EEG maps of alcohol-dependent patients differ significantly from those of normal controls and patients suffering from other mental disorders and thus EEG mapping may be used for diagnostic purposes. Moreover, the quantitative EEG may also be of prognostic value as relapsing patients differ from abstaining ones, since they show a significantly more pronounced hyperarousal of the CNS.

The purpose of this paper is to review the effects of selective serotonin (5-HT) reuptake inhibitors on objective and subjective sleep and awakening quality measures. Polysomnography (PSG) demonstrated in both healthy volunteers and depressed patients a decrease in sleep efficiency and total sleep time, a lengthening of sleep latency and a deterioration in sleep continuity, including an increase in the number of awakenings and wake time during the total sleep period. Sleep architecture mostly showed an increase in S1 and S2 and a decrease in S3, S4 and REM sleep as well as a lengthening of REM latency. Objective awakening quality, if measured at all by psychometry, generally showed no decrements. Concerning subjective sleep and awakening quality, normals demonstrated either no changes or a tendency towards a deterioration, while in patients some improvement was observed. Reasons for this discrepancy will be discussed. Novel 5-HT reuptake inhibitors with additional modes of action such as 5-HT2 antagonism (e.g. trazodone, nefazodone) are more likely to improve objective and subjective sleep quality, although some shortcomings may be inherent in regard to comorbidity (e.g. sleep-related breathing disorders). Thus, PSG seems to be a necessity for diagnosis and treatment of complex sleep disorders.

The restless legs syndrome (RLS) is a common sensorimotor disorder which leads to severe sleep disturbances and showed a prevalence of 7.9% in our sleep laboratory. The aim of this study was to investigate periodic leg movements (PLM), arousal and respiratory variables in 12 untreated RLS patients and to measure the acute effects of 0.5 mg ropinirole, a nonergoline dopamine agonist, as compared with placebo. In the target variable PLM/h of total sleep time (PLM/h TST), RLS patients showed an increased value of 40/h (normal 0–5/h). Further, we found an increased number of PLM (368), PLM/h of time in bed (49/h), PLM/h of REM sleep (11), PLM/h of non-REM sleep (46) and PLM/h awake (61). The arousal index was also increased (32/h; normal 0–25/h), as were arousals due to PLM. In the confirmatory part of our descriptive data analysis, ropinirole 0.5 mg significantly improved, as compared with placebo, the index PLM/h TST by 75%. In the descriptive part, all the other PLM variables were improved as well. Arousals due to PLM decreased, while spontaneous arousals increased. Respiratory variables, which had a priori been in the normal range, showed a slight but significant improvement after the dopamine agonist. Thus, 0.5 mg ropinirole significantly improved the target variable PLM/h TST, along with objective and subjective sleep quality and morning noopsychic performance, as described in the preceding paper. Our data encourage further sleep studies including all above-mentioned variables in a larger group of RLS/PLM during sleep patients as well as long-term efficacy trials.

Objective and subjective sleep and awakening quality was investigated in 11 drug‐free patients (4 females, 7 males) aged 30–55 (mean: 44±9) years with nonorganic insomnia (F 51·0) related to panic disorder (F 41·0) as compared with 11 age‐ and sex‐matched normal controls aged 30–58 (mean: 44±9) years, utilising polysomnography (PSG) and psychometry. PSG demonstrated decreased sleep efficiency (primary target variable), total sleep time (TST) and S2 as well as increased middle and late insomnia, S1, S3+S4, snoring and PLM in patients. There were no intergroup differences in REM variables. Subjective sleep quality deteriorated, as did drive and fine motor activity in the morning, while concentration increased. Blood pressure in the evening and morning and pulse rate in the evening were elevated. These differences as compared with normals were distinct from those observed in other sleep disorders. In a subsequent acute, placebo‐controlled cross‐over design study, patients received alprazolam 0·5 mg (Xanor®;) and placebo. As compared with placebo, alprazolam induced an increase in sleep efficiency (primary target variable), TST and S2, a decrease in wakefulness during the total sleep period, S3+S4 and the oxygen desaturation and PLM indices, and improved subjective sleep quality, somatic complaints, drive, affectivity and drowsiness in the morning. There were no changes in REM variables. Thus, alprazolam induced changes that were opposite to the differences observed between patients and controls before treatment, thereby normalizing sleep and awakening quality. As observed in insomnia related to GAD and subsequent benzodiazepine therapy, the present study also points to a key‐lock principle in the treatment of insomnia caused by anxiety disorders and neurophysiologically visualizes processes at the receptor level (e.g. benzodiazepine agonists versus inverse agonists). Copyright © 2000 John Wiley & Sons, Ltd.

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