脑血管痉挛(cerebral vasospasm,CVS)是蛛网膜下腔出血(subarachnoid hemorrhage,SAH)急性期常见并发症之一,严重时引起迟发性缺血性神经功能损伤(delayed ischemic neurological deficits ,DIND),是导致SAH 致死、致残的重要原因.本文就CVS 病因、发病机制、诊断、药物治疗作一综述.
In this study, we hypothesized that total flavonoid of Litsea coreana leve (TFLC) protects against focal cerebral ischemia/reperfusion injury. TFLC (25, 50, 100 mg/kg) was administered oral y to a rat model of focal ischemia/reperfusion injury, while the free radical scavenging agent, edaravone, was used as a positive control drug. Results of neurological deficit scoring, 2,3,5-triphenyl tetrazolium chloride staining, hematoxylin-eosin staining and biochemical tests showed that TFLC at different doses significantly al eviated cerebral ischemia-induced neurological deficits and histopathological changes, and reduced infarct volume. Moreover, it suppressed the increase in the levels of nitrates plus nitrites, malondialdehyde and lactate dehydrogenase, and it diminished the reduction in gluta-thione, superoxide dismutase and catalase activities induced by cerebral ischemia/reperfusion in-jury. Compared with edaravone, the protective effects of TFLC at low and medium doses (25, 50 mg/kg) against cerebral ischemia/reperfusion injury were weaker, while the protective effects at high dose (100 mg/kg) were similar. Our experimental findings suggest that TFLC exerts neuroprotective effects against focal cerebral ischemia/reperfusion injury in rats, and that the effects may be asso-ciated with its antioxidant activities.
短暂头痛、神经功能缺损伴脑脊液淋巴细胞增多综合征(syndrome of transient headache and neurological deficits with cerebrospinal fluid lymphocytosis,HaNDL),曾被称为偏头痛伴脑脊液淋巴细胞增多、假性偏头痛伴脑脊液淋巴细胞增多~([1]),最早由Bartleson于1981年提出.近年来,国外HaNDL综合征病例报道逐渐增多~([2-4]),但国内尚未见报道.
延迟性缺血性神经功能障碍(delayed ischemic neurological deficits,DIND) 是蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后继发脑组织缺血而出现的神经功能缺损[1-3],常表现为新发的偏瘫、失语、癫痫以及不同程度的昏迷,严重者可导致死亡,其与颅内动脉瘤破裂再出血均是动脉瘤性SAH的严重并发症,随着早期外科开颅动脉瘤夹闭和血管内动脉瘤栓塞治疗的开展,再出血率下降,DIND已成为SAH后致死致残的重要原因,临床上发生率约为32.4%～42.0%[1].
