Headaches related to triptans therapy in patients of migrainous vertigo

Dizziness and vertigo are frequently reported by patients with migraine. In migrainous vertigo (MV), vertigo is causally related to migraine. Patients of MV usually have an attenuated or absent headache with their vertigo as compared with their usual headache of migraine. Here we report three female patients of MV in which administration of triptan was associated with induction (two patients) or exacerbation (one patient) of headache with disappearance of vertigo. We suggest that headache and vertigo of migraine may be inversely related to each other and suppression of one may induce or aggravate the other.     

Headache and ischemic stroke

Migraine is a common neurological condition affecting yearly 1%–10% of all men and 3%–20% of all women. Focal neurological symptoms (auras), most commonly visual and sensory, occur in 4% of migraine attacks. Migraine with and without aura seems to be associated with an increased stroke risk. Migraine with aura may mimic transient ischemic attacks and may induce stroke (migrainous stroke). Headache is also a common symptom during ischemic stroke In this review, we present the evidence about each of these circumstances to better understand the relationship between headache, especially migraine, and ischemic stroke. Received: 27 September 2001 / Accepted in revised form: 27 December 2001     

Migrainous cerebral infarction in the Sagrat Cor Hospital of Barcelona stroke registry

Nine of 2000 consecutive stroke patients included in the Sagrat Cor Hospital of Barcelona Stroke Registry over a 10-year period fulfilled the strictly defined International Headache Society criteria for migrainous stroke and in whom other causes of stroke were ruled out. They accounted for 13% of all first-ever ischaemic stroke of unusual cause. Migrainous stroke was more common in women (67%) and in patients aged 45 years or younger (78%) compared to the remaining ischaemic strokes of unusual cause. No patient died during hospital stay and 67% were symptom-free at discharge. In the multivariate analysis, nausea or vomiting (odds ratio (OR) 8.40, 95% confidence interval (CI) 1.49-47.21) and age (OR 0.95, 95% CI 0.91-0.99) were predictors of migrainous stroke. Migrainous stroke is a rare entity. Vascular risk factors are uncommon and the prognosis is generally good. Patients with migrainous stroke present some different clinical features from other ischaemic strokes of unusual aetiology.     

Cortical inhibition and habituation to evoked potentials: relevance for pathophysiology of migraine

Dysfunction of neuronal cortical excitability has been supposed to play an important role in etiopathogenesis of migraine. Neurophysiological techniques like evoked potentials (EP) and in the last years non-invasive brain stimulation techniques like transcranial magnetic stimulation (TMS) and transcranial direct current stimulation gave important contribution to understanding of such issue highlighting possible mechanisms of cortical dysfunctions in migraine. EP studies showed impaired habituation to repeated sensorial stimulation and this abnormality was confirmed across all sensorial modalities, making defective habituation a neurophysiological hallmark of the disease. TMS was employed to test more directly cortical excitability in visual cortex and then also in motor cortex. Contradictory results have been reported pointing towards hyperexcitability or on the contrary to reduced preactivation of sensory cortex in migraine. Other experimental evidence speaks in favour of impairment of inhibitory circuits and analogies have been proposed between migraine and conditions of sensory deafferentation in which down-regulation of GABA circuits is considered the more relevant pathophysiological mechanism. Whatever the mechanism involved, it has been found that repeated sessions of high-frequency rTMS trains that have been shown to up-regulate inhibitory circuits could persistently normalize habituation in migraine. This could give interesting insight into pathophysiology establishing a link between cortical inhibition and habituation and opening also new treatment strategies in migraine.     

