Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury: What Is Important to Know?

Abstract

Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality. The etiologies of TBI are varied and its complications can lead to paroxysmal sympathetic hyperactivity that was first described as a "sympathetic storm" or "diencephalic autonomic seizure." The clinical manifestations are rapid and sudden onset of sympathetic hyperactivity characterized by tachycardia, systolic hypertension, hyperthermia, tachypnea, and diaphoresis, all summarized in the latest and most accepted diagnostic criteria. The pathophysiology remains controversial with many theories proposed. Given the clinical manifestations, the complications, outcomes, and lack of popularity of the syndrome, we report a case treated in our institution and review the current pathophysiology and treatment options.

Keywords: dysautonomia; paroxysmal sympathetic hyperactivity; psh; sympathetic storm; traumatic brain injury.

Figure 1. Preoperative axial non-injected CT scan showing the subdural hematoma, brain edema, and frontal contusions.

A: Red arrow showing the fronto-temporal-occipital subdural hematoma. B: Red arrow showing the frontal contusion and brain edema. CT: computed tomography

Figure 2. PSH pathophysiology showing the summary of the physiology of the sympathetic hyperactivity according to the excitatory/inhibitory ratio model and the impact on the organs.

PSH: paroxysmal sympathetic hyperactivity