A 43-year-old patient with well healthy in the past was admitted after a accidental falling down injury. Upon arrival at the Emergent Department, he was unresponsive. (Glasgow coma scale = E1V1M1). The continuous Electrocardiological monitor demonstrated ventricular fibrillation without pulse, and the defibrillation (360 J) with intravenous Epinephrine (1 mg) push was given. The electrocardiogram (ECG) returned to sinus tachycardia. The endotracheal tube was intubated to keep airway patent and ventilation under the unstable vital sign. Ten minutes later, the polymorphic ventricular tachycardia (torsade de pointes) were recorded by continuous ECG. After defibrillation (360 J) twice with intravenous Epinephrine (1 mg) and Amiodarone (150 mg), the rhythm returned to normal sinus rhythm, and the vital sign recovered gradually. The laboratory evaluation showed no abnormality. The cranial computed tomography was done thereafter which showed occipital bone fracture with subarachnoid hemorrhage, subdural hemorrhage and epidural hemorrhage (Figure 2, arrows indicated hemorrhage). Clinical study has shown increased sympathetic activity in patients with acute intracranial hemorrhage. The increased level of catecholamines would lead to QT prolongation or hypokalemia, which are the predisposing factors of the development of torsade de pointes. Although, the definitive confirmation of a cause and effect relationship about intracranial hemorrhage and torsade de pointes is still controversial, the life-threatening arrhythmia, including atrioventricular blocks, ventricular tachycardia, and fibrillation, which accompany acute cerebral accidents in patients without cardiac disease is observed in many case reports. In our experience and clinical observation, patients should be constantly monitored after acute cerebral events. Besides, the treating team should be familiar with and well-trained in the diagnosis and treatment of cardiac arrhythmias.