脑血管储备对缺血性卒中的预测价值

目的探讨脑血管储备的改变是否能预测有颈动脉或者大脑中动脉狭窄或闭塞患者的缺血性卒中的发生。方法采用灌注CT和吸入5％CO2方法测定脑血管储备。研究对象为37例颈内动脉或大脑中动脉狭窄或者闭塞的患者,平均年龄（58．0±11．9）岁。分为两组：储备下降组（脑血管储备〈10％）和储备正常组（脑血管储备≥10％）。所有患者采用药物治疗,通过定期门诊或者电话随访。结果脑血管储备下降组17例,脑血管储备正常组20例。在平均56．9个月的随访中,总共有7例发生缺血性卒中,均发生于脑血管储备下降侧的脑组织,并且都属于脑血管储备下降组（7／17）。缺血性脑卒中的年发生率在脑血管储备下降组和正常组分别是8．7％和0％。Kaplan—Meier生存分析提示脑血管储备下降组发生卒中的风险显著高于正常组（P=0．002,Log-rank法）。结论对于颈内动脉、大脑中动脉狭窄或闭塞的患者,脑血管储备的下降可能预示着未来易于发生缺血性卒中。     

Tumor necrosis factor B gene polymorphism contributes to susceptibility to migraine without area

Migraine without aura (MWOA) and migraine with aura (MWA) are disorders in which multiple factors, including environmental and genetic factors, are involved. In a previous study we hypothesized a protective role of HLA-DR2 antigen, providing additional basis for the proposed genetic heterogeneity between MWOA and MWA. The cytokines TNFA and TNFB are polypeptide effectors of inflammatory reaction and endothelial function. To better define the involvement of HLA region genes in migraine, we performed an association study of the tumor necrosis factor (TNF) genes, located in the HLA class III region, with MWOA and MWA. TNFB alleles 1 and 2 were analyzed by PCR-RFLP in 30 MWOA patients, in 47 MWA patients and in 101 random controls. The frequency of TNFB*2 was significantly increased in MWOA patients as compared with controls (78.72% vs. 61.4%, p _c = 0.004), while no significant differences were found between MWA patients and controls. The distribution of TNFB genotypic frequencies showed a significant decrease of TNFB 1,1 homozygotes in MWOA patients (p _c = 0.0201). The observed increase of TNFB*2 in MWOA is dustributed in TNFB 2,2 and TNFB 1,2 genotypes, meaning that the susceptibility allele could act as “dominant”: people with TNFB 1,1 genotype are less predisposed to the disease. While more studies are needed in larger migraine samples to reinforce the statistical power of the reported data, the present study supports the hypothesis that TNFB is a susceptibility gene in MWOA. Received: 21 August 2000, Accepted in revised form: 18 October 2000     

改良PASS评分在急性大动脉闭塞性脑梗死中的应用

目的 探讨改良院前急性卒中严重程度量表（mPASS）在急性大动脉闭塞性脑梗死中的应用效果。方法采用回顾性分析方法,收集急性脑梗死患者112例,根据是否为大动脉闭塞性脑梗死将患者分为闭塞组（59例）和非闭塞组（53例）,收集患者入院时的神经功能评分：美国国立卫生研究院卒中量表（NIHSS）、PASS及mPASS评分,以及临床预后评价结果：改良Rankin量表（mRS）评分。各评分预测价值以受试者操作特征（ROC）曲线的曲线下面积（AUC）表示,计算敏感度、特异度,采用约登指数评价最佳阈值。采用logistic回归分析大动脉闭塞与mPASS各子项之间的关系。结果 闭塞组各量表的神经功能评分及mRS评分均高于非闭塞组（P均<0.01）。mPASS评分的AUC、敏感度、特异度、约登指数及准确率均高于PASS评分。Logistic回归分析显示皮质症状凝视最具有参考意义（P <0.001）,mRS评分与mPASS各子项呈正相关（mRS评分=0.554+0.037意识水平+1.965凝视+0.206肢体运动+0.193语言功能,F=25.361,P <0.001）。结论 相较于NI...     

