Journal
NEUROLOGY
Volume 69, Issue 14, Pages 1424-1433Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/01.wnl.0000277461.06713.23
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Funding
- NCRR NIH HHS [M01-RR0079] Funding Source: Medline
- NIA NIH HHS [R01-AG22985, K23 AG021606, P50-AG03006, P01-AG019724, P01 AG019724] Funding Source: Medline
- NIMH NIH HHS [R25 MH060482] Funding Source: Medline
- PHS HHS [DHS 04-35516, DHS 03-75271] Funding Source: Medline
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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.
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