Most strokes are caused by a narrowing or blood clot that impedes the flow of blood through a cerebral artery, cutting off the supply of oxygen and glucose to a brain region. Occasionally the loss of blood flow to a brain region is caused by the rupture of a blood vessel. In either case, brain cells begin to die. At present, we don’t know how to induce the adult brain to produce new neurons to replace those that die, so an important consideration in the management of stroke is to try to prevent as much neuronal death as possible.
One obvious strategy is to unblock the blood vessel as soon as possible, and various thrombolytics (literally “clot dissolvers”; from the Greek thrombos, “clot,” and lytikos, “able to loosen”) have been shown to be effective in restoring circulation. There is a growing consensus that part of the neuronal death following stroke results from the overexcitation of neurons, which causes them to produce too many action potentials and leads to death (Lo et al., 2003; Rossi et al., 2000). New treatment strategies are being developed to suppress this excitotoxicity (see Figure 1).
Lo, E. H., Dalkara, T., and Moskowitz, M. A. (2003). Mechanisms, challenges and opportunities in stroke. Nature Reviews. Neuroscience 4: 399–415.
Rossi, D. J., Oshima, T., and Attwell, D. (2000). Glutamate release in severe brain ischaemia is mainly by reversed uptake. Nature 403: 316–321.