Dyssomnias are primary disorders of initiating or maintaining sleep or of excessive sleepiness and are characterized by a disturbance in the amount, quality, or timing of sleep. This section includes Primary Insomnia, Primary Hypersomnia, Narcolepsy, Breathing-Related Sleep Disorder, Circadian Rhythm Sleep Disorder, and Dyssomnia Not Otherwise Specified.
Dyssomnias (Insomnia) Classification & Clinical Findings
Patients may complain of difficulty getting to sleep or staying asleep, intermittent wakefulness during the night, early morning awakening, or combinations of any of these. Transient episodes are usually of little significance. Stress, caffeine, physical discomfort, daytime napping, and early bedtimes are common factors.
Psychiatric disorders are often associated with persistent insomnia. Depression is usually associated with fragmented sleep, decreased total sleep time, earlier onset of REM sleep, a shift of REM activity to the first half of the night, and a loss of slow wave sleep - all of which are nonspecific findings. In manic disorders, sleeplessness is a cardinal feature and an important early sign of impending mania in bipolar cases. Total sleep time is decreased, with shortened REM latency and increased REM activity. Sleep-related panic attacks occur in the transition from stage 2 to stage 3 sleep in some patients with a longer REM latency in the sleep pattern preceding the attacks.
Difficulty Initiating and Maintaining Sleep (DIMS, Insomnia). Inability to sleep may take the form of prolonged initial latency to sleep, recurrent nocturnal awakenings, or early morning awakening without the ability to return to sleep. Insomnia is an extremely common complaint that causes high levels of frustration and significant misery. For reasons that are inexplicable, insomnia is frequently trivialized by the clinician and treated pharmacologically without attention to the underlying cause of the complaint. Inability to initiate or maintain sleep is a symptom that must be explored with the same approach the clinician uses to assess other medical complaints. As in most disorders, a careful history is the most significant diagnostic tool. Exploring the patient's daily schedule in an orderly fashion is often markedly revealing. A sleep log helps document patterns that suggest specific disease. The schedule of daily activities gives insight into the patient's personality and discloses habits that contribute to poor sleep hygiene. All medical history is relevant, and illnesses that may cause nocturnal arousal are particularly important. A family history of sleep disorder and history of childhood sleep behavior are useful. A review of drug use, including prescription medications, home remedies, caffeine, alcohol, and illicit drugs, is critical.
Excessive Daytime Sleepiness (DOES). Excessive daytime sleepiness is defined as the tendency to fall asleep inappropriately when sedentary. Patients with excessive daytime sleepiness may or may not demonstrate hypersomnolence, that is, excessive sleep during a 24-hour period. Patients with chronic disorders of excessive daytime sleepiness often accept their sleepiness as normal. The clinician should look for a history of excessive daytime sleepiness in any situation presenting as chronically reduced performance, including dementia, or in situations suggesting episodic inattention, such as automobile accidents. Instead of complaining of sleepiness, many patients cite blackouts, forgetfulness, poor concentration, automatic behavior, and amnestic spells. Children may have poor school performance or behavioral problems, including apparent hyperactivity. These situations require the taking of a sleep history that includes questioning the patient as to whether or not sleeping occurs during sedentary activities, social activities, driving, and eating. Sleepiness needs to be distinguished from fatigue and disorders of consciousness secondary to encephalopathy.
Within the classification of the dyssomnias, the sleep abnormalities must be fundamental to the existence of the disorder. Psychiatric and medical disorders that influence sleep, as only one component of the clinical presentation, are not included in the ICSD definition of dyssomnia. The dyssomnias are further divided into three groups: the intrinsic sleep disorders, the extrinsic sleep disorders, and the circadian rhythm sleep disorders. Intrinsic sleep disorders are thought to originate within the body; examples are narcolepsy and obstructive sleep apnea. Extrinsic sleep disorders originate outside the body; these include poor sleep hygiene and environmental disruption. Circadian rhythm sleep disorders represent disorders of the timing of the sleep-wake cycle within the 24-hour day.
Intrinsic Sleep Disorders. "Psychophysiologic insomnia is a disorder of somatized tension and learned sleep-preventing associations that results in a complaint of insomnia and associated decreased functioning during wakefulness." These patients usually do not have evidence of underlying psychiatric disease but may be highly focused on their insomnia. Overconcern with the process of going to sleep is alerting, induces increased tension, and becomes a sleep-preventing association. The precipitant for this disorder may be a period of acute insomnia associated with an external stressor (see the discussion of adjustment sleep disorder). A characteristic pattern emerges: inability to obtain satisfactory sleep for a few nights induces fear that another sleepless night will follow. Patients report that they feel alert as soon as they try to initiate sleep. They toss and turn, watch the clock, and become frustrated and angry that they are unable to sleep. Often sleep improves in a new environment that is free of the usual external sleep-onset associations.
