Abstract
The lateral hypothalamic syndrome of feeding disorders may not involve the hypothalamus per se, nor is it simply an impairment of feeding behavior. Recent work has forced revisions in traditional concepts regarding the role of the hypothalamus in the control of feeding. At present, it seems clear that hypothalamic damage disrupts nonspecific contributions to feeding behavior, by damaging dopaminergic and other fibers of passage coursing through the ventral diencephalon, and that the resultant aphagia reflects a general disruption of all voluntary behavior that includes feeding but is not restricted to it. Neurological dysfunctions such as akinesia, catalepsy, and sensory neglect are prominent and indicate a broad activational disorder reminiscent of Parkinson's disease. In the absence of a clear notion of how feeding is controlled by the brain, it seems premature to consider animals with experimental lesions in the hypothalamus (or elsewhere in the brain) as appropriate models of anorexia nervosa.
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