Dysautonomia after Severe Traumatic Brain Injury

Abstract

This study found persistent sympathetic overactivity in response to nociceptive stimuli in dysautonomic subjects (mean, 5 yrs postinjury). This significantly extends the duration over which such sympathetic overactivity has been quantified in this group, contributing to the accumulating empirical evidence that dysautonomic paroxysms result from sympathetic overresponsiveness. Given that sympathetic overactivity has now been observed from day 7 through 5 yrs postinjury, quantitative evaluation of patients for overresponsiveness to stimuli should be added to current diagnostic procedures at all stages of recovery.

Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

“…Changes in the neurotransmitter system, driven by stimuli, highlight the importance of considering the triggering event in pathogenetic research. To summarize, the triggering of paroxysm, a sudden exaggerated response originating in the afferent stimulation of the sympathetic nervous system, is responsible for the core pathophysiological features (38,39).…”

“…In TBI patients, negative microbial cultivation of blood, cerebrospinal fluid, airway secretion, or urine provides clues for exclusion. In addition, normal electroencephalograms (EEGs) in PSH patients can help to exclude epilepsy and other nervous system diseases (7,39,63,64). In brief, those examinations could improve the efficiency of diagnosis before the preliminary symptoms and validation have occurred (64).…”

Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury

“…demonstrated that changes in heart rate variability associated with nociceptive stimuli accompany the onset of sympathetic storming. [ 5 7 ] Retrospective reviews indicate that those with diffuse axonal injury on imaging studies are at highest risk for developing sympathetic storming. [ 3 14 ] Symptoms are thought to persist for months to years, with one study revealing a mean duration of 5 years post-injury.…”

“…[ 3 14 ] Symptoms are thought to persist for months to years, with one study revealing a mean duration of 5 years post-injury. [ 5 ]…”

Treatment Progress of Paroxysmal Sympathetic Hyperactivity after Acquired Brain Injury

“…The model indicates that there exist inhibitory centers in the brainstem and diencephalon which can suppress the sensitization and amplification of afferent sensory information processed by circuits in the spinal cord. Afferent stimuli from the spinal cord could modulate the balance of the sympathetic and parasympathetic systems by input (such as noxious stimuli) from the environment [17,18]. The change of spinal cord circuits amplifies the mild noxious stimuli.…”