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July 1966

Neurogenic Hypernatremia

Author Affiliations

From the Department of Neurology of the College of Physicians and Surgeons, Columbia University, and the Neurological Institute of the Presbyterian Hospital, New York.

Arch Neurol. 1966;15(1):78-87. doi:10.1001/archneur.1966.00470130082009

CENTRAL nervous system dysfunction has been implicated in disorders of water and osmolar balance, including diabetes insipidus, inappropriate secretion of antidiuretic hormone (ADH),1 hypodipsia,2,3 and neurogenic hypernatremia.4,5 The physiologic basis of diabetes insipidus is comparatively well understood, and hypodipsia and inappropriate secretion of ADH have been studied with the aid of experimental models.1,6-8 However, the existence of hypernatremia and hyperosmolarity due to hypothalamic disease and not attributable to diabetes insipidus or hypodipsia has been questioned.9,10 One difficulty in the recognition of this syndrome arises from the close proximity of the ADH secretion, thirst, and osmoreceptor centers in the anterior hypothalamus so that lesions in this area may produce various combinations of diabetes insipidus, hypodipsia, and hypernatremia.4,5

A clinical definition of primary neurogenic hypernatremia must distinguish this syndrome from the far more frequent hyperosmolarity of dehydration, resulting from diabetes insipidus, hypodipsia, and gastrointestinal or renal

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