Cortical thinning in patients with persistent insomnia and its relation with insomnia progression

Abstract

Introduction Previous studies have demonstrated that insomnia is associated with cortical atrophy, but the impact of progressive decline in sleep quality to such structural changes has not been investigated, which can be assessed accurately through a longitudinal study. Materials and methods Sixty patients presenting persistent insomnia at three time points spaced two years apart (PI, age = 51.13 ± 8.06, males = 60%) and 44 good sleepers (GS, age = 48.09 ± 6.47, males = 56.8%) were randomly selected from a larger population-based study. All participants underwent 1.5 Tesla MRI at the endpoint. Outer and inner cortical interfaces were extracted using the CIVET image processing pipeline developed at Montreal Neurological Institute. A total of 80,492 points were sampled on these surfaces, and cortical thickness was measured as the shortest distance between the two interfaces. Participants also completed the Pittsburgh Sleep Quality Index (PSQI) and Beck Depression Inventory (BDI) at each visitation. We defined longitudinal change of PSQI scores as ‘PSQI at the 3rd –1st time point’. Linear regression analysis was conducted with insomnia progression, insomnia groups, and an interaction as independent variables, and cortical thickness as the dependent variable. All statistical tests included age, sex, and depression as covariates. Multiple comparisons were corrected based on a random field theory for image data. Results The PI group presented cortical thinning in the precentral cortex of both hemispheres and the superior/mid frontal areas ( p p r = −.44, p F = 3.1, p = 0.001). Conclusion We found cortical atrophy in multiple brain regions, including bilateral frontal lobes in the PI group relative to GS groups. Additionally, having PI had implications for regions in the parietal and frontal lobe, especially with progressive decline in sleep quality over time. Further studies using neuropsychological assessments may reveal cognitive deficits that are secondary to structural brain changes resulting from PI. Acknowledgements This study was performed at the Korea University Hospital, Ansan, Republic of Korea. This study was supported by grants from the Korean Center for Disease Control, Prevention and the Korean Ministry for Health and Welfare, and the National Research Foundation of Korea Grant funded by the Korean Government. [Grants 2005-E71001-00, 2006-E71005-00, 2007-E71001-00, 2008-E71001-00, 2009-E71002-00, 2010-E71001-00, 2011- E71004-0, 2011-E71005-00, 2012-E71005-00, 2013-E71005-00, NRF-2012-S1A5BA01].