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Cited by 158Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroprotection in Cerebral Ischemia

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A Review of Neuroprotection Pharmacology and Therapies in Patients with Acute Traumatic Brain Injury

McConeghy, Kevin W., Hatton, Jimmi, Hughes, Lindsey, Cook, Aaron M.·2012·CNS Drugs
DOI 10.2165/11634020-000000000-00000
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Abstract

Traumatic brain injury (TBI) affects 1.6 million Americans annually. The injury severity impacts the overall outcome and likelihood for survival. Current treatment of acute TBI includes surgical intervention and supportive care therapies. Treatment of elevated intracranial pressure and optimizing cerebral perfusion are cornerstones of current therapy. These approaches do not directly address the secondary neurological sequelae that lead to continued brain injury after TBI. Depending on injury severity, a complex cascade of processes are activated and generate continued endogenous changes affecting cellular systems and overall outcome from the initial insult to the brain. Homeostatic cellular processes governing calcium influx, mitochondrial function, membrane stability, redox balance, blood flow and cytoskeletal structure often become dysfunctional after TBI. Interruption of this cascade has been the target of numerous pharmacotherapeutic agents investigated over the last two decades. Many agents such as selfotel, pegorgotein (PEG-SOD), magnesium, deltibant and dexanabinol were ineffective in clinical trials. While progesterone and ciclosporin have shown promise in phase II studies, success in larger phase III, randomized, multicentre, clinical trials is pending. Consequently, no neuroprotective treatment options currently exist that improve neurological outcome after TBI. Investigations to date have extended understanding of the injury mechanisms and sites for intervention.…

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Metadata

Authors
McConeghy, K. W., Hatton, J., Hughes, L., & Cook, A. M.
Affiliations
  • University of Kentucky HealthCare (US)
  • University of Kentucky (US)
Corresponding author
Cook, Aaron M.
ORCID
Venue
CNS Drugs
Publisher
Springer Science and Business Media LLC
Published
2012-07
Volume
26
Issue
7
Pages
613-636
ISSN
1172-7047 (ISSN-L)
DOI
10.2165/11634020-000000000-00000
OpenAlex
W2006925820
Cited by
158
References
0
Citations by year
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FWCI
2.29
Type
journal article
Language
en
Open access
closed
Locations
  • CNS Drugs (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
  • Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords
traumatic brain injury, neuroprotection, secondary brain injury, intracranial pressure, cerebral perfusion, calcium influx, mitochondrial dysfunction, redox homeostasis, blood flow, cytoskeleton, magnesium, progesterone, cyclosporine, biomarkers, clinical trial design
MeSH terms
Animals, Brain Injuries, Clinical Trials as Topic, Humans, Prognosis, Multicenter Studies as Topic, Randomized Controlled Trials as Topic, Neuroprotective Agents

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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