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Pathophysiology of Epidemic St. Louis Encephalitis: I. Inappropriate Secretion of Antidiuretic Hormone: II. Pituitary-Adrenal Function: III. Cerebral Blood Flow and Metabolism

MARTIN G. WHITE, M.D.; NORMAN W. CARTER, M.D.; FLOYD C. RECTOR, M.D.; DONALD W. SELDIN, M.D., F.A.C.P.; S. JAN DREWRY, M.D.; JAY P. SANFORD, M.D., F.A.C.P.; JAMES P. LUBY, M.D.; ROGER H. UNGER, M.D.; NORMAN M. KAPLAN, M.D., F.A.C.P.; WILLIAM SHAPIRO, M.D.; and SEYMOUR EISENBERG, M.D.
Ann Intern Med. 1969;71(4):691-702. doi:10.7326/0003-4819-71-4-691
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SUMMARY:

Studies of pathophysiology in epidemic St. Louis encephalitis were undertaken during the 1966 Dallas epidemic. Eighteen of 52 patients were hyponatremic during their acute illness. Of this group, 13 patients appeared to have hyponatremia due to inappropriate secretion of antidiuretic hormone; the remaining patients were probably hyponatremic from salt depletion. Water loading in some of these patients showed that the defect (persistent elaboration of antidiuretic hormone) was only partial, allowing excretion of the water load with urine not maximally dilute.

Severely ill patients tended to have 8 AM plasma 17-hydroxycorticoid (17-HOCS) values that were elevated or at the upper limit of normal. Normal diurnal variation in plasma 17-HOCS levels was absent. Plasma 17-HOCS rose after adrenocorticotrophic hormone (ACTH) administration but did not respond to dexamethasone suppression. An insulin-induced fall in blood sugar caused a rise in both plasma 17-HOCS and growth hormone. Patients had an increase in either urinary or plasma 11-deoxycorticoids (11-DOCS) after the administration of metyrapone. These findings probably represent the response to severe stress. The hypothalamic-pituitary-adrenal axis appeared to be functionally intact in these patients.

Cerebral blood flow and metabolism were measured in five patients, one of whom was comatose when studied. In two of the conscious patients cerebral blood flow was normal despite normal arterial oxygen tension and systemic hypocapnia; inflammatory cerebral vasodilatation may have accounted for the findings. Inflammatory changes affecting the respiratory centers and an associated metabolic acidosis may have accounted, in part, for lowered carbon dioxide tensions found in at least two of the patients. In the comatose patient, although the cerebral blood flow was normal, the cerebral metabolic rate for oxygen was markedly depressed; this patient's findings represent what has been termed the "luxury-perfusion syndrome." Cerebral blood flow abnormalities per se were not responsible for the altered sensorium in these patients.

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