Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury.

作者: Rui-Zhe Zheng , Zhong-Qi Lei , Run-Ze Yang , Guo-Hui Huang , Guang-Ming Zhang

DOI: 10.3389/FNEUR.2020.00081

关键词:

摘要: 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 driven by loss inhibition excitation in nervous system without parasympathetic involvement. Recently, advances clinical diagnostic TBI patients have reached a broad consensus many neurology departments. These should provide more unanimous foundation for systematic research on this syndrome its clear management. Clinically, great deal attention paid to definition criteria, epidemiology pathophysiology, symptomatic treatment, prevention control secondary patients. Potential benefits treatment may result from three main goals: eliminating predisposing causes, mitigating excessive outflow, supportive therapy. However, individual pathophysiological differences, therapeutic responses outcomes, precision medicine approaches management are varied inconsistent between studies. Further, potential drugs might suppress manifestations process treatment. The purpose review present current comprehensive studies identification early stage framework PSH.

参考文章(92)
Stephen Welle, Ronald G. Schwartz, Marcia Statt, Reduced metabolic rate during β-adrenergic blockade in humans Metabolism. ,vol. 40, pp. 619- 622 ,(1991) , 10.1016/0026-0495(91)90053-Y
Holly E Hinson, Louis Puybasset, Nicolas Weiss, Vincent Perlbarg, Habib Benali, Damien Galanaud, Mike Lasarev, Robert D Stevens, Neuro Imaging for Coma Emergence, Recovery (NICER) Consortium, None, Neuroanatomical basis of paroxysmal sympathetic hyperactivity: a diffusion tensor imaging analysis. Brain Injury. ,vol. 29, pp. 455- 461 ,(2015) , 10.3109/02699052.2014.995229
Antonio De Tanti, Giulio Gasperini, Mauro Rossini, Paroxysmal episodic hypothalamic instability with hypothermia after traumatic brain injury Brain Injury. ,vol. 19, pp. 1277- 1283 ,(2005) , 10.1080/02699050500309270
F. Beissner, K. Meissner, K.-J. Bar, V. Napadow, The autonomic brain: an activation likelihood estimation meta-analysis for central processing of autonomic function. The Journal of Neuroscience. ,vol. 33, pp. 10503- 10511 ,(2013) , 10.1523/JNEUROSCI.1103-13.2013
KimberlyS Meyer, Understanding paroxysmal sympathetic hyperactivity after traumatic brain injury Surgical Neurology International. ,vol. 5, pp. 490- 492 ,(2014) , 10.4103/2152-7806.144632
Christian Woiciechowsky, Khusru Asadullah, Dirk Nestler, Beatrice Eberhardt, Cornelia Platzer, Britta Schöning, Frauke Glöckner, Wolfgang R. Lanksch, Hans-Dieter Volk, Wolf-Diatrich Döcke, Sympathetic activation triggers systemic interleukin-10 release in immunodepression induced by brain injury. Nature Medicine. ,vol. 4, pp. 808- 813 ,(1998) , 10.1038/NM0798-808
Ian J. Baguley, Roxana E. Heriseanu, Ian D. Cameron, Melissa T. Nott, Shameran Slewa-Younan, A critical review of the pathophysiology of dysautonomia following traumatic brain injury Neurocritical Care. ,vol. 8, pp. 293- 300 ,(2008) , 10.1007/S12028-007-9021-3
R N Russo, S O'Flaherty, Bromocriptine for the management of autonomic dysfunction after severe traumatic brain injury. Journal of Paediatrics and Child Health. ,vol. 36, pp. 283- 285 ,(2000) , 10.1046/J.1440-1754.2000.00485.X