New pharmacological agents are being sought that offer neuroprotection in the immediate aftermath of the injury, thus preventing some of the extensive damage caused in the 'second injury' of TBI.
Apart from the physical tearing of axonal connections that often result from acceleration and/or impact, much damage is caused by biochemical events that immediately follow the TBI. Cascades of the neurotransmitter Glutamate released throughout the brain can cause damage to neurons through the process of excitotoxicity (literally excited to death). Other neurons may be necrotised or undergo a pre-programmed death or apoptosis.
Research is underway into how we can chemically interfere with these processes, e.g. by limiting the cascade of glutamate release; by blocking the effects that glutamate has on certain receptor-types (in particular the NMDA receptor); by preventing neuron necrosis and disrupting the genes that are responsible for apoptosis. A number of agents have been tested both in vitro and in vivo but movement from the R&D labs to clinical application is slow and no new pharmacological treatments have made it to the 'market' as yet.
Neuroprotectives are usually only useful if given in the earliest stages after brain injury but one potential neuroprotective, Erythropoietin or EPO, has been shown in one study to offer some restoration of spatial memory in TBI'd rats when given daily for 14 days post-TBI.
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