Subcortical brain anatomy in anorexia and bulimia

Abstract

Many studies have reported a generalized decrease in brain volume (pseudoatrophy) in patients with anorexia nervosa and bulimia (Enzmann and Lane 1977; Heinz et al 1977; Hoffman et al 1989a and b; Krieg et al 1989b). To some degree this change is reversible, but some enlargement of cerebrospinal fluid (CSF) spaces appears to persist despite normalization of weight and eating habits (Artmann et al 1985; Krieg et al 1986, 1988). Change that persists after successful treatment might be due to residual damage to the brain or persistent abnormal metabolism; however, it might also represent underdeveloped or involuted areas that were originally responsible for the behavioral pathology (Artmann et al 1985). However, previous in vivo anatomic studies have focused only on the gross finding of CSF space enlargement or have used techniques with poor spatial resolution and partial voluming problems (i.e., single photon emission computed tomography (SPECT); Krieg et al 1989a). Limited studies of regional cerebral metabolism have shown focal changes: one small positron