A critical review of the literature on the ventromedial hypothalamic (VMH) syndrome suggests several problems with the available explanations. In particular, explanations of finickiness and hyperphagia fail to account for essential metabolic changes and obesity that occur even when food intake is controlled. Alternatively, hypotheses that offer an account of essential metabolic changes and obesity are unable to explain finickiness satisfactorily. Some mechanism that directly couples sensory events to metabolic responses is apparently responsible for elements of the syndrome. Based on the review, a hypothesis that can account for the finickiness, hyperphagia, and obesity seen in the VMH syndrome is formulated. This hypothesis suggests that VMH lesions produce their major effects on feeding behavior by directly heightening the phasic autonomic and endocrine responses triggered by oropharyngeal contact with food stimuli-the cephalic reflexes of digestion. This proposal can account for finickiness, explain the paradoxes associated with the operant behavior of the lesioned animal, and elucidate the reasons food-restricted VMH animals still fatten. As a working hypothesis, it is parsimonious, empirically testable, and consistent with physiological observations on the VMH syndrome.The feeding disturbances associated with hypothalamic lesions are major models for the physiological analysis of "drive," "motivation," or "emotion." The ventromedial hypothalamic (VMH) synodrome, characterized by dramatic finickiness, hyperphagia, and obesity, is the most completely studied of these models. One reason for the experimental interest in the VMH syndrome is that it evidences a paradoxical dissociation of "hunger" and "food intake" (Miller,