Abstract
Cerebral white matter, which is composed of myelinated axons and glials, is demonstrated to be as vulnerable as grey matter to ischemia, and the mechanisms of white matter damage are distinct in some points from those of grey matter damage. However, attention has focused almost exclusively on the damage to grey matter in rodent models of brain injury while the assessment of white matter damage has been neglected. Because an explanation for the lack of efficacy of most of neuroprotective drugs for clinical use is that neuroprotective strategies have primarily targeted grey but not white matter damage, the efficacy of a drug or a method should be dependent on its ability to protect against not only grey but also white matter damage.
