Manuela Russo1, Katie Mahon1, Megan Shanahan1, Elizabeth Ramjas1, Carly Solon1, Shaun M Purcell1, Katherine E Burdick2. 1. Icahn School of Medicine at Mount Sinai, Departments of Psychiatry and Neuroscience, United States. 2. Icahn School of Medicine at Mount Sinai, Departments of Psychiatry and Neuroscience, United States; James J Peters VA Medical Center Bronx, NY, United States. Electronic address: Katherine.burdick@mssm.edu.
Abstract
BACKGROUNDS: Sleep and circadian rhythm disruptions are prominent, trait-like features of bipolar disorder (BD) which precede the onset of mood episodes. Neurocognitive impairments also characterize BD not only during acute phases of the illness but also during remission. Although the relationship between these two debilitating aspects of the illness might seem intuitive, very little is known about their relationship. We examined the association between sleep dysfunction and neurocognition in BD. METHODS: In a sample of 117 BD patients (mean age=45.0±10.7; 59.0% (n=69) male), neurocognitive functioning was assessed using the MATRICS Consensus Cognitive Battery (MCCB). Sleep quality data were collected using the Epworth Sleepiness Scale (ESS) and the Pittsburgh Sleep Quality Index (PSQI). Partial Pearson correlations tested for a relationship between sleep and neurocognition. Path analyses were conducted to examine the hypothesized direct influence of sleep disruption on neurocognition. RESULTS: Higher levels of sleep disruptions were associated with a more severe clinical presentation and poorer performance in social cognition, visual learning and working memory. Social cognition and working memory were directly (negatively) predicted by sleep disruptions. LIMITATIONS: The study was limited by a relatively small sample size and the lack of behavioral and biological objectives measure of activity/rest cycles. CONCLUSIONS: Our study suggests that in patients with BD, sleep disruptions have a detrimental effect on general level of psychopathology and contribute directly to impaired cognitive functioning in the domains of social cognition and working memory. More research using objective measurement of sleep should be pursued to support these data and to further investigate the causal relationship between these disabling aspects of the illness. Published by Elsevier B.V.
BACKGROUNDS: Sleep and circadian rhythm disruptions are prominent, trait-like features of bipolar disorder (BD) which precede the onset of mood episodes. Neurocognitive impairments also characterize BD not only during acute phases of the illness but also during remission. Although the relationship between these two debilitating aspects of the illness might seem intuitive, very little is known about their relationship. We examined the association between sleep dysfunction and neurocognition in BD. METHODS: In a sample of 117 BD patients (mean age=45.0±10.7; 59.0% (n=69) male), neurocognitive functioning was assessed using the MATRICS Consensus Cognitive Battery (MCCB). Sleep quality data were collected using the Epworth Sleepiness Scale (ESS) and the Pittsburgh Sleep Quality Index (PSQI). Partial Pearson correlations tested for a relationship between sleep and neurocognition. Path analyses were conducted to examine the hypothesized direct influence of sleep disruption on neurocognition. RESULTS: Higher levels of sleep disruptions were associated with a more severe clinical presentation and poorer performance in social cognition, visual learning and working memory. Social cognition and working memory were directly (negatively) predicted by sleep disruptions. LIMITATIONS: The study was limited by a relatively small sample size and the lack of behavioral and biological objectives measure of activity/rest cycles. CONCLUSIONS: Our study suggests that in patients with BD, sleep disruptions have a detrimental effect on general level of psychopathology and contribute directly to impaired cognitive functioning in the domains of social cognition and working memory. More research using objective measurement of sleep should be pursued to support these data and to further investigate the causal relationship between these disabling aspects of the illness. Published by Elsevier B.V.
Authors: J Volkert; J Kopf; J Kazmaier; F Glaser; K C Zierhut; M A Schiele; S Kittel-Schneider; A Reif Journal: Eur Neuropsychopharmacol Date: 2014-08-15 Impact factor: 4.600
Authors: Junghee Lee; Lori Altshuler; David C Glahn; David J Miklowitz; Kevin Ochsner; Michael F Green Journal: Am J Psychiatry Date: 2013-03 Impact factor: 18.112
Authors: Lauren B Marangell; Ellen B Dennehy; Sachiko Miyahara; Stephen R Wisniewski; Mark S Bauer; Mark Hyman Rapaport; Michael H Allen Journal: J Affect Disord Date: 2008-08-15 Impact factor: 4.839
Authors: Anabel Martínez-Arán; Eduard Vieta; María Reinares; Francesc Colom; Carla Torrent; Jose Sánchez-Moreno; Antonio Benabarre; José Manuel Goikolea; Mercè Comes; Manel Salamero Journal: Am J Psychiatry Date: 2004-02 Impact factor: 18.112
Authors: Jiajun Shi; Jacqueline K Wittke-Thompson; Judith A Badner; Eiji Hattori; James B Potash; Virginia L Willour; Francis J McMahon; Elliot S Gershon; Chunyu Liu Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2008-10-05 Impact factor: 3.568
Authors: Molly Patapoff; Marina Ramsey; Madison Titone; Christopher N Kaufmann; Atul Malhotra; Sonia Ancoli-Israel; David Wing; Ellen Lee; Lisa T Eyler Journal: J Psychiatr Res Date: 2022-04-03 Impact factor: 5.250
Authors: Heather A Bruce; Peter Kochunov; Joshua Chiappelli; Anya Savransky; Kathleen Carino; Jessica Sewell; Wyatt Marshall; Mark Kvarta; Francis J McMahon; Seth A Ament; Teodor T Postolache; Jeff O'Connell; Alan Shuldiner; Braxton Mitchell; L Elliot Hong Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2021-03-01 Impact factor: 3.568
Authors: Andrea Polo; Sakshi Singh; Anna Crispo; Marilina Russo; Aldo Giudice; Maurizio Montella; Giovanni Colonna; Susan Costantini Journal: Oncol Lett Date: 2017-09-29 Impact factor: 2.967