BackgroundDisturbance in sleep quality is a symptom of Major Depressive Disorder (MDD) and Bipolar Disorder (BD) and thus improving quality of sleep is an important aspect of successful treatment. Here, a prospective, double-blind, randomized, placebo-controlled study examined the effect of olanzapine (an atypical antipsychotic) augmentation therapy on sleep architecture, specifically slow wave sleep (SWS), in the treatment of depression. The effect of olanzapine augmentation therapy on other features of sleep (e.g., sleep continuity) and depression (e.g., illness severity and cognitive function) were also determined.MethodsPatients currently experiencing a major depressive episode and who were on a stable medication were included. Sleep architecture was measured by overnight ambulatory polysomnography. Illness severity was determined using the Montgomery-Asberg Depression Rating Scale (MADRS). 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 tests were administered at baseline, after 2–4 days of treatment and after 28–31 days of treatment. Twenty-five patients participated in the study (N = 10, N = 15 for placebo and olanzapine treated groups respectively).ResultsThe primary objective of the study was to assess the objective (polysomnographic) changes in sleep quality, defined as changes in SWS, following olanzapine treatment for depression. Latency to but not duration of SWS was found to significantly differ between olanzapine- and placebo-treated participants (Hedge’s g: 0.97, 0.13 respectively). A significant improvement in olanzapine-treated participants over placebo-treated participants was observed in secondary outcome measures, including sleep efficiency, total sleep time, and sleep latency. Secondary objectives assessed the subjective changes in sleep quality parameters and correlated them with measures of illness severity and changes in cognition. MADRS scores were significantly improved in olanzapine-treated participants over time but not more than placebo treatment. There was no significant difference between olanzapine- and placebo-treated participants in SWM, SSP or RTI tasks.ConclusionsOlanzapine augmentation treatment generally did not improve SWS but did improve sleep continuity and depression. Olanzapine may be one of few medications that improve sleep continuity, thus directly targeting symptoms of depression.Trial registrationClinicalTrials.gov, NCT00520507.

Recent behavioral studies have shown that color imagery can benefit visual search when it is congruent with an upcoming target.In the present study we investigated whether this color imagery benefit was due to the processes underlying attentional guidance, as indicated by the electrophysiological marker known as the N2pc component. Participants were instructed to imagine a color prior to each trial of a singleton search task. On some trials, the imagined color was congruent with the target, and on other trials, it was congruent with the distractors. The analyses revealed that the N2pc was present when color imagery was congruent with the search target, and absent when it was congruent with the distractors. Further, there was preliminary evidence that attentional guidance depended on the vividness of color imagery and the frequency at which participants implemented the imagery instruction. Overall, the results of the present study indicate that color imagery can influence the attentional guidance processes underlying visual search.

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Self-motion perception relies primarily on the integration of the visual, vestibular, proprioceptive, and somatosensory systems. There is a gap in understanding how a temporal lag between visual and vestibular motion cues affects visual–vestibular weighting during self-motion perception. The beta band is an index of visual–vestibular weighting, in that robust beta event-related synchronization (ERS) is associated with visual weighting bias, and robust beta event-related desynchronization is associated with vestibular weighting bias. The present study examined modulation of event-related spectral power during a heading judgment task in which participants attended to either visual (optic flow) or physical (inertial cues stimulating the vestibular, proprioceptive and somatosensory systems) motion cues from a motion simulator mounted on a MOOG© Stewart Platform. The temporal lag between the onset of visual and physical motion cues was manipulated to produce three lag conditions: simultaneous onset, visual before physical motion onset, and physical before visual motion onset. There were two main findings. First, we demonstrated that when the attended motion cue was presented before an ignored cue, the power of beta associated with the attended modality was greater than when visual–vestibular cues were presented simultaneously or when the ignored cue was presented first. This was the case for beta ERS when the visual-motion cue was attended to, and beta event-related desynchronization when the physical-motion cue was attended to. Second, we tested whether the power of feature-binding gamma ERS (demonstrated in audiovisual and visual–tactile integration studies) increased when the visual–vestibular cues were presented simultaneously versus with temporal asynchrony. We did not observe an increase in gamma ERS when cues were presented simultaneously, suggesting that electrophysiological markers of visual–vestibular binding differ from markers of audiovisual and visual–tactile integration. All event-related spectral power reported in this study were generated from dipoles projecting from the left and right motor areas, based on the results of Measure Projection Analysis.