Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

Abstract

A 35-year-old male was the unrestrained driver in a rollover motor vehicle accident from which he was ejected. He was initially comatose, with anisocoria and bilaterally unreactive pupils, absent oculocephalic, corneal, cough and gag reflexes, and no motor response to painful stimulus, but initiating respirations on his own (GCS 3T, FOUR score E0 M0 B0 R1 [1]). Shortly after admission, he developed extensor posturing, elevating his exam to GCS 4T, FOUR score E0 M1 B0 R1. However, his exam did not improve further. Head CT demonstrated small petechial hemorrhages at the gray/white junction, corpus callosum, basal ganglia, and in the interpeduncular cistern, consistent with diffuse axonal injury (Fig. 1). An intracranial pressure monitor was placed, and intracranial pressures were wellcontrolled over the next several days without requiring any interventions. Three days after the accident, the patient developed intermittent episodes of tachycardia with tachypnea, hypertension, fever, profuse sweating, and brisk extensor posturing, consistent with paroxysmal sympathetic hyperactivity [2, 3] (Video in Supplementary material).Paroxysmal sympathetic hyperactivity (PSH) can occur following traumatic brain injury with axonal shear injury, due to disinhibition of subcortical sympathoexcitatory structures [3]. This may have an early and late onset, and is most frequently seen in younger patients. The classic features of these episodes include at least four of the following: profuse sweating, tachycardia, hypertension, tachypnea, fever and extensor posturing, and occur transiently without any other cause [4]. PSH has been previously called diencephalic seizures, but EEGs in these patients have always been normal. The typical clinical features were present in our patient, and were never associated with twitches or decrease in responsiveness that may indicate seizures.PSH typically responds most effectively to a combination of opiate agonist and nonselective beta blockade [4,5]. Bromocriptine and clonidine may also be used, but with less consistent results [4,5], and gabapentin is gaining more widespread use for long term effectiveness. In our patient, the episodes were initially treated with beta blockade with propranolol, but did not respond. A combination of clonidine and morphine given during acute episodes was most effective in halting them. Gabapentin was started two days later for longer-term control. However, his neurologic exam failed to improve, care was withdrawn at the strong request of the family and he expired soon after extubation. Paroxysmal sympathetic hyperactivity is a common occurrence in catastrophic neurologic injuries leading to persistent vegetative state. These manifestations are often mistaken for rigors or convulsions and are commonly inadequately treated.Electronic supplementary material The online version of this article (

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