Background We investigated whether the combination of multimodal behaviour therapy (BT) with fluvoxamine is superior to BTand placebo in the acute treatment of severely ill in-patients with obsessive-compulsive disorder (OCD).Method In a randomised, double-blind design, 30 patients were treated for nine weeks with BT plus placebo and 30 patients with BT plus fluvoxamine (maximum dosage 300 mg, mean dose 288.1 mg). BT included exposure with response prevention, cognitive restructuring and development of alternative behaviours.Results Both groups showed a highly significant symptom reduction after treatment. There were no significant differences between the groups concerning compulsions. Obsessions were significantly more reduced in the fluvoxamine and BT group than in the placebo and BT group. Furthermore, the group BT plus fluvoxamine showed a significantly higher response rate (87.5 v. 60%) according to a previously defined response criterion. Severely depressed patients with OCD receiving BT plus placebo presented a significantly worse treatment outcome (Y–BOCS scores) than all other groups.Conclusions The results suggest that BTshould be combined with fluvoxamine when obsessions dominate the clinical picture and when a secondary depression is present.

PSG and CPC measures differentiated no from moderate to severe OSA groups and HFC ≥ 50 % discriminated successful from unsuccessful CPAP therapy. The HFC ≥ 50 % cutoff showed clinical value in identifying sleep quality disturbance among CPAP users.

No abstract

Depression could be an independent risk factor for cardiovascular disease. We assessed bupropion response in depressed patients by polysomnography (PSG) and cardiopulmonary coupling (CPC) variables. Nineteen subjects participated in a two-session, two consecutive night PSG protocol. Participants received either placebo or bupropion-SR 150 mg, orally, in a randomized, double-blind cross-over fashion on night two. Outcome variables were: sleep stages, REM latency, stable, unstable sleep and very low frequency coupling (VLFC). CPC analysis uses heart rate variability and the electrocardiogram’s R-wave amplitude fluctuations associated with respiration to generate frequency maps. Bupropion increased REM latency (p=0.043) but did not impact PSG sleep continuity, architecture and CPC variables. A trend (p=0.092) was observed towards increasing VLFC duration. Bupropion increased the number of stable-unstable sleep transitions (p=0.036). Moderate to strong correlations between PSG and CPC variables were found on placebo and bupropion nights. Limitations include a small sample size, limited power to detect CPC changes and lack of normal controls for comparison. Increased stable-unstable sleep transitions and VLFC duration may indicate vulnerability to cardiovascular disease due to their association with low heart rate variability that has been associated with increased mortality raising the question whether the beneficial effects of the antidepressant medication outweighs the impact on cardiopulmonary dynamics.

Baseline electroencephalographic (EEG) sleep and the EEG sleep response to scopolamine were studied in 10 adult female patients with unipolar major depressive disorder. Subjects were studied twice for two consecutive nights while depressed and, again, during remission. On the second night of each two-night session, normal saline or scopolamine (1.5 microg/kg, i.m.) was administered in a randomized, double-blind, cross-over fashion. Nocturnal urinary free cortisol (NUFC) measures also were collected. Compared to the depressed state, NUFC was significantly lower during remission. In contrast, baseline EEG sleep measures did not differ from episode to remission. Scopolamine suppressed rapid eye movement (REM) sleep to a comparable extent during the depressive episode and in remission. Scopolamine also reduced NUFC secretion during both clinical states, but to a lesser extent than REM sleep suppression. The findings suggest that the dysregulation in cholinergic systems associated with depressive illness may be persistent during remission, at least for some cholinergic systems. The results also suggest that the central cholinergic system(s) that regulate(s) REM sleep may be more sensitive to dysregulation than the cholinergic system(s) that control(s) nocturnal cortisol secretion.