There is a general consensus that the aetiology of eating disorders is multidetermined, affected by biological, psychological and social factors that interact in a complex fashion (Garfinkel, Kennedy and Kaplan, 1995). And while it is clear that no one cause for eating disorders will be discovered, the role of the central nervous system (CNS) deserves special attention as the CNS must play a central role in mediating and maintaining eating behaviours. A fuller understanding of CNS control of eating may lead to improvements in the medical treatment of various disorders of eating. For these reasons, direct and non-invasive analytic methods of brain imaging are now widely applied in the study of eating disorders (Ellison and Foog, 1998; Krishnan and Gadde, 1998; Grady, 1999; Demaerel, 2000; Hendren, De Backer and Pandina, 2000).
This chapter will review the research findings from brain imaging techniques focusing on anorexia nervosa and bulimia nervosa, and categorizing the studies as either structural or functional. The literature on obesity will also be reviewed, as a substantial proportion of the obese in weight control programs have bingeeating behaviour (De Zwaan et al., 1994) and are reported to have many characteristics in common with patients suffering from eating disorders (Stunkard, 1996).
Tables XXIII-8.1 and XXIII-8.2 present a brief summary of the studies reviewed in this chapter according to the brain imaging techniques used.
Table XXIII-8.1 Brain imaging studies of eating disorders: structural brain imaging studies
Table XXIII-8.2 Brain imaging studies of eating disorders: functional brain imaging studies
Numerous important findings in patients with anorexia nervosa were detected by computed tomography (CT) in studies performed in the 1980s. These structural changes are characterized by an enlargement of the cortical and cerebellar sulci, the interhemispheric fissure and the cisterns, and a widening of internal cerebrospinal fluid (CSF) spaces (Datlof et al., 1986; Lankenau et al., 1985). According to these studies, as body weight increased, these changes, labelled 'pseudoatrophy' returned to normal (Kohkmeyer, Lemkuhl and Poutska, 1983; Artmann et al., 1985).
However, there may be different patterns of recovery for the cortical sulci and ventricles over the course of weight restoration. In one of these studies, 15 anorexic patients out of 25 displayed enlarged ventricles and cortical sulci. After 3 month's treatment, the cortical sulci returned to normal while the ventricles remained enlarged (Dolan, Mitchell and Wakeling, 1988). The authors suggested that ventricular enlargement might require longer than 3 months to recover, or that with sufficient chronicity the observed changes in ventricular size might be irreversible. The observed reversal of sulcal widening following refeeding was interpreted as upholding a hypothesis that the observed changes are secondary to malnourishment.