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Sleep laboratory and outpatient studies of the hypnotic efficacy of the amino acid L-tryptophan are reviewed, with particular emphasis on evaluation of therapeutic effectiveness in the treatment of insomnia. In younger situational insomniacs, whose sleep problem consists solely of longer than usual sleep latencies, L-tryptophan is effective in reducing sleep onset time on the first night of administration in doses ranging from 1 to 15 g. In more chronic, well-established sleep-onset insomnia or in more severe insomnias characterized by both sleep onset and sleep maintenance problems, repeated administration of low doses of L-tryptophan over time may be required for therapeutic improvement. In these patients, hypnotic effects appear late in the treatment period or, as shown in some studies, even after discontinuation of treatment. The improvement in sleep measures post-treatment has given rise to use of a treatment regimen known as "interval therapy", in which L-tryptophan treatment alternates with an L-tryptophan-free interval until improvement occurs. The absence of side effects and lack of development of tolerance in long-term use are important factors in the decision to embark upon a trial of L-tryptophan treatment. In addition, L-tryptophan administration is not associated with impairment of visuomotor, cognitive, or memory performance, nor does it elevate threshold for arousal from sleep.

A considerable proportion of chronic non-organic pain patients suffer from insomnia, and alpha sleep has been suggested to be specifically associated with fibromyalgia. However, the clinical significance of those symptoms is not clear. This study was carried out to investigate this question. Twenty-six middle-aged, non-organic pain patients complaining of persistent insomnia were compared with 25 chronic primary insomniacs in a polysomnographic investigation. Alpha sleep was measured by automatic EEG analysis. A postsleep inventory allowed a separation of those pain patients with actual pain in the recording night to examine its possible influence on sleep. Both groups of patients displayed severe disturbance of sleep maintenance. The pain group did not differ in any of the insomnia variables or in sleep stages from chronic primary insomniacs. The occurrence of alpha sleep was high in either group which suggests that this is not a phenomenon specifically related to pain syndromes. A comparison of the pain subgroups revealed no difference between those with or without actual pain in the recording night. It is concluded that insomnia in chronic pain is of the same type and degree as primary insomnia. Apparently, the chronic process made insomnia so persistent that there was no response to actual night-time pain. Our study suggests that the interpretation of insomnia as secondary to pain, as it is usually made by the pain patients themselves, is a misattribution. It is suggested that insomnia in chronic pain patients should be taken seriously and treated by its specific methods.

Psychobiological aspects of low-dose benzodiazepine dependence (LBD) and drug withdrawal were investigated in 76 middle-aged and elderly chronic insomniacs in a sleep laboratory. Comparison with drug-free insomniacs showed that LBD leads to a complete loss of hypnotic activity and substantial suppression of delta and REM sleep. Only small differences were found between benzodiazepines with different half-life time. Upon withdrawal, recovery from this suppression, especially in REM sleep, occurred, while insomnia did not increase. The patients, however, reported sleeping longer while taking the drug compared with withdrawal. This misperception seems to be a specific effect of benzodiazepines, and contrasts with the full awareness of insomnia upon withdrawal. It is concluded that these effects play a leading role in the patients' inability to escape their sleeping pills. The response of REM sleep to withdrawal should make this a useful measure to objectively confirm low-dose benzodiazepine dependence.

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