关于椎基底动脉缺血与眩晕的讨论

据国外报道，由耳石漂浮导致的眩晕综合征很常见，占所有占眩晕病因的40%左右。但国内常常忽视这种综合征，而且在李焰生教授的讲座中也未提及，请问这种综合征是否包括在良性阵发性变位性眩晕中？另外，Dix-Hallpike检查对良性阵发性位置性眩晕的特异性和敏感性如何？良性阵发性位置性眩晕有什么立竿见影的治疗方法吗？     

椎基底动脉缺血的早期诊断─ENG、BAEP与SPECT的对照研究

对５０例临床诊断为椎基底动脉缺血的病人行ＥＮＧ（４４例）、ＢＡＥＰ（４９例）和ＳＰＥＣＴ（５０例）检查，异常率分别为 ８６． ４％、７３． ５％和 ７８％，差异无显著性。与 ＳＰＥＣＴ对照研究更进一步证实 ＥＮＧ和 ＢＡＥＰ对本病早期诊断有肯定价值，ＥＮＧ更敏感，ＳＰＥＣＴ准确直观。三项检查互相补充可提高诊断率。     

椎基底动脉供血不足BAEP检查结果分析

目的：探讨脑干听觉诱发电位（ＢＡＥＰ０在椎基底动脉供血不足（ＶＢＩ）诊断中的意义。方法：对１０９例ＶＢＩ患者做常规ＢＡＥＰ检查，并对其结果按年龄、病程进行分析。结果：１０９便中异常８１例，异常表现为各主波的波间期延长。其中病程〈２年者异常率为４０．６％，２－５年者为８７．８％，〉５年者为８８．９％。结论：ＶＢＩ２的ＢＡＥＰ异常率有随病程延长而增高的倾向。ＢＡＥＰ对ＶＢＩ缓解期间病例诊断有一定参考意     

纳络酮对动脉粥样硬化性椎-基底动脉缺血的疗效观察及机理探讨

目的观察纳络酮治疗动脉粥样硬化性椎－基底动脉缺血（ＡＳＶＢＩ）的临床疗效,探讨其机理。方法将４０例ＡＳＶＢＩ患者随机分成常规治疗组（低分子右旋糖酐＋丹参）和纳络酮治疗组,检测治疗前后脑干听觉诱发电位（ＢＡＥＰ）、血清丙二醛（ＭＤＡ）含量及超氧化物歧化酶（ＳＯＤ）活性变化情况;同时选取３０名健康人作为正常对照组,并检测上述指标。结果纳络酮治疗组与常规治疗组相比疗效更佳,临床症状、ＭＤＡ、ＳＯＤ及ＢＡＥＰ均有显著差异（Ｐ＜０．０１）。结论纳络酮有清除自由基的作用,能有效改善ＡＳＶＢＩ患者脑部缺血、缺氧症状。     

椎基底动脉短暂缺血发作、椎基底动脉供血不足与慢性脑供血不足

18 8 9年Ｐｅａｂｏｄｙ首先对一组高血压或 /及动脉粥样硬化的患者突然出现一过性半身不遂、失语或失明等神经功能障碍发作 ,历时 2 4小时至数日自愈者称为“脑血管痉挛”。1 951年Ｄｅｎｎｙ Ｂｒｏｗｎ提出 ,由于中毒性肺炎或心源性休克等各种原因引起全身血压下降 ;或由于脑血管狭窄致脑内血流量的不足 ,出现的一过性神经功能障碍 ,命名为脑供血不足(ＣＶＩ)。 1 955年Ｍｉｌｌｉｋａｎ发现 ,临床表现为反复可逆性短暂发作的神经功能缺失的病例 ,大多数可能是由于大动脉粥样硬化斑块溃疡表面的微栓子脱落引起的微栓塞所致。其后 ,由于Ｆ…     

轻微椎—基底动脉缺血性眩晕的rCBFM与BAEP对比观察

对３０例轻微椎－基底动脉（ＶＢＡ）缺血性眩晕患者进行了ｒＣＢＦＭ与ＢＡＥＰ检查的对比观察，认为前者在显示ＶＢＡ系统缺血方面可以直接明确诊断，阳性率高，可直观地显示缺血的部位和范围，且可了解动脉系统代偿供血情况，但不能完全取代ＢＡＥＰ。     

