天麻素联合盐酸氟桂利嗪治疗偏头痛的疗效观察

目的探讨天麻素联合氟桂利嗪治疗偏头痛的临床疗效。方法将58例偏头痛患者随机分为对照组与研究组,对照组26例患者接受氟桂利嗪治疗,研究组32例患者在氟桂利嗪治疗基础上给予天麻素治疗,对比分析2组患者的临床治疗效果及头痛程度、头痛持续时间、头痛频率。结果研究组总有效率(84.37%)明显高于对照组(65.38%),差异有统计学意义(P0.05),研究组在头痛的发作时间、频次及程度上均小于对照组,差异有统计学意义(P0.05)。结论天麻素联合氟桂利嗪治疗偏头痛临床疗效显著,可明显降低头痛程度,缩短头痛持续时间和头痛频率,效果优于单用氟桂利嗪治疗,值得临床推广应用。     

氟桂利嗪和托吡酯单用及合用预防偏头痛发作的临床研究

目的观察氟桂利嗪、托吡酯及氟桂利嗪合用托吡酯对偏头痛发作的预防作用。方法将101例偏头痛患者随机分为氟桂利嗪合用托吡酯组(34例,A组)、氟桂利嗪组(34例,B组)及托吡酯组(33例,C组),疗程2个月,观察上述3组治疗前后头痛发作程度、头痛发作频率及头痛持续时间的变化。结果A组、B组治疗前后上述3项指标均有改善,评分差值均有统计学意义,P< 0.05;而C组治疗前后仅头痛发作的程度、频率有改善,评分差值有统计学意义,P<0.05;3组间治疗前后比较;上述3项指标F值分别为24.23、12.44、9.86,P均小于0.05;其中A组3方面改善均最为明显;而B组及C组之间没有明显差异。结论氟桂利嗪、氟桂利嗪合用托吡酯对偏头痛发作的程度、频率及持续时间均有较好的预防作用,而托吡酯对偏头痛持续时间没有减少的作用;氟桂利嗪合用托吡酯较单独应用其中的一种有更好的预防偏头痛的效果。     

氟桂利嗪对青霉素致痈效应和海马神经元单位放电的影响

目的：探讨Ca^2＋拮抗剂氟桂利嗪对青霉素致效应和海马神经元单位放电的影响.方法：Wistar大鼠随机分成3组.正常对照组;癫癎模型组：用青霉素钠按6 000 000 U·kg^-1腹腔注射;癫癎预处理组：造模前用盐酸氟桂利嗪 20 mg·kg^-1每隔12 h灌胃,共2次,于第2次给药2 h后制作模型.观察癫癎发作并记录海马神经元单位放电.结果： ①正常对照组大鼠共记录到24个单位海马神经元放电;②癫癎模型组共记录到78个单位海马神经元放电,癫癎发作程度强,发作频率高;③癫癎预处理组共记录到47个单位海马神经元放电,癫癎发作程度减轻,发作频率减少.结论：氟桂利嗪可抑制青霉素致效应,减少海马神经元的单位放电.     

盐酸氟桂利嗪胶囊治疗月经期偏头痛的临床疗效观察

目的探讨盐酸氟桂利嗪胶囊治疗月经期偏头痛的临床疗效及最佳治疗方案。方法将68例月经期偏头痛患者随机分为两组,A组为常规治疗组(每周服用盐酸氟桂利嗪胶囊5天,停用2天),B组为按生物节律周期治疗组(在月经来临前十天服用盐酸氟桂利嗪胶囊,连续服用20天)。所有患者均于睡前服用5mg盐酸氟桂利嗪胶囊,并记录头痛日记和药物不良反应;根据头痛程度、发作频率、持续时间和伴随症状的变化情况,经量化记分,于用药1个月、3个月、6个月进行疗效判定,同时比较药物不良反应的发生率。结果 1个月和3个月两组间盐酸氟桂利嗪胶囊疗效无明显差异(P>0.05),但6个月时,B组患者头痛程度、发作频率、持续时间、伴随症状与A组相比,明显减轻/减少(P<0.001);两组间药物不良发应发生率无差异(P>0.05)。结论盐酸氟桂利嗪胶囊能够有效的防治月经期偏头痛;根据生物节律周期即女性雌激素分泌水平变化给予盐酸氟桂利嗪胶囊防治月经期偏头痛疗效更佳。     

氟桂利嗪联合血塞通治疗偏头痛的临床疗效

目的探讨氟桂利嗪与血塞通联合治疗偏头痛的临床疗效。方法 108例偏头痛患者随机分为观察组(n=54)与对照组(n=54),对照组给予氟桂利嗪治疗,观察组在对照组基础上加用血塞通治疗,对比2组治疗效果。结果 2组偏头痛发作频率及VAS评分较治疗前均显著降低(P0.01),疼痛持续时间显著缩短(P0.01),且治疗后观察组显著优于对照组(P0.01);观察组治愈率33.3%,显著高于对照组的16.7%;观察组有效率94.4%,显著高于对照组的75.9%。结论氟桂利嗪与血塞通联合治疗偏头痛,有较好的治愈率与有效率,值得临床推广。     

