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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 and Methods: 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.
Conclusion: 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.
Glossary: AD = Alzheimer disease; FTD = frontotemporal dementia; GCRC = General Clinical Research Center; MMSE = Mini-Mental State Examination; OFC = orbitofrontal cortex; PA = progressive aphasia; PSP = progressive supranuclear palsy; ROI = region of interest; SemD = semantic dementia; VBM = voxel-based morphometry.
Footnotes
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jwoolley{at}memory.ucsf.edu
Supplemental data at www.neurology.org
Editorial, see page 1389
Supported by grant no. UL1 RR024131-01 from the National Center for Research Resources, a component of the NIH, and NIH Roadmap for Medical Research and by the following grants: NIH/NIA P01-AG019724, P50-AG03006 AD Research Center, M01-RR0079 General Clinical Research Center; DHS 03-75271 (Miller, Johnson); and National Institute of Neurological Disorders and Stroke R01-AG22985 and DHS 04-35516 (Gorno-Tempini).
Disclosure: The authors report no conflicts of interest.
The content of the paper is the responsibility of the authors and does not necessarily represent the official view of the National Center for Research Resources or NIH.
Received January 13, 2007. Accepted in final form April 23, 2007.
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