西比灵和血磁疗法治疗椎—基底动脉供血不足的临床探讨

目的：探讨椎－基底动脉供血不足（VBI）患者在服用西比灵等基因上，应用血磁疗法治疗后脑血流动力学和血液流变学的变化。方法：60例VIB患者分成治疗组和常规组，在治疗前及治疗2周后分别行经颅多普勒（TCD）和血流变学检查。结果：在常规治疗（西比灵）基础上合用血磁疗法能改善全血粘度，能使椎－基底动脉系统区血流速度增加，以使其供血区的脑血流量增加。结论：血磁疗与西比灵等综合治疗能改善VBI患者脑循环，疗效显著，安全可靠。     

椎－基底动脉供血不足的SPECT与临床

本文对８０例椎—基底动脉供血不足（ＶＢＩ）患者及６０例健康对照组进行￣（９９ｍ）Ｔｃ—ＥＣＤ—ＳＰＥＣＴ检查，ＳＰＥＣＴ诊断ＶＢＩ的灵敏性为７３，８％，特异性为７８．３％，总符合率为７５．７％。５９例ＳＰＥＣＴ阳性者，出现相应临床症状者４３例（７２．９％）。ＶＢＩ组缺血灶的缺血程度较对照组明显（Ｐ＜０．０１）。８０例ＶＢＩ患者均在距ＶＢＩ最后一次发作１６ｄ内进行ＳＰＥＣＴ检查，３ｄ以内与４ｄ后检查的两组阳性率相差不明显（Ｐ＞０．０５）。     

脑血管性痴呆局部脑血流的定量分析

目的探讨血管性痴呆的脑循环变化。方法采用单光子发射计算机断层显像（ＳＰＥＣＴ），９９ｍ－ＥＣＤ标记，定量测定血管性痴呆（ＶＤ）、多发性脑梗塞（ＭＩ）及正常老年人各１０例的局部脑血流量。结果ＶＤ组各脑叶及基底节区平均脑血流量均显著低于对照组（Ｐ＜０．０１）；ＶＤ组比ＭＩ组额颞叶皮质血流量明显减少（Ｐ＜０．０１，Ｐ＜０．０５）；ＶＤ额叶皮质脑血流量改变与神经心理测试ＭＭＳＥ呈正相关（ｒ＝０．６９２，Ｐ＜０．０５）。结论ＶＤ存在全脑广泛的脑血流灌注降低。额叶皮质血流灌注降低与痴呆的发生及痴呆的严重程度密切相关。ＳＰＥＣＴ局部脑血流定量测定对于ＶＤ的预测及早期发现有重要意义     

椎基底动脉供血不足、腔隙性脑梗死的CDS改变

目的：探讨椎基底动脉供血不足（ＶＢＩ）、腔隙性脑梗死（腔梗）的临床及ＣＤＳ改变的异同。方法：对患者进行眼底、颈椎Ｘ线片、脑血管彩色多谱勒超声（ＣＤＳ）扫描。结果：ＶＢＩ组、腔梗组,眼底动脉硬化Ⅰ度、Ⅱ度之间有显著性差异,有无颈椎骨质增生之间也有显著性差异。ＣＤＳ检查两组均有明显的脑动脉硬化,ＶＢＩ组椎动脉（ＶＡ）、基底动脉（ＢＡ）血流速度减慢,腔梗组大脑前动脉（ＡＣＡ）、大脑中动脉（ＭＣＡ）血流速度异常增快。结论：颈椎病与ＶＢＩ密切相关;脑动脉硬化确是缺血性脑血管的病理基础;ＣＤＳ检查有助于ＶＢＩ和腔梗的诊断。     

椎基底动脉供血不足性眩晕患者ENG,BAEP与rCBF的对照研究

目的 探讨眼震电图（ＥＮＧ）,脑干听觉诱发电位（ＢＡＥＰ）,局部脑血流（ｒＣＢＦ）地椎基底动脉供血不足（ＶＢＩ）性眩晕的诊断价值,方法 对６０例ＶＢＩ眩晕患者进行ＥＮＧ,ＢＡＥＰ与ｒＣＢＦ检测,结果 本病ＥＮＧ异常率为９８．４％ＢＡＥＰ异常率５８．３％,ｒＣＢＦ异常率国６１％,结论 三项检查均为较理想的非创伤性检查,对ＶＢＩ眩晕的诊断三者相互补充,可提高早期确诊率,并有助于定位诊断。     

