be associated with some morbidity. Compared with transient insomniacs or normal control subjects, chronic insomniacs re-ported greater difficulty enjoying family and social relationships, greater difficulty concentrating, more problems with memory, greater frequency of falling asleep while visiting friends, and more automobile accidents due to sleepiness. Nevertheless, only about 5% of patients with chronic insomnia ever sought medical attention specifically for insomnia. Only a minority of patients have ever used prescription sleeping pills. On the other hand, most psychiatrists do not routinely inquire about difficulties with sleep and wakefulness. If these patients with chronic or serious insomnia are to be helped, psychiatrists must be proactive and ask specific questions about sleep and its disorders


The prevalence of primary insomnia is not known. Treat-such as temperament and lifestyle, ineffective coping and de-fense mechanisms, inappropriate use of alcohol or other sub-stances, maladaptive sleep–wake schedules and excessive worry about poor sleep. The harder these individuals try to sleep, the worse it is. They keep themselves awake by their apprehensions: “If I don’t get to sleep right now, I’ll make a bad impression to-morrow”. Cognitive–behavioral therapy (CBT) therefore is very effective, as shown by Morin and colleagues (1993). An 8-week group intervention aimed at changing maladaptive sleep habits and altering dysfunctional beliefs and attitudes about sleepless-ness was effective in reducing sleep latency, waking up after sleep onset, and early morning awakening, and in increasing sleep effi-ciency. In a second study, Morin and colleagues (1999) found that CBT and pharmacological approaches were both effective for the short-term management of insomnia but that improvement was better sustained over time with the behavioral treatment.




Diagnosis and treatment of chronic insomnia are often challeng-ing and difficult. Both the psychiatrist and the patient must be for-bearing and realistic as they jointly explore the evolution, causes, manifestations and ramifications of the sleep complaint. In part, the diagnosis of primary insomnia is reached by exclusion after a careful differential diagnosis of other causes. Simple answers and simple solutions are rare. Even if insomnia is initially precip-itated by a single event or condition, chronic insomnia is usually maintained by various predisposing and perpetuating factors. For example, a business woman in her early thirties had insomnia during a period of intense stress in her business, but it continued long after the stress had been satisfactorily resolved. Factors that contributed to chronicity included her lifelong somewhat obses-sive, anxious personality structure and after the onset of her in-somnia, her gradually escalating concerns about her insomnia; these resulted in advanced sleep phase as she tried to spend more time in bed for “rest” and use of wine and sleeping pills at bed-time to sleep. If all these factors can be properly sorted out and dealt with, both the psychiatrist and the patient will be gratified.



Treatment of Chronic Primary Insomnia


Clinical management is often multidimensional, involving psy-chosocial, behavioral and pharmacological approaches. The relationship with the psychiatrist can often be important since many insomniac patients are skeptical that they can be helped overtly. They are focused on the symptom rather than the un-derlying causes, and are not psychologically minded. Behavioral treatments, in combination with addressing sleep hygiene, may be helpful in treating psychophysiological and other insomnias. Relaxation training (progressive relaxation, autogenic training, meditation, deep breathing) can all be effective if overtaught to become automatic. Two other behavioral therapies have been shown to be effective for insomnia: stimulus control and sleep restriction therapy (Bootzin and Nicassio, 1978; Spielman et al., 1987; Morin et al., 1994).


The aim of stimulus control therapy is to break the nega-tive associations of being in bed unable to sleep (Table 59.5). It is especially helpful for patients with sleep-onset insomnia and prolonged awakenings. Sleep restriction therapy (Table 59.6) is based on the observation that more time spent in bed leads to more fragmented sleep. Both therapies may take 3 to 4 weeks or longer to be effective.


