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In high-altitude areas (HAA), oxygen in inspired air is at a lower partial pressure. The ensuing hypoxia elicits neurohumoral and hemodynamic responses in both brain and lungs with varying severity of cerebral and pulmonary syndromes [1,2]. While there is data on the risk of developing certain pathophysiological conditions at high altitude, such as cerebral or pulmonary edema, there is a paucity of literature detailing the incidence of seizures after ascent to HAA [3].