ReviewFrontiers in neurology
Ketamine as a potential cognitive enhancer in neurological disorders: evidence from preclinical and clinical studies.
Review in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subanesthetic ketamine shows rapid neuroplastic and antidepressant effects in psychiatric conditions, prompting interest in its potential relevance for cognitive dysfunction in neurological disorders. Cognitive deficits are widespread across traumatic brain injury, stroke, epilepsy, and neurodegenerative diseases, yet treatments remain primarily compensatory. Ketamine's actions on glutamatergic signaling, synaptogenesis, and neuroinflammation suggest possible cognitive implications, but its specific effects on cognition in neurological populations remain unclear. This systematic review evaluated evidence on the effects of ketamine on cognitive functioning in neurological diseases and injuries characterized by cognitive impairment. A systematic search of three databases through February 10, 2024, was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analysis 2020 guidelines, including animal or human studies administering ketamine or its derivatives with cognitive outcome measures. Twenty-two studies met inclusion criteria: twenty-one animal studies and one human study. In animal models of traumatic brain injury, epilepsy, cerebrovascular disease, Parkinson's disease, and infectious encephalopathy, a subject-level vote count in rodents indicated positive cognitive effects in 93.2% of subjects, particularly in working memory and spatial learning, while null effects appeared in 4.1% and negative effects in 2.7%. The only human study, conducted in patients with Huntington's disease, reported short-term, dose-dependent cognitive worsening after escalating intravenous ketamine. Overall, preclinical evidence indicates potential cognitive effects in animal models of neurological injury; however, human evidence remains extremely limited and does not currently support clinical cognitive enhancement. Further controlled clinical studies are needed to clarify safety, mechanisms, and translational relevance in neurological rehabilitation.
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