Psychophysiologic insomnia can be treated with relaxation techniques in combination with methods that "decondition" the patient's negative associations with sleep onset. A technique known as stimulus-control therapy, proposed by Bootzin, is highly effective. The patient is instructed to (1) go to bed only if sleepy; (2) use the bed only for sleeping and sexual relations, not as a place to read, write, or watch television; (3) get up and leave the bedroom if not asleep within 10 to 15 minutes and engage in a nonstimulating activity until sleepiness is perceived; (4) repeat this step as many times as necessary throughout the night; (5) maintain a fixed schedule of awakening each morning; and (6) take no naps during the day.
"Sleep state misperception is a disorder in which a complaint of insomnia or excessive sleepiness occurs without objective evidence of sleep disturbance." There is a small but distinct group of patients who complain of insomnia because of inability to recognize that they have slept. These patients are most clearly identifiable when there is a report of absolute lack of sleep. Polysomnographic recording reveals normal sleep latency, a normal number of arousals and awakenings, and normal sleep duration, but the patient perceives poor or absent sleep. This disorder needs to be distinguished from the phenomenon of paradoxical improvement in sleep during overnight recording in the sleep laboratory, which occurs in patients with psychophysiologic insomnia. In the latter disorder, sleep may improve in a novel environment, such as the sleep laboratory, and this improvement is appreciated by the patient.
Sometimes patients report sleepiness that cannot be verified on objective testing with the multiple sleep latency test (MSLT, discussed later), and this may be a sleep state misperception. Sleepiness, however, is more difficult to measure than presence or absence of sleep.
The underlying pathophysiologic mechanisms of sleep state misperception are not understood. Many patients who report near-absence of sleep are mistakenly treated with hypnotic medications for years without improvement. The existence of this disorder underscores the importance of polysomnographic evaluation of patients with chronic sleep complaints.
"Idiopathic insomnia is a lifelong inability to obtain adequate sleep that is presumably due to an abnormality of the neurological control of the sleep-wake system." This disorder may also be termed childhood-onset insomnia. Unlike "short sleepers," who feel rested despite short sleep duration, patients with this disorder complain of chronically poor performance caused by poor sleep. Polysomnographic evaluation reveals increased sleep latency, decreased efficiency, and increased arousals, but the cause of the disrupted sleep is not apparent. Because of the chronicity of the disorder, secondary sleep disorders such as psychophysiologic insomnia and hypnotic dependence often develop. There is no effective treatment except directing attention to conditions that may aggravate the underlying insomnia.
"Narcolepsy is a disorder of unknown etiology which is characterized by excessive sleepiness that typically is associated with cataplexy and other REM sleep phenomena such as sleep paralysis and hypnogogic hallucinations." Narcolepsy was first defined as a distinct disorder in 1880 by Gelineau, who described the syndrome as a "rare, little known neurosis characterized by imperative need to sleep." It is now known that the disorder is not rare. The prevalence is estimated at between 2 and 16 per 10,000 persons. The onset of symptoms occurs typically in the second or third decade, and both sexes are equally affected. A family history is noted in approximately one third of cases.
The discovery of REM sleep was followed by the finding that patients with narcolepsy have abnormal REM physiology. It is now accepted that the major manifestations of narcolepsy represent a disorder of control mechanisms that regulate REM sleep. Episodes of REM occur at the wrong time, intruding on wakefulness, and the physiologic components of this sleep state dissociate and appear independently. These major symptoms are referred to as the narcolepsy tetrad: (1) excessive daytime sleepiness, (2) cataplexy, (3) hypnogogic hallucinations, and (4) sleep paralysis. Few patients report all of these symptoms, especially in the early stages of the disorder, but almost all narcoleptic patients have evidence of excessive daytime sleepiness.
The cardinal symptom of narcolepsy is excessive daytime sleepiness, and approximately 10% of patients complain of this symptom alone. The tendency to sleep inappropriately may have a gradual or an abrupt onset. History taking typically reveals that patients remember brief lapses of attention in sedentary situations years before presentation to a physician. With time, sleepiness is evident in clearly inappropriate situations, such as during driving, holding business conversations, eating, or engaging in sexual intercourse. Patients are frequently able to recognize impending drowsiness and take measures to alert themselves. Irresistible sleep attacks are characteristic, however, and tend to occur when the urge to sleep has been delayed. Two features are unique to the naps of narcoleptics: (1) dreaming during naps is common and (2) brief naps of 5- to 10-minute duration are remarkably refreshing.
Cataplexy is a sudden, usually brief, loss of muscle tone induced by emotion. The presence of cataplexy is considered diagnostic of narcolepsy, but only 60% to 80% of patients experience this symptom, and it may occur years after the onset of sleepiness. Rarely, cataplexy is the presenting symptom of the disorder. Idiopathic cataplexy may exist but is poorly described. Laughter and anger are the most common precipitants, but the emotional trigger may be specific to the patient. The weakness that develops usually involves the muscles of the face or the supporting muscles of the legs; it may be so mild as to give only the sense that the face will not move properly or so profound as to cause a sudden fall. The appearance of facial tremulousness can be confused with seizure activity. Occasionally, patients have difficulty speaking. Consciousness is maintained during a cataplectic episode, but prolonged episodes may be immediately followed by REM sleep. Cataplexy is the result of sudden skeletal muscle atonia, sparing extraocular eye movements and diaphragm motion. Deep tendon reflexes are absent during the episode. This atonia is similar to that which occurs during normal REM sleep. Cataplexy thus seems to represent a dissociation of normal REM phenomena, occurring inappropriately during waking.
