Post‐traumatic Hypothalamic Obesity—an Autopsy Case—†

Abstract

A 45‐year‐old housewife sustained a blow to the occipital region In a traffic accident about 2 years and 3 months prior to death. Autopsy revealed lesions of softening in the hypothalamus, left thalamus, frontal lobe (especially on the left), and base of the left temporal lobe. Following the head trauma, a marked Increase of appetite was noted, with obesity, hypogonadism, and mild elevation of temperature. No diabetes insipidus was noted whatsoever. Based on data from physical and pathological examination, the relationship between function and morphology in the human hypothalamus was discussed.

Conjugated Linoleic Acid Administration Induces Amnesia in Male Sprague Dawley Rats and Exacerbates Recovery from Functional Deficits Induced by a Controlled Cortical Impact Injury

“…The decline in P 4 following a TBI was similar to that reported by Wright and colleagues [ 80 ]. These results are similar to those reported in humans, where early studies demonstrated that TBI could alter hypothalamic morphology and induce hypogonadism and hypothryoidism [ 81 , 82 ]. Subsequent studies demonstrated that the post-traumatic hypopituitarism, initially unresponsive to GnRH in severe TBI, could eventually be reversed with GnRH treatment and indicated a hypothalamic cause for hypogonadism [ 83 ].…”

Changes in weight after traumatic brain injury in adult patients: A longitudinal study

“…Obese passengers are more likely to suffer a more severe head injury after frontal motorvehicle crashes 1 . After traumatic brain injury (TBI), changes in weight and (or) food behavior have been reported in short studies 2,3 and various clinical case-reports 4,5 . Some reports have described hyperphagia and reduction of satiety 6 .…”

Hypogonadism induced by surgical stress and brain trauma is reversed by human chorionic gonadotropin in male rats: A potential therapy for surgical and TBI‐induced hypogonadism?

“…Our data are consistent with early studies in humans demonstrating that TBI could alter hypothalamic morphology and induce hypogonadism and hypothyroidism. 76,77 However, while our study implicates isoflurane in the induction of hypogonadism and hypopituitarism via suppression of HP function, human studies suggest that TBI-induced hypogonadism and hypopituitarism is mediated via suppression of HP function by elevated circulating cortisol. 78,79 Ranganathan et al 79 demonstrated that the stress of TBI results in anovulation and central hypothalamic-pituitary-ovarian axis suppression, with menstruation resuming among pre-menopausal women when serum cortisol normalized to luteal phase control levels.…”

“…It is apparent that TBI‐induced HH, even when limited to the anterior hypothalamus, 13,80 is a system problem commonly involving both the HPG axis and the HPA axis 81 . From our study, it is not possible to determine whether the CCI injury had an impact beyond that of craniectomy on promoting hypogonadism or hypoadrenalism, as has been reported for human TBI 6–8,10,14,76–78,82–96 . These results demonstrate that future studies need to take into account the effects of isoflurane alone in any model of TBI‐induced hypogonadism.…”

“…81 From our study, it is not possible to determine whether the CCI injury had an impact beyond that of craniectomy on promoting hypogonadism or hypoadrenalism, as has been reported for human TBI. [6][7][8]10,14,[76][77][78][82][83][84][85][86][87][88][89][90][91][92][93][94][95][96] These results demonstrate that future studies need to take into account the effects of isoflurane alone in any model of TBI-induced hypogonadism.…”