A wide variety of sedating medications have com-monly been used as sleeping pills including benzodiazepinesment of insomnia should, insofar as possible, be directed at iden-tifiable causes, or those factors that perpetuate the disorders.



imidazopyridines (zolpidem), pyrazolopyrimidines (zaleplon), chloral hydrate, antihistamines (diphenhydramine, hydroxyzine, doxylamine), certain antidepressants (amitriptyline, doxepin, trimipramine, and trazodone), barbiturates and over-the-counter medications. However, they do vary in their pharmacokinetic properties and side effects (Table 59.7). The ideal sleeping pill would shorten latency to sleep; maintain normal physiological sleep all night without blocking normal behavioral responses to the crying baby or the alarm clock; leave neither hangover nor withdrawal effects the next day; and be devoid of tolerance and side effects such as impairment of breathing, cognition, ambula-tion and coordination. Furthermore, sleeping pills should not be habit-forming or addictive. Unfortunately, the ideal sleeping pill has not yet been found. Sleeping pills, if given in appropriate doses, are effective compared with placebo at least from a few days to a few weeks. More recent, developed sleeping pills (such as zaleplon) have demonstrated their superiority after 1 year in double-blind studies with a parallel placebo group. The question, however, is what is the lowest adequate dose for an individual patient, that is, the dose that will promote sleep with the least number of side effects.


The duration of action of these medications is important for several reasons (Table 59.8). Drugs with long half-life me-tabolites may have next-day hangover effects and tend to ac-cumulate with repeated nightly administration, especially in the elderly, who metabolize and excrete the drugs more slowly than do the young. In addition, long half-life metabolites may act addictively or synergistically the next day with alcohol, with drugs with sedative side effects, or during periods of decreased alertness, such as the afternoon dip in arousal levels. Because the elderly are more sensitive to both the benefits and the side effects at a given dose than are younger patients, a dose for the elderly



and debilitated patient should normally be about half of that for young and middle-aged patients.


Short half-life hypnotics usually produce less daytime sedation than long half-life drugs, but they often result in more rebound insomnia when they are discontinued. Whereas nearly all hypnotics and sedatives can produce amnesia, the problem may be more common with some short half-life drugs, especially for material that is learned during the periods of peak concentra-tions of drugs, for example, if the subject is awakened during the middle of the night. Administration of zaleplon 4 hours or more before arising in the morning does not appear to be associated with impairment in motor performance.


Patients should be educated about the anticipated benefits and limitations of sleeping pills, side effects and appropriate use, and should be followed up by office visits or phone calls regularly if prescriptions are renewed. Although hypnotics are usually pre-scribed for relatively short periods of time (2–6 weeks at most), about 0.5 to 1% of the population uses a hypnotic nearly every night for months or years. Whether this practice is good, useless, or bad remains controversial. Treatment of these patients should focus on the lowest possible effective dose – intermittently if pos-sible – for the treatment of insomnia.


Hypnotics are relatively contraindicated in patients with sleep-disordered breathing; during pregnancy; in substance abus-ers, particularly alcohol abusers; and in those individuals who may need to be alert during their sleep period (e.g., physicians on call). In addition, caution should be used in prescribing hypnotics to patients who snore loudly; to patients who have renal, hepatic, or pulmonary disease; and to the elderly.




Melatonin is synthesized and released from the pineal gland un-der dark ambient conditions at a time that is determined by the individual’s internal biological clock located within the SCN at the anterior portion of the hypothalamus. For individuals who are synchronized with the local light–dark environment, melatoninis usually secreted at night. The duration of secretion is approxi-mately 8 to 12 hours, depending partially on age, season of the year and lighting conditions. Bright light prevents or terminates secretion of melatonin. For these reasons, melatonin has some-times been called the “hormone” of the night or of sleep. In ad-dition, nocturnal melatonin secretion appears to be blunted with normal aging, with administration of beta-adrenergic blockers (propranolol, pindolol, metoprolol), and in some populations of patient (including patients with mood disorders, premenstrual depression and panic disorder).


The functions of melatonin in humans are poorly under-stood, although in animals it has been implicated in seasonal behaviors, breeding, reproductive physiology and timing of adolescence.


