Background Weight gain and obesity after brain damage have been described in both children and adults. Most commonly, they are caused by damage to the hypothalamus. We report here a case of hyperphagia and rapid weight gain after surgical removal of brainstem cavernoma, followed by resolution after gastric bypass surgery.
Case Presentation A 30-year-old woman presented with acute onset of facial paresthesias, left-side weakness, and double vision. Brain MRI disclosed a 1.5 × 1.7 × 2.3 cm heterogeneous lesion in the posterior right pons with signs of recent bleeding and an intact hypothalamus. The lesion was resected, and the histologic examination confirmed the suspected diagnosis of cavernous hemangioma. Immediately after surgery, she noted onset of a voracious appetite and lack of satiety. She had no symptoms suggestive of hypothalamic dysfunction, such as abnormal thermoregulation, water balance, sleep-wake cycles, and aggressive behavior. Despite extreme dietary counseling, 10 months postoperatively, her weight had increased 120 pounds, at a rate of 10 to 15 pounds per month. Her brain MRI revealed hypertrophic olivary degeneration with no hypothalamic damage. Treatment with centrally acting stimulants, phentermine and sibutramine, partially decreased her appetite but only lowered the rate of weight gain to 2 lb per month. One and a half years after initial surgery, she underwent Roux-en-Y gastric bypass (RYGP), followed by immediate resolution of hyperphagia, weight loss, and return to baseline body weight within 3 years.
Discussions Energy homeostasis involves interactions between afferent hormonal and neuronal signals, the central nervous system and brainstem, and efferent pathways. Unregulated appetite and weight gain after brain damage have, until now, been exclusively reported in those with ventromedial hypothalamus lesions. Previous reports of brainstem lesions often described paraparesis and weight loss. This is the first report of unwanted weight gain in humans with an exclusive brainstem lesion. Destruction of the brainstem ventral noradrenergic bundle (VNAB) has been shown to cause hyperphagia and obesity in rats. Therefore, we hypothesize that the surgery resulted in damage to the VNAB, or its ascending projections to the hypothalamus. Other potential mechanisms may involve damage to the nucleus of solitary or vagal projections carrying satiety signals from the gut (CCK, GLP-1, PYY, oxyntomodulin) to the NTS. Restoration of satiety and body weight after RYGP suggests correction of this defect via alterations in the levels of gut hormones, vagal signaling, or both.
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