<p>Early-onset restrictive eating disorders (rEO-ED) encompass a heterogeneous group of conditions, including early-onset anorexia nervosa (EO-AN) and avoidant/restrictive food intake disorders (ARFID). However, the impact of rEO-ED on brain morphometry remains largely unknown. Here we performed the largest magnetic resonance imaging-derived brain features comparison of children and early adolescents (&lt;13 years) with EO-AN (<i>n</i> = 124) or ARFID (<i>n</i> = 50) versus typically developing individuals (TD, <i>n</i> = 116). EO-AN was associated with widespread cortex thinning, while underweight patients with ARFID exhibited reduced surface area and volumes compared with TD. Despite similar body mass index distributions, EO-AN and ARFID showed distinct structural patterns, suggesting independent brain mechanisms. Finally, we identified overlapping patterns of brain thickness differences between EO-AN and obsessive–compulsive disorder and between ARFID and autism spectrum disorder. Future studies are required to partition the contribution of body mass index versus rEO-ED mechanisms, as well as to identify shared mechanisms with other neurodevelopmental conditions toward a multidimensional approach of eating disorders.</p>

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Neuroimaging insights into brain mechanisms of early-onset restrictive eating disorders

  • Clara A. Moreau,
  • Anael Ayrolles,
  • Christopher R. K. Ching,
  • Robin Bonicel,
  • Alexandre Mathieu,
  • Coline Stordeur,
  • Clara El Khantour,
  • Pierre Bergeret,
  • Nicolas Traut,
  • Lydie Tran,
  • David Germanaud,
  • Marianne Alison,
  • Monique Elmaleh-Bergès,
  • Stefan Ehrlich,
  • Paul M. Thompson,
  • Thomas Bourgeron,
  • Richard Delorme

摘要

Early-onset restrictive eating disorders (rEO-ED) encompass a heterogeneous group of conditions, including early-onset anorexia nervosa (EO-AN) and avoidant/restrictive food intake disorders (ARFID). However, the impact of rEO-ED on brain morphometry remains largely unknown. Here we performed the largest magnetic resonance imaging-derived brain features comparison of children and early adolescents (<13 years) with EO-AN (n = 124) or ARFID (n = 50) versus typically developing individuals (TD, n = 116). EO-AN was associated with widespread cortex thinning, while underweight patients with ARFID exhibited reduced surface area and volumes compared with TD. Despite similar body mass index distributions, EO-AN and ARFID showed distinct structural patterns, suggesting independent brain mechanisms. Finally, we identified overlapping patterns of brain thickness differences between EO-AN and obsessive–compulsive disorder and between ARFID and autism spectrum disorder. Future studies are required to partition the contribution of body mass index versus rEO-ED mechanisms, as well as to identify shared mechanisms with other neurodevelopmental conditions toward a multidimensional approach of eating disorders.