大鼠基底动脉闭塞所致神经症状及缺血范围观察

目的:观察大鼠脑干缺血后的神经症状及缺血范围。方法:两点电凝大鼠基底动脉制作脑干缺血动物模型,应用亚甲兰和TTC(2,3,5-氯化三苯基四氮唑)染色确定缺血范围及程度。结果:两点电凝基底动脉后大鼠出现不同程度神经缺失症状。亚甲兰及TTC染色显示缺血区主要位于桥脑及延髓上部小部分区域。结论:两点电凝基底动脉后大鼠出现的神经功能障碍与临床脑干梗塞患者所出现的症状有相似之处,缺血部位恒定,可用来模拟某些临床病理过程。     

大鼠基底动脉闭塞对脑干血流影响的实验研究

目的：观察大鼠基底动脉闭塞后对脑干血流变化的影响。方法：两点凝闭基底动脉，应用激光多普勒技术测量基底动脉闭塞前及闭塞后30、60、120分钟血流值。结果：基底动脉闭塞后脑干局部血流较闭塞前显著降低。结论：两点闭塞基底动脉效果可靠，激光多普勒可用来观察局部血流动力学变化。     

实验性脑干缺血动物模型的建立

实验性脑干缺血动物模型的建立赵士福，王东武，张基谟，郑健椎基底动脉系统存在丰富供血与侧支循环，难以造成缺血可靠、方法简便、与人发病相似的动物模型．以前研究中，曾有关犬、猫、兔基底动脉（ＢＡ）不同水平阻塞报导［１］．但并未产生神经功能障碍和梗塞。我们于...     

椎基底动脉系缺血时植物神经作用的实验研究

目的 通过不同方法建立椎基镀动脉系缺血动物模型，对缺血病灶区超微结构进行研究，比较与血管伴行的交感神经损伤与否、病灶内的病理形成的差异，探讨交感神经在缺血时的作用机理。方法 通过电凝和直接栓塞兔小脑后下动脉，建立不同的椎基底动脉系缺血的模型，对模型进行动态的脑干诱发电位监测，并以光镜、透射电镜检查病灶内的病理变化，结果 病理检查显示电凝损害了闭塞部位的植物神经后，沿血管走行的对血管起支配作用的植物神经部分发生溃变，梗塞灶内充血性、缺血性梗塞同时存在，而栓塞组梗塞灶内毛细血管旁的交感神经纤维形态完整，梗塞均表现为缺血性，动态的脑干听觉诱发电位检查发现，由于支配血管的交感神经损害，发生了脑干的继发性损害，缺血性损害范围增大，预后恶化，结论 交感神经对脑血管的支配作用在缺血性中风的病理过程中起着重要的作用。它维持了正常情况下脑血管的张力，在 缺血、缺氧时能有效地增加脑血流，限制局灶性梗塞范围的扩大，对邻近的脑组织起着保护性作用。     

海风藤对犬脑干缺血后细胞内钙含量和超微病理改变影响的研究

本研究选用犬基底动脉全段结扎脑干缺血模型，观察了海风藤对犬脑干缺血后脑组织细胞内钙含量和超微病理改变的影响，我们发现海风藤０．３ｇ／ｋｇ可明显降低犬脑干局灶性缺血后细胞内钙含量，改善缺血后神经元超微结构的损害，提示海风藤对脑干缺血具有保护作用。     

家兔椎基底动脉供血不足动物模型的BAEP变化

目的 为了探讨家兔椎基底动脉缺血后的脑干听觉诱发电位(brainstem auditory evoked potentials，BAEP)变化及其在临床工作中的意义。方法 通过结扎家兔单侧椎动脉从而造成脑干缺血，并连续记录结扎后一小时内的BAEP的变化过程。结果 I、Ⅲ、V潜伏期逐渐延长，以V波延长最明显，I～Ⅲ、Ⅲ～V、I～V峰间期均明显延长，I波、V波波幅改变无统计意义。结论 本实验表明在椎基底动脉供血不全时BAEP有显著异常，可作为椎基底动脉梗死溶栓治疗后脑干功能变化的观察指标。     

BAEP与MRA在椎基底动系统TIA中的应用研究

目的:探讨脑干听觉诱发电位(BAEP)及磁共振血管成像(MRA)检查对椎基底动脉系统TIA的早期诊断价值。方法:对60例椎基底动脉系统TIA患者进行BAEP和MRA检查。BAEP异常患者治疗1周后复查,分析其前后变化。同时选取36例健康人行BAEP检查作对照。结果:治疗前患者组BAEP异常44例(73.3%),MRA异常35例(58.3%);治疗后患者组BAEP异常14例(23.3%)。对照组两项检查均正常。结论:BAEP、MRA对椎基底动脉系统TIA早期诊断具有重要价值,二者联合检测有助于缺血定位。     

