Sudden death amidst powerful emotional arousal is a familiar and dramatic event in the literature, history, and folklore of most cultures. Although physicians and laymen have accepted this association of mind and mortality for centuries, the arrhythmogenic potential of strong emotions only recently has been physiologically explained. Lown et al1 have shown that psychological stress may be associated with increased sympathetic activity that can provoke ventricular arrhythmias and may lower the threshold of ventricular fibrillation. The relationship between the CNS and cardiac arrhythmias is not limited to moments of strong emotions, however. Structural disease of the CNS also may be associated with life-threatening arrhythmias, distinctive ECG changes, and histopathologic changes. These alterations can occur in the absence of organic heart disease, hypoxia, or electrolyte imbalance.2-9 This association, though less familiar, is of importance to the clinician who may be misled into administering therapy for the cardiac manifestation, while