San Diego Veterans Affairs Health Care System

San Diego, United States

San Diego Veterans Affairs Health Care System

San Diego, United States
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Kaye W.H.,University of California at San Diego | Wagner A.,University of California at San Diego | Fudge J.L.,University of Rochester | Paulus M.,University of California at San Diego | Paulus M.,San Diego Veterans Affairs Health Care System
Current Topics in Behavioral Neurosciences | Year: 2011

Objectives: This chapter reviews brain imaging findings in anorexia and bulimia nervosa which characterize brain circuitry that may contribute to the pathophysiology of eating disorders (EDs). Summary of recent findings: Recent imaging studies provide evidence of disturbed gustatory processing in EDs which involve the anterior insula as well as striatal regions. These results raise the possibility that individuals with anorexia nervosa have altered appetitive mechanism that may involve sensory, interoceptive, or reward processes. Furthermore, evidence of altered reward mechanisms is supported by studies that suggest that individuals with anorexia nervosa and bulimia nervosa share a trait toward similar anterior ventral striatal pathway dysregulation. This shared trait disturbance of the modulation of reward and emotionality may create a vulnerability for dysregulated appetitive behaviors. However, those with anorexia nervosa may be able to inhibit appetite and have extraordinary self-control because of exaggerated dorsal cognitive circuit function, whereas individuals with bulimia nervosa are vulnerable to overeating when they get hungry, because they have less ability to control their impulses. Future directions: Current therapeutic interventions have modest success. Better understanding of neurocircuits that may be related to altered appetite, mood, impulse control, and other symptoms underlying the pathophysiology of EDs might improve psychotherapeutic and drug treatment strategies. © Springer-Verlag Berlin Heidelberg 2010.


Oberndorfer T.A.,University of California at San Diego | Oberndorfer T.A.,University of Colorado at Denver | Oberndorfer T.A.,San Diego Veterans Affairs Health Care System | Oberndorfer T.A.,University of Rochester | And 32 more authors.
American Journal of Psychiatry | Year: 2013

Objective: Recent studies suggest that altered function of higher-order appetitive neural circuitry may contribute to restricted eating in anorexia nervosa and overeating in bulimia nervosa. This study used sweet tastes to interrogate gustatory neurocircuitry involving the anterior insula and related regions that modulate sensory-interoceptive-reward signals in response to palatable foods. Method: Participants who had recovered from anorexia nervosa and bulimia nervosa were studied to avoid confounding effects of altered nutritional state. Functional MRI measured brain response to repeated tastes of sucrose and sucralose to disentangle neural processing of caloric and noncaloric sweet tastes. Whole-brain functional analysis was constrained to anatomical regions of interest. Results: Relative to matched comparison women (N=14), women recovered from anorexia nervosa (N=14) had significantly diminished and women recovered from bulimia nervosa (N=14) had significantly elevated hemodynamic response to tastes of sucrose in the right anterior insula. Anterior insula response to sucrose compared with sucralose was exaggerated in the recovered group (lower in women recovered from anorexia nervosa and higher in women recovered from bulimia nervosa). Conclusions: The anterior insula integrates sensory reward aspects of taste in the service of nutritional homeostasis. One possibility is that restricted eating and weight loss occur in anorexia nervosa because of a failure to accurately recognize hunger signals, whereas overeating in bulimia nervosa could represent an exaggerated perception of hunger signals. This response may reflect the altered calibration of signals related to sweet taste and the caloric content of food and may offer a pathway to novel and more effective treatments.


Raj Rajasekaran M.,San Diego Veterans Affairs Health Care System | Sinha S.,University of California at San Diego | Seo Y.,San Diego Veterans Affairs Health Care System | Salehi M.,San Diego Veterans Affairs Health Care System | And 2 more authors.
American Journal of Physiology - Gastrointestinal and Liver Physiology | Year: 2014

Obstetrical trauma to external anal sphincter (EAS) is extremely common; however, its role in the development of anal incontinence is not clear. We examined the regenerative process and functional impact of experimental surgical trauma to EAS muscle in an animal model. Surgical myotomy, a craniocaudal incision extending along the entire length and thickness of the EAS, was performed in rabbits. Animals were allowed to recover, and anal pressures were recorded at weekly intervals for 12 wk using a custom-designed probe system to determine the length-tension property of EAS muscle. Animals were killed at predetermined time intervals, and the anal canal was harvested for histochemical studies (for determination of muscle/connective tissue/collagen) and sarcomere length measurement. In addition, magnetic resonance diffusion tensor imaging (MR-DTI) and fiber tracking was performed to determine myoarchitectural changes in the EAS. Myotomy of the EAS muscle resulted in significant impairment of its length-tension property that showed only partial recovery during the 12-wk study period. Histology revealed marked increase in the fibrosis (connective tissue = 69% following myotomy vs. 28% in controls) at 3 wk, which persisted at 12 wk. Immunostaining studies confirmed deposition of collagen in the fibrotic tissue. There was no change in the sarcomere length following myotomy. MR-DTI studies revealed disorganized muscle fiber orientation in the regenerating muscle. We conclude that, following experimental injury, the EAS muscle heals with an increase in the collagen content and loss of normal myoarchitecture, which we suspect is the cause of impaired EAS function. © 2014 the American Physiological Society.

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