Autonomic Dysfunction After Acute Brian Injury

Autonomic Dysfunction After
Acute Brain Injury

Emerging evidence implicates autonomic dysfunction after acute brain injury as a potential cause of secondary brain injury. One such manifestation of dysautonomia is “Paroxysmal Sympathetic Hyperactivity” (PSH). PSH, commonly called “storming”, is a poorly understood clinical syndrome that manifests as episodic alterations of vital signs.

We have approached this clinical problem from two perspectives, 1) clinical description and treatment, and 2) neuro-anatomical localization.

Collaborating with a group of anesthesiologists and neuroradiologists in France, we were the first to use diffusion tensor imaging (DTI) to investigate an anatomical localization for PSH and recognize PSH in Anti-NMDA receptor encephalitis. Our group also found that early fever was associated with the development of PSH after TBI.

 

 

Figure: PSH In ICH 
Gao. Annals of Clinical and Translational Neurology 2014; 1(3): 215–219

 

 

Notable publications:

  1. Hinson HE, Puybasset L, Weiss N, Perlbarg V, Benali H, Galanaud D, Lasarev M, Stevens RD. Neuroanatomical basis of paroxysmal sympathetic hyperactivity: a diffusion tensor imaging analysis. Brain Inj. 2015 Jan 7:1-7
  2. Hinson HE, Schreiber MA, Amber L. Laurie AL, Baguley IJ, Bourdette D, Ling GSF. Early Fever as a Predictor of Paroxysmal Sympathetic Hyperactivity in Traumatic Brain Injury. J Head Trauma Rehabil. 2017 Sep/Oct;32(5):E50-E54.
  3. Hinson HE, Takahashi C, Altowaijri G, Baguley IJ, Bourdette D. Anti-NMDA receptor encephalitis with paroxysmal sympathetic hyperactivity: an under-recognized association? Clinical Autonomic Research. 2013 Apr;23(2):109-11.
  4. Hinson HE, Sheth KN. Manifestations of the hyperadrenergic state after acute brain injury. Curr Opin Crit Care. 2012 Apr;18(2):139-45. doi:10.1097/MCC.0b013e3283513290.PMID: 22322258 Review.
  5. Paroxysmal sympathetic hyperactivity in hemispheric intraparenchymal hemorrhage. Gao B, Pollock JA, Hinson HE.Ann Clin Transl Neurol. 2014 Mar 1;1(3):215-219. doi: 10.1002/acn3.44.PMID: 24904923