The limited database available suggests that melatonin may eventually have a role in the prevention and treatment of circadian and sleep disturbances. Some evidence suggests that it has intrinsic hypnotic effects. Laboratory studies suggest that people are more likely to sleep during the period of endogenous melatonin secretion than during periods of the day without melatonin secretion. Furthermore, some but not all studies suggest that melatonin (0.3–10.0 mg) may induce and maintain sleep when administered to normal subjects or, in a few studies, to individuals with insomnia, jet lag, or other circadian rhythm disturbances. In addition, it is possible that melatonin administration can shift the phase position of the underlying biological clock. The entraining effects of a dose of 0.5 mg melatonin act like a “dark pulse”, that is, the phase-response curve is nearly opposite that of light. Melatonin-induced phase-advanced rhythms when administered in the late afternoon or early evening, and it delayed the circadian clock when administered in the early morning. Future research is needed to fulfill the promise that melatonin can be used to prevent or treat some forms of insomnia or other sleep disorders, especially in the elderly, or in cases associated with circadian rhythm disorders (jet lag, shift work, the non-24-hour-day syndrome, phase displacement), neurological disorders, or psychiatric disorders.


The scientific clinical database for the use of melatonin in humans is limited at this time. Few well-designed clinical trials exist to establish clinical benefits or risks in specific disorders or conditions. Little is known about optimal doses, timing of me-latonin administration, duration of treatment, drug interactions, or populations at risk, if any. The safety of melatonin, especially melatonin available in health food stores, is unknown. Melatonin is currently treated by the US Food and Drug Administration as a nutritional supplement rather than a medication. Therefore, pu-rity of the product, safety, efficacy, and claims by manufacturers are not carefully regulated in the USA. Physicians are advised to maintain a watchful eye at this time and to be prudently cautious about recommendations to patients and the public about the uses and benefits of melatonin.


Because the timing of melatonin secretion is regulated by the SCN, investigators and clinicians can measure plasma levels of melatonin in dim light conditions to determine the phase position of the circadian clock. A useful revision of this technique is called the dim light melatonin onset (DLMO, pronounced “dil-mo”) (Lewy and Sack, 1989). Using repeated measures of DLMO over periods of weeks, Lewy and Sack (1989) demonstrated that the circadian clock was “free-running” in a significant proportion of totally blind individuals, that is, the time of day at which melatonin secretion began completely drifted around the clock in a clockwise direction about every 3 weeks. Since the patientstried to maintain a conventional bedtime (approximately 11PM– 7AM), their wake–sleep cycle was in and out of synchrony with their own internal clock, creating significant difficulties in sleep and alertness at times during the month. Furthermore, Lewy and Sack found that appropriately-timed administration of melatonin synchronized the internal clock with the external light–dark cycle.


As footnoted in Table 59.7, the US FDA has very recently approved the first noncontrolled medication to offer a unique mechanism of action that permits extended use for problems with sleep onset in adults. Through the selective binding of melatonin receptors in the SCN, the alerting signal is dampened thereby facilitating sleep onset. The recommended dosage for ramelteon is 8 mg. It is rapidly absorbed from the stomach and and broken down by first-pass metabolism in the liver through the CYP1A2 enzyme. Ramelteon should not be taken with high fat foods which apparently decrease absorption.


Primary Hypersomnia


A specific diagnostic category for primary hypersomnia exists in DSM-IV-TR, defining a disorder characterized by clinically significant excessive sleepiness of at least 1 month’s duration, with significant distress or impairment. The hypersomnia is not caused by another primary sleep disorder, a psychiatric disorder, a medical disorder, or a substance. Patients with primary hyper-somnia usually present with complaints of long and nonrestora-tive nocturnal sleep, difficulty awakening (“sleep drunkenness”), and daytime sleepiness and intellectual dysfunction; do not expe-rience the accessory symptoms of narcolepsy such as cataplexy, sleep paralysis and hypnagogic hallucinations; and often report frequent headaches and Raynaud’s phenomena.



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