By Frederick A. Zeiler
First Online: 05 January 2021
Over the past two decades, there has been a dramatic expansion of cerebral physiologic monitoring devices in neurocritical care [1,2,3,4]. This type of monitoring can take many forms, including, but not limited to, intracranial pressure (ICP), cerebral perfusion pressure (CPP), brain tissue oxygen (PbtO2), near-infrared spectroscopy (NIRS) regional cerebral oxygen saturations, transcranial Doppler (TCD) cerebral blood flow velocity assessments, thermal diffusion-based cerebral blood flow (CBF), and cerebral microdialysis. Such devices have seen a large uptake in the multimodal monitoring (MMM) of cerebral physiology in adult traumatic brain injury (TBI), with support from international experts [1, 3], adoption within recent renditions of guideline-based therapeutic strategies [5,6,7], and sparking ongoing randomized control trials on therapeutic targets based on the raw data provided from such devices [8, 9].
Aside from the raw cerebral physiologic information provided from these data, advances in offline and bedside bio-signal analytic platforms and techniques have led to derivation of additional indices of cerebral physiologic function. Again, the majority of the literature in this area pertains to adult TBI populations, with derived measures including those related to cerebrovascular reactivity (i.e., cerebral autoregulation) [10, 11], cerebral compensatory reserve [12, 13], signal complexity (i.e., entropy) [14, 15], and autonomic function [16, 17], to name a few. Cerebrovascular reactivity monitoring, taking the form of continuously updating Pearson correlation coefficients, derived from the relationship between slow-wave vasogenic fluctuations in a driving pressure for CBF and a surrogate measure of pulsatile cerebral blood volume/CBF, has seen increasing adoption within MMM of the TBI patient [11, 18]. The pressure reactivity index (PRx) is one such example, and the most commonly recognized cerebrovascular reactivity metric, derived from the relationship between ICP and mean arterial pressure (MAP) .
PRx has a strong independent association with 6-month outcome in TBI, beyond that of ICP, when adjusting for baseline admission characteristics [19,20,21,22,23]. In addition, PRx has received some validation in experimental models as a measure of the Lassen autoregulatory curve [24,25,26], with defined thresholds associated with outcome in the adult TBI populations [20, 27]. Further, recent analysis suggests that during the current era of guideline-based therapeutics in TBI, the majority of cerebral physiologic derangement is related to impaired cerebrovascular reactivity [28, 29], which remains independent to current therapeutic interventions . In corollary, such cerebrovascular reactivity metrics can be used to derive other personalized physiologic targets in TBI care, with optimal CPP (CPPopt) being the exemplar [31, 32], with time spent away from CPPopt demonstrating a stronger association with outcome, compared to Brain Trauma Foundation (BTF)-based CPP thresholds . This has sparked ongoing phase II studies on CPPopt vs BTF-based CPP targets in adult TBI . Finally, dosing or exposure time to certain cerebral physiologic derangements is emerging as an increasingly important factor dictating outcome in TBI care [34,35,36].
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