Abstract
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. Despite the pathophysiology of PSH not being completely understood, most researchers gradually agree that PSH is driven by the loss of the inhibition of excitation in the sympathetic nervous system without parasympathetic involvement. Recently, advances in the clinical and diagnostic features of PSH in TBI patients have reached a broad clinical consensus in many neurology departments. These advances should provide a more unanimous foundation for the systematic research on this clinical syndrome and its clear management. Clinically, a great deal of attention has been paid to the definition and diagnostic criteria, epidemiology and pathophysiology, symptomatic treatment, and prevention and control of secondary brain injury of PSH in TBI patients. Potential benefits of treatment for PSH may result from the three main goals: eliminating predisposing causes, mitigating excessive sympathetic outflow, and supportive therapy. However, individual pathophysiological differences, therapeutic responses and outcomes, and precision medicine approaches to PSH management are varied and inconsistent between studies. Further, many potential therapeutic drugs might suppress manifestations of PSH in the process of TBI treatment. The purpose of this review is to present current and comprehensive studies of the identification of PSH after TBI in the early stage and provide a framework for symptomatic management of TBI patients with PSH.
Highlights
There is a subgroup of patients with simultaneously paroxysmal transient increases in sympathetic activity involved in heart rate, blood pressure, respiratory rate, temperature, sweating, and posturing activity, which may persist over time, and are associated with worse outcomes [1]
It is generally known that paroxysmal sympathetic hyperactivity (PSH) is mostly prevalent in traumatic brain injury (TBI) patients, and the understanding of advanced pathophysiological, clinical features, and recognition methods of PSH in TBI patients is necessary
Some features detected from the evidence-based clinical practice will provide predictors for early identification of PSH in TBI patients
Summary
There is a subgroup of patients with simultaneously paroxysmal transient increases in sympathetic activity involved in heart rate, blood pressure, respiratory rate, temperature, sweating, and posturing activity, which may persist over time, and are associated with worse outcomes [1]. An unambiguous definition and diagnostic criterion for the syndrome was proposed by an expert group in 2014. The outbreaks of PSH were traditionally described in severe acquired brain injury (ABI) patients [e.g., traumatic brain injury (TBI), anoxic brain injury, stroke, tumors, infections, or unspecified causes], the prevalence of PSH of 33% after TBI compared with 6% after other causes suggests that the dominant underlying cause in PSH is TBI [4]. In the past decade, about 80% of PSH cases have been reported to occur after TBI [5, 6]. Its wide incidence rates reported ranging from 8 to 33% of PSH reveal the underlying discrepancy of current diagnostic and admission criteria as well as ignorance on disease identification [7]
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