Impact of transcranial direct current stimulation (tDCS) on cerebral vasospasm after subarachnoid hemorrhage (SAH) in an experimental rat model.

急性，非创伤性蛛网膜下腔出血（SAH）是在十分之八的情况下破裂的颅内动脉瘤的结果。发病率为每年每10万居民6-8例。出血的总体年风险约为1% /年，取决于伴随的风险因素和动脉瘤大小。尽管诊断和治疗策略得到了优化，但动脉瘤破裂后的死亡率和严重发病率仍然高得令人无法接受。在出血后的头两周内，死亡和严重发病的主要原因是脑血管痉挛，导致缺血性梗死，这是迟发性缺血性神经功能缺损（DIND）的主要原因。脑血管痉挛主要是由于血液产物的释放和蛛网膜下腔的炎症反应。迄今为止，血管痉挛的药物治疗和介入治疗成功率有限。我们的目的是评估经颅直流电刺激（tDCS）对动脉瘤性SAH后脑血管痉挛的影响。本课课组目前的研究结果证明，tDCS以极性特异性的方式调节脑血流量，其中调节的程度取决于所应用的刺激参数。因此，tDCS可能对血管痉挛及其后遗症有积极作用，这似乎是可行的。因此，我们的目的是评估tDCS对脑血管痉挛的影响，以及其对脑血管痉挛相关缺血的影响。此外，如果我们能够检测到tDCS对脑血管痉挛的影响，下一步将是建立最大反应的刺激参数。因此，证明tDCS对血管痉挛和/或血管痉挛相关缺血的疗效将具有重要的临床意义，因为它将为动脉瘤性SAH后临床相关血管痉挛患者的治疗开辟一条新的无创途径。

An acute, non-traumatic subarachnoid hemorrhage (SAH) is in eight out of ten cases the result of a ruptured intracranial aneurysm. The incidence is 6-8 cases per 100 000 residents per year. The overall annual risk of bleeding is approximately 1% / year, depending on accompanying risk factors and the aneurysm size. Despite an optimization of diagnostic and treatment strategies, the mortality and severe morbidity after an aneurysm rupture is still unacceptably high. In the first two weeks after the bleeding, the major cause of death and severe morbidity is the cerebral vasospasm, leading to ischemic infarctions, which are the major cause for delayed ischemic neurological deficits (DIND). Cerebral vasospasms are predominantly the result of released blood products and an inflammatory reaction in the subarachnoid space. Up to date, vasospasm is treated pharmacologically and interventionally with limited success. Aim of our project is to evaluate the effects of transcranial direct current stimulation (tDCS) on cerebral vasospasm after aneurysmal SAH. Current results of our research group proved that tDCS modulates cerebral blood flow in a polarity-specific way, in which the extent of modulation depends on the stimulation parameters applied. Hence, it appears feasible, that tDCS might have a positive effect on vasospasm and its sequel. Therefore, it is our aim to evaluate the effects of tDCS on cerebral vasospasm, respectively its influence on vasospasm-associated ischemia. Furthermore, if we are able to detect an influence of tDCS on cerebral vasospasm, the establishment of stimulation parameters with maximal response will be the next step. Herefrom, the proof of efficacy of tDCS on vasospasm and / or vasospasm-related ischemia would be of substantial clinical importance, because it would open a new noninvasive avenue in the treatment of patients with clinically relevant vasospasm after aneurysmal SAH.