Preliminary studies show brain anomalies in AN diminish with weight rehabilitation.
Reprinted from Eating Disorders Review
March/April Volume 26, Number 2
©2015 iaedp
It has been clear for some time that brain volume is diminished in people with AN, and some studies suggest it may be reversible. Until recently, neuroscientists studying the effects of anorexia nervosa (AN) on the brain were hampered by an inability to measure cortical structure anomalies well enough to fully define the changes. Now researchers from the Translational Developmental Neuroscience Lab at University Hospital Carl Gustav Carus, Dresden, Germany, have reported that widespread thinning of gray matter in the cortex of the brain that is seen in acutely ill adolescent patients can be completely reversed with successful weight rehabilitation (Biol Psychiatry. 2014; doi:10.1016).
Dr. Stefan Ehrlich and the Dresden researchers used structural magnetic resonance imaging (MRI) to study a large sample of both acutely ill and long-term recovered patients with AN. Newer techniques allowed for extremely precise measurement of cortical gray matter.
Forty female patients underwent MRI scanning within 4 days after they were admitted to specialized eating disorder clinics and again following successful therapy with complete restoration to normal weight, eating behavior, and return of menstruation. Structural MRI data were also obtained among 34 recovered patients after long-term weight restoration and an equal number of age-matched healthy control subjects. Dr. Ehrlich’s group reported that the magnitude of cortical gray matter thinning in acute AN was similar, comparable to that typically seen in Alzheimer’s disease, and significant thinning of the cortical gray matter was seen over 85% of the cortical surface. Severity of low weight did not correlate with cortical thinning but there also was a strong negative correlation between drive for thinness and gray matter volume/thickness in extrastriate regions that play a role in body perception.
The authors concluded that the results show that structural brain anomalies in AN are primarily the result of malnutrition and are not likely to reflect premorbid trait markers or permanent scars.
