ing the first week in 36% of cases and within 4 weeks in 85%. The rates of clinical recovery at 1 and 4 weeks, 6, 12 and 24 months were 4, 24, 57, 70 and 82%, respectively. The chance of recovery was significantly affected by age, antecedent gastroenteritis, disability, electrophysiological signs of axonopathy, latency to nadir and duration of active disease. The main treatments did not seem to affect the chance of recovery20:T443,HYPONATREMIA is a widely recognized complication of several central nervous system (CNS) disorders. Recent reports of hyponatremia in subarachnoid hemorrhage¹and herpes simplex encephalitis²have added to a long list which includes meningitis,³head injuries,⁴brain tumors,⁵and a variety of other CNS illnesses.^6-8The recognition of this complication is clinically important since hyponatremia per se may cause delirium, tremor, and convulsions, and thus create a problem in diagnosis or additionally insult an already damaged nervous system. It is less widely recognized that hyponatremia complicates "acute para-infectious" polyneuropathy, an illness usually considered to be restricted to the peripheral nervous system.⁹To our knowledge, only three such cases have been reported;^10-12and in all, the lowered serum sodium produced no symptoms. This paper reports four cases of severe hyponatremia associated with, and complicating the course of, pareinfectious polyneuropathy. The evidence suggests that21:T402,Studies in which plasma osmolality was altered acutely by oral water loading and hypertonic sodium chloride infusion were performed to further identify the mechanisms involved in the pathogenesis of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Guillain-Barré syndrome. Although resetting of the osmotic threshold for vasopressin release was demonstrated in these studies, this does not seem to have been a primary factor in the development of SIADH in this patient. Downward resetting of the osmotic threshold by sustained hypoosmolality has been previously demonstrated, and it is possible that this may account for the initially low osmotic threshold identified by our studies. These studies suggest that inappropriate antidiuresis, as shown by the absence of a diuretic response to low threshold suppression of the plasma arginine vasopressin concentration was due either to a vasopressin-independent mechanism or to markedly increased renal tubular sensitivity to vasopressin.

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