Optimal Treatment of Dysautonomia

Autonomic dysfunction following traumatic brain injury is a frequent complication that occasionally persists as a clinical syndrome now known as paroxysmal sympathetic hyperactivity (PSH) in as many as 10% of TBI patients. While the pathophysiology of PSH is relatively unknown, it is believed to be a result of a loss of inhibitory modulation on nociceptive spinal afferents due to brain injury, leading to a disproportionate sympathetic response. Clinical features of this syndrome include tachycardia, hypertension, hyperhidrosis, hyperthermia, and tachypnea as well as muscle dystonia and posturing. Symptoms of PSH are typically managed with pharmacologic agents such as beta-blockers, morphine, gabapentin, bromocriptine, and, rarely, intrathecal baclofen therapy. While PSH is thought to result in detrimental short-term outcomes, it is not clear to what extent these patients suffer long-term consequences. Nevertheless, PSH is an important complication of TBI, and recognition of this syndrome is necessary for managing autonomic dysfunction in the post-TBI patient.