Polysomnographic effects of adjuvant ginkgo biloba therapy in patients with major depression medicated with trimipramine.

Sleep disturbance and cognitive impairment are frequent complaints of depressed patients under standard antidepressant medication. Therefore, additional therapies are required which specifically focus on the improvement of these deficits without exerting major side effects. Ginkgo biloba extract (EGb) has been shown to improve cognitive abilities in elderly subjects and in patients with disorders of the dementia spectrum. Animal studies surmise that EGb may reduce CRH activity, which is substantially related to depressive mood and behavior, predominantly cognition and sleep. An open non-randomized pilot study has been conducted to investigate the effects of ginkgo biloba extract (EGb Li 1370) on cognitive performance and sleep regulation in depressed inpatients. 16 patients were treated with a trimipramine (T)-monotherapy (200 mg) for six weeks. In eight of the 16 patients, an adjunct EGb therapy (240 mg/d) was applied for four weeks after a baseline week, the other eight patients remained on trimipramine monotherapy (200 mg) during the entire study. Polysomnography, cognitive psychomotor performance and psychopathology were assessed at baseline, after short-term and long-term adjunct EGb treatment, and after one week of ginkgo discontinuation (at the respective evaluation times in the eight patients on T-monotherapy). This report focuses on the results of EGb on sleep EEG pattern. EGb significantly improved sleep pattern by an increase of sleep efficiency and a reduction of awakenings. In addition, sleep stage 1 and REM-density were reduced, while stage 2 was increased. Non-REM sleep, predominantly slow wave sleep in the first sleep cycle, was significantly enhanced compared to trimipramine monotherapy. Discontinuation of EGb reversed most of these effects. Based on the animal data, these results suggest that EGb may improve sleep continuity and enhance Non-REM sleep due to a weakening of tonic CRH-activity. The compensation of the deficient Non-REM component in depression by the EGb application may provide a new additional treatment strategy, especially in the treatment of the depressive syndrome with sleep disturbance.

Effect of zopiclone and temazepam on sleep EEG parameters, psychomotor and memory functions in healthy elderly volunteers.

RATIONALE: The increased prevalence of sleep disturbance in old age is accompanied by a higher prescription rate of hypnotics, predominantly benzodiazepines in the elderly. In young volunteers zopiclone exerts a beneficial effect on sleep continuity without suppression of SWS and REM sleep; psychomotor performance and vigilance seemed to be less impaired than under classical benzoediazepines. OBJECTIVE: The present study investigates the effects of zopiclone on sleep EEG and cognitive performance in comparison to temazepam and placebo in the elderly population. METHODS: Single oral doses of zopiclone (7.5 mg), temazepam (20 mg) and placebo were administered in a randomized double-blind, completely counterbalanced cross-over design to 12 healthy elderly men and women (65.9 +/- 3.6 years, range 60-70 years). On each of the 3 study nights a sleep EEG was registered from 10 p.m. to 6.30 a.m. and cognitive performance tests were applied at 8 p.m., 2 a.m. (when subjects were awake for 30 min), 7 a.m. and 9 a.m. RESULTS: After zopiclone treatment, sleep continuity had significantly improved and sleep stage 4 was increased compared to temazepam and placebo. In addition, both active substances significantly reduced REM density. Neither active compound substantially altered psychomotor and memory performance. CONCLUSIONS: Zopiclone and temazepam can be considered as effective hypnotics in elderly subjects when administered in that dosage. The superiority of zopiclone on sleep architecture may be related to a more specific action of zopiclone at the GABA-A benzodiazepine receptor complex. The suppression of REM density by both compounds and their subtle effects on cognition may reflect a GABAergic mediated reduction of cholinergic neuro-transmission.

[C-reactive protein and relative lymphocytopenia: early markers of acute myocardial infarction?]. / C-reaktives Protein und relative Lymphozytopenie: Frühmarker des akuten Myokardinfarkts?

OBJECTIVE: Recent data suggest that relative lymphocytopenia and elevated C-reactive protein (CRP) are early markers of myocardial infarction. We tested these two parameters to predict myocardial infarction before elevation of creatine kinase. METHODS: Over a two-year period, 260 patients presented at the emergency room of Männedorf Hospital with suspicion of unstable angina or myocardial infarction. 197 patients were excluded because of intercurrent conditions associated with an acute-phase response or changes in leukocyte counts, as well as patients with established myocardial infarction (creatine kinase elevation at entry). The remaining 63 patients were reviewed for relative lymphocytopenia (< 20.3%) and C-reactive protein levels > 5 mg/l at admission. RESULTS: Elevated levels of C-reactive protein were found in 8 of 20 patients (40%) with unstable angina and in 29 of 43 patients (67%) with myocardial infarction. A value for C-reactive protein > 5 mg/l on admission had a sensitivity of 67% and a predictive value of 78% for subsequent myocardial infarction. Relative lymphocytopenia was found in 2 patients (10%) with unstable angina and in 19 patients (44%) with myocardial infarction. The positive predictive value of both markers diagnosing myocardial infarction was 93% compared to 78% of elevated CRP or 90% of relative lymphocytopenia. In contrast, the sensitivity of both markers combined was 33%. CONCLUSIONS: At present, elevation of C-reactive protein and relative lymphocytopenia allow early diagnosis of myocardial infarction. However, the markers' sensitivity is relatively low.