[Physiopathology of vertebrobasilar ischemia].
Although most of the studies concerning physiopathology of ischemia refer to cerebral hemispheres, it seems reasonable to consider that cellular and biochemical changes due to ischemia are similar in cerebellum and brain stem, which receive blood flow from vertebral and basilar arteries. Anyway, it must be noted that arterial distribution and anatomical structure of this part of the brain are quite distinct, so there might be differences in tissue vulnerability according to severity and duration of ischemia. Cellular injury from ischemia results, at first, as a consequence of energy failure that leads to loss of ionic homeosthasis and membrane potential. This runs a cascade of reactions which is responsible of injury progression. Reperfusion may potentiate this reactions if it does not occur early enough. Main mediators of these reactions are acidosis, citoplasmic calcium overload and excess of free radicals. Development of an inflammatory response and injury to microcirculation contribute to perpetuate the process.
Alonso de Leciñana
M
M
Servicio de Neurología, CM La Zarzuela, Madrid, España.
Díez-Tejedor
E
E
D000138:Acidosis / Q000209:etiology; D001488:Basilar Artery / Q000503:physiopathology*; D002545:Brain Ischemia / Q000209:etiology* / Q000503:physiopathology*; D001933:Brain Stem / Q000098:blood supply; D002118:Calcium / Q000032:analysis; D002531:Cerebellum / Q000098:blood supply; D003593:Cytoplasm / Q000737:chemistry; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D014711:Vertebral Artery / Q000503:physiopathology*; D014715:Vertebrobasilar Insufficiency / Q000150:complications* / Q000503:physiopathology*
D005609:Free Radicals; D002118:Calcium
Fisiopatología de la isquemia vertebrobasilar.