That anorexia nervosa is practically confined to females must figure in any acceptable explanation of the syndrome. Among psychiatric disorders, only hysteria has this sex predilection. Probably important is that anorexia nervosa has its onset in relation to menarche, at a time when the female exhibits rather large fluctuations in appetite and weight. This has suggested to some an imbalance between the satiety center, believed to lie in the ventromedial hypothalamus, and the feeding center, in the lateral hypothalamus.
An association of anorexia with structural disease involving the appetite centers has not been established, although the cases of acquired anorexia reported by Lewin and colleagues and of White and Hain are informative. Martin and Reichlin, in citing these rare cases, attribute the anorexia and cachexia to lesions of the lateral hypothalamus. A disorder of infants described under the title of “diencephalic syndrome” causes progressive and ultimately fatal emaciation (“failure to thrive”) despite normal food intake in an otherwise alert and cheerful infant. The causative lesion has usually proved to be a low-grade astrocytoma of the anterior hypothalamus or optic nerve region (Burr et al). Also interesting is a case in which profound and long-standing anorexia nervosa resolved after a left thalamic stroke (Dusoir et al). See Chap. 26 for further discussion and references.
Treatment Treatment at the moment consists of winning the patient’s confidence, supportive psychotherapy, assignment of one individual to sit with the patient as each meal is eaten, and a gradual increase of a balanced diet (Anderson). Extreme cases require hospitalization. If the patient refuses to eat, tube feeding is the only alternative. As weight is gained over several weeks, the patient usually becomes more normal in her attitude toward eating and will continue to recover on this regimen at home. The menses do not return until considerable weight has been gained (approximately 10 percent above the weight at the time of the menarche). Our colleagues report better success with such a regimen when imipramine or fluoxetine is added. Others have found these drugs to be ineffective except in patients with prominent symptoms of depression.
Becker and colleagues emphasized the potentially devastating medical complications to which severely anorectic patients are prone and the need to evaluate and treat these problems at the same time that nutritional therapy is undertaken. In particular, an electrocardiogram is essential in order to exclude a prolonged QT interval—the presence of which contraindicates the use of tricyclic antidepressants and increases the risk of ventricular tachycardia.
On average, 50 percent of patients recover completely or almost completely (Steinhausen and Seidel). In the remainder, the outcome is quite unfavorable. They either relapse after an initial period of improvement or remain chronically anorectic. Many patients are said to lapse into a chronic dysfunctional state characterized by a persistent preoccupation with food, weight, and dieting. It is not generally appreciated that chronic anorexia nervosa significantly shortens life; after a mean followup period of 12 years, 11 percent of a group of 84 patients had died (Deter and Herzog), and 15 percent after 20 years (Ratnasuriya et al). Suicide is a major contributor to this high mortality rate (Sullivan). The addition of antidepression drugs to a behavioral regimen has been tried with generally disappointing results.
The few adolescent boys who we have seen with this syndrome recovered on antidepressant medication. Cases caused by tumors within the hypothalamus were mentioned earlier and in Chap. 26.
In general, the therapeutic benefit of these drugs is considerably greater in cases of bulimia than it is in anorexia nervosa. A review of the problem of bulimia nervosa, binge eating followed by purging, is given by Mehler. The medical complications of either component disorder may be seen but particularly hypokalemia and alkalosis.