Structural aspects of ischemic brain damage.
The structural changes during cerebal ischemia are reviewed. In the acute phase the neurons may show either pale or dark type of ischemic injury. The former is usually associated with complete ischemia and the structural alterations are fairly inconspicious, while the latter is seen in incomplete ischemia or ischemia with recirculation and is characterized by shrinkage of neurons with extensive mitochondrial swelling and astrocytic edema. Both types of injury may be irreversible, but long post-ischemic period is usually necessary to see the final outcome of the insult, all the more since the neurons may not die until after a free postischemic interval (even with resumed function) of several hours to days. The delayed death is preceded by peculiar proliferation of cytoplasmic membranes before the doomed neurons become shrunken and disintegrate. This "maturation phenomenon" or "delayed neuronal death" is understandably important since it suggests that a longer postischemic interval for therapeutic interventions may exist. Several factors both during and after the ischemic insult can modify the changes and affect the severity of the damager among the most important ones are the degree of lactic acidosis during the ischemic period, as well as the characteristics of the neurons, since excitoxic damage by transmitter substances released by the ischemic insult has been suggested to be responsible for the delayed neuronal death.
Kalimo
H
H
Smith
M L
ML
D000140:Acidosis, Lactic / Q000473:pathology; D000818:Animals; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000473:pathology*; D002470:Cell Survival; D007425:Intracellular Membranes / Q000473:pathology; D009474:Neurons / Q000473:pathology; D013997:Time Factors