An Investigation of Sleep Architecture and Consequent Cognitive Changes in Olanzapine Treated Patients with Depression
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Objective: Primarily, to determine the effect of olanzapine augmentation therapy on sleep architecture, specifically slow wave sleep (SWS), in the treatment of depression. Secondarily, to determine the effect of olanzapine augmentation therapy on illness severity and cognitive function. Finally, to examine the correlation between sleep architecture, illness severity and cognition. Methods: Prospective, double-blind, randomized, placebo-controlled study. Patients with major depressive disorder or bipolar disorder currently experiencing a major depressive episode were included. Patients were on a stable medication regime for 4 weeks prior and throughout the study. Sleep architecture was measured by overnight, ambulatory, polysomnography. Illness severity was determined using the Hamilton Depression Rating Scale (HDRS), Montgomery Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Rating Scale (HARS). Cognitive function was examined using Cambridge Neuropsychological Test Automated Battery (CANTAB): Spatial Working Memory (SWM), Spatial Span (SSP), and Reaction Time (RTI) tasks. Polysomnographs, clinical measures and cognitive test were administered at baseline, after 2-4 days of treatment and after 28-31 days of treatment. Results: Twenty-five patients participated in the study. There was no significant difference between olanzapine and placebo treated groups on age, gender, diagnosis, education level, employment or marital status and number of children. Latency to SWS, duration of SWS, sleep efficiency, total sleep time, total wake time and sleep latency significantly improved in olanzapine treated participants over placebo treated participants. Latency to and duration of rapid eye movement sleep was not significantly different between olanzapine and placebo treated participants. HDRS scores were significantly improved in olanzapine treated versus placebo treated participants. No significant difference between treatment groups was seen in MADRS, HARS, and subjective sleep quality scores. There was no significant difference between olanzapine and placebo treated participants in SWM, SSP or RTI tasks. Change in sleep architecture was not significantly correlated to clinical change or change in SWM, SSP or RTI. Clinical change was not significantly correlated to SWM or SSP. Clinical change, however, was significantly correlated to change in RTI, in the placebo treated group only. Conclusion: Olanzapine augmentation treatment improves SWS, sleep continuity and depressive symptoms.