海风藤对犬脑干缺血后细胞内钙含量和超微病理改变影响的…

本研究选用犬基底动脉全段结扎脑缺血模型，观察了海风藤对犬脑干缺血后脑组织细胞内钙含量和超微病理改变的影响，我们发现海风藤０．３ｇ／ｋｇ，可明显降低犬脑干避灶性的因后细胞内钙含量，改善缺血后神经超微结构的损害，提示海风藤对脑干缺血具有保护作用。     

脑干梗死患者超早期动脉接触溶栓治疗的护理体会

椎-基底动脉系统，又称后循环，由椎动脉、基底动脉、大脑后动脉及其各级分支组成，主要分支供应脑干、小脑、枕叶、颞叶后部和丘脑等。后循环脑血流受损会引起脑干缺血，如果不及时恢复供血可导致脑干梗死。由于后循环解剖学和生理学的复杂性，后循环缺血梗死病情危重且难以治疗，患者常出现昏迷、四肢瘫痪以及急性呼吸循环衰竭症状，预后极差。     

后循环缺血与眩晕

后循环又称椎基底动脉系统，由椎动脉、基底动脉和大脑后动脉（posterior cerebral artery，PCA）组成，主要向脑干、小脑、丘脑、枕叶、部分颞叶等结构供血。后循环缺血（posterior circulation ischemia,PCI）是常见的缺血性脑血管病。与前循环缺血一样，PCI也可按缺血程度和持续时间的不同分为短暂性脑缺血发作（transient ischemic attack,TIA）和脑梗死。其同义词包括椎基底动脉系统缺血、后循环TIA和脑梗死、椎基底动脉疾病、椎基底动脉血栓栓塞性疾病。     

椎-基底动脉形态、血流量与脑干梗死的关系

目的研究椎-基底动脉形态、血流量与脑干梗死的关系。方法本研究分脑干梗死组与非脑干梗死组,用彩色多普勒超声分别测量两组患者椎动脉的血流量及管径,用颅脑MRA分别判定两组患者基底动脉弯曲度,通过统计分析,判定两组患者椎动脉血流量及管径、基底动脉弯曲度是否存在统计学差异。结果脑干梗死组双侧椎动脉血流量之和低于正常及一侧椎动脉管径低于正常时,与非脑干梗死组相比存在统计学差异。脑干梗死组基底动脉弯曲度分级与非脑干梗死组基底动脉弯曲度分级相比无统计学差别。结论脑干梗死与椎动脉形态、血流量相关,与基底动脉弯曲程度不相关。     

Ischemia in the territory of a hypoplastic vertebrobasilar system

BACKGROUND: Congenital variations in the configuration and size of the cerebral vessels may predispose to ischemic stroke. OBJECTIVES/METHODS: To illustrate that a hypoplastic basilar artery may lead to posterior circulation ischemia in adults, eight cases are reported from two university medical centers. RESULTS: Five men and three women with a mean age of 49.8 years are reported. Four of the patients had other conventional stroke risk factors. Two patients had brainstem strokes, and six had TIA. All patients had hypoplastic basilar arteries. Seven patients had at least one hypoplastic vertebral artery (bilateral in five cases), and six patients had both posterior cerebral arteries originating from the internal carotid arteries. CONCLUSIONS: A hypoplastic basilar artery is frequently accompanied by vertebral artery hypoplasia, and this can predispose adults to posterior circulation ischemia. This entity can be suspected on the basis of MR angiogram, but conventional angiography will provide definitive diagnosis. Optimal medical and surgical treatment of this condition is unresolved.     

Diffuse cerebral ischemia in the cat: III. Neuropathological sequelae of severe ischemia.

The neuropathological consequences of sever diffuse cerebral ischemia were investigated in an animal model in which postischemic alterations of regional brain blood flow and energy metabolism had been previously characterized. Pentobarbital-anesthetized cats received either 15 or 30 minutes of ischemia produced by basilar artery and bilateral carotid artery occlusions plus mild hypotension; this was followed by 60 to 90 minutes of normotensive recirculation. The brains were perfusion-fixed for light microscopy. Both insult durations resulted in unequivocal ischemic cell change affecting neurons of the cerebral neocortex, striatum, thalamus, and hippocampus and portions of the rostral brainstem. Animals with 30 minutes of prior ischemia differed from those with 15 minutes of ischemia in showing a more apparent regional accentuation of ischemic change in the parasagittal cortical gyri--the sites of previously documented focal postischemic heterogeneities of blood flow and metabolism. In other respects, however, the overall distribution and spectrum of severity of the ischemic alterations were similar for the two insult durations. These data support the view that significant permanent neuronal injury may result from a period of cerebral ischemia as brief as 15 minutes.     

