Paroxysmal sympathetic hyperactivity occurs primarily after severe traumatic brain injury and is characterized by abnormal paroxysmal surges in sympathetic nervous system activity. The clinical symptoms of paroxysmal sympathetic hyperactivity may resemble those of epilepsy or sepsis, leading to delayed diagnosis and inadequate treatment. A 16-year-old male individual suffered a severe brain injury following a traffic accident. His Glasgow Coma Scale score was 4/15 (E1V1M2). Magnetic resonance imaging revealed cerebral contusion in bilateral frontal lobes, genu, and splenium of the corpus callosum, and diffuse axonal injury was diagnosed. Pharmacological therapy with medication to reduce cerebral edema, analgesics, sedatives, and antiepileptic drugs was initiated. On the 7th day, the sedatives were temporarily discontinued, the patient's limbs were held in an extended position with muscle contractions, and also exhibited hyperthermia, tachycardia, sweating, and hypertension, which lasted approximately 30 minutes and occurred multiple times a day. Blood, sputum, and urine cultures were negative, and two electroencephalograms did not detect epileptic discharges, so sepsis and epilepsy were excluded. Baclofen and dantrolene slightly improved muscle stiffness, but the continuous intravenous infusion of sedatives could not be discontinued for more than 40 days because it caused a recurrence of attacks. Propranolol 30 mg/day was added, and paroxysmal sympathetic hyperactivity attacks disappeared. Therefore, sedatives could be discontinued and the patient was transferred to a rehabilitation hospital. Propranolol, an oral β-adrenergic blocker, is one of the effective treatments for paroxysmal sympathetic hyperactivity.