Illnesses in which anxiety and fear are prominent symptoms also result in difficulty in falling asleep and in light, fitful, or intermittent sleep. Disturbing dreams are frequent in these situations and may awaken the patient. Exceptionally, a patient may even try to stay awake in order to avoid them. In contrast, depressive illness produces early morning waking and inability to return to sleep; the quantity of sleep is reduced, and nocturnal motility is increased. REM sleep in depression, although not always reduced, comes earlier in the night. If anxiety is combined with depression, there is a tendency for both the above patterns to be observed. Yet another common pattern of disturbed sleep can be discerned in individuals who are under great tension and worry or are overworked and tired out. These people sink into bed and sleep through sheer exhaustion, but they awaken early with their worries and are unable to get back to sleep.
Chronic and even short-term use of alcohol, barbiturates, and certain nonbarbiturate sedative-hypnotic drugs markedly reduces REM sleep as well as stages 3 and 4 of NREM sleep (N3). Following withdrawal of these drugs, there is a rapid and marked increase of REM sleep, sometimes with vivid dreams and nightmares. “Rebound insomnia,” a worsening of sleep compared with pretreatment levels, has also been reported upon discontinuation of short-half-life benzodiazepine hypnotics, notably triazolam (Gillin et al) and including the newer sleep agents mentioned below. Furthermore, a form of drug-withdrawal or rebound insomnia may actually occur during the same night in which the drug is administered. The drug produces its hypnotic effect in the first half of the night and a worsening of sleep during the latter half of the night, as the effects of the drug wear off; the patient and the physician may be misled into thinking that these latter symptoms require more of the hypnotic drug or a different one. Alcohol taken in the evening acts in the same way. Rebound insomnia must be distinguished from the early morning awakening that accompanies anxiety and depressive states.
A wide variety of other pharmacologic agents may give rise to sporadic or persistent disturbances of sleep.
Caffeine-containing beverages, corticosteroids, bronchodilators, central adrenergic-blocking agents, amphetamines, certain “activating” antidepressants such as fluoxetine, and cigarettes are the most common offenders. Others are listed in the extensive review of Kupfer and Reynolds.
Acroparesthesias, a predominantly nocturnal tingling and numbness of the fingers and palms caused by tight carpal ligaments (carpal tunnel syndrome), may awaken the patient at night (see in the following text, under “Sleep Palsies and Acroparesthesias”). Cluster headaches characteristically awaken the patient within 1 to 2 h after falling asleep (see Chap. 9 for a fuller discussion). In a few patients, cluster headaches occur only during or immediately after the REM period.
The sleep rhythm is totally deranged in acute confusional states and especially in delirium, and the patient may doze for only short periods, both day and night, the total amount and depth of sleep in a 24-h period being reduced. Frightening hallucinations may prevent sleep. The senile patient tends to catnap during the day and to remain alert for progressively longer periods during the night, until sleep is obtained in a series of short naps throughout the 24 h; the total amount of sleep may be increased or decreased.
Treatment of Insomnia