title: Binge eating is associated with right orbitofrontal-insular-striatal atrophy in frontotemporal dementia.
abstract: BACKGROUND
  Neurophysiologic studies on human and nonhuman primates implicate an orbitofrontal-insular-striatal circuit in high-level regulation of feeding. However, the role of these areas in determining feeding disturbances in neurologic patients remains uncertain.
  
  
  OBJECTIVE
  To determine brain structures critical for control of eating behavior, we performed a prospective, laboratory-based, free-feeding study of 18 healthy control subjects and 32 patients with neurodegenerative disease. MR voxel-based morphometry (VBM) was used to identify regions of significant atrophy in patients who overate compared with those who did not.
  
  
  RESULTS
  Despite normal taste recognition, 6 of 32 patients compulsively binged, consuming large quantities of food after reporting appropriate satiety. All six patients who overate were clinically diagnosed with frontotemporal dementia (FTD), a disorder previously associated with disordered eating, while the nonovereaters were diagnosed with FTD, semantic dementia, progressive aphasia, progressive supranuclear palsy, and Alzheimer disease. VBM revealed that binge-eating patients had significantly greater atrophy in the right ventral insula, striatum, and orbitofrontal cortex.
  
  
  CONCLUSIONS
  Binge eating can occur despite reported satiety and is associated with damage to a right-sided orbitofrontal-insular-striatal circuit in humans. These findings support a model in which ventral insular and orbitofrontal cortices serve as higher-order gustatory regions and cooperate with the striatum to guide appropriate feeding responses.
authors.affiliation: Memory and Aging Center, Department of Neurology, University of California San Francisco, 1779 Turk St., San Francisco, CA 94115, USA. jwoolley@memory.ucsf.edu
authors.forename: J D
authors.initials: JD
authors.lastname: Woolley
authors.forename: M-L
authors.initials: ML
authors.lastname: Gorno-Tempini
authors.forename: W W
authors.initials: WW
authors.lastname: Seeley
authors.forename: K
authors.initials: K
authors.lastname: Rankin
authors.forename: S S
authors.initials: SS
authors.lastname: Lee
authors.forename: B R
authors.initials: BR
authors.lastname: Matthews
authors.forename: B L
authors.initials: BL
authors.lastname: Miller
mesh_terms: D000368:Aged; D001066:Appetite / Q000502:physiology; D001284:Atrophy / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D052018:Bulimia Nervosa / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology; D003342:Corpus Striatum / Q000473:pathology / Q000503:physiopathology; D003704:Dementia / Q000150:complications / Q000473:pathology* / Q000523:psychology; D005247:Feeding Behavior / Q000502:physiology; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D001523:Mental Disorders / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D008875:Middle Aged; D009434:Neural Pathways / Q000473:pathology* / Q000503:physiopathology; D009483:Neuropsychological Tests; D011237:Predictive Value of Tests; D017397:Prefrontal Cortex / Q000473:pathology / Q000503:physiopathology; D012201:Reward; D012528:Satiety Response