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  • Title: Subcortical volume and cortical surface architecture in women with acute and remitted anorexia nervosa: An exploratory neuroimaging study.
    Author: Miles AE, Voineskos AN, French L, Kaplan AS.
    Journal: J Psychiatr Res; 2018 Jul; 102():179-185. PubMed ID: 29680574.
    Abstract:
    BACKGROUND: Anorexia nervosa (AN) is a highly heritable psychiatric disorder characterized by starvation and emaciation and associated with changes in brain structure. The precise nature of these changes remains unclear, as does their developmental time course and capacity for reversal with weight-restoration. In this comprehensive neuroimaging study, we sought to characterize these changes by measuring subcortical volume and cortical surface architecture in women with acute and remitted AN. METHODS: Structural magnetic resonance imaging data was acquired from underweight women with a current diagnosis of AN (acAN: n = 23), weight-recovered women with a past diagnosis of AN (recAN: n = 24), and female controls (HC: n = 24). Subcortical segmentation and cortical surface reconstruction were performed with FreeSurfer 6.0.0, and group differences in regional volume and vertex-wise, cortex-wide thickness, surface area, and local gyrification index (LGI), a measure of folding, were tested with separate univariate analyses of covariance. RESULTS: Mean hippocampal and thalamic volumes were significantly reduced in acAN participants, as was mean cortical thickness in four frontal and temporal clusters. Mean LGI was significantly reduced in acAN and recAN participants in five frontal and parietal clusters. No significant group differences in cortical surface area were detected. CONCLUSIONS: Reductions in subcortical volume, cortical thickness, and right postcentral LGI were unique to women with acute AN, indicating state-dependence and pointing towards cellular remodeling and sulcal widening as consequences of disease manifestation. Reductions in bilateral frontal LGI were observed in women with acute and remitted AN, suggesting a role of atypical neurodevelopment in disease vulnerability.
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