脑卒中后的神经可塑性
中山大学附属第一医院神经科脑血管专科 (510080)
脑卒中后梗塞灶或血肿中心区神经细胞死亡后导致的神经功能缺损，至今尚缺乏真正有效的治疗措施和药物。尽管如此，这种神经功能缺损可在一定时期内不同程度地自发性改善。这种功能改善目前被认为与神经可塑性(Neural plasticity)有关。已经知道，脑卒中后的神经可塑性包括结构和功能两方面。前者包括突触囊泡蛋白(Synaptophysin, SYN)、生长关联蛋白(Growth associated protein-43, GAP-43) 和钙/降钙素依赖蛋白激酶II(Ca2+/calmodulin-dependent protein kinase II, CaMKII)等基因表达和这些蛋白含量的变化，并直接影响到相互联系的突触数目，甚至神经元数目量。后者是指神经功能缺损的自发性改善，可能与皮层的功能代偿有关。一侧大脑皮层运动感觉区梗塞后，与皮层运动区有密切纤维联系的丘脑可发生继发性萎缩。神经移植补充脑源性神经营养因子(BDNF)后，可减轻这种继发性损害并改善神经可塑性。因此，脑卒中后导致的神经损害不仅是病灶局部的，可能波及到整个神经系统的相关部位。这可能是脑卒中后神经功能恢复困难和治疗效果差的原因。
Neuroplasticity after Stroke
ZENG Jinsheng
Stroke Center, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China
The death of neural cells in the center of the cerebral infarcts or hematoma after stroke leads to the dysfunction of central nervous system. No effective management is available until now. However, the neurologic dysfunction can be improved spontaneously over time, which is considered to be related to neural plasticity including the plasticity in both structure and function. Structural plasticity means the changes of the expression of synaptophysin (SYN), growth associated protein-43 (GAP-43), Ca2+/calmodulin-dependent protein kinase II (CaMKII), etc, and the resulting changes of the number of synapse and neuron. Functional plasticity refers to the automatic improvement of neurologic dysfunction involving the compensation of the cortical function of the brain. In addition, atrophy of the thalamencephalon which presents close connection with the motor-sensory cortex of the brain may occur secondary to the unilateral cerebral cortical infarction. Supplement of brain derived neural factor (BDNF) can alleviate this secondary pathological change and enhance the neural plasticity. Therefore, the dysfunction after stroke is not only due to ischemic or hemorrhagic lesion, but also related to the whole central nervous system, which may be the underlying reason why the rehabilitation of neural function is so difficult and why the treatment is usually unsatisfied., http://www.100md.com(曾进胜)
脑卒中后梗塞灶或血肿中心区神经细胞死亡后导致的神经功能缺损，至今尚缺乏真正有效的治疗措施和药物。尽管如此，这种神经功能缺损可在一定时期内不同程度地自发性改善。这种功能改善目前被认为与神经可塑性(Neural plasticity)有关。已经知道，脑卒中后的神经可塑性包括结构和功能两方面。前者包括突触囊泡蛋白(Synaptophysin, SYN)、生长关联蛋白(Growth associated protein-43, GAP-43) 和钙/降钙素依赖蛋白激酶II(Ca2+/calmodulin-dependent protein kinase II, CaMKII)等基因表达和这些蛋白含量的变化，并直接影响到相互联系的突触数目，甚至神经元数目量。后者是指神经功能缺损的自发性改善，可能与皮层的功能代偿有关。一侧大脑皮层运动感觉区梗塞后，与皮层运动区有密切纤维联系的丘脑可发生继发性萎缩。神经移植补充脑源性神经营养因子(BDNF)后，可减轻这种继发性损害并改善神经可塑性。因此，脑卒中后导致的神经损害不仅是病灶局部的，可能波及到整个神经系统的相关部位。这可能是脑卒中后神经功能恢复困难和治疗效果差的原因。
Neuroplasticity after Stroke
ZENG Jinsheng
Stroke Center, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China
The death of neural cells in the center of the cerebral infarcts or hematoma after stroke leads to the dysfunction of central nervous system. No effective management is available until now. However, the neurologic dysfunction can be improved spontaneously over time, which is considered to be related to neural plasticity including the plasticity in both structure and function. Structural plasticity means the changes of the expression of synaptophysin (SYN), growth associated protein-43 (GAP-43), Ca2+/calmodulin-dependent protein kinase II (CaMKII), etc, and the resulting changes of the number of synapse and neuron. Functional plasticity refers to the automatic improvement of neurologic dysfunction involving the compensation of the cortical function of the brain. In addition, atrophy of the thalamencephalon which presents close connection with the motor-sensory cortex of the brain may occur secondary to the unilateral cerebral cortical infarction. Supplement of brain derived neural factor (BDNF) can alleviate this secondary pathological change and enhance the neural plasticity. Therefore, the dysfunction after stroke is not only due to ischemic or hemorrhagic lesion, but also related to the whole central nervous system, which may be the underlying reason why the rehabilitation of neural function is so difficult and why the treatment is usually unsatisfied., http://www.100md.com(曾进胜)