Citation

Khalid F, Yang GL, McGuire JL, Robson MJ, Foreman B, Ngwenya LB, Lorenz JN. Neurosurg. Focus 2019; 47(5): e8.

Affiliation

Departments of1Pharmacology and Systems Physiology and.

Copyright

(Copyright © 2019, American Association of Neurological Surgeons)

DOI

10.3171/2019.8.FOCUS19517

PMID

31675718

Abstract

Although there is a substantial amount of research on the neurological consequences of traumatic brain injury (TBI), there is a knowledge gap regarding the relationship between TBI and the pathophysiology of organ system dysfunction and autonomic dysregulation. In particular, the mechanisms or incidences of renal or cardiac complications after TBI are mostly unknown. Autonomic dysfunction following TBI exacerbates secondary injury and may contribute to nonneurologial complications that prolong hospital length of stay. Gaining insights into the mechanisms of autonomic dysfunction can guide advancements in monitoring and treatment paradigms to improve acute survival and long-term prognosis of TBI patients. In this paper, the authors will review the literature on autonomic dysfunction after TBI and possible mechanisms of paroxysmal sympathetic hyperactivity. Specifically, they will discuss the link among the brain, heart, and kidneys and review data to direct future research on and interventions for TBI-induced autonomic dysfunction.

Language: en

Keywords

AKI = acute kidney injury; ANP = atrial natriuretic peptide; ANS = autonomic nervous system; ARC = augmented renal clearance; CKD = chronic kidney damage; ICP = intracranial pressure; NTS = nucleus tractus solitarius; PSH = paroxysmal sympathetic hyperactivity; RVLM = rostral ventrolateral medulla; SAH = subarachnoid hemorrhage; SFO = subfornical organ; TBI = traumatic brain injury; autonomic dysfunction; autoregulation; cardiovascular; kidney; traumatic brain injury