Hiratani M, Munesue T, Terai K, Haruki S
Department of Pediatrics, Center of Developmental Medicine and Education for Handicapped Children, Fukui Prefecture.
No To Hattatsu. 1997 Sep;29(5):367-72.
The syndrome of water intoxication, resulting from dilutional hyponatremia and characterized by lethalgy, confusion, seizures, and coma was seen in two autistic boys living in the institution for mentally retarded children. Patient 1, a 19 year-old autistic boy showed loss of attention, inactiveness, sleepiness and delirium and then followed by overbreathing, severe vomiting and finally convulsive seizures several times, or coma, since October 1985. In August 1988, he was admitted with generalized tonic clonic convulsion associated with frequent vomiting EEG showed diffuse spike and wave complex with slow background activity. Laboratory data showed inappropriately high serum ADH level (8.5 pg/ml), low sodium concentration (121 mOsm/m/l), serum osmolality (237 mOsm/l) which was lower than urine osmolality (334 mOsm/l), and remarkable body weight gain (8.5 kg). He was diagnosed as water intoxication due to compulsive water drinking and SIADH. Diminished GH secretion to insulin-induced hypoglycemia and exaggerated prolactin response to LHRH stimulation suggested a hypothalamic lesion. Patient 2, a 17-year-old autistic boy, showed essentially the same symptoms and laboratory data as Patient 1, except that he had no epileptic discharge in EEG, and curious GH response to insulin-induced hypoglycemia. A remarkable daily body weight change suggested excessive water drinking and a possible episodic release of ADH. With mild water restriction, this became smaller. Since Patient 1 had epileptic attacks several times without hyponatremia and his EEG showed epileptic discharges, he was diagnosed as having epilepsy. Patient 2 has been seizure-free until now. Abnormality of hypothalamic or pituitary defects and polydipsia and possibility of water intoxication should always be considered when an autistic patients shows recurrent epileptic attacks or episodic strange behaviors with hyponatremia.
水中毒综合征由稀释性低钠血症引起,表现为嗜睡、意识模糊、癫痫发作和昏迷,在两名居住于智障儿童机构的自闭症男孩中被观察到。患者1,一名19岁的自闭症男孩,自1985年10月起出现注意力丧失、活动减少、嗜睡和谵妄,随后出现呼吸急促、严重呕吐,最终多次抽搐发作或昏迷。1988年8月,他因频繁呕吐伴全身性强直阵挛性惊厥入院。脑电图显示弥漫性棘波和慢波复合波,背景活动缓慢。实验室检查数据显示血清抗利尿激素水平异常升高(8.5 pg/ml)、钠浓度降低(121 mOsm/m/l)、血清渗透压(237 mOsm/l)低于尿渗透压(334 mOsm/l),且体重显著增加(8.5 kg)。他被诊断为因强迫饮水和抗利尿激素分泌异常综合征导致的水中毒。胰岛素诱导低血糖时生长激素分泌减少以及促黄体生成素释放激素刺激时催乳素反应过度提示下丘脑病变。患者2,一名17岁的自闭症男孩,表现出与患者1基本相同的症状和实验室检查数据,只是脑电图无癫痫放电,且对胰岛素诱导低血糖有奇特的生长激素反应。每日体重显著变化提示饮水过多以及抗利尿激素可能间歇性释放。轻度限制饮水后,体重变化变小。由于患者1在无低钠血症时多次癫痫发作且脑电图显示癫痫放电,他被诊断为患有癫痫。患者2至今未发作。当自闭症患者出现反复癫痫发作或伴有低钠血症的间歇性奇怪行为时,应始终考虑下丘脑或垂体缺陷异常以及烦渴和水中毒的可能性。