Paroxysmal sympathetic hyperactivity (PSH) is a disorder in the regulation of autonomic function most commonly observed in patients with acute brain injury, most notably severe traumatic brain injury (TBI) [1,2].
Paroxysmal sympathetic hyperactivity (PSH) is a pattern of recurrent bursts of dysregulated sympathetic activity following severe, diffuse brain injury. These episodes of sympathetic activation are short, dramatic, and often triggered by stimulation.
Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that causes episodes of increased activity of the sympathetic nervous system. Hyperactivity of the sympathetic nervous system can manifest as increased heart rate, increased respiration, high blood pressure, perspiration, and hyperthermia. [1] .
Paroxysmal sympathetic hyperactivity (PSH) has predominantly been described after traumatic brain injury (TBI), which is associated with hyperthermia, hypertension, tachycardia, tachypnea, diaphoresis, dystonia (hypertonia or spasticity), and even motor features such as extensor/flexion posturing.
PSH onset is typically 5-7 days after brain injury + after completion of acute ICP management (but may occur as early as 24 hours post-injury or as late as several weeks following injury)
The unifying term for the syndrome—paroxysmal sympathetic hyperactivity (PSH)—and clear diagnostic criteria defined by expert consensus were only recently established. PSH has predominantly been described after traumatic brain injury (TBI), in which it is associated with worse outcomes.
Paroxysmal Sympathetic Hyperactivity (PSH) is a syndrome of disproportionate and pathological sympathetic overreaction that can be triggered by nociceptive or environmental stimuli, 1 which occurs after severe acquired brain injury.
In children, PSH can be a recognized complication of an underlying degenerative neurologic condition. More than 30 prior terms have been used for PSH, including sympathetic or autonomic storm, autonomic dysfunction, dysautonomia, and diencephalic seizure (1,3,4).