Eating disorders are relatively frequent psychiatric disorders that can produce serious consequences at the brain level. In an effort to clarify the neurobiological mechanisms of their pathogenesis, some studies have suggested the existence of modifications of the cortical architecture in eating disorders, but it is unknown whether the alterations described are a cause or consequence of eating disorders. The main objective of this systematic review is to collect the evidence available about the volumetric alterations of the cerebral cortex in eating disorders in adults and their apparent relationship with the pathogenesis of the disease. Initially, 91 articles were found by a search that included the terms anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder, gray matter, cortical thickness (CT), and brain volume. To pare down the articles, the following inclusion criteria were applied: (1) cortical thickness and/or gray matter volume (GMV) in patients with anorexia, bulimia nervosa, or binge-eating disorder was the main measure of the study; and (2) the sample was adult patients aged 18–65. The exclusion criteria were as follows: (1) articles that did not analyze cortical thickness or gray matter volume; (2) studies with patients with comorbidities; and (3) studies in patients who did not meet the DSM-IV/DSM-V criteria. In the first phase of selection, we proceeded to read the titles and abstracts as a first screen, thereby excluding 62 studies, followed by a complete critical reading of the 29 remaining articles. In this last phase, nine studies were excluded because they did not specify the eating disorder subtype, they included adolescents, or they did not measure GMV or CT. Finally, after the above systematic selection process, 20 articles were included in this review. Despite the methodological heterogeneity of the studies, there was some agreement between them. They showed an overall reduction in GMV in eating disorders, as well as alterations in certain regions of the cerebral cortex. Some of the most often mentioned cortical areas were the frontal, cingulate, and right orbitofrontal cortices, the precuneus, the right insula, and some temporoparietal gyri in cases of AN, with greater cortical involvement in frontotemporal and medial orbitofrontal regions in BN and binge eating disorder. Likewise, certain cortical regions, such as the left inferior frontal gyrus, the precuneus, the right superior motor area, the cingulate cortex, the insula, and the medial orbitofrontal sulcus, often remained altered after recovery from AN, making them potential cortical areas involved in the etiopathogenesis of AN. A reduction in GMV in specific areas of the CNS can inform us about the neurobiological mechanisms that underlie eating disorders as well as give us a better understanding of their possible consequences at the brain level.
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