Autonomic dysfunction following traumatic brain injury: translational insights.
Neurosurg Focus
; 47(5): E8, 2019 11 01.
Article
em En
| MEDLINE
| ID: mdl-31675718
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.
Palavras-chave
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
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Doenças do Sistema Nervoso Autônomo
/
Lesões Encefálicas Traumáticas
Limite:
Humans
Idioma:
En
Revista:
Neurosurg Focus
Assunto da revista:
NEUROCIRURGIA
Ano de publicação:
2019
Tipo de documento:
Article