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

Citation
U. Hemmeter et al., Polysomnographic effects of adjuvant ginkgo biloba therapy in patients with major depression medicated with trimipramine, PHARMACOPS, 34(2), 2001, pp. 50-59
Citations number
62
Categorie Soggetti
Neurosciences & Behavoir
Journal title
PHARMACOPSYCHIATRY
ISSN journal
01763679 → ACNP
Volume
34
Issue
2
Year of publication
2001
Pages
50 - 59
Database
ISI
SICI code
0176-3679(200103)34:2<50:PEOAGB>2.0.ZU;2-N
Abstract
Sleep disturbance and cognitive impairment are frequent complaints of depre ssed patients under standard antidepressant medication. Therefore, addition al therapies are required which specifically focus on the improvement of th ese deficits without exerting major side effects. Ginkgo biloba extract (EG b) has been shown to improve cognitive abilities in elderly subjects and in patients with disorders of the dementia spectrum. Animal studies surmise t hat EGb may reduce CRH activity, which is substantially related to depressi ve mood and behavior, predominantly cognition and sleep. An open non-random ized pilot study has been conducted to investigate the effects of ginkgo bi loba extract (EGb Li 1370) on cognitive performance and sleep regulation in depressed inpatients, 16 patients were treated with a trimipramine (T)-mon otherapy (200 mg) for six weeks. In eight of the 16 patients, an adjunct EG b therapy (240 mg/d) was applied for four weeks after a baseline week, the other eight patients remained on trimipramine monotherapy (200 mg) during t he entire study. Polysomnography, cognitive psychomotor performance and psy chopathology were assessed at baseline, after short-term and long-term adju nct EGb treatment, and after one week of ginkgo discontinuation (at the res pective evaluation times in the eight patients on T-monotherapy). This repo rt focuses on the results of EGb on sleep EEG pattern. EGb significantly im proved 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 mono therapy. Discontinuation of EGb reversed most of these effects. Based on th e 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 com pensation of the deficient Non-REM component in depression by the EGb appli cation may provide a new additional treatment strategy, especially in the t reatment of the depressive syndrome with sleep disturbance.