TY - JOUR
T1 - Paroxysmal sympathetic hyperactivity
T2 - the storm after acute brain injury
AU - Meyfroidt, Geert
AU - Baguley, Ian J.
AU - Menon, David K.
PY - 2017/9
Y1 - 2017/9
N2 - A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. 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. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials
AB - A substantial minority of patients who survive an acquired brain injury develop a state of sympathetic hyperactivity that can persist for weeks or months, consisting of periodic episodes of increased heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli. 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. The pathophysiology of the condition is not completely understood, although most researchers consider it to be a disconnection syndrome with paroxysms driven by a loss of inhibitory control over excitatory autonomic centres. Although therapeutic strategies to alleviate sympathetic outbursts have been proposed, their effects on PSH are inconsistent between patients and their influence on outcome is unknown. Combinations of drugs are frequently used and are chosen on the basis of local custom, rather than on objective evidence. New rigorous tools for diagnosis could allow better characterisation of PSH to enable stratification of patients for future therapeutic trials
UR - http://www.scopus.com/inward/record.url?scp=85026898259&partnerID=8YFLogxK
U2 - 10.1016/S1474-4422(17)30259-4
DO - 10.1016/S1474-4422(17)30259-4
M3 - Article
C2 - 28816118
AN - SCOPUS:85026898259
SN - 1474-4422
VL - 16
SP - 721
EP - 729
JO - The Lancet Neurology
JF - The Lancet Neurology
IS - 9
ER -