Manifestations of the hyperadrenergic state after acute brain injury.
OBJECTIVE
Hyperadrenergic activity leading to autonomic dysfunction after acute brain injury is an underrecognized, yet important source of complications following a variety of neurologic injuries. Autonomic dysfunction may prolong ICU stay and increase healthcare costs driven by extensive diagnostic workups and/or ensuing complications. In this review article, we intend to illustrate commonalities between various hyperadrenergic states in acquired brain injury. Specifically, this review will focus on autonomic dysfunction in two common conditions in the neurocritical care unit, traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH).


RESULTS
Elevated levels of catecholamines have been well documented in SAH and to a lesser extent in paroxysmal sympathetic hyperactivity, hinting at the underlying increased sympathetic tone in both disease states. The resultant hyperadrenergic state may manifest with vital sign alterations, or end-organ dysfunction such as heart failure. Neuroimaging and limited clinical data have elucidated some information regarding underlying mechanisms, but the gaps in understanding have thus far limited prospective clinical trials. A multitude of therapeutic options to reduce adrenergic tone have been employed with varying degrees of success.


CONCLUSIONS
The pathophysiology of autonomic dysfunction is incompletely understood and treatment options are few. However, recognizing hyperadrenergic commonality in disparate neurologic disease may facilitate novel inquiries into lesion localization and therapeutics. It is possible that adrenergic blockade may diminish or abrogate end-organ dysfunction in TBI and SAH.
Department of Neurology and Neurocritical Care, Oregon Health and Science University, Portland, Oregon 97239, USA. hinson@ohsu.edu
Holly E
HE
Hinson
Kevin N
KN
Sheth
D018674:Adrenergic Antagonists / Q000494:pharmacology*; D001930:Brain Injuries / Q000150:complications / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D002319:Cardiovascular System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D011941:Receptors, Adrenergic / Q000187:drug effects*; D012039:Regional Blood Flow; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*
D018674:Adrenergic Antagonists; D011941:Receptors, Adrenergic