Seiler R W, Grolimund P, Zurbruegg H R
Acta Neurochir (Wien). 1987;85(1-2):7-16. doi: 10.1007/BF01402363.
70 consecutive patients admitted within four days after the first aneurysmal subarachnoid haemorrhage (SAH) were evaluated by daily transcranial Doppler ultrasound (TCD) measurement of the blood flow velocities (BFVs) of both middle cerebral arteries (MCAs) and by daily recordings of their clinical grade (Hunt and Hess). Patients with no or only little subarachnoid blood in the first CT after admission were classified as low-risk for the development of symptomatic vasospasm (VSP), and patients with big subarachnoid clots or thick layers of subarachnoid blood were graded as high-risk patients for symptomatic VSP. The first series of 33 patients received no nimodipine whereas the second series of 37 patients were treated with nimodipine 2 mg/h intravenously, starting within 24 hours after the SAH in the majority of patients. 7-14 days postoperatively, the intravenous dose was changed to oral nimodipine 60 mg/q4h for one week and then discontinued. A mean BFV curve of the side with the higher flow velocities correlated with the mean clinical status (Hunt and Hess) was calculated by computer analysis for the patients treated without nimodipine and for those receiving nimodipine in each risk group. The mean BFV curves of the same risk groups were compared in order to evaluate the effect of nimodipine for the prevention of vasospasm following SAH. The delayed neurological deficits (DIND) and the functional outcome six months after the SAH were recorded in each group and compared. Nimodipine given within four days after the SAH did not prevent vasospasm evaluated by TCD, but it significantly reduced the severity of the vasoconstriction, especially in high-risk patients. It reduced significantly the incidence of DIND in high-risk patients and improved their functional outcome. Although nimodipine may have a reduced efficacy in preventing vasospasm after early operation of high-risk patients, it probably protects the brain by increasing its tolerance to focal ischaemia.
连续70例在首次动脉瘤性蛛网膜下腔出血（SAH）后4天内入院的患者，通过每日经颅多普勒超声（TCD）测量双侧大脑中动脉（MCA）的血流速度（BFV）以及每日记录其临床分级（Hunt和Hess分级）进行评估。入院后首次CT显示蛛网膜下腔无血或仅有少量血液的患者被归类为发生症状性血管痉挛（VSP）的低风险患者，而蛛网膜下腔有大血凝块或蛛网膜下腔血液厚层的患者被分级为症状性VSP的高风险患者。第一组33例患者未接受尼莫地平治疗，而第二组37例患者在SAH后24小时内开始静脉滴注尼莫地平2mg/h，大多数患者如此。术后7 - 14天，静脉剂量改为口服尼莫地平60mg/每4小时，持续一周，然后停药。通过计算机分析，为未接受尼莫地平治疗的患者以及每个风险组中接受尼莫地平治疗的患者计算出流速较高一侧的平均BFV曲线与平均临床状态（Hunt和Hess分级）的相关性。比较相同风险组的平均BFV曲线，以评估尼莫地平对预防SAH后血管痉挛的效果。记录每组SAH后6个月的延迟性神经功能缺损（DIND）和功能结局并进行比较。SAH后4天内给予尼莫地平并不能预防通过TCD评估的血管痉挛，但它显著降低了血管收缩的严重程度，尤其是在高风险患者中。它显著降低了高风险患者中DIND的发生率并改善了他们的功能结局。尽管尼莫地平在预防高风险患者早期手术后的血管痉挛方面可能疗效降低，但它可能通过增加大脑对局灶性缺血的耐受性来保护大脑。
