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. 2025 Feb 20;6(1):232-241.
doi: 10.1089/neur.2024.0146. eCollection 2025.

High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury

Davis McClarty  1 , Logan Froese  2 , Tobias Bergmann  3 , Kevin Y Stein  3 , Amanjyot S Sainbhi  3 , Abrar Islam  3 , Nuray Vakitbilir  3 , Noah Silvaggio  4 , Izabella Marquez  5 , Alwyn Gomez  4   6 , Frederick A Zeiler  2   3   6   7
Affiliations

High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury

Davis McClarty et al. Neurotrauma Rep. .

Abstract

Acute traumatic neural injury, also known as traumatic brain injury (TBI), is a leading cause of death. TBI treatment focuses on the use of sedatives, vasopressors, and invasive intracranial pressure (ICP) monitoring to mitigate ICP elevations and maintain cerebral perfusion pressure (CPP). While common sedatives such as propofol and fentanyl have significant side effects, ketamine is an attractive alternative due to its rapid onset and cardiovascular stability. Despite these benefits, ketamine's use remains controversial due to historical concerns about increasing ICP. Using high-frequency monitoring, this retrospective study compared cerebral pressure-flow dynamics in patients with moderate/severe TBI who received ketamine with those who did not. Statistical analysis included descriptive statistics, comparisons within and between patients receiving ketamine, and evaluation of physiological response around incremental dose changes in ketamine. Various cerebral physiological indices were analyzed, including ICP, CPP, regional cerebral oxygen delivery, intracranial compliance, and cardiovascular reactivity metrics. A total of 122 patients were studied, with 17 receiving ketamine (median age: 37 years) and 105 not receiving ketamine (median age: 42 years). Results indicated higher median ICP in the ketamine group compared with the no ketamine group (9.05 mmHg and 14.00 mmHg, respectively, p = 0.00017); however, this is likely due to differences in patient characteristics and injury severity between the groups. No significant differences were observed in any other index of cerebral pressure-flow dynamics or between any incremental dose change condition. These findings suggest that ketamine does not significantly impact cerebral pressure-flow dynamics, challenging historical concerns about its use in patients with TBI.

Keywords: acute brain injuries; ketamine; sedation; traumatic brain injury.

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Figures

FIG. 1.
FIG. 1.
Graphical representation of windowing for incremental dose change analysis. Mean index was calculated in both the “pre-window” and “post-window.”
FIG. 2.
FIG. 2.
(A–C) Interpatient analysis between the no ketamine and ketamine groups: (A) Mean ICP. (B) Percentage time above ICP of 20 mmHg. (C) Percentage time above ICP of 22 mmHg. (D–F) Intrapatient analysis between zero ketamine infusion and ketamine infusion: (D) Mean ICP. (E) Percentage time above ICP of 20 mmHg (C) Percentage time above ICP of 22 mmHg. ICP, invasive intracranial pressure.
FIG. 3.
FIG. 3.
Mean hourly data for select indices of cerebral pressure-flow dynamics, illustrated with a LOESS curve with the 95% confidence interval. For rSO2, COx, and COx_a, only results for the left side are displayed. However, results for the right side showed similar trends. LOESS, locally estimated scatterplot smoothing; rSO2, regional cerebral oxygen saturation.
FIG. 4.
FIG. 4.
Mean index value pre- and post-infusion dose increase for select indices of cerebral pressure-flow dynamics. For rSO2, COx, and COx_a, only results for the left side are displayed. However, results for the right side showed similar trends. rSO2, regional cerebral oxygen saturation.
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