Janjua Nazli, Mayer Stephan A
Neurocritical Care, Department of Neurology, Neurological Intensive Care Unit, Columbia-Presbyterian Medical Center, Neurological Institute, New York, New York 10032, USA.
Curr Opin Crit Care. 2003 Apr;9(2):113-9. doi: 10.1097/00075198-200304000-00006.
To summarize new pathophysiologic insights and recent advances in the diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage.
Important, newly recognized mediators of cerebral arterial spasm after subarachnoid hemorrhage include superoxide free radicals, ferrous hemoglobin (which acts as a nitric oxide scavenger), endothelins, protein kinase C, and rho kinase. Microvascular dysfunction and autoregulatory failure also has been an area of increasing research focus in recent years. New diagnostic modalities include measures of cerebral blood flow such as single-photon emission computed tomography and perfusion computed tomography, magnetic resonance imaging, intracranial brain oxygen tension probes, and jugular venous oxygen saturation monitors. Proton magnetic resonance spectroscopy and microdialysis can detect tissue biochemical abnormalities, but these techniques have not found their way into routine clinical practice as of yet. In addition to nimodipine and hypertensive hypervolemic therapy, promising new treatments for vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia. Balloon angioplasty has emerged as the primary weapon for treating medically refractory ischemia from vasospasm and in many centers is being used as a first-line treatment or even prophylactically.
The neurointensive care management of vasospasm after subarachnoid hemorrhage has evolved significantly over the past 10 years, with many new diagnostic modalities and promising treatments now available. Clinical trials are needed to evaluate the efficacy of these new techniques and to further define the optimal management of this often devastating complication.
总结动脉瘤性蛛网膜下腔出血后脑血管痉挛诊断和治疗方面新的病理生理学见解及近期进展。
蛛网膜下腔出血后新确认的重要脑动脉痉挛介质包括超氧自由基、亚铁血红蛋白（作为一氧化氮清除剂）、内皮素、蛋白激酶C和rho激酶。近年来，微血管功能障碍和自动调节功能衰竭也一直是研究日益关注的领域。新的诊断方法包括脑血流量测量，如单光子发射计算机断层扫描和灌注计算机断层扫描、磁共振成像、颅内脑氧分压探头和颈静脉血氧饱和度监测仪。质子磁共振波谱和微透析可检测组织生化异常，但这些技术尚未进入常规临床实践。除尼莫地平和高血压高血容量疗法外，治疗血管痉挛或其缺血性并发症的有前景的新疗法包括硫酸镁、盐酸法舒地尔、甲磺酰替拉扎特、促红细胞生成素和诱导低温。球囊血管成形术已成为治疗血管痉挛所致药物难治性缺血的主要手段，在许多中心正被用作一线治疗甚至预防性治疗。
过去10年中，蛛网膜下腔出血后血管痉挛的神经重症监护管理有了显著进展，现在有许多新的诊断方法和有前景的治疗方法。需要进行临床试验来评估这些新技术的疗效，并进一步明确这种常常具有毁灭性的并发症的最佳管理方法。
