High-Frequency Analysis of the Cerebral Physiological Impact of Ketamine in Acute Traumatic Neural Injury.
Davis McClarty, Logan Froese, Tobias Bergmann, Kevin Y Stein, Amanjyot S Sainbhi, Abrar Islam, Nuray Vakitbilir, Noah Silvaggio, Izabella Marquez, Alwyn Gomez, Frederick A Zeiler
Neurotrauma reports 2025 DOI: 10.1089/neur.2024.0146 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Retrospective study Peer reviewed |
|---|---|
| Sample size | 122 |
| Population | Patients with moderate/severe traumatic brain injury |
| Intervention | Ketamine |
| Topics | Ketamine Esketamine |
| Keywords | Acute brain injuries Traumatic brain injury #brain-trauma head injury Tbi Brain damage #ketamine ketamine therapy Ketamine treatment Ketamine sedation #neurology brain medicine Neurological treatment |
| Citations | 1 |
| Key points | Ketamine does not significantly affect cerebral pressure-flow dynamics in patients with moderate to severe TBI, contradicting historical concerns about increased intracranial pressure. |
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.
Comparable studies
Other observational and cohort studies on ketamine, most cited first.
| Study | Year | Design | Participants |
|---|---|---|---|
| Taming the Ketamine Tiger Volunteers from a prison population | 2010 | Observational study | n = 20 |
| Increased spontaneous MEG signal diversity for psychoactive doses of ketamine, LSD and psilocybin Humans | 2017 | Observational study | |
| Disruption of Frontal–Parietal Communication by Ketamine, Propofol, and Sevoflurane Surgical patients undergoing induction of anesthesia with intravenous ketamine | 2013 | Observational cohort | n = 30 |
| Do the dissociative side effects of ketamine mediate its antidepressant effects? Treatment-resistant inpatients with major depressive disorder or bipolar disorder | 2014 | Observational cohort | n = 108 |
| Concomitant BDNF and sleep slow wave changes indicate ketamine-induced plasticity in major depressive disorder Patients with treatment-resistant major depressive disorder | 2012 | Observational cohort | n = 30 |