Schneider-Helmert D
Medical Center Mariastein, Basel, Switzerland.
Acta Psychiatr Scand. 1988 Dec;78(6):706-11. doi: 10.1111/j.1600-0447.1988.tb06408.x.
Psychobiological aspects of low-dose benzodiazepine dependence (LBD) and drug withdrawal were investigated in 76 middle-aged and elderly chronic insomniacs in a sleep laboratory. Comparison with drug-free insomniacs showed that LBD leads to a complete loss of hypnotic activity and substantial suppression of delta and REM sleep. Only small differences were found between benzodiazepines with different half-life time. Upon withdrawal, recovery from this suppression, especially in REM sleep, occurred, while insomnia did not increase. The patients, however, reported sleeping longer while taking the drug compared with withdrawal. This misperception seems to be a specific effect of benzodiazepines, and contrasts with the full awareness of insomnia upon withdrawal. It is concluded that these effects play a leading role in the patients' inability to escape their sleeping pills. The response of REM sleep to withdrawal should make this a useful measure to objectively confirm low-dose benzodiazepine dependence.
在睡眠实验室对76名中老年慢性失眠患者进行了低剂量苯二氮䓬依赖(LBD)和药物戒断的心理生物学方面的研究。与未使用药物的失眠患者相比,结果显示LBD会导致催眠活性完全丧失以及对δ波睡眠和快速眼动睡眠的显著抑制。在不同半衰期的苯二氮䓬之间仅发现了微小差异。戒断时,这种抑制作用尤其是在快速眼动睡眠中的抑制作用会恢复,而失眠并未加重。然而,患者报告称服药时比戒断时睡眠时间更长。这种错误认知似乎是苯二氮䓬的一种特殊效应,与戒断时对失眠的完全感知形成对比。得出的结论是,这些效应在患者无法摆脱安眠药的情况中起主导作用。快速眼动睡眠对戒断的反应应使其成为客观确认低剂量苯二氮䓬依赖的一项有用指标。