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LETTER TO EDITOR |
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Year : 2013 | Volume
: 61
| Issue : 3 | Page : 320-321 |
Unusual presentation of hyperphagia after surgery for fourth ventricular ependymoma: Accessory satiety center or hypothalamic seedlings?
Sivashanmugam Dhandapani1, Madhivanan Karthigeyan1, Manju Dhandapani2
1 Department of Neurosurgery, Post Graduate Institute of Medical Education and Research, Chandigarh - 12, India 2 Department of NINE, Post Graduate Institute of Medical Education and Research, Chandigarh - 12, India
Date of Submission | 31-May-2013 |
Date of Decision | 31-May-2013 |
Date of Acceptance | 04-Jun-2013 |
Date of Web Publication | 16-Jul-2013 |
Correspondence Address: Sivashanmugam Dhandapani Department of Neurosurgery, Post Graduate Institute of Medical Education and Research, Chandigarh - 12 India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.115086
How to cite this article: Dhandapani S, Karthigeyan M, Dhandapani M. Unusual presentation of hyperphagia after surgery for fourth ventricular ependymoma: Accessory satiety center or hypothalamic seedlings?. Neurol India 2013;61:320-1 |
How to cite this URL: Dhandapani S, Karthigeyan M, Dhandapani M. Unusual presentation of hyperphagia after surgery for fourth ventricular ependymoma: Accessory satiety center or hypothalamic seedlings?. Neurol India [serial online] 2013 [cited 2021 Mar 1];61:320-1. Available from: https://www.neurologyindia.com/text.asp?2013/61/3/320/115086 |
Sir,
Abnormal eating behavior is known to occur with central nervous system (CNS) lesions. [1],[2],[3] In this report, we describe probably the first case of hyperphagia following surgery for fourth ventricular ependymoma.
An 8-year-old girl child presented with clinical features of raised intracranial pressure. Neuroimaging revealed fourth ventricular ependymoma with hydrocephalus [Figure 1]. Her symptoms improved following ventriculo-peritoneal shunt and transvermian tumor excision. Postoperatively the child was noted to have excessive appetite, almost the double of her previous intake with no satiety. There were no speech or behavioral abnormalities. Physical examination revealed no features of endocrine dysfunction and her hormone profile was unremarkable. Histopathological examination confirmed the diagnosis of ependymoma. Postoperative magnetic resonance imaging (MRI) did not show significant residual or obvious subarachnoid seedlings [Figure 2]. Hyperphagia persisted for a month, and gradually got stabilized. | Figure 1: Preoperative contrast CT and MRI showing fourth ventricular ependymoma
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 | Figure 2: Postoperative CT and contrast MRI showing no significant residual tumor
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CNS tumors located around the third ventricular region or hypothalamus and hydrocephalus have been reported to cause hyperphagia. [1],[2],[3] Dysfunction of bilateral ventromedial hypothalamic nuclei, which contain the satiety center leads to hyperphagia and obesity in these patients. [1],[2] In our patient, the hyperphagia could only be explained by either hypothalamic tumor seedlings or injury to accessory satiety center situated around the fourth ventricle during tumor resection. Though there were no radiological features of hypothalamic seedlings, microscopic tumor seedlings could have got displaced retrograde to the third ventricle possibly affecting ventromedial nuclei. There has been a report of leukemic infiltration of ventromedial nucleus of hypothalamus and disturbance in neuro-endocrine function with subsequent hyperphagia and obesity. [3] The other possibility of accessory satiety center around fourth ventricle is also to be considered due to the common embryological origin of hypothalamus and cerebellum from alar plates. [4] This atypical presentation widens the pathophysiology of eating disorders away from the usual hypothalamic location, and needs further corroboration.
» References | |  |
1. | Celesia GG, Archer CR, Chung HD. Hyperphagia and obesity. Relationship to medial hypothalamic lesions. JAMA 1981;246:151-3.  [PUBMED] |
2. | Bray GA, York DA. Hypothalamic and genetic obesity in experimental animals: An autonomic and endocrine hypothesis. Physiol Rev 1979;59:719-809.  [PUBMED] |
3. | Zhang LD, Li YH, Ke ZY, Huang LB, Luo XQ. Obesity as the initial manifestation of central nervous system relapse of acute lymphoblastic leukemia: Case report and literature review. J Cancer Res Ther 2012;8:151-3.  [PUBMED] |
4. | Sadler TW. Langman's Medical Embryology. 12 th ed. Philadelphia: Lippincott Williams and Wilkins; 2012.  |
[Figure 1], [Figure 2]
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