椎—基底动脉供血不足的SPECT与临床

本文对８０例椎－基底动脉供血不足（ＶＢＩ）患者及６０例健康对照组进行＾９９ｍＴｃ－ＥＣＤ－ＳＰＥＣＴ检查，ＳＰＥＣＴ诊断ＶＢＩ的灵敏性为７３．８％，特异性为７８．３％，总符合率为７５．７％，５９例ＳＰＥＣＴ阳性者，出现相应临床症状者４３例（７２．９％），ＶＢＩ组缺血灶的缺血程度较对照明显（Ｐ〈０．０１）。８０例ＶＢＩ患者均在距ＶＢＩ最后一次发作１６ｄ内进行ＳＰＥＣＴ检查，３ｄ以内与４ｄ后检查的两组     

BAEP转颈试验与椎—基底动脉供血不足预后的相关性研究

本文对３９例Ｖ－ＢＡＩ脑干听觉诱发电位（ＢＡＥＰ）异常者（Ａ组）与３０例ＢＡＥＰ转颈试验异常者（Ｂ组）作了西比灵治疗的前瞻性随访分析。结果表明：ＢＡＥＰ转颈试验可使Ｖ－ＢＡＩ的ＢＡＥＰ异常率由转颈前的４４．８３％提高到７９．３１％（Ｐ＜０．０１）；Ａ组Ⅲ、Ⅴ（ＰＬ）及Ⅰ～Ⅲ、Ⅰ～Ⅴ（ＩＰＬ）延长（Ｐ＜０．０１），Ｂ组Ⅲ（ＰＬ）和Ⅰ～Ⅲ（ＩＰＬ）延长为著（Ｐ＜０．０５）；西比灵治疗后Ⅲ、Ⅴ（ＰＬ）、Ⅰ～Ⅲ、Ⅰ～Ⅴ（ＩＰＬ）有明显恢复（Ｐ＜０．０５），且与病情改善程度密切相关。     

西比灵和血磁疗法治疗椎-基底动脉供血不足的临床探讨

目的 :探讨椎 -基底动脉供血不足 (VBI)患者在服用西比灵等基础上 ,应用血磁疗法治疗后脑血流动力学和血液流变学的变化。方法 :60例VBI患者分成治疗组和常规组 ,在治疗前及治疗 2周后分别行经颅多普勒 (TCD)和血流变学检查。结果 :在常规治疗 (西比灵 )基础上合用血磁疗法能改善全血粘度 ,能使椎 -基底动脉系统区血流速度增加 ,以使其供血区的脑血流量增加。结论 :血磁疗与西比灵等综合治疗能改善VBI患者脑循环 ,疗效显著 ,安全可靠     

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     

椎─基底动脉供血不足的BAEP和TCD变化

本文对３７例椎－基底动脉供血不足ＣＴ为阴性的病人，进行了ＢＡＥＰ和ＴＣＤ检查，异常率为８３．８％和７０．３％，（Ｐ＞０．０５），主要异常表现分别为：Ⅲ—Ⅴ＞Ⅰ─Ⅲ间期，Ⅰ／Ⅴ波幅比＞１和椎基底动脉血流异常，证明ＢＡＥＰ、ＴＣＤ对椎─基底动脉供血不足的诊断很有价值。     

Pathogenesis of transient ischemic attacks within the vertebrobasilar arterial system.

Regional cerebral blood flow (rCBF) was measured by xenon 133 inhalation in 36 patients with vertebrobasilar arterial insufficiency (VBI), three patients with brain stem infarction, and 15 age-matched normal controls before and after inducing postural hypotension. Probes mounted over the suboccipital area by means of a helmet were used to measure rCBF over the brain stem and cerebellar regions. When lying flat, rCBF values measured over both cerebral hemispheres and the brain stem-cerebellar regions in patients with VBI were not significantly different from normal controls. Unlike carotid transient ischemic attacks, regional flow reduction rarely persisted for three weeks after transient ischemic symptoms in patients with VBI. When postural hypotension was induced, rCBF became significantly reduced in patients with VBI whether or not they were treated with papaverine. Dysautoregulation was restricted to vertebral, basilar, and posterior cerebral arterial distribution in patients with VBI of 1 to 12 months' duration, but was more widespread and involved both cerebral hemispheres in long-standing VBI. Hemodynamic factors and dysautoregulation appear to play a part in the pathogenesis of symptoms of VBI.     

