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Brain tissue oxygen (PbtO₂) monitoring in traumatic brain injury (TBI) has demonstrated strong associations with globaloutcome. Additionally, PbtO₂ signals have been used to derive indices thought to be associated with cerebrovascular reactivityin TBI. However, their true relationship to slow-wave vasogenic fuctuations associated with cerebral autoregulation remainsunclear. The goal of this study was to investigate the relationship between slow-wave fuctuations of intracranial pressure(ICP), mean arterial pressure (MAP) and PbtO₂ over time. Using the Collaborative European NeuroTrauma EfectivenessResearch in Traumatic Brain Injury (CENTER-TBI) high resolution ICU sub-study cohort, we evaluated those patients withrecorded high-frequency digital intra-parenchymal ICP and PbtO2 monitoring data of a minimum of 6 h in duration. Digitalphysiologic signals were processed for ICP, MAP, and PbtO₂ slow-waves using a moving average flter to decimate the highfrequency signal. The frst 5 days of recording were analyzed. The relationship between ICP, MAP and PbtO₂ slow-wavesover time were assessed using autoregressive integrative moving average (ARIMA) and vector autoregressive integrativemoving average (VARIMA) modelling, as well as Granger causality testing. A total of 47 patients were included. The ARIMAstructure of ICP and MAP were similar in time, where PbtO₂ displayed diferent optimal structure. VARIMA modellingand IRF plots confrmed the strong directional relationship between MAP and ICP, demonstrating an ICP response to MAPimpulse. PbtO₂ slow-waves, however, failed to demonstrate a defnite response to ICP and MAP slow-wave impulses. Theseresults raise questions as to the utility of PbtO₂ in the derivation of cerebrovascular reactivity measures in TBI. There isa reproducible relationship between slow-wave fuctuations of ICP and MAP, as demonstrated across various time-seriesanalytic techniques. PbtO₂ does not appear to reliably respond in time to slow-wave fuctuations in MAP, as demonstratedon various VARIMA models across all patients. These fndings suggest that PbtO₂ should not be utilized in the derivationof cerebrovascular reactivity metrics in TBI, as it does not appear to be responsive to changes in MAP in the slow-waves.These fndings corroborate previous results regarding PbtO₂ based cerebrovascular reactivity indices.