June 1997

Cerebral Gray Matter Volume Deficits After Weight Recovery From Anorexia Nervosa

Author Affiliations

From the Institute of Medical Science (Ms Lambe) and the Departments of Pediatrics (Dr Katzman), Medical Imaging (Dr Mikulis), and Psychiatry (Drs Kennedy and Zipursky), University of Toronto School of Medicine, Toronto, Ontario. Ms Lambe is now with the Interdepartmental Neuroscience Program, Yale University, New Haven, Conn.

Arch Gen Psychiatry. 1997;54(6):537-542. doi:10.1001/archpsyc.1997.01830180055006

Background:  Structural changes have been observed in the brains of low-weight patients with anorexia nervosa (AN), including increased cerebrospinal fluid (CSF) volumes and decreased gray matter and white matter volumes. We hypothesized that subjects who are weight-recovered from AN would show elevated CSF volumes and reduced gray matter volumes compared with controls.

Methods:  We used magnetic resonance imaging to compare the brains of 12 subjects who are weight-recovered from AN (time since weight recovery, 1-23 years) with those of 18 healthy control subjects and 13 low-weight patients with AN. Axial, dual-echo scans of the whole brain were segmented into gray matter, white matter, and CSF compartments by means of a computerized volumetric approach. Brain measures were corrected for the significant effects of intracranial volume and age, based on regression analysis of a larger group of 30 healthy female controls.

Results:  t Tests showed that the weight-recovered group had significantly greater CSF volumes and smaller gray matter volumes than the control group. By comparison with low-weight patients, the weight-recovered subjects had significantly smaller CSF volumes and significantly larger gray matter and white matter volumes. In the weight-recovered group, neither the CSF elevations nor gray matter deficits were correlated with the length of time since weight recovery.

Conclusions:  The persistent gray matter volume deficits in subjects who are weight-recovered from AN suggest that there may be an irreversible component to the brain changes associated with the illness. The neuropathological features of this irreversible component have yet to be characterized.