Ketamine in acute phase of severe traumatic brain injury “an old drug for new uses?”

Yang

et al. 2022

JCM

Background: Pregnant women are more likely to suffer post-puncture symptoms such as headaches and nausea due to the outflow of cerebrospinal fluid after spinal anesthesia. Because ketamine has the effect of raising intracranial pressure, it may be able to improve the symptoms of perioperative hypocranial pressure and effectively prevent the occurrence of hypocranial pressure-related side effects. Method: Keywords such as ketamine, cesarean section, and spinal anesthesia were searched in databases including Medline, Embase, Web of Science, and Cochrane from 1976 to 2021. Thirteen randomized controlled trials were selected for the meta-analysis. Results: A total of 12 randomized trials involving 2099 participants fulfilled the inclusion criteria. There was no significant association between ketamine and the risk of headaches compared to the placebo (RR = 1.12; 95% CI: 0.53, 2.35; p = 0.77; I² = 62%). There was no significant association between ketamine and nausea compared to the placebo (RR = 0.66; 95% CI: 0.40, 1.09; p = 0.10; I² = 57%). No significant associations between ketamine or the placebo and vomiting were found (RR = 0.94; 95% CI: 0.53, 1.67; p = 0.83; I² = 72%). Conclusion: Intravenous ketamine does not improve the symptoms caused by low intracranial pressure after spinal anesthesia in patients undergoing cesarean section.

Section: Discussionmentioning

confidence: 99%

Effect of Intravenous Ketamine on Hypocranial Pressure Symptoms in Patients with Spinal Anesthetic Cesarean Sections: A Systematic Review and Meta-Analysis

Yang

et al. 2022

JCM

“…Though these are a novel class of drugs deserving close study, more data are necessary to prove their efficacy for treatment of brain injury, as historically many compounds have seemed promising in vitro , including likely hundreds of compounds thought to facilitate neuroplasticity and neuroprotection, but have not borne out in clinical trials ( 61 , 62 ). There is already mixed evidence to suggest the use of non-classical psychedelics ketamine ( 63 , 64 ), as well as tetrahydrocannabinol (THC) ( 65 , 66 ) and cannabidiol ( 67 , 68 ), as neuroprotectants after TBI and stroke. Presence of THC on urine drug screen is associated with decreased mortality in adult patients sustaining TBI ( 65 ).…”

Section: Discussionmentioning

confidence: 99%

Psychedelics for Brain Injury: A Mini-Review

Khan

Carter²,

Aggarwal

et al. 2021

Front. Neurol.

Objective: Stroke and traumatic brain injury (TBI) are among the leading causes of disability. Even after engaging in rehabilitation, nearly half of patients with severe TBI requiring hospitalization are left with major disability. Despite decades of investigation, pharmacologic treatment of brain injury is still a field in its infancy. Recent clinical trials have begun into the use of psychedelic therapeutics for treatment of brain injury. This brief review aims to summarize the current state of the science's relevance to neurorehabilitation, and may act as a resource for those seeking to understand the precedence for these ongoing clinical trials.Methods: Narrative mini-review of studies published related to psychedelic therapeutics and brain injury.Results: Recent in vitro, in vivo, and case report studies suggest psychedelic pharmacotherapies may influence the future of brain injury treatment through modulation of neuroinflammation, hippocampal neurogenesis, neuroplasticity, and brain complexity.Conclusions: Historical data on the safety of some of these substances could serve in effect as phase 0 and phase I studies. Further phase II trials will illuminate how these drugs may treat brain injury, particularly TBI and reperfusion injury from stroke.

“…Additionally, many of these studies reported no change in ICP in healthy individuals and did not report concurrent changes in mean arterial pressure and calculated cerebral perfusion pressure 48 . As such, current opinions consider the rise in ICP caused by ketamine to be a myth 33,56,57 . In fact, in more recent preclinical trials modeling increases in ICP, racemic ketamine (10 mg/kg) was shown to decrease ICP by a maximum of 10.8% 58 .…”

Section: Discussionmentioning

confidence: 99%

The use of ketamine as a neuroprotective agent following cardiac arrest: A scoping review of current literature

et al. 2022

Aims The objective of this article is to summarize the state of the literature surrounding the use of ketamine as a neuroprotective agent following cardiac arrest. Methods Five electronic databases were used to search for studies related to the use of ketamine for neuroprotection following cardiac arrest. This search was performed once in May 2020, and an updated search was conducted in May 2021 and March 2022. Results All searches combined retrieved 181 results; no clinical trials were identified. As such, the authors were limited to writing a scoping review of the literature rather than a systematic review. Conclusions The current state of the literature describes the mechanism of action of ketamine as a neuroprotective agent through its action as an NMDA antagonist. There is evidence of its efficacy as a neuroprotective agent in preclinical models of cardiac arrest. Current published clinical work supports the use of ketamine ameliorating neurologic outcomes in other conditions such as epilepsy, traumatic brain injury, and depression. The current state of the literature is reflective of the notion that the use of ketamine following cardiac arrest may result in improved neurologic outcomes. Future research directions should focus on the use of ketamine as a possible clinical intervention following cardiac arrest.