Ischemia leads to excessive activation of excitatory amino acid receptors and accumulation of intracellular calcium, which cause cellular injury. Rather than dissolving the thrombus, neuro-protective agents use a variety of mechanisms to attempt to save ischemic neurons in the brain from irreversible injury. These therapies target the neurons in the penumbra region, or rim, of the infarct, which are less likely to be irreversibly injured at early time points than are the neurons in the infarct core. Because they do not directly affect clotting and blood flow, neuroprotective agents are not expected to exhibit the risk of hemorrhage seen with the use of thrombolytic agents.

Despite the completion of multiple clinical trials to investigate neuroprotective agents, no drug has yet been proven to be efficacious in the treatment of acute clinical stroke. In fact, several studies have shown adverse treatment effects. We will review the results of the major neuro-protective trials in clinical stroke, highlighting the factors that could be changed to improve outcome in future studies. Two such factors include modification of drugs in classes associated with prominent side effects, and improvement of patient selection criteria to target those groups that are most likely to respond to individual therapies.

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