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Summary Differences in sleep and awakening quality between 51 insomniac postmenopausal syndrome patients and normal controls were evaluated. In a subsequent double-blind, placebo-controlled, comparative, randomized, three-arm trial (Climodien 2/3 = estradiol valerate 2 mg + the progestogen dienogest 3 mg = regimen A, estradiol valerate 2 mg = regimen EV, and placebo = regimen P), the effects of 2 months of hormone replacement therapy were investigated, followed by a 2-month open-label phase in which all patients received Climodien[sup ®] 2/2 (EV 2 mg + dienogest 2 mg = regimen A*). Polysomnography at baseline demonstrated significantly deteriorated sleep initiation and maintenance, increased S1 and decreased S2 in patients. Subjective sleep and awakening quality, well-being, morning drive, wakefulness, memory and reaction time performance were deteriorated too. Treatment with both regimen A and regimen EV induced a moderate, although nonsignificant, improvement in the primary efficacy variable wakefulness during the total sleep period compared with baseline, while under placebo no changes occurred. Secondary efficacy variables concerning sleep initiation and maintenance, and sleep architecture showed similar findings. The apnea and apnea–hypopnea indices improved significantly under regimen A, compared with both baseline and placebo. Subjective sleep and awakening quality improved significantly after regimen A and EV compared with baseline, with the drug-induced changes being superior to those induced by placebo. In the open-label phase, subjective sleep quality improved further, significantly in the former regimen A group. Awakening quality, somatic complaints and morning thymopsyche did not yield any significant findings. Concerning morning noopsychic performance, memory improved significantly after regimen A compared with baseline, fine motor activity after regimen EV. Reaction time performance increased with all three compounds. In conclusion, Climodien significantly improved subjective sleep quality, the apnea and apnea–hypopnea indices of insomniac postmenopausal syndrome patients, while it only marginally improved variables concerning objective sleep and awakening quality. [ABSTRACT FROM AUTHOR]

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[sup ®] ;) 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. [ABSTRACT FROM AUTHOR]

Recent investigations in our sleep outpatient clinic demonstrated that 30% of patients exhibited organic and 70% nonorganic sleep disorders, with 41% showing as an additional diagnosis neurotic, stress-related, and somatoform disorders, 31% affective disorders and 15% mental and behavioral disorders due to psychoactive substance use. Thus, the aim of the study was to investigate the acute effects of the imidazopyridine zolpidem on objective and subjective sleep and awakening quality in the largest of the above-mentioned groups. In this single-blind, placebo-controlled cross-over study, 15 patients (9 females and 6 males aged 51.1 + 11.3 years) diagnosed as having nonorganic insomnia (ICD–10: F 51.0) related to neurotic and stress-related disorders (F 1.1:12, F 41.2:2 and F 43.2:1) were included. Objective and subjective sleep and awakening quality measures were investigated in 3 subsequent nights in the sleep laboratory (adaptation, baseline/placebo and zolpidem 10 mg night), utilizing clinical, polysomnographic, psychometric and psychophysiological methods. The drug-free patients were matched according to age and sex with 15 normal healthy controls (age 51.2 + 11.8 years). Statistical analysis of polysomnographic variables demonstrated a significant lengthening of the total sleep period (TSP) and total sleep time (TST), an improvement in sleep efficiency and a shortening of sleep latencies after zolpidem as compared with placebo. These changes were opposite to the differences between patients and controls. Concerning sleep architecture, zolpidem increased the length of S4 and S3 + S4 as compared with placebo. Subjective sleep and awakening quality and the thymopsychic variables drive, mood, affectivity and wakefulness in the morning showed no significant changes, as a significant improvement had already occurred from the adaptation to the baseline/placebo night. Noopsychic variables (attention, concentration, attention variability, numerical memory, fine motor activity, reaction time measures) showed similar findings. Moreover, subjective sleep and awakening quality, thymopsychic and noopsychic measures during baseline/placebo recordings did not differ significantly from normative data (except for fine motor activity). Psychophysiological measures did not show any significant alterations either, except for a decrease in systolic blood pressure in the evening. Conclusion: As compared with placebo, zolpidem induced a significant improvement in objective sleep quality, mainly by increasing TSP, TST and sleep efficiency and shortening sleep latencies, thereby normalizing the disorder of initiating and maintaining sleep. Deep sleep stages S3 + S4 increased (although at baseline/placebo these stages did not differ from controls), while S1, S2 and SREM did not change significantly. Subjective sleep and awakening quality as well as thymopsychic and noopsychic performance in the morning mainly showed a placebo and ‘first- night effect’ phenomenon in these patients. Thus, the changes induced by zolpidem were somewhat different from those after classical benzodiazepines.Copyright © 2000 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]