Comparing Neural Responses to Food Images in EDNOS Patients and Healthy Controls Using fMRI

Overview

Currently, there is not a robust, testable neural model available that sufficiently explains the development and maintenance of anorexia nervosa (AN) a severe, often fatal, adolescent-onset eating disorder. Using state of the art neuroimaging and neuropsychological techniques, our objective is to identify neural mechanisms in the adolescent brain underlying AN. This is of high clinical relevance in as much as it will provide a robust platform for a diagnostic battery so that physicians can identify those who are prone to develop AN at a very early stage of life. The aim of this research plan is: 1) To develop knowledge of cognitive dysfunction in adolescents who have recently been diagnosed with AN, with a battery of cognitive tests during a series of clinical visits. 2) To provide a scientific basis for our knowledge about how the brain of an adolescent with an eating disorder differs from that of a healthy adolescent, by conducting functional and structural magnetic resonance imaging on adolescent females with AN.

Adolescents with eating disorders have debilitating cognitive disturbances that impact on their social, educational and physical health. One cognitive trait that is found to form core cognitive disturbances in AN is superior working memory (WM). WM is the ability to ruminate on a cognitive strategy while attending to the details of another task, excluding non-relevant stimuli, and is linked to activation of the dorsolateral prefrontal cortex (DLPFC). By administering functional Magnetic Resonance Imaging (fMRI) we have recently found that females with AN have increased activation in the DLPFC and reduced appetitive brain responses when thinking about eating food shown in visual images. This suggests that the increased WM capacity in AN may serve to suppress food intake, but this has not yet been clarified. In line with this assumption, we have also shown that restraint of appetite in those with AN was linked to greater plasticity in the DLPFC. Furthermore, Transcranial Magnetic Stimulation (TMS) of the DLPFC reduces appetitive responses to food stimuli in adults with eating disorders. Conversely, we have shown that being obese is linked to reduced structure and abnormal function in the DLPFC, as well as reduced attentional control/WM performance. Therefore, it is likely that DLPFC-related WM function is associated with eating disorders, particularly cognitive restraint of appetite. It is likely that the interaction between appetitive brain regions and specific prefrontal cortex (PFC) cognitions determines whether an adolescent develops anorexia nervosa. We aim to provide neuropsychological and brain imaging measures showing how a specific cognitive function is linked to early-onset disordered eating behaviour, and we will do this before and after standard clinical treatment. We suggest that such understanding could enable school nurses to use the unique paradigm we use in our fMRI study, to detect illness before it damages the child's life and becomes difficult to treat. The study has now been increased to include genetic components to examine the genetic and epigenetic variation for genes found to be linked with eating disorders.