The lateral hypothalamic syndrome

With the early application of stereotaxic surgery to neurological studies in experimental animals, Anand and Brobeck (1951) first reported that bilateral lesions of small nuclei in the hypothalamus could disrupt feeding behavior with medial hypothalamic lesions causing obesity and lateral lesions aphagia. In the latter syndrome, the lesioned animals would completely stop eating to the extent that if not maintained 

Regulates food intake and body weight on wet palatable foods 

Drinks water prandially, Survives on dry food and water 

Regulates food intake to dilution, temperature and deprivation 

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Levitt DR, Teitelbaum P (1975) Somnolence, akinesia and sensory activation of motivated behavior in the lateral hypothalamic syndrome. Proc Natl Acad Sci USA 72 2819-2823. 

Marshall JF, Richardson JS, Teitelbaum P (1974) Nigrostriatal bundle damage and the lateral hypothalamic syndrome. J Comp Physiol Psychol 7 808-830. 

Teitelbaum P, Epstein AN (1962a) The lateral hypothalamic syndrome recovery of feeding and drinking after lateral hypothalamic lesions. Physiol Rev 69 74-90. 

Ungerstedt U (1970) Is interruption of the nigro-striatal dopamine system producing the lateral hypothalamic syndrome Acta Physiol Sccmd 80 35A-36A. 

Lesions of the lateral hypothalamic area (LHA) cause anorexia, whereas ablation of the paraventricular nucleus (PVN) cause a hyperphagic obesity syndrome. Consistent with these results, LHA neurons express the orexigenic neuropeptides MCH and orexin. PVN neurons produce several neuropeptides that are anorex-igenic when administered directly into the brain (CRH, TRH, oxytocin), in addition to their better known roles as endocrine regulators. LHA and PVN receive rich inputs from axons of NPY/AgRP and aMSH/CART-producing neurons in the arcuate nucleus. 

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