A study to compare independent groups of patients with episodic migraine who were treated preventively with flunarizine or nadolol

INTRODUCTION. Flunarizine, with level of evidence A, and nadolol, with evidence level C, would be indicated as preventive treatment of migraine. Yet, no previous studies have been conducted to compare the effectiveness of the two drugs. AIM. To compare the effectiveness parameters in independent groups of patients treated preventively with one of the pharmaceuticals from the study, the same protocol being applied in both cases. PATIENTS AND METHODS. The subjects selected for the study were patients with episodic migraine (according to 2004 International Headache Society criteria) who had undergone preventive treatment for the first time, with flunarizine (5 mg/day) or nadolol (20-40 mg/day). The main effectiveness variables (reduction in the number of seizures at four months of treatment and responder rates) were analysed. RESULTS. The study included 227 patients who intended to receive treatment: 155 with flunarizine (80.5% females; mean age: 38.3 ± 12.1 years) and 72 with nadolol (63.8% females; mean age: 37.1 ± 12.0 years). The mean number of seizures prior to treatment was 6.09 ± 2.6 in the flunarizine group and 5.1 ± 1.7 in the nadolol group (p = 0.0079); at four months of treatment it was 2.61 ± 2.4 in the flunarizine group and 2.77 ± 2.4 in the nadolol group (p = NS). Percentage of reduction of migraines: 55.2% with flunarizine and 50.4% with nadolol (p = NS). The responder rate was 69% with flunarizine and 67% with nadolol (p = NS). The excellent response rate (reduction in the number of seizures by 75% or more) was 52.2% with flunarizine and 36.1% with nadolol (p = 0.0077). Percentage of adverse side effects: 48.3% with flunarizine and 25% with nadolol (p = 0.0009). The satisfaction rate was similar in both groups, 68%. CONCLUSIONS. Both flunarizine and nadolol proved to be effective in the preventive treatment of episodic migraine. Flunarizine is used more often in our milieu and was less well tolerated.     

Effect of flunarizine on electroencephalogram recovery and brain temperature in gerbils after brain ischemia.

BACKGROUND AND PURPOSE: This study was designed to determine whether flunarizine enhances the rate of brain recovery as measured by electroencephalography after cerebral ischemia and whether these effects are attributable to changes in brain temperature. METHODS: Male gerbils (n = 81) were treated with either 10 mg/kg flunarizine or its vehicle, beta-cyclodextrin, intraperitoneally, 60 minutes before bilateral carotid occlusion of either 4 or 6 minutes' duration. The electroencephalogram was continuously recorded in the preischemic, ischemic, and postischemic stages of the experiment and rated for the time necessary for the return of 4-6, 7-10, and 11-15 Hz activity. In a second set of experiments, intracerebral temperature was monitored for 60 minutes before ischemia, during 10 minutes of carotid occlusion, and for 60 minutes after ischemia. RESULTS: Flunarizine pretreatment resulted in significantly more rapid return of electroencephalographic activity in each of the three frequency categories monitored when compared with those animals pretreated with vehicle alone (p less than 0.001). Flunarizine had no effect on brain temperature before, during, or up to 60 minutes after termination of ischemia. CONCLUSIONS: Flunarizine, which has been of efficacy in reducing neuronal death, mortality, and functional impairment when administered after ischemic insults, may have prophylactic value in accelerating brain recovery from ischemia, but does not have this effect as a result of altered brain temperature.     

Flunarizine in stroke treatment (FIST): a double-blind, placebo-controlled trial in Scandinavia and the Netherlands

Introduction - An international, multicenter trial was conducted in 331 patients to determine the effect of a large dose of flunarizine (a calcium entry blocker) in the treatment of acute ischemic stroke in the territory of the Middle cerebral artery. Methods - The administration of the trial medication should start within 24 h after the initial symptoms of stroke. According to a random schedule, the patients were assigned to a 4-weeks double-blind treatment with either flunarizine ( n = 166) or placebo ( n = 165): one week intravenous administration (50 mg daily), followed by 3 weeks oral treatment (week 2, 21 mg daily; week 3–4, 7 mg daily). All patients had to be investigated by computerized tomography (CT) within 7 days after stroke onset; 36 patients were secundarily excluded because the CT showed another pathology. During the treatment period, other "stroke therapies" were not allowed. Patients were followed up for 24 weeks. Results - After the 24 weeks trial period, the percentage of patients who were dead or pendent (modified Rankin score 3–5) was similar in both treatment groups (flunarizine 67%, placebo 65%). During the trial, the scores for handicap severity (modified Rankin scale), neurological status (Orgogozo) and activities of daily living (modified Barthel index) strongly improved in both treatment groups, but no differences were found between the treatment groups. In this trial, the administration of trial treatment started relatively late after stroke onset (flunarizine group: mean time interval 13.5 h; placebo 12.3 h). A subgroup of patients received trial medication within 6 h after stroke onset (flunarizine n = 31; placebo n = 29). Also in this subgroup, no differences were found between the flunarizine and placebo group. Conclusion - Flunarizine did not improve neurologic and functional outcome in patients with acute ischemic stroke.     

