Authors: Chanju Fritch; Chanju Fritch, BS; Adarsh Vangala, BS; Fares Qeadan, PhD; Bill Shuttleworth, PhD; Andrew Carlson (Albuquerque, NM)
Recovery from acute neurologic injury (traumatic brain injury (TBI), stroke, and subarachnoid hemorrhage (SAH)) is often complicated by secondary injury, which can significantly influence a patient’s outcome. Cerebral autoregulation and its disturbance are known factors for vulnerability to these secondary injuries. Cortical spreading depolarization (SD) is recognized to occur commonly after acute neurologic injury and is likely induced in regions of metabolic instability. We hypothesize that SD may be in regions of impaired autoregulation and may be a surrogate measure for autoregulatory disturbance.
Adult patients undergoing clinically indicated triggered craniotomy were prospectively enrolled in an observational study of factors affecting SD. A subdural electrode was placed at the time of surgery and monitored for SD. MAP and CBF data were collected in a time locked multiparametric monitoring system (Moberg CNS). Physiology data was gathered in 1m intervals, filtered for spurious values, and re-binned into 20 min sections. Probability of SD was plotted versus falling MAP. Loss of autoregulation (defined as correlation of CBF and MAP>0.7) was then also tested for association with SD.
A total of 31 patients were enrolled. Per 1mmHg of MAP increase, SD occurrence probability changed by 0.955 (95%CI=.944-.966) with a p<.0001. Dichotomized odds of SD for MAP less than 90mmHg demonstrated OR of 2.717 (95%CI 1.979-3.730) compared to MAP values above 90. Furthermore, the odds of SD were significantly increased with loss of autoregulation (OR=2.238, 95%CI=1.044-4.800).
These data confirm that risk of SD increases with lower MAP, with a strong inflection point around 90mmHg. Significant association of SD with loss of autoregulation suggests that SD may reflect autoregulatory instability, either globally, or focally in regions that would not be detected by standard global measures such as PRx. These results have potential implications in monitoring and prevention of secondary brain injury.