Difficulty with the initiation and maintenance of SLEEP is so common a problem as to be considered normal when it is situational, short-lived, and followed by refreshing compensatory sleep. From an evolutionary point of view, it is clear that adaptation to such environmental uncertainties as temperature fluctuation and the threat of predation often require the temporary postponement of sleep. In modern life the social equivalents of such environmental uncertainties are the ANXIETY and STRESS of urban life both of which cause AROUSAL which counteracts sleep.
When stress and anxiety become chronic, sleep may become so disrupted as to constitute a functionally significant disability, warranting symptomatic treatment by psychotherapy, behavioural manipulation (see COGNITIVE-BEHAVIOURAL THERAPY) or medication with SEDATIVES. But before any of these treatments is instituted, a thorough medical investigation, including special inquiry about specific sleep disorders, should be undertaken. This is because almost any medical or psychiatric disease may present with, or be complicated by, non-specific insomnia and these underlying specific conditions must be recognized and treated first. In the case of such specific sleep disorders as sleep APNOEA which can present as the excessive daytime sleep that insomniacs may complain of, treatment with sedatives is actually contraindicated because it may be harmful. And when insomnia is symptomatic, treatment of the underlying cause relieves the symptoms without recourse to sedatives.
Most normal individuals are able to fall asleep within 5–10 minutes with occasional increases in sleep latency to 30 minutes. Depending on the subject’s age, sleep is then maintained for 6–8 hours with one to three brief interruptions. In evaluating deviations from these norms, it should be recognized that (1) sleep, like all other biological variables, is extremely variable in that normal people may need as few as 4 or as many as 10 hours of sleep to feel rested; (2) that insomniacs often grossly exaggerate their sleeplessness (see PSEUDINSOMNIA); and (3) that the dynamic response to sleep deprivation protects the insomniac from harm due to sleep loss itself. Chronically anxious individuals typically complain of difficulty falling asleep while depressed subjects more typically go to sleep promptly only to awaken early in the morning (see DEPRESSION). For anxiety insomnia the treatment of choice is relaxation and sleep hygiene training and this naturalistic approach should be vigorously pursued before turning to sedative medication. There is, as yet, no physiological sedative and all of the available medications incur some risk with the frequently prescribed BENZODIAZE PINES being particularly problematic. If the insomnia is due to a major affective disorder the medications of choice are the TRICYCLICANTIDEPRESSANTS or amine reuptake blockers rather than sedatives.
Understanding insomnia in anxiety and depression is helped by recognizing the dynamics of sleep-wake neurophysiology. Waking is mediated by the AMINERGIC modulatory systems of the subcortical brain which energize the THALAMUS and CEREBRAL CORTEX. These systems are brought further into play by the anxiety and stress of real and imagined threats to an individual’s security. When so exaggerated, the aminergic systems oppose the CHOLINERGIC modulation of sleep and thus impair both deep NON-REM SLEEP and REM SLEEP preventing the profound physical and psychic restoration conferred by those sleep phases. The result is an unhealthy interaction which traps the patient in an endless cycle of anxious days and restless nights until the process can be reversed by the interventions discussed below.
Because of the discrepancy between the subjective experience and objective signs of insomnia and because of the difficulty managing such cases, the evaluation of a patient’s complaint should begin with an alliance-building inquiry into the patient’s lifestyle. This investigative process is abetted by scrupulous sleep charting with notation of other significant behaviours such as the time of getting up in the mornings, daily activity and exercise, exercise, food, and DRUG intake. Bed partners or family member collaborators are particularly helpful allies, and should be recruited early in the evaluation period. They are in an ideal position to inform the clinician about the objective signs of sleep disorder, to assure compliance with diagnostic or treatment programs, and to evaluate the efficacy of interventions. Sleep laboratory studies have their place in the ruling out of specific sleep disorders and in reassuring the patient that his symptom, while upsetting, is not indicative of organic disease but the sleep laboratory is not an end in itself and is no substitute for a sound behavioural approach. The strongest antidotes to insomnia are a positive mental attitude and a vigorous physical activity pattern, two attributes that are notoriously difficult to inculcate in chronically anxious insomniac people. Before prescribing drugs it is also critical to restrict the intake of CAFFEINE, a potent opponent of sleep that is often taken in excess by anxious insomniacs to counteract sleepiness and improve mood. NICOTINE, taken via cigarette smoking, is another problematic stimulant chemical which is easily available and difficult to withdraw from anxious subjects especially if they have become functionally disabled. Finally, ALCOHOL must not be used as a sedative because of its propensity to interrupt sleep later in the night when the ALDEHYDE products of its hepatic degradation are produced after sleep onset. Recent evidence indicates that chronic insomnia is best treated by behavioural means. When carefully screened subjects are seen in groups led by therapists well-versed in sleep hygiene and relaxation response training techniques, significant improvement in symptoms can be obtained in 95% of the patients within eight weeks.
J.ALLAN HOBSON
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