Hypoglycemia presenting as basilar artery thrombosis.

BACKGROUND AND PURPOSE: Following our treatment of a patient with hypoglycemia-induced brain stem symptoms, we examined the possible mechanisms for hypoglycemia presenting as basilar artery disease. CASE DESCRIPTION: We describe a patient who had progressive brain stem symptoms due to a diet-induced hypoglycemia initially diagnosed as basilar artery thrombosis. Symptoms ceased immediately after intravenous glucose. CONCLUSIONS: Before invasive diagnostic and thrombolytic strategies are considered, hypoglycemia as a rare but important cause of acute brain stem dysfunction must be considered in patients suspected to suffer from basilar artery thrombosis.     

Early diagnosis of basilar artery occlusion using magnetic resonance imaging

Three patients with a clinical diagnosis of pontine infarction probably due to basilar artery occlusion were studied with magnetic resonance imaging within 24 hours after onset or latest progression of symptoms. The earliest changes on magnetic resonance images were an absence of signal void in the basilar artery suggestive of severe reduction of blood flow or occlusion (flow-void phenomena). The presumed basilar artery thrombosis was best demonstrated as a linear structure isointense or hyperintense with the brainstem in the pontine cistern on T1-weighted parasagittal images and as either absence of flow-void phenomena or higher signal intensity at various levels corresponding to the course of the basilar artery on the axial T2-weighted images. Brainstem parenchymal changes characteristic of infarction were not obvious for at least 12 hours after onset or 90 minutes after latest progression of symptoms and were best shown by both axial and coronal T2-weighted images. Recognition of these magnetic resonance imaging findings may allow earlier diagnosis and treatment of acute ischemia in the vertebrobasilar system.     

Basilar artery giant fusiform aneurysms caused by congenital defect of the internal elastic lamina and media

Giant fusiform aneurysms of the basilar artery were found in a 6-year-old boy who subsequently died after rupture of the aneurysm, and in a 64-year-old man who showed signs of ischemia and compression of the brain stem. Autopsy disclosed strikingly similar abnormalities of the wall of the basilar artery, consisting of a defect of the internal elastic lamina and absence of the media. A congenital anomaly may play a role in the pathogenesis of this abnormality, in both young and some elderly patients.     

Basilar artery occlusion in rats

The basilar artery is one of the three major sources of blood supply to the circle of Willis. To investigate the effects of basilar artery occlusion, we surgically exposed and coagulated the basilar artery in 25 rats. Basilar artery occlusion at any single point between the foramen magnum and the circle of Willis in 11 rats did not produce histologically detectable infarcts in the brain at 12-24 hours. Two-point occlusions of the basilar artery in 12 rats produced variable infarcts between the occlusion sites but no ischemic lesions elsewhere. After either single- or double-point occlusions, the proximal basilar artery refilled within 2-3 minutes. When the basilar artery was occluded above and below the origins of the anterior inferior cerebellar arteries, the artery segments between the occlusion points initially collapsed but refilled within 2-3 minutes in two rats. Basilar artery occlusions invariably suppressed cortical somatosensory evoked potentials by greater than 50%. Regardless of whether a brain stem infarct developed, somatosensory evoked potential amplitudes recovered to greater than baseline levels by 4 hours in seven of 17 rats and returned to baseline levels by 24 hours in every rat tested. We conclude that the occluded basilar artery receives extensive retrograde collateral blood flow and that somatosensory evoked potentials are exquisitely sensitive to basilar artery occlusion but are insensitive to whether brain stem infarcts develop.     

Long term survival after basilar artery occlusion. 4 cases

Four cases of basilar artery occlusion with a follow-up from 7 to 12 years are reported. The first patient, a 60 year old woman, had a proximal occlusion which was revealed by an acute brain stem ischemia. The second case was a 63 year old man with an aortic aneurysm who had a single episode of vertebro-basilar insufficiency. Cerebral angiography demonstrated a lower basilar artery occlusion. The third patient, a 60 year-old woman, had been operated from right carotid artery and left vertebral artery stenosis; 8 years later, without clinical manifestations, a left carotid artery stenosis and an occlusion of the lower part of the basilar artery were discovered. The evolution was eventless after a left carotid endarterectomy. The last case was a 60 year old man who had a lower basilar artery occlusion associated with a left internal carotid occlusion. There was a full recovery after a hemiplegic stroke. From our personal cases and the review of the literature, long term survival after basilar artery occlusion may occur in occlusions restricted to the lower or middle part of the basilar artery and with a good collateral supply from carotid and cerebellar arteries.