椎基底动脉供血不足患者的脑干听觉诱发电位与经颅多普勒检查

目的：探讨椎基底动脉供血不足（ＶＢＩ）患者的脑干听觉诱发电位（ＢＡＥＰ）与经颅多普勒（ＴＣＤ）的相关性。方法：地５８例临床诊断ＶＢＩ眩晕的患者及３０例非ＶＢＩ眩晕的患者进行ＢＡＥＰ和ＴＣＤ检测。结果：ＶＢＩ组ＢＡＥＰ异常率为５９％,ＴＣＤ异常率为６１５,χ＾２检验差异无显著意义;非ＶＢＩ组ＢＡＥＰ异常率８％,ＴＣＤ异常率为４７％,χ＾２检验差异有显著意义。ＶＢＩ组ＢＡＥＰ及ＴＣＤ皆异常者为６４／１     

Emergence of lung-inflation-related sympathetic nerve activity in spinal cord transected neonatal swine

Sympathetic (SYMP) nerve activity in spinal intact neonatal swine is comprised of prominent bursts reflecting modulation by supraspinal structures involved in shaping central respiratory and baroreceptor activity. After spinal cord transection (SCT), we found no evidence of such modulation. SYMP activity was now related to the ventilatory cycle, exhibiting bursts only during lung inflation. Such activity suggests the emergence of latent spinal circuits which may have the capacity to regulate cardiovascular activity.     

The effect of transient cerebral ischemia on the vascular permeability to protein tracers

Summary A study was made on the effect of ischemia on the vascular permeability to proteins in the cat brain. Evans blue and horseradish peroxidase were used as protein tracers. They were intravenously injected and localized by fluorescence and electron microscopy.Acute complete cerebral ischemia produced by arterial ligations for 15 min to 3h did not induce extravasation of the tracers. Electron microscopical observations on the cortical vessels showed that this was due to a maintained barrier function of the vascular endothelium.Incomplete cerebral ischemia of corresponding duration produced by an arteriovenous shunt (between one common carotid artery and one femoral vein) caused exceptionally extravasation around cortical vessels. Some cats with long shunting time showed signs of increased vascular permeability in the thalamus where the tracers had accumulated in neurons.Severe swelling of capillary endothelial and perivascular glial cells and changes of their cytoplasmic organelles were present in animals without signs of increased vascular permeability to proteins. A discrepancy therefore exists between the maintained impermeability of the capillary endothelium to protein tracers and the ultrastructural changes of the endothelial cell cytoplasm following acute ischemia.Presented at the 45th Annual Meeting, American Association of Neuropathologists, New Haven, Conn., June 20, 1969.     

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。     

The effect of intravascular saline perfusion on the sequelae of transient cerebral ischemia

Summary Transient global ischemia was produced in cats by interrupting the arterial blood supply to the brain under direct observation of the pial vessels. The pial circulation could be restored only for a brief period after ischemia but intravascular rinsing of the brain during ischemia with various saline solutions considerably improved the postischemic circulation.The functional status of neuronal activity was assessed by recording the EEG and the pyramidal response (PR) after electrical stimulation of the motor cortex. Perfused and nonperfused cats were compared with regard to the structure and function of the motor cortex in the early postischemic period. The neurophysiological signals recovered after ischemia of much longer duration in the perfused animals than in the nonperfused cats. Severe structural alterations were seen in capillaries, neurons and glial cells when ischemia was long enough to suppress the PR. In the perfused animals these changes were virtually absent even after ischemia up to 30 min duration.The increased tolerance of the brain to ischemia produced by the intravascular rinsing appears to result from at least two different mechanisms. Elimination of metabolic waste products presumably reduces tissue damage during ischemia and the improved postischemic circulation prevents secondary ischemic lesions.

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Zuammenfassung Passagere Globalischämie wurde an Katzen durch Unterbrechung der Blutversorgung des Gehirns unter direkter Beobachtung der Piagefäße erzeugt. Die piale Zirkulation konnte nur kurzfristig nach der Ischämie wiederhergestellt werden, doch wurde die postischämische Zirkulation durch intravasale Perfusion des Gehirns mittels verschiedener Salzlösungen beträchtlich verbessert.Der Funktionszustand der neuronalen Aktivität wurde mittels EEG und Pyramidenreaktion (PR) nach elektrischer Reizung des motorischen Cortex geprüft. Perfundierte und nichtperfundierte Katzen wurden im Hinblick auf die Struktur und Funktion des motorischen Cortex in der frühen postischämischen Periode verglichen. Bei perfundierten Tieren kamen die neurophysiologischen Signale nach Ischämie von wesentlich längerer Dauer wieder, als ber nichtperfundierten Katzen. Schwere strukturelle Veränderungen fanden sich an Capillaren, Neuronen und Gliazellen, wenn die Ischämie lange genug anhielt, um die PR zu unterdrücken. Bei perfundierten Tieren fehlten solche Veränderungen selbst nach Ischämie bis zu 30 min Dauer.Die gesteigerte Toleranz des Gehirns gegenüber Ischämie infolge intravasaler Durchströmung erscheint durch zumindest zwei verschiedene Mechanismen bedingt. Die Eliminierung metabolischer Schlackenstoffe verringert vermutlich die Gewebsschäden während der Ischämie und die verbesserte postischämische Zirkulation verhindert sekundäre ischämische Schäden.