帕罗西汀联合氟桂利嗪防治更年期偏头痛的疗效观察

目的 观察帕罗西汀联合氟桂利嗪防治更年期偏头痛的疗效.方法 将120例更年期偏头痛患者随机分成两组,帕罗西汀联合氟桂利嗪为研究组,单用氟桂利嗪为对照组,观察治疗前后偏头痛发作次数、持续时间的变化,同时采用汉密尔顿抑郁量表(HAMD)和汉密尔顿焦虑量表(HAMA)进行评定.共观察8周.结果 治疗8周末,研究组每周偏头痛发作次数(0.5±0.3)比治疗前减少(1.1±0.5),差异有统计学意义(t=8.0,P<0.01);偏头痛持续时间(h/次)比治疗前短(2.7±0.7,7.6±3.1,t=11.9,P<0.01).治疗8周末,对照组发作次数也比治疗前减少,差异有统计学意义(0.7±0.3,2.7±0.7,t=8.0,P<0.01),偏头痛持续时间(h/次)比治疗前短(2.7±0.7,7.4±3.1,t=11.5,P<0.01);治疗8周末,研究组的发作次数少于对照组(t=3.7,P<0.05),两组偏头痛持续时间差异无统计学意义(t=0,P>0.05).治疗8周末研究组HAMD和 HAMA低于对照组(HAMD:5.9±1.8,8.7±2.3,t=7.3,P<0.01;HAMA:4.9±1.7,8.8±2.1,t=11.2,P<0.01).结论 帕罗西汀联合氟桂利嗪对预防更年期偏头痛发作优于单用氟桂利嗪.     

氟桂利嗪对癫痫鼠痫性发作和脑电活动的影响

目的研究氟桂利嗪对青霉素致癎大鼠癎性发作和脑电活动的影响.方法用60只Wistar大鼠分4组,即对照组及氟桂利嗪10、20、40 mg·kg-1组,2 h后对照组和各实验组给同样剂量青毒素300 万U·kg-1腹腔注射,观察大鼠行为表现及EEG改变.结果氟桂利嗪能明显降低青霉素致癎大鼠癎性发作程度,明显缩短癎性发作持续时间,显著延长癎性发作的潜伏期,明显提高存活率;明显延长大脑皮质、海马癎性放电潜伏期,缩短其持续时间,明显减少癎性放电的数量.结论氟桂利嗪对青霉素致癎大鼠的癎性行为和大脑皮质、海马的癎性电活动均有抑制作用.     

联合氟哌噻吨美利曲辛治疗偏头痛的临床观察

目的探讨盐酸氟桂利嗪、阿司匹林联合氟哌噻吨美利曲辛治疗偏头痛的疗效和安全性。方法 62例确诊为偏头痛的患者,根据是否应用氟哌噻吨美利曲辛分为2组。观察组32例予以盐酸氟桂利嗪、阿司匹林联合氟哌噻吨美利曲辛治疗;对照组30例予以盐酸氟桂利嗪、阿司匹林治疗。疗程均8w,以治疗前、治疗后第4周末和第8周末为观察节点,观察症状消失及缓解情况、睡眠质量以及不良反应的发生情况,并做对比分析。结果观察组与对照组比较,治疗后第4周末和第8周末,头痛发作次数和持续时间明显减少,头痛程度明显减轻,PSQI评分明显减少(P<0.05);治疗前后两组患者TESS评分无明显差异。结论盐酸氟桂利嗪、阿司匹林联合氟哌噻吨美利曲辛治疗偏头痛疗效确切,能显著降低发作频率、减轻发作程度,能改善患者精神状态和生活质量,并且安全可靠。     

氟桂利嗪分别联合普萘洛尔与托吡酯治疗偏头痛的临床价值分析

目的对比氟桂利嗪联合普萘洛尔与氟桂利嗪联合托吡酯治疗偏头痛的临床效果。方法选取2016年7月至2018年2月收治的偏头痛患者92例为研究对象,以随机数字表法分为观察组46例,对照组46例,观察组应用氟桂利嗪联合托吡酯治疗,对照组应用氟桂利嗪联合普萘洛尔治疗,观察两组治疗前、治疗3个月后头痛改善情况、脑血管血流情况,治疗后脑电图(EEG)变化及用药期间不良反应发生情况。结果治疗前两组头痛情况差异无统计学意义(P0.05),治疗后均有改善,观察组治疗3个月后头痛发作频率、头痛程度及头痛持续时间与同期对照组对比,P0.05;治疗前两组脑血流情况差异无统计学意义(P0.05),治疗后均有好转,观察组治疗3个月后基底动脉(BA)、椎动脉(VA)、大脑中动脉(MCA)血流速度与同期对照组对比,P0.05;观察组治疗后EEGθ波增多、δ波增多、α波频率变慢比率分别为54.35%、63.04%、80.43%,与对照组30.43%、39.13%、58.70%对比,差异有统计学意义(P0.05);观察组用药期间不良反应发生率为19.57%,同对照组39.13%对比,明显减少,P0.05。结论相比于氟桂利嗪联合普萘洛尔,氟桂利嗪联合托吡酯能明显减少头痛发作次数,缩短头痛持续时间,减轻头痛程度,对患者脑血管血流及异常神经元放电改善作用显著,且安全性较高,更值得推广。     

托吡酯单药治疗癫癎的临床观察

目的观察托吡酯(TPM)单药治疗癫癎的临床疗效和不良反应.方法应用TPM治疗64例癫癎患者,平均日剂量为138 mg,服药6～36个月,将每例患者治疗最后3个月的发作次数与基础期比较,并观察记录其不良反应.结果本组总有效率为78.1%,其中控制率为42.2%.不良反应的发生率为70.3%,中枢神经系统的不良反应占57.1%,多数较轻微且持续时间较短.10例(15.6%)因治疗无效、不良反应或经济等原因终止治疗.结论 TPM长期单药治疗癫癎疗效明显,耐受性好,较为安全.     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.