Abuse of alcohol may cause or be secondary to the sleep disturbance. There is a tendency to use alcohol as a means of getting to sleep without realizing that it disrupts the normal sleep cycle. Acute alcohol intake produces a decreased sleep latency with reduced REM sleep during the first half of the night. REM sleep is increased in the second half of the night, with an increase in total amount of slow wave sleep (stages 3 and 4). Vivid dreams and frequent awakenings are common. Chronic alcohol abuse increases stage 1 and decreases REM sleep (most drugs delay or block REM sleep), with symptoms persisting for many months after the individual has stopped drinking. Acute alcohol or other sedative withdrawal causes delayed onset of sleep and REM rebound with intermittent awakening during the night.
Heavy smoking (more than a pack a day) causes difficulty falling asleep - apparently independently of the often associated increase in coffee drinking. Excess intake near bedtime of caffeine, cocaine, and other stimulants (eg, over-the-counter cold remedies) causes decreased total sleep time - mostly NREM sleep - with some increased sleep latency.
Sedative-hypnotics - specifically, the benzodiazepines, which are the most commonly prescribed drugs to promote sleep - tend to increase total sleep time, decrease sleep latency, and decrease nocturnal awakening, with variable effects on NREM sleep. Withdrawal causes just the opposite effects and results in continued use of the drug for the purpose of preventing withdrawal symptoms. Antidepressants decrease REM sleep (with marked rebound on withdrawal in the form of nightmares) and have varying effects on NREM sleep. The effect on REM sleep correlates with reports that REM sleep deprivation produces improvement in some depressions.
Persistent insomnias are also related to a wide variety of medical conditions, particularly delirium, pain, respiratory distress syndromes, uremia, asthma, and thyroid disorders. Adequate analgesia and proper treatment of medical disorders will reduce symptoms and decrease the need for sedatives.
In general, there are two broad classes of treatment for insomnia, and the two may be combined: psychological (cognitive-behavioral) and pharmacologic. In situations of acute distress, such as a grief reaction, pharmacologic measures may be most appropriate. With primary insomnia, however, initial efforts should be psychologically based. This is particularly true in the elderly to avoid the potential adverse reactions of medications. The elderly population is at risk for complaints of insomnia because sleep becomes lighter and more easily disrupted with aging. Medical disorders that become more common with age may also predispose to insomnia.
Psychological strategies should include educating the patient regarding good sleep hygiene: (1) Go to bed only when sleepy. (2) Use the bed and bedroom only for sleeping and sex. (3) If still awake after 20 minutes, leave the bedroom and only return when sleepy. (4) Get up at the same time every morning regardless of the amount of sleep during the night. (5) Discontinue caffeine and nicotine, at least in the evening if not completely. (6) Establish a daily exercise regimen. (7) Avoid alcohol as it may disrupt continuity of sleep. (8) Limit fluids in the evening. (9) Learn and practice relaxation techniques. A recent study suggests that cognitive behavioral therapy for insomnia was as effective as zolpidem with benefits sustained 1 year after treatment.
The clinician should also discuss any myths or misconceptions about sleep that the patient may hold.
When the above measures are insufficient, medications may be useful. Pharmacologic measures currently rely primarily on safe hypnotic medications that are difficult to overdose with. Lorazepam (0.5 mg nightly), temazepam (7.5-15 mg nightly), zolpidem (5-10 mg nightly), and zaleplon (5-10 mg nightly) are often effective for the elderly population and can be given in larger doses - twice what is prescribed for the elderly - in younger patients. It is important to note that short-acting agents like triazolam or zolpidem may lead to amnestic episodes if used on a daily ongoing basis. Longer-acting agents such as flurazepam (half-life of > 48 hours) may accumulate in the elderly and lead to cognitive slowing, ataxia, falls, and somnolence. In general, it is appropriate to use medications for short courses of 1-2 weeks. The medications described above have largely replaced barbiturates as hypnotic agents because of their greater safety in overdose and their lesser hepatic enzyme induction effects. Antihistamines such as diphenhydramine (25 mg nightly) or hydroxyzine (25 mg nightly) may also be useful for sleep, as they produce no pharmacologic dependency; their anticholinergic effects may, however, produce confusion or urinary symptoms in the elderly. Trazodone, an atypical antidepressant, is a non-habit-forming, effective sleep medication in lower than antidepressant doses (25-150 mg at bedtime). Priapism is a rare side effect requiring emergent treatment.
Triazolam has achieved popularity as a hypnotic drug because of its very short duration of action. Because it has been associated with dependency, transient psychotic reactions, anterograde amnesia, and rebound anxiety, it has been removed from the market in several European countries. If used, it must be prescribed only for short periods of time.