氟桂嗪治疗Tourette综合征的临床疗效观察

目的探讨氟桂嗪是否有治疗Tourette综合征(多发性抽动秽语综合征)的作用.方法163例患儿分为3组:泰必利组和泰必利加氟桂嗪治疗组以及单用氟桂嗪治疗组,用药和观察时间至少为6个月,用"不自主运动量表(AIMS)"评分法来评定治疗后抽动症状的改善程度.结果66例泰必利组中有24例抽动症状消失,痊愈率为36.36%;66例泰必利加氟桂嗪治疗组中有36例抽动症状消失,痊愈率为54.55%,两者痊愈率相比差异有显著性意义(P＜0.05).31例单用氟桂嗪治疗组中"轻度"患儿的痊愈率达100%,即病情偏轻者效果较佳,病情严重者效果较差.结论氟桂嗪对Tourette综合征确有治疗作用,其药理机制可能与氟桂嗪的抗多巴胺能活性作用有关.     

氟桂利嗪和倍他司汀治疗良性位置性眩晕及其伴随症状的临床疗效比较

目的观察氟桂利嗪与倍他司汀治疗良性位置性眩晕(BPPV)及其伴随症状的临床疗效。方法将182例BPPV的患者随机分为氟桂利嗪治疗组和倍他司汀治疗组。氟桂利嗪治疗组给予氟桂利嗪进行常规治疗,倍他司汀治疗组施以倍他司汀治疗。两组均治疗8周为1个疗程并进行随访。比较两种药物治疗眩晕及伴随症状的疗效。结果治疗8周后,氟桂利嗪治疗眩晕的疗效高于倍他司汀(χ2=4.4138,P<0.05),在治疗头痛、自主神经伴随症状方面,氟桂利嗪的疗效也均高于倍他司汀(均P<0.01),而在治疗耳鸣方面,两组疗效比较无统计学差异(χ2=3.3442,P>0.05)。结论氟桂利嗪治疗BPPV及其伴随症状具有较好的疗效。     

Flunarizine reduces cerebral infarct size after photochemically induced thrombosis in spontaneously hypertensive rats

The cerebroprotective effect of flunarizine was studied in a minimally invasive model of photochemically induced cerebral infarction in spontaneously hypertensive rats. Intravenous administration of the photosensitizing dye rose bengal and intense focal illumination of the brain produced a deep cortical infarction that resulted from singlet oxygen-induced peroxidative injury to the endothelial membrane, subsequent platelet adhesion, and eventual thrombus formation. The infarct size was calculated from area measurements on consecutive histologic sections prepared from the brain cortex 4 hours after the onset of the insult. Oral treatment with 40 mg/kg flunarizine 3 hours before photoexcitation resulted in a significant reduction of the median infarct size from 11.75 mm3 in the untreated group to 6.40 mm3 in the treated group (n = 13, p less than 0.001). At this dose, flunarizine had no effect on systemic blood pressure. In a separate experiment the area of thrombotic obstruction was quantified 30 minutes after the onset of light exposure. Flunarizine did not significantly reduce early thrombus formation (2.28 mm3 in the untreated and 1.78 mm3 in the treated group) (n = 12, p = 0.2). The infarcted area at 4 hours was considerably larger than the initial thrombotic area. Protection with flunarizine against development of cortical infarction has been unequivocally shown. Although some effect may already be present at the early stage of lesion formation, the major protective action admittedly occurred in the later postinsult period when the lesion was expanding.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of a new vasodilator (flunarizine) on the cerebral circulation.