脑梗塞并发多器官衰竭患者肿瘤坏死因子含量的观察

目的：检测脑梗塞并发多器官功能衰竭（ＭＯＦ）患者血清肿瘤坏死因子（ＴＮＦ）的含量变化并探讨其意义。方法：单纯急性脑梗塞患者（ＡＣＩ组）２１例，脑梗塞并发多器官功能衰竭患者（ＭＯＦ组）２４例（其中伴上消化道出血１１例，心功能衰竭７例，肾功能衰竭６例）。采用放射免疫方法检测２组患者血清ＴＮＦ的含量。结果：脑梗塞并发ＭＯＦ组ＴＮＦ含量〔（２．４７±０．３９）μｇ／Ｌ〕明显高于ＡＣＩ组〔（１．８９±０．２４）μｇ／Ｌ〕，Ｐ＜０．０１。脑梗塞并发ＭＯＦ组中各亚组间ＴＮＦ〔上消化道出血组（２．５３±０．４３）μｇ／Ｌ，心功能衰竭组（２．０１±０．２８）μｇ／Ｌ，肾功能衰竭组（２．４１±０．３２）μｇ／Ｌ〕差异显著（Ｐ均＜０．０１），尤以上消化道出血组升高明显。结论：ＴＮＦ参与了脑梗塞并发上消化道出血的发病；监测ＴＮＦ变化有助于对脑梗塞并发ＭＯＦ患者的病情观察和预后估计。     

急性脑梗塞时肿瘤坏死因子的变化及其意义

目的：研究肿瘤坏死因子（ＴＮＦ）在急性脑梗塞时的变化及其意义。方法：用放射免疫方法测定３２例急性脑梗塞患者的血清ＴＮＦ水平及白细胞（ＷＢＣ）计数。结果：急性脑梗塞时患者血清ＴＮＦ显著增高〔（２３．６７±３．３２）ｐｍｏｌ／Ｌ〕，与正常对照组〔（８．１６±３．５６）ｐｍｏｌ／Ｌ〕比较有显著性差异（Ｐ＜０．０１）；ＴＮＦ在梗塞发生后第１、５、１０及１４日呈持续性增高，其中以第５日为最高（３０．７４±６．３３）ｐｍｏｌ／Ｌ；第１日时ＴＮＦ与ＷＢＣ呈一致性改变。结论：急性脑梗塞后的ＴＮＦ持续性增高与脑梗塞后的ＴＮＦ双重合成有关，ＴＮＦ引发的血管内皮细胞白细胞血小板环路激活过程是脑缺血性损害的基本病理过程。     

Relationship among trunk control,activities of daily living,and upper extremity function during the first week after stroke in patients with acute cerebral infarction

[Purpose] We aimed to identify the relationship among trunk control, activities of daily living, and upper extremity function during the first week after stroke in patients with acute cerebral infarction. [Participants and Methods] Ninety-five patients with first cerebral infarction were included. Trunk control was assessed using the Postural Assessment Scale for Stroke. Additionally, activities of daily living were evaluated using the Functional Independence Measure, and upper extremity function was assessed using the upper extremity component of the Fugl-Meyer Assessment. Correlation analysis was performed to examine the relationships among these three measures. Furthermore, stepwise multiple regression analysis was performed to investigate the factors affecting activities of daily living. [Results] The total score and two subcategories of the Postural Assessment Scale for Stroke were significantly correlated with the Functional Independence Measure motor values. Stepwise multiple regression analysis revealed age and the Postural Assessment Scale for Stroke as factors influencing the Functional Independence Measure. Moreover, the Postural Assessment Scale for Stroke and upper extremity component of Fugl-Meyer Assessment showed a high correlation. [Conclusion] The trunk control ability assessed using the Postural Assessment Scale for Stroke is strongly correlated with activities of daily living estimated using the Functional Independence Measure in the first week after stroke in patients with acute cerebral infarction. The upper extremity component of Fugl-Meyer Assessment was not identified as a factor affecting the Functional Independence Measure.     

