Castillo J
Servicio de Neurología, Hospital Xeral de Galicia, Universidad de Santiago de Compostela, España.
Rev Neurol. 2000;30(5):459-64.
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.
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.
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.
了解生理病理机制有助于理解脑缺血各阶段的神经影像学变化以及许多治疗方法所基于的作用机制。
脑缺血的生理病理学在脑白质和灰质中有所不同。在灰质中,血管阻塞会导致缺血梯度。在更外周的区域,即缺血半暗带,神经元和神经胶质会发生功能改变,尽管结构完整性会维持一段时间。谷氨酸的释放和钙进入细胞会引发一系列生化过程,最终导致神经元死亡。在白质中,能量丧失会改变离子交换泵的方向,导致钙进入轴突。γ-氨基丁酸的释放会激活特定受体,保护神经纤维免受缺氧后果的影响。
伴随缺血的脑水肿有双重机制:最初是细胞毒性的,然后是血管源性的。两者都有助于增加脑缺血造成的神经损伤。