Shibuya M, Suzuki Y, Enomoto H, Okada T, Ogura K, Sugita K
Department of Neurosurgery, Nagoya University, Japan.
Acta Neurochir (Wien). 1994;131(1-2):19-25. doi: 10.1007/BF01401450.
Calcium antagonists are currently most widely used for chronic cerebral vasospasm after aneurysmal subarachnoid haemorrhage (SAH). However, the vasodilatory effects of systemically administered calcium antagonists can be limited secondary to hypotension. We previously compared intrathecal and intravenous routes of administration of nicardipine. Intrathecal administration of nicardipine significantly dilated spastic basilar arteries on day 7 in a two-haemorrhage canine model of vasospasm. In the present communication, the effects of prophylactic, serial administration of intrathecal nicardipine on vasospasm was examined in 50 patients. Patients were classified as Fisher SAH group 3 and all had their aneurysms clipped within 3 days of SAH. Following placement of a cisternal drain, 2 mg of nicardipine was injected, three times each day for an average of 10 days. The control group consisted of 91 similar patients with cisternal drainage not treated with nicardipine. Intrathecal administration of nicardipine decreased the incidence of symptomatic vasospasm by 26%, angiographic vasospasm by 20% and increased good clinical outcome at one month after the haemorrhage by 15%. Postoperative angiograms revealed that patients in the nicardipine group showed less vasospasm of major cerebral arteries, near the tip of a drain in the basal cistern, but vasospasm in the A2 and M2 segments was not decreased. Radio-isotope cisternography suggested that nicardipine might not reach the subarachnoid space around A2 and M2 segments. Nine patients complained of headache probably secondary to nicardipine induced vasodilation. Two patients suffered from meningitis, both were successfully treated. Intrathecal administration nicardipine appears to be effective in the treatment of vasospasm, but side effects were significant.
钙拮抗剂目前是动脉瘤性蛛网膜下腔出血（SAH）后慢性脑血管痉挛最广泛使用的药物。然而，全身给药的钙拮抗剂的血管舒张作用可能会因低血压而受到限制。我们之前比较了尼卡地平鞘内和静脉给药途径。在双次出血的犬血管痉挛模型中，鞘内注射尼卡地平在第7天可显著扩张痉挛的基底动脉。在本报告中，对50例患者进行了鞘内预防性、连续注射尼卡地平对血管痉挛影响的研究。患者被归类为Fisher SAH 3级，且均在SAH后3天内夹闭动脉瘤。在放置脑池引流管后，注射2mg尼卡地平，每天3次，平均10天。对照组由91例接受脑池引流但未用尼卡地平治疗的类似患者组成。鞘内注射尼卡地平使症状性血管痉挛的发生率降低了26%，血管造影显示的血管痉挛降低了20%，并使出血后1个月时良好临床结局的比例提高了15%。术后血管造影显示，尼卡地平组患者大脑主要动脉的血管痉挛较少，在基底脑池引流管尖端附近，但A2和M2段的血管痉挛并未减轻。放射性同位素脑池造影表明，尼卡地平可能无法到达A2和M2段周围的蛛网膜下腔。9例患者抱怨头痛，可能继发于尼卡地平引起的血管扩张。2例患者患脑膜炎，均成功治愈。鞘内注射尼卡地平似乎对血管痉挛的治疗有效，但副作用明显。
