SUMMARY1. Age changes in spontaneous and evoked transmitter release, in receptor number and in ultrastructure at the neuromuscular junction were studied in the CBF-1 mouse strain, which stays physically active and relatively free of organ pathology into advanced age.

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The clinical and pathologic findings in 20 patients with hypertensive encephalopathy were reviewed. The dominant central nervous system (CNS) symptoms were altered state of consciousness and severe headache. Nausea, vomiting, and visual disturbances were less common. Seizures and focal signs were infrequent. The changes seen were invariably accompanied both by the characteristic ophthalmoscopic alterations of malignant hypertension and by uremia. The neuropathologic changes consisted of severe vascular alterations (fibrinoid necrosis of arterioles, thrombosis of arterioles and capillaries), and of parenchymal lesions (microinfarcts, petechial hemorrhages) secondary to the vascular lesions. The vascular changes were not confined to the brain but were diffuse, affecting the eyes, kidneys, and other organs. In the CNS the brainstem was most severely affected. Cerebral edema was not observed, even in those patients who had increased cerebrospinal fluid pressure and papilledema.

The rapid correction or over-correction of hyponatremia is believed by many to be the crucial factor in the causation of central pontine myelinolysis (CPM). Over a 17-year period we found CPM in 10 (7%) of the 139 burn patients examined postmortem but in only 10 (0.28%) of the 3,528 patients in the general autopsy population (p less than 0.001). Each of the burn patients with CPM had suffered a prolonged, nonterminal episode of extreme serum hyperosmolality, whereas most burn patients without CPM had not suffered such an episode. The histologic age of the lesions correlated with the duration of time between the hyperosmolar episode and death. Hypernatremia, hyperglycemia, and azotemia, alone or combined, accounted for the hyperosmolality. No single electrolyte or metabolic derangement was essential, as in at least one burn patient with CPM the serum sodium, glucose, or blood urea nitrogen was normal during the hyperosmolar episode. Hyponatremia was not present in any burn patient with CPM. We conclude that severely burned patients, like alcoholics, are especially susceptible to CPM, and that in burn patients with CPM there is a striking association with serum hyperosmolality. The data also suggest that the rapid correction of hyponatremia exerts its effects by causing an osmotic shift and not because of any specific property of the sodium ion.