Context.-Because of its onset in generally remote environments, high-altitude cerebral edema (HACE) has received little scientific attention. Understanding the pathophysiology might have implications for prevention and treatment of both this disorder and the much more common acute mountain sickness. Objectives.-To identify a clinical imaging correlate for HACE and determine whether the edema is primarily vasogenic or cytotoxic. Design.-Case-comparison study. Setting.-Community hospitals accessed by helicopter from mountains in Colorado and Alaska. Patients.-A consecutive sample of 9 men with HACE, between 18 and 35 years old, 8 of whom also had pulmonary edema, were studied after evacuation from highaltitude locations; 5 were mountain climbers and 4 were skiers. The control group, matched for age, sex, and altitude exposure, consisted of 3 subjects with highaltitude pulmonary edema only and 3 who had been entirely well at altitude. Four patients with HACE were available for follow-up imaging after complete recovery. Main Outcome Measures.-Magnetic resonance imaging (MRI) of the brain during acute, convalescent, and recovered phases of HACE, and once in controls, immediately after altitude exposure. Results.-Seven of the 9 patients with HACE showed intense T 2 signal in white matter areas, especially the splenium of the corpus callosum, and no gray matter abnormalities. Control subjects demonstrated no such abnormalities. All patients completely recovered; in the 4 available for follow-up MRI, the changes had resolved entirely. Conclusions.-We conclude that HACE is characterized on MRI by reversible white matter edema, with a predilection for the splenium of the corpus callosum. This finding provides a clinical imaging correlate useful for diagnosis. It also suggests that the predominant mechanism is vasogenic (movement of fluid and protein out of the vascular compartment) and, thus, that the blood-brain barrier may be important in HACE.

MR imaging of high-altitude cerebral edema shows reversible WM edema, especially in the corpus callosum and subcortical WM. Recent studies have revealed hemosiderin deposition in WM long after high-altitude cerebral edema has resolved, providing a high-altitude cerebral edema "footprint." We wished to determine whether these microbleeds are present acutely and also describe the evolution of all MR imaging findings. In 8 patients with severe high-altitude cerebral edema, we obtained 26 studies: 18 with 3T and 8 with 1.5T scanners, during the acute stage, recovery, and follow-up in 7 patients and acutely in 1 patient. Imaging confirmed reversible cytotoxic and vasogenic WM edema that unexpectedly worsened the first week during clinical improvement before resolving. The 3T SWI, but not 1.5T imaging, showed extensive microbleeds extending beyond areas of edema seen acutely, which persisted and with time coalesced. These findings support cytotoxic and vasogenic edema leading to capillary failure/leakage in the pathophysiology of high-altitude cerebral edema and provide imaging correlation to the clinical course.ABBREVIATIONS: HACE ϭ high-altitude cerebral edema; HAPE ϭ high-altitude pulmonary edema; MB ϭ microbleed

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Autopsy in a patient with severe hyponatremia showed central pontine myelinolysis. Review of our patients with central pontine myelinolysis and those described in the English literature to data disclosed that 61 percent had documented hyponatremia. While the exact mechanism involving hyponatremia and central pontine myelinolysis cannot be defined, a circumstantial relationship is apparent. The purpose of this paper is to emphasize this relationship and to suggest that the possibility of central pontine myelinolysis be considered in any patient with hyponatremia and neurologic dysfunction.

Among 472 adult seizure admissions to a municipal hospital, 41% had a history of alcohol abuse. Those were predominantly men aged 40 to 50 years. The primary underlying conditions were the alcohol withdrawal state (59%) and posttraumatic seizures. The nonalcohol groups included men and women equally, commonly between 20 and 40 years old, and frequent causes were vascular disease and posttraumatic seizures. However, many patients (24% in the alcohol and 39% in the nonalcohol groups) had no demonstrable cause. Focal sizures comprised 24% of the alcohol and 20% of the nonalcohol groups. Nonalcoholic focal seizures had a tumor or vascular lesion in 47%; above age 50 the association was 60%. Alcohol-related focal seizures had such a lesion in 15%, and only 19% above age 50. Conditions associated with alcoholic focal seizures were alcohol withdrawal and posttrauma sequelae.