Autonomic Dysfunction and Associations with Functional and Neurophysiological Outcome in Moderate/Severe Traumatic...

The quantification and objective documentation of autonomic dysfunction in traumatic brain injury (TBI) is neither well studied nor extensively validated. Most of the descriptions of autonomic dysfunction in the literature are in the form of vague non-specific clinical manifestations. Few studies propose the use of objective measures of assessing the extent of autonomic dysfunction to link them to the outcome of TBI. Our goal was to perform a scoping systematic review of the literature on the objective documentation of autonomic dysfunction in terms of functional and physiological variables to be linked to outcome of TBI. PubMed/MEDLINE^®, BIOSIS, Scopus, Embase, Cochrane Libraries, and Global Health databases were searched. Two reviewers independently screened the results. Full texts for citations passing this initial screen were obtained. Inclusion and exclusion criteria were applied to each article to obtain final articles for review. The initial search yielded 2619 citations. Of 69 articles selected for final review, 14 were chosen based on the inclusion and exclusion criteria and are included in the results of this article. 9 of these articles assessed autonomic dysfunction using functional variables and 7 assessed autonomic dysfunction using physiological variables. Some studies included both functional and physiological variables. Of the nine studies linking autonomic dysfunction to functional variables, nine included heart rate variability (HRV), three included baroreflex sensitivity (BRS), and two included blood pressure variability (BPV). A total of 2714 adult patients were studied. Although the nature of association between autonomic dysfunction and outcome is unclear, the objective quantification of autonomic dysfunction seems to be associated with global patient outcome and other neurophysiological measures. Further studies are needed to validate its use and explore the underlying molecular mechanisms of the described associations.