Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.
Take-home message:In adult and paediatric patients suffering from severe traumatic brain injury, an approximately exponential curve describes the relationship between intensity and duration of episodes of increased intracranial pressure (ICP) and worse clinical outcomes. In children, compared to adults, this occurs at lower ICP thresholds of shorter duration. Electronic supplementary materialThe online version of this article (doi:10.1007/s00134-015-3806-1) contains supplementary material, which is available to authorized users. To assess the impact of the duration and intensity of episodes of increased intracranial pressure on 6-month neurological outcome in adult and paediatric traumatic brain injury. Methods:Analysis of prospectively collected minute-by-minute intracranial pressure and mean arterial blood pressure data of 261 adult and 99 paediatric traumatic brain injury patients from multiple European centres. The relationship of episodes of elevated intracranial pressure (defined as a pressure above a certain threshold during a certain time) with 6-month Glasgow Outcome Scale was visualized in a colour-coded plot. Results:The colour-coded plot illustrates the intuitive concept that episodes of higher intracranial pressure can only be tolerated for shorter durations: the curve that delineates the duration and intensity of those intracranial pressure episodes associated with worse outcome is an approximately exponential decay curve. In children, the curve resembles that of adults, but the delineation between episodes associated with worse outcome occurs at lower intracranial pressure thresholds. Intracranial pressures above 20 mmHg lasting longer than 37 minutes in adults, and longer than 8 minutes in children, are associated with worse outcomes. In a multivariate model, together with known baseline risk factors for outcome in severe traumatic brain injury, the cumulative intracranial pressure-time burden is independently associated with mortality. When cerebrovascular autoregulation, assessed with the low-frequency autoregulation index, is impaired, the ability to tolerate elevated intracranial pressures is reduced. When the cerebral perfusion pressure is below 50 mmHg, all intracranial pressure insults, regardless of duration are associated with worse outcome. Conclusions:The intracranial pressure-time burden associated with worse outcome is visualised in a colour-coded plot. In children, secondary injury occurs at lower intracranial pressure thresholds as compared to adults. Impaired cerebrovascular autoregulation reduces the ability to tolerate intracranial pressure insults. Thus, 50 mmHg might be the lower acceptable threshold for cerebral perfusion pressure.
The definition of cerebral perfusion pressure (CPP) secondary insults in severe traumatic brain injury remains unclear. The purpose of the present study is to visualize the association of intensity and duration of episodes below or above CPP thresholds and outcome. The analysis was based on prospectively collected minute-by-minute intracranial pressure (ICP) and blood pressure data and outcome from 259 adult patients. The relationship of episodes of CPP below or above a certain threshold for certain duration with the 6-month Glasgow Outcome Score was visualized separately for episodes of active or deficient autoregulation (AR). In adults ≤65 years, an almost exponential transition curve separates the episodes of CPP associated with better outcomes from the episodes of low CPP associated with worse outcomes, indicating that lower CPP could only be tolerated for a brief time. Analysis of episodes of high CPP again showed a time-intensity dependent association with outcome. When combining the two plots, a safe CPP zone between 60 and 70 mm Hg could be delineated—however, only for AR active insults. The AR status predominantly affected the transition curve for insults of low CPP. Episodes with ICP >25 mm Hg were associated with poor outcome regardless of CPP. In the present study, the CPP pressure-time burden associated with poor outcome was visualized. A safe zone between 60 and 70 mm Hg could be identified for adults ≤65 years, provided AR was active and ICP was ≤25 mm Hg. Deficient AR reduces the tolerability for low CPP.
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