[Physiopathology of cerebral ischemia].
BACKGROUND
Knowledge of physiopathological mechanisms permits understanding of neuro-imaging changes during the various phases of cerebral ischaemia and the mechanisms of action on which many aspects of treatment are based.


METHODS
The physiopathology of cerebral ischemia is different in the white and grey matter of the brain. In the grey matter, obstruction of a blood vessel causes an ischemic gradient. In the more peripheral zones, known as the ischemic penumbra, functional alterations occur in the neurons and the glia, although the structural integrity is maintained for some time. Liberation of glutamate and the entrance of calcium into the cells leads to a series of biochemical processes which end in neurone death. In the white matter, loss of energy alters the direction of the ion exchange pumps, resulting in calcium entering the axon. Liberation of GABA activates specific receptors which protect the nerve fibres from the consequences of anoxia.


CONCLUSIONS
The cerebral oedema which accompanies ischemia has a double mechanism: initially it is cytotoxic and then vasogenic. Both contribute to increase the neurological damage caused by cerebral ischaemia.
Castillo
J
J
Servicio de Neurología, Hospital Xeral de Galicia, Universidad de Santiago de Compostela, España. mecasti@usc.es
D000818:Animals; D001921:Brain / Q000098:blood supply / Q000503:physiopathology*; D001929:Brain Edema / Q000209:etiology; D002545:Brain Ischemia / Q000150:complications / Q000503:physiopathology*; D015220:Calcium Channels / Q000378:metabolism; D016923:Cell Death / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D009474:Neurons / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D015220:Calcium Channels; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid