SLOW WAVE SLEEP AND RESPONSE TO COGNITIVE BEHAVIORAL THERAPY FOR INSOMNIA

Introduction Cognitive Behavioral Therapy for Insomnia (CBT-I) is recognized to be the first-choice treatment for chronic insomnia. Since the subjective evaluation of nocturnal sleep in mandatory for the diagnosis of insomnia, the efficacy of CBT-I has been mostly investigated with subjective measures. Only few studies examined the efficacy of CBT-I with an objective evaluation. However, polysomnography (PSG) could provide important information regarding objective sleep phenotypes and its influence on CBT-I response. Aim of our study was to evaluate if PSG variables before treatment could predict CBT-I outcomes. Methods 29 chronic insomnia patients (15 females and 14 males, mean age 40.8±12.0) underwent an ambulatory PSG recording before CBT-I treatment. Patients also reported subjective sleep by means of sleep diary during PSG evaluation and throughout the duration of CBT-I (9 weeks). PSG data were used as primary outcomes to evaluate possible different response to CBT-I. Moreover, we used a general linear model to assess if any PSG sleep measures could predict patients’ response to CBT-I in terms of Insomnia Severity Index (ISI) or subjective sleep diary variables. Results All patients demonstrated a significant improvement after CBT-I both at ISI (19.1±3.7 vs 10.8±4.9; p=.000) and at sleep variables (Sleep Latency: 38.1±28.6 vs 22.9±22.5, p=.005; Wake after Sleep Onset (WASO): 98.6±79.9 vs 51.7±52.1, p=.002; Sleep Efficiency: 67.2±19.1 vs 82±11.9, p=.000).The general linear model analysis with PSG data showed that only Slow Wave Sleep (SWS) % predicted the decrease of WASO subjectively reported at Sleep Diaries. In particular, patients by a higher SWS % were the ones showing a greater improvement at WASO after CBT-I (98.6±79.9 vs 51.7±52.2; p= .032). Conclusion Our study demonstrated that SWS % before treatment predict a better response to CBT-I. This result might support the hypothesis of a possible phenotype of insomnia characterized by % of SWS that could be the natural mediator of “process S” pressure that would result in a greater improvement of subjectively reported WASO and therefore in a better outcome after CBT-I

Traumatic brain injury as a trigger of neurodegeneration

Although millions of individuals suffer a traumatic brain injury (TBI) worldwide each year, it is only recently that TBI has been recognized as a major public health problem. Beyond the acute clinical manifestations, there is growing recognition that a single severe TBI (sTBI) or repeated mild TBIs (rTBI) can also induce insidious neurodegenerative processes, which may be associated with early dementia, in particular chronic traumatic encephalopathy (CTE). Identified at autopsy examination in individuals with histories of exposure to sTBI or rTBI, CTE is recognized as a complex pathology featuring both macroscopic and microscopic abnormalities. These include cavum septum pellucidum, brain atrophy and ventricular dilation, together with pathologies in tau, TDP-43, and amyloid-β. However, the establishment and characterization of CTE as a distinct disease entity is in its infancy. Moreover, the relative "dose" of TBI, such as the frequency and severity of injury, associated with risk of CTE remains unknown. As such, there is a clear and pressing need to improve the recognition and diagnosis of CTE and to identify mechanistic links between TBI and chronic neurodegeneration