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Monoaminergic agonists for acute traumatic brain injury

Lookup NU author(s): Dr Rob ForsythORCiD

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Abstract

Although there have been considerable gains in understanding the cascade of events that lead to secondary injury after traumatic brain injury (TBI), efforts to translate this understanding into new therapeutic, so-called neuroprotective approaches, have so far proven disappointing. As an alternative, there is growing interest in approaches to enhance brain repair after injury. Animal models suggest that agents enhancing monoaminergic ( MA) transmission, particularly amphetamines, promote motor recovery from focal brain injury and it is proposed that this might represent a complementary means of therapeutic intervention in the later post-injury phase. To evaluate the evidence that MAs improve final outcome after TBI. We searched CENTRAL (The Cochrane Library, Issue 2, 2005), the Cochrane Injuries Group's Specialised Register ( to May 2005), MEDLINE (1966 to May 2005), EMBASE (1980 to May 2005) and the Science Citation Index (1992 to June 2005). We contacted researchers and authors of published and unpublished trials. Searches were updated in May 2005. Randomised controlled trials comparing the use of a MA (together with conventional non-pharmacological rehabilitative therapy) versus conventional non-pharmacological rehabilitative therapy alone. Two authors independently screened records, extracted data and assessed trial quality. Although there is a limited clinical literature addressing this topic, none of the studies identified fully met inclusion criteria for this review. At present there is insufficient evidence to support the routine use of MAs to promote recovery after TBI.


Publication metadata

Author(s): Forsyth RJ, Jayamoni B, Paine TC

Publication type: Review

Publication status: Published

Journal: Cochrane Database of Systematic Reviews

Year: 2006

Issue: 4

Pages: CD003984

ISSN (electronic): 1469-493X

URL: http://dx.doi.org/10.1002/14651858.CD003984.pub2

DOI: 10.1002/14651858.CD003984.pub2


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