Department of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Korányis Fasor 9, H-6720, Szeged, Hungary; Department of Neurology Faculty of Medicine, University of Szeged, Semmelweis u. 6, H-6725, Szeged, Hungary.
Department of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Korányis Fasor 9, H-6720, Szeged, Hungary.
Neurochem Int. 2019 Jul;127:125-136. doi: 10.1016/j.neuint.2018.10.010. Epub 2018 Oct 15.
Secondary injury following acute brain insults significantly contributes to poorer neurological outcome. The spontaneous, recurrent occurrence of spreading depolarization events (SD) has been recognized as a potent secondary injury mechanism in subarachnoid hemorrhage, malignant ischemic stroke and traumatic brain injury. In addition, SD is the underlying mechanism of the aura symptoms of migraineurs. The susceptibility of the nervous tissue to SD is subject to the metabolic status of the tissue, the ionic composition of the extracellular space, and the functional status of ion pumps, voltage-gated and other cation channels, glutamate receptors and excitatory amino acid transporters. All these mechanisms tune the excitability of the nervous tissue. Aging has also been found to alter SD susceptibility, which appears to be highest at young adulthood, and decline over the aging process. The lower susceptibility of the cerebral gray matter to SD in the old brain may be caused by the age-related impairment of mechanisms implicated in ion translocations between the intra- and extracellular compartments, glutamate signaling and surplus potassium and glutamate clearance. Even though the aging nervous tissue is thus less able to sustain SD, the consequences of SD recurrence in the old brain have proven to be graver, possibly leading to accelerated lesion maturation. Taken that recurrent SDs may pose an increased burden in the aging injured brain, the benefit of therapeutic approaches to restrict SD generation and propagation may be particularly relevant for elderly patients.
急性脑损伤后的二次损伤极大地导致了更差的神经学预后。自发性、复发性的脑扩散性去极化事件（SD）已被认为是蛛网膜下腔出血、恶性缺血性中风和创伤性脑损伤的一种强有力的二次损伤机制。此外，SD 是偏头痛患者先兆症状的潜在机制。神经组织对 SD 的易感性取决于组织的代谢状态、细胞外空间的离子组成以及离子泵、电压门控和其他阳离子通道、谷氨酸受体和兴奋性氨基酸转运体的功能状态。所有这些机制都调节神经组织的兴奋性。研究还发现，衰老会改变 SD 的易感性，这种易感性在年轻成年时似乎最高，随着衰老过程而下降。老年大脑中灰质对 SD 的较低易感性可能是由于与离子在细胞内外间隙之间的转移、谷氨酸信号以及多余钾和谷氨酸清除相关的机制的年龄相关性损伤所致。尽管衰老的神经组织因此更难以维持 SD，但 SD 在老年大脑中的复发后果被证明更为严重，可能导致病变成熟加速。考虑到复发性 SD 可能会给衰老损伤的大脑带来更大的负担，限制 SD 产生和传播的治疗方法的益处可能对老年患者特别相关。