Cortical spreading depression can be triggered by sensory stimulation in primed wild type mouse brain: a mechanistic insight to migraine aura generation

BackgroundUnlike the spontaneously appearing aura in migraineurs, experimentally, cortical spreading depression (CSD), the neurophysiological correlate of aura is induced by non-physiological stimuli. Consequently, neural mechanisms involved in spontaneous CSD generation, which may provide insight into how migraine starts in an otherwise healthy brain, remain largely unclear. We hypothesized that CSD can be physiologically induced by sensory stimulation in primed mouse brain.MethodsCortex was made susceptible to CSD with partial inhibition of Na⁺/K⁺-ATPase by epidural application of a low concentration of Na⁺/K⁺-ATPase blocker ouabain, allowing longer than 30-min intervals between CSDs or by knocking-down α2 subunit of Na⁺/K⁺-ATPase, which is crucial for K⁺ and glutamate re-uptake, with shRNA. Stimulation-triggered CSDs and extracellular K⁺ changes were monitored in vivo electrophysiologically and a K⁺-sensitive fluoroprobe (IPG-4), respectively.ResultsAfter priming with ouabain, photic stimulation significantly increased the CSD incidence compared with non-stimulated animals (44.0 vs. 4.9%, p < 0.001). Whisker stimulation also significantly increased the CSD incidence, albeit less effectively (14.9 vs. 2.4%, p = 0.02). Knocking-down Na⁺/K⁺-ATPase (50% decrease in mRNA) lowered the CSD threshold in all mice tested with KCl but triggered CSDs in 14.3% and 16.7% of mice with photic and whisker stimulation, respectively. Confirming Na⁺/K⁺-ATPase hypofunction, extracellular K⁺ significantly rose during sensory stimulation after ouabain or shRNA treatment unlike controls. In line with the higher CSD susceptibility observed, K⁺ rise was more prominent after ouabain. To gain insight to preventive mechanisms reducing the probability of stimulus-evoked CSDs, we applied an A1-receptor antagonist (DPCPX) to the occipital cortex, because adenosine formed during stimulation from ATP can reduce CSD susceptibility. DPCPX induced spontaneous CSDs but only small-DC shifts along with suppression of EEG spikes during photic stimulation, suggesting that the inhibition co-activated with sensory stimulation could limit CSD ignition when K⁺ uptake was not sufficiently suppressed as with ouabain.ConclusionsNormal brain is well protected against CSD generation. For CSD to be ignited under physiological conditions, priming and predisposing factors are required as seen in migraine patients. Intense sensory stimulation has potential to trigger CSD when co-existing conditions bring extracellular K⁺ and glutamate concentrations over CSD-ignition threshold and stimulation-evoked inhibitory mechanisms are overcome.     

实验性大脑皮层梗死后中枢神经系统相关部位的神经可塑性

目的 :探讨实验性大脑皮层梗塞后同侧纹状体、丘脑及对侧脊髓前角的神经结构可塑性。方法 :采用易卒中型肾血管性高血压大鼠制作右侧大脑中动脉皮层支闭塞模型 ,分别于术后第 1周、2周、3周和 4周 ,取鼠脑行免疫组化检查 ,检测大鼠不同时点纹状体、丘脑腹后外侧核及对侧脊髓前角的微管相关蛋白 2 (MAP 2 )、突触生长素(SYN)和生长相关蛋白 (GAP 43)表达的变化。结果 :大脑皮层梗塞后第 1周 ,同侧纹状体、丘脑腹后外侧核和对侧脊髓前角GAP 43阳性信号开始增加 ,第 2周达到高峰 ,之后增加幅度逐渐减弱 ;这些部位SYN阳性信号第 1周较对照组高 ,至第 2周恢复正常 ,第 3周和第 4周逐渐降低 ,且显著低于对照组 ;脑皮层梗塞后第 2周 ,同侧纹状体和丘脑腹后外侧核MAP 2阳性细胞数开始减少 ,至 3周、4周显著低于对照组。结论 :大脑皮层梗死后早期远离梗塞灶的相关神经组织有明显的可塑性 ,后期神经细胞继发性死亡且可塑减缓     

