Dyssomnias
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.
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.
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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