     

The role of vertebral and internal carotid artery disease in the pathogenesis of vertebrobasilar transient ischemic attacks

Summary Color-coded duplex sonography has improved the evaluation of the hemodynamics of the vertebral arteries (VA). A reliable differentiation between a normal vessel, hypoplasia, stenosis and occlusion of VA can now be made. We studied two groups of patients in a prospective study with isolated carotid artery disease (n=48), and with a combination of carotid and vertebral artery disease (n=14), to determine the role of VA in the pathogenesis of transient ischemic attacks (TIAs) in the vertebrobasilar system. Apart from the existing arteriosclerotic changes of the internal carotid arteries, the condition of the VA was of importance for the occurrence of TIAs in the vertebrobasilar territory. We found that 8% of the patients with isolated hemodynamically relevant stenosis or occlusion of one or both internal carotid arteries had a TIA in the vertebrobasilar territory. Patients with combined carotid and vertebral artery disease had an increase of TIAs in the same region in 71%. The high rate of TIAs in this group might be attributed to the combined effect of carotid and vertebral artery disease, as a third group (n=30) with isolated vertebral artery disease showed TIAs in only 13%.     

Degeneration of cardiac sympathetic nerve can occur in multiple system atrophy

Decreased cardiac uptake of meta-iodobenzylguanidine (MIBG) on [¹²³I] MIBG myocardial scintigraphy, a sensitive biological marker for Parkinson’s disease (PD), is related to cardiac sympathetic denervation in patients with PD. A slight decrease in cardiac uptake of MIBG has also been reported in some patients with multiple system atrophy (MSA). However, the pathophysiological mechanism accounting for the slight decrease in MIBG uptake in MSA remains to be elucidated. For confirmation, we examined cardiac tissue and sympathetic ganglia from patients with MSA. We immunohistochemically examined each specimen of 15 patients with MSA together with 10 control subjects using antibodies against tyrosine hydroxylase (TH) and neurofilament (NF). The number of TH-immunoreactive nerve fibers in the epicardium was preserved in 8 of 15 patients with MSA as well as in 10 control subjects. The number of TH-immunoreactive, but not of NF-immunoreactive nerve fibers in the epicardium was mildly or moderately decreased in six patients with MSA, of whom four showed a decrease of TH immunoreactivity in the neuronal somata in the sympathetic ganglia. Moreover, TH- and NF-immunoreactive nerve fibers almost entirely disappeared in the heart of one patient with MSA, in whom Lewy body pathology was present in the sympathetic ganglia. These findings suggest that mild degeneration of the cardiac sympathetic nerve can occur in MSA which is closely related to the pathological change of neurons in the sympathetic ganglia, accounting for the slight decrease in cardiac uptake of MIBG. Moreover, concurrent Lewy body pathology in the sympathetic ganglia might accelerate cardiac sympathetic denervation even in MSA.     

Inhibition of RVLM synaptic activation at peak hyperthermia reduces visceral sympathetic nerve discharge

Hyperthermia is an environmental stressor that produces marked increases in visceral sympathetic nerve discharge (SND) in young rats. The brainstem in rats contains the essential neural circuitry for mediating visceral sympathetic activation; however, specific brainstem sites involved remain virtually unknown. The rostral ventral lateral medulla (RVLM) is a key central nervous system region involved in the maintenance of basal SND and in mediating sympathetic nerve responses evoked from supraspinal sites. In the present study we tested the hypothesis that inhibition of RVLM synaptic activation at peak hyperthermia (internal body temperature, Tc, increased to 41.5 °C) would affect heating-induced visceral sympathetic activation. Experiments were completed in chloralose–urethane anesthetized, baroreceptor-intact and sinoaortic-denervated, 3–6 month-old Sprague–Dawley rats. Bilateral inhibition of RVLM synaptic activation produced by muscimol microinjections (400 and 800 pmol) at 41.5 °C resulted in immediate and significant reductions in peak heating-induced renal and splenic sympathoexcitation. Interruption of RVLM synaptic activation and axonal transmission by lidocaine microinjections (40 nmol) at 41.5 °C produced significant reductions in hyperthermia-induced sympathetic activation to similar levels produced by RVLM muscimol microinjections. The total amount of SND inhibited by RVLM muscimol and lidocaine microinjections was significantly more during hyperthermia (41.5 °C) than normothermia (38 °C). These findings demonstrate that maintenance of sympathetic activation at peak hyperthermia is dependent on the integrity of RVLM neural circuits.     

