Nocturnal attacks are symptomatic of numerous primary headache syndromes. It has proven possible to verify, with polygraphic sleep recordings, a strict correlation between the onset of headache attacks and the rapid eye movements (REM) stage for migraineurs, patients with chronic paroxysmal hemicrania and cluster headache (CH). The purpose of this study was to investigate the correlation between attack onset of chronic CH and sleep stages, the REM stage in particular. Nine patients from our headache outpatient service with a diagnosis of CH were examined in this study. All medication was discontinued at least one week prior to sleep polygraphias, which were conducted in a sleep laboratory on two consecutive nights. Any attacks were treated with oxygen inhalation during the drug-free period. EEG, EMG, and EOG were continuously monitored during the sleep polygraphias. Eight patients had 25 CH attacks during 12 of the 17 nights recorded. Only three of these patients had arousals with attacks in the REM stage and these amounted to five of the 25 recorded attacks. Eleven attacks were in stage 2, four in stage 1 and two in stage 3. These results correlate with recent findings according to which headache attacks were often related to REM in episodic CH, but rarely in the chronic type. Whether or not different pathogenic mechanisms are involved in the episodic and the chronic type of CH is a matter for further discussion.
The 24-h sleep-wake pattern of plasma LH was studied in 18 patients with severe weight loss. Sixteen patients had anorexia nervosa, one suffered from schizophrenia and one had a gastric ulcer. The age of the patients ranged from 13 to 31 years. Seventeen women and one boy participated in the study. Their weight ranged from 51 to 73 % of the ideal body weight (IBW) at the first 24-h study which was at one week after admission to the hospital. Blood was taken through an indwelling venous catheter every 30 min. The patients' weight increased under behavioural therapy and they were re-studied when they had gained approximately 10 % IBW and again prior to release from the psychiatric ward. The LH patterns were classified as infantile, pubertal or adult. All patients except for two had an iniantile pattern at the first study. Except for the two patients who had no anorexia nervosa, all developed a pubertal and/or an adult pattern. All patients whose weight was below 69 % IBW had an infantile LH pattern. Adult patterns were only seen when the body weight was greater than 80 % IBW. The increase of the average 24-h LH values was slower the older the patients were and the longer they had been anorectic.
Previous research has demonstrated that in healthy subjects sit uat ional strain may provoke not only sleep disturbances characteristic of depression (e.g., shortened REM latencies), but also alterations in dream content. Nevertheless, there are some controversial results. The aim or our study was to clarify these inconsistencies by developing a design which might avoid some methodological problems which were present in some of these previous studies. Eleven male subjects slept in the laboratory for 7 consecutive nights. During 1 evenings they saw a stressful and a neutral movie in randomized order. The subsequent nights included REM sleep awakenings for the purpose of dream collections. Whereas the subjects were demonstrably affected by the disturbing films, the patterns of subsequent sleep remained unchanged. In contrast manifest content of the initial dreams were clearly altered. Whereas the modes of dreaming were quite different within post‐stress nights, mood was unproved the next morning in all subjects. The results are discussed within the framework of several prevailing concepts about sleep, dreams, and psychological strain.
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