Proceedings of the 2015 ISNR Conference: Poster Presentations

Abstract

Background: Insomnia is common in patients with major depressive disorder (MDD); they complain of falling asleep and awakening in the daytime. One of the neuropsychopathological mechanisms of insomnia is cortical hyperarousal. Previous studies explored cortical activities at pre-sleep and sleep stages among patients with primary insomnia and MDD, as well as the physiological arousal in the daytime among patients with chronic insomnia. There were few studies that explored clearly the psychopathological mechanism among patients comorbid with MDD and insomnia. The purpose of this study was to explore the daytime cortical arousal among patients comorbid with MDD and insomnia.Methods: Fifty patients comorbid with MDD and insomnia were the MDD group that was compared with 35 healthy controls in beta power of electroencephalogram (EEG). All of the participants filled out the Pittsburgh Sleep Quality Index (PSQI). The resting EEG with eye-closed were measured for 5 min via 19-channel BrainMaster equipment (BrainMaster Technologies, Inc., Bedford, Ohio), where the spectrum analyses showed the beta power (13-32 Hz; as a cortical hyperarousal index) at Fz and Cz.Results: This study found that: (1) After controlling the medication effects, there were positive correlations between PSQI total score, the habitual sleep efficiency, use of sleep medications, and beta power at Fz and Cz.(2) There were higher absolute and relative beta power at Fz and Cz in the MDD group than that of in healthy controls. (3) After controlling the medication effect, the MDD group with high sleep disturbance had higher relative beta power at Fz and Cz than that of the MDD group with low sleep disturbance. Conclusion:This study indicated that poor sleep quality was associated with daytime cortical arousal. Patients with MDD had higher cortical arousal at the frontal and central areas than that of healthy controls. These phenomena may reflect the daytime cortical hyperarousal that was found among patients comorbid with MDD and insomnia. Background: The study is based on an underlying neuropathological model of autism, which emphasizes "minicolumnar" pathology (Casanova, 2007;Casanova et al., 2006) and cortical lateral inhibition deficits resulting in behavioral abnormalities and executive dysfunctions. We propose that neuromodulation based on lowfrequency repetitive TMS over prefrontal area will enhance lateral inhibition through activation of inhibitory double bouquet interneurons and will be accompanied by EEG alteration that can be operantly conditioned using neurofeedback (NFB) immediately after rTMS session. In prior studies in children with ASD we demonstrated post-TMS improvements in executive functions Sokhadze, El-Baz, Sears, Opris, & Casanova, 2014), as well as positive effects of prefrontal neurofeedback in ASD (Wang et al., 2014). In the current study each rTMS session was followed by NFB training that we predicted to result in a synergetic response. References Objectives:The overall aim of the study was to investigate behavioral respon...