交感神经纤维减少对胃癌患者术后护理及临床预后的影响

目的探讨胃癌患者中局部组织内交感神经纤维减少对癌症进展、术后护理及临床预后的影响。方法采用回顾性研究,临床获得120例胃癌患者的术中组织样本并进行酪氨酸羟化酶(TH)的免疫组织化学染色,显微镜下对组织内的交感神经纤维的分布进行评估,并与患者的病理学诊断、临床护理及相关预后进行关联分析。结果正常胃壁组织内的动脉完全被交感神经纤维覆盖,而胃癌组织内围绕动脉周围组织的TH免疫活性显著降低;交感神经纤维缺失程度与癌症细胞的侵袭深度(P0.01)、淋巴结转移(P0.01)及微血管密度(P=0.043)呈显著相关性;同时交感神经纤维缺失严重的患者显示出明显较高的临床护理要求和难度,且临床预后更差,多变量分析显示具有独立关联性。结论胃癌患者局部组织动脉周围交感神经纤维的缺失可能与微血管的生成及胃癌侵袭性增强相关,可作为潜在的临床标记物,提示患者的护理要求及相关临床预后。     

椎基底动脉压迫型前庭阵发症的磁共振特点分析

目的探讨椎基底动脉压迫型前庭阵发症的磁共振影像学特征。方法共收集前庭阵发症(vestibular paroxysmia,VP)患者64例,分为非椎基底动脉压迫型组(对照组)32例和椎基底动脉压迫型组(观察组)32例,应用三维时间飞跃法磁共振血管成像技术,判断64例患者的前庭蜗神经周围有无神经血管交互压迫(neurovascular cross-compression,NVCC)及其压迫类型,并对两组间NVCC压迫点至前庭蜗神经出脑干处的最短距离、基底动脉及双侧椎动脉血管直径、双侧椎动脉间血管直径变异度进行统计学分析。结果在观察组NVCC压迫点距前庭蜗神经出脑干处距离为(6.26±2.02)mm明显小于对照组(8.17±1.98)mm(t=-3.872,P=0.000,P0.01);而观察组椎动脉血管直径(3.53±0.42)mm与对照组(3.44±0.31)mm无明显差异(t=0.962,P=0.340,P0.05);两组的基底动脉血管直径观察组(3.74±0.41)mm与对照组(3.65±0.29)mm间亦无统计学意义(t=0.992,P=0.326,P0.05);而观察组的双侧椎动脉血管直径变异度(1.09±0.31)mm明显高于对照组(0.82±0.35)mm(t=3.330,P=0.001,P0.05)。结论椎基底动脉压迫型VP患者NVCC压迫点距前庭蜗神经出脑干处距离较近且双侧椎动脉血管直径变异度较大。     

大鼠面神经缺血后面神经核磷酸化CREB水平的变化

目的探讨大鼠面神经缺血损伤后面神经元内环磷腺苷反应元件结合蛋白（CREB）磷酸化水平的变化及其与氧化应激的关系。方法 55只成年雄性SD大鼠随机分为正常组（5只）、假手术组（25只）和面神经缺血组（25只）,后两组又根据时间分为术后1、3、7、14、21 d 5个亚组,每亚组5只大鼠。显微手术阻断大鼠鼓室段岩动脉建立大鼠面神经缺血损伤模型。采用分光光度法测定面神经核丙二醛（MDA）含量;利用免疫印迹法测定面神经元内锰超氧化物歧化酶（Mn SOD）和磷酸化CREB（p-CREB）表达水平。结果面神经缺血后,面神经核MDA含量先增高,7 d达峰值,随后降低;而面神经元Mn SOD和p-CREB表达水平先降低,7 d达最低值,随后逐渐增高。面神经缺血组每个时间点MDA水平、Mn SOD和p-CREB表达水平均与正常组和假手术组差异显著（P〈0.05）,而假手术组与正常组之间无显著差异（P〉0.05）。结论面神经缺血损伤后造成面神经元氧化应激损伤,导致p-CREB水平先降低后增高,p-CREB水平的增高可降低ROS对面神经元的氧化损伤能力。