In order to clarify the effects of flunarizine, a newly-synthesized derivative of piperazine on cerebral circulation and metabolism, cerebrocortical oxygen tension, carbon dioxide tension and cerebrocortical blood flow were continuously recorded, along with a simultaneous monitoring of arterial blood pressure in 11 cats. Maximal changes in cerebrocortical oxygen tension induced by intravenous administration of flunarizine (0.6-1.0 mg/kg) were compared with those of papaverine hydrochloride (1 mg/kg). Flunarizine caused increases in cerebrocortical oxygen tension as well as cerebrocortical blood flow and a decrease in cerebrocortical carbon dioxide tension despite a fall in blood pressure, indicating an increase of cerebral blood flow presumably due to cerebral vasodilatation. Since the increase of cerebrocortical oxygen tension induced by flunarizine was comparable to that induced by papaverine, it was concluded that flunarizine appears to be a potent vasodilator of cerebral vessels.     

Comparison of the efficacy and safety of flunarizine to propranolol in the prophylaxis of migraine.

This study was designed to compare flunarizine, a cerebro-specific calcium channel antagonist, and propranolol in the prophylaxis of migraine with or without aura. Following a 1 month single-blind placebo baseline period, 94 patients were equitably randomised under double-blind conditions to take flunarizine 10 mg daily or propranolol 80 mg twice daily for 4 months. Both treatments led to a significant reduction in the frequency of migraines and use of rescue analgesics with a significantly greater decrease in number of attacks for flunarizine after 1 and 4 months. Neither treatment affected the severity nor duration of migraines. Overall, 67% of flunarizine patients and 51% of propranolol patients responded positively. Propranolol significantly reduced blood pressure and heart rate; flunarizine had no effect on cardiovascular function. Weight gain was noted with both treatments. Flunarizine is at least as effective as propranolol in the prophylactic treatment of migraine and may have a better safety profile.     

Nitrogen monoxide vector of ultrasonic atomizing inhalation improves vertebro-basilar artery insufficiency Hemodynamic changes are detected by transcranial Doppler test

BACKGROUND: Latest researches at home and abroad indicate that glycerol trinitrate plays its function because it can metabolize into nitrogen monoxide (NO) in vivo. OBJECTIVE: To study the therapeutic effects of NO vector of ultrasonic atomizing inhalation on vertebro-basilar artery insufficiency (VBI) through transcranial Doppler (TCD) detection and serum NO content and indirect effect of TCD on cerebral blood flow changes. DESIGN: Randomized grouping and controlled clinical study. SETTING: Department of Neurology, the Fourth People's Hospital of Jinan. PARTICIPANTS: A total of 130 patients who were diagnosed as VBI were selected from Department of Neurology, the Fourth People's Hospital of Jinan from December 2001 to December 2005. The involved inpatients were checked by CT and MRI, and met the VBI diagnostic standard enacted by the Fourth National Academic Meeting of Cerebrovascular Disease in 1995. All patients and their relatives provided the confirmed consent. They were randomly divided into low-dose treatment group (n =60), high-lose treatment group (n =30) and control group (n =40). METHODS: Patients in the low-dose and high-dose treatment groups were given ultrasonic atomizing inhalation of 3 mg and 5 mg glycerol trinitrate, respectively, for 20 minutes, once a day. In addition, ligustrazine and energy mixture were used once a day for three days in a course. Cases in the control group were only given ligustrazine and energy mixture. All selected cases accepted TCD, blood NO content was checked at the time of beginning, after the first time and after a period of treatment.　According to the TCD test, VBI patients were divided into two groups (high-low flow velocity). The vertebral artery (VA) and basal artery (BA) of left or right sides were detected by 2 Hz detector via occipital window. MAIN OUTCOME MEASURES: ① Blood flow velocity of systolic phase, blood flow velocity of diastole phase and vascular resistance in left and right VA and BA detected by using TCD before treatment, after treatment for one course; ② content of serum NO indirectly measured by using nitric acid disoxidation technique. RESULTS: All 130 VBI patients were involved in the final analysis. ① Changes of hemodynamic indexes: Systolic phase of VA and diastole phase of BA were higher in low-dose treatment group than that in the control group after first treatment, and there was significant difference (P < 0.05); meanwhile, systolic phase and diastole phase of VA and systolic phase of BA were also higher in treatment group than that in the control group after one course (P < 0.05). However, both systolic phase and diastole phase of VA and BA were lower in high-dose treatment group than that in the control group after first treatment and one course, and there was significant difference (P < 0.05). ② Content of serum NO: After first treatment, there was no significant difference between low-dose treatment group and high-dose treatment group (P > 0.05); but both groups were higher than control group, and there was significant difference (P < 0.05, 0.01). CONCLUSION: NO vector of ultrasonic atomizing inhalation can improve VBI so as to improve cerebral blood-supply state.