Case study Hypodipsic hypernatremia and diabetes insipidus following anterior communicating artery aneurysm clipping: diagnostic and therapeutic challenges in the amnestic rehabilitation patient BENJAMIN N. NGUYEN { , STUART A. YABLON { and CHRISTINE Y. CHEN ‡ { Mississippi Methodist Rehabilitation Center, Jackson, MS, USA ‡ Kaiser Permanante, Baldwin Park Medical Center, Baldwin Park, CA, USA (Received 16 March 2001; accepted 27 April 2001 ) Hypodipsic hypernatremia (HH) represents a pathological increase in serum sodium due to a lack of thirst and defect in hypothalamic osmoreceptors. While 15% of patients with HH have a vascular aetiology, few cases have been described. Moreover, the presence of such abnormalities in the amnestic patient can have particularly threatening implications, as HH tends to recur unless the patient complies with a regimen of water intake. This study reports the case of a 46-year-old male admitted for rehabilitation of functional deficits following subarachnoid haemorrhage (SAH), with clipping of an anterior communicating artery (ACoA) aneurysm. Clinical examination was remarkable for profound short-term memory loss and inability to retain new information. Blood chemistry on admission showed a serum sodium level of 160 mEq/L, increasing to 167 mEq/L the following day. The patient denied thirst, and showed no clinical signs of dehydration. Neuroendocrine evaluation revealed diabetes insipidus (DI) and HH. Treatment initially included DDAVP and intravenous hydration, later supplemented with chlorpropramide. Stabilization of serum sodium and osmolality did not ensue until the treatment regimen included hydrochlorothiazide and supervision of enforced fluid intake. Endocrine abnormalities may be encountered among patients with vascular lesions adjacent to the hypothalamus. Rehabilitation interventions include establishing a structured medication regimen with fluid administration in the amnestic patient with hypothalamic dysfunction. Introduction ACoA aneurysm rupture with associated SAH represents the second most common cause among the more than 18 000 cases of aneurysmal rupture/SAH reported yearly [1]. It is responsible for 30% of fatal aneurysmal rupture in one recent study [2]. Survivors of SAH secondary to ACoA aneurysmal rupture may develop an amnestic syndrome characterized by significant short-term memory deficits, changes in intellectual function, and conceptual learning [3]. Additionally, pituitary and hypothalamic abnormalities frequently occur among these patients, with one Brain Injury ISSN 0269±9052 print/ISSN 1362±301X online # 2001 Taylor & Francis Ltd http://www.tandf.co.uk/journals DOI: 10.1080/02699050110063459 BRAIN INJURY, 2001, VOL. 15, NO. 11, 975±980 Correspondence to: Benjamin N. Nguyen, MD, Drake Center, Inc., 151 West Galbraith Road, Cincinnati, OH 45216, USA. e-mail: quangmmrc@yahoo.com