A 58-year-old man with a history of a seizure disorder was hospitalized with acute-onset shortness of breath immediately following a tonic-clonic seizure. He was afebrile; in respiratory distress; and hypoxic, with an oxygen saturation of 84% on room air. Auscultation revealed bibasilar crackles and an S3 gallop. The patient was given noninvasive mechanical ventilatory support, oxygen, and diuretics. A chest film (A) and a CT scan (B) showed the perihilar butterfly pattern of alveolar infiltrate of pulmonary edema. A 2-dimensional echocardiogram demonstrated normal systolic and diastolic function with an ejection fraction of 65%. The patient showed significant improvement; a second chest film taken 2 days after the seizure revealed complete resolution of the edema (C). Drs Bijoy E. John and Amado Freire of the University of Tennessee College of Medicine, Memphis, diagnosed neurogenic pulmonary edema (NPE). Acute pulmonary edema has been reported following epileptic seizure, head injury, and intracranial hemorrhage. Such a report appeared in the literature as early as 1908.1 NPE occurs within minutes of seizure activity and— with symptomatic therapy—resolves within hours. Acute onset of postseizure dyspnea is a clue to NPE, but the disorder is easily confused with aspiration pneumonitis. However, aspiration pneumonitis has a slower onset and resolution and is associated with fever and focal infiltrates. The pathophysiology of NPE is poorly understood. It is believed to be a neurohumeral response after seizure or brain injury with release of α-adrenergic agonists and an increase in pulmonary capillary hydrostatic pressure.2 Increased pulmonary capillary permeability also is thought to be a component of this process.3 These 2 mechanisms result in acute pulmonary edema.