Abstract
At its core, insomnia is the inability to sleep when expecting to do so. The behavioral and cognitive factors associated with insomnia have been extensively studied but the pathophysiology of insomnia remains unclear. This study investigated structural brain differences in a well-characterized sample of individuals who met DSM-IV-TR criteria for insomnia disorder (n = 58) and controls (n = 67) using high-dimensional surface-based mapping procedures. MRI scans were collected at the University of Pittsburgh at either 1.5 or 3 Tesla. We harmonized these scans using neuroComBat procedures. Image processing included the FreeSurfer toolkit and large-deformation diffeo-morphic metric mapping (LDDMM). We hypothesized that the insomnia group would demonstrate altered volume, cortical thickness, and shape relative to a control group in regions predicted by prior genetic analyses and MRI studies: orbitofrontal cortex, prefrontal cortex, temporal cortex, precuneus, hippocampus, thalamus, cingulate, caudate nucleus, and cerebellum. Repeated measures general linear models were conducted for extracted values of all regions, with group status as the between-subjects effect and hemisphere as the within-subjects effect. We found that compared to controls, individuals with insomnia had significantly greater cerebellar gray matter volume than controls with a rightward volumetric asymmetry, thinner anterior cingulate cortices, inward deformations in the head of the right caudate, and outward deformation in the right CA1 region of the hippocampus. Structural differences may represent individual differences that confer vulnerability to insomnia. Alternatively, insomnia may result in brain alterations through regional sleep disruption or chronic daytime use differences.