高血压性脑出血患者伴新发无症状性脑梗死的相关危险因素分析及预后的探讨

目的: 探讨急性高血压性脑出血患者的新发无症状性脑梗死（silent brain infarction,SBI）的发生率及相关危险因素,同时探讨伴发新发SBI的脑出血患者发生临床脑血管事件或血管相关性死亡的情况。方法: 采用前瞻性研究,观察100例在发病3 d内经CT诊断为高血压性脑出血的患者,所有患者在发病第5天行MRI检查以明确新发SBI及脑微出血（cerebral microbleeds,CMBs）病灶,并在1年内定期随访后续的临床脑血管事件或血管相关性死亡。结果: 100例患者中,观察到11例（11%）共有14个新发SBI病灶。经单因素分析发现,基线水平中伴有CMBs和脑白质疏松是新发SBI的危险因素。在随访的1年内,14例患者发生了临床脑血管事件或血管相关性死亡,其中9例发生脑梗死,1例再发脑出血,4例发生血管相关性死亡。Cox比例风险模型显示,高龄、房颤和伴有新发SBI为发生临床脑血管事件或血管相关性死亡的独立预测因素。结论: 新发SBI在脑出血的急性期阶段常见,与CMBs及脑白质疏松相关。伴有新发SBI的高血压性脑出血患者未来1年内发生临床脑血管事件或血管相关性死亡的风险增加。     

紫外线照射充氧自血回输对急性脑梗塞患者肿瘤坏死因子及血浆内 …

目的　探讨紫外线照射充氧自血回输(UBIO)对急性脑梗塞患者循环血中肿瘤坏死因子(TNF)、内皮素(ET)含量的影响。方法　60例急性脑梗塞患者随机分为UBIO综合治疗组与常规治疗组各30例,采用放免法分别测定两组患者治疗前及治疗20 d 后TNF、ET含量。结果　UBIO组治疗前TNF、ET含量分别为(0.98±0.56)ng/ml、(74.86±25.72)pg/ml,治疗20 d 后TNF、ET含量显著下降,分别为(0.61±0.45)ng/ml、(56.32±21.33)pg/ml(P＜0.01),而常规治疗组下降无显著性(P＞0.05)。结论　UBIO能从多方面干预TNF、ET的释放。     

颅脑损伤术后发生脑梗死的相关高危因素探讨

目的探讨颅脑损伤术后患者发生脑梗死的相关高危因素。方法选取2010年6月至2014年6月收治的颅脑损伤术后的800例患者为研究对象,对患者的年龄、性别、格拉斯哥昏迷评分(GCS)、脑血管痉挛、是否并发脑疝、脑挫裂伤、糖尿病、入院时血压等临床资料进行回顾性分析。采用描述性统计和Logistic回归分析颅脑损伤术后患者发生脑梗死的影响因素。结果 800例临床资料完整的颅脑损伤术后发生脑梗死的患者有45例,发生率为5.63%,死亡2例,病死率为4.44%,年龄、GCS评分、脑血管痉挛、并发脑疝、脑挫裂伤、糖尿病及低血压这7个因素经统计学检验差异有统计学意义(P0.05);经多因素Logistic回归分析发现颅脑损伤术后患者发生脑梗死与低龄、低GCS、低收缩压、脑血管痉挛、并发脑疝、脑损伤类型中的脑挫裂伤、糖尿病及低血压等因素关系密切。结论低龄、低GCS、低收缩压、脑血管痉挛、并发脑疝、脑损伤类型中的脑挫裂伤、糖尿病及低血压等因素可能是颅脑损伤患者术后发生脑梗死的危险因素,需要采取合理措施降低其对患者预后的影响,提高患者的生活质量。     

血小板参数、NIHSS评分与中国缺血性卒中亚型分型的关系

目的探讨血小板参数、NIHSS评分与中国缺血性卒中亚型（CISS）分型中大动脉粥样硬化性（LAA）及穿支动脉病变（PAD）的关系。方法 2012年1月至2014年5月急性脑梗死住院患者213例。依据临床症状、体征、头颅核磁共振、头颈部CTA、颈动脉超声、脑血管造影结果分为LAA组（113例）、PAD组（100例）。均进行血小板检测,参数包括血小板计数（PLT）、平均血小板体积（MPV）、血小板体积分布宽度（PDW）、血小板比积（PCT）,记录入出院时NIHSS评分,并进行比较。结果与PAD组比较,LAA组PLT和PCT明显减少（P均〈0.05）;PDW和MPV略升高,差异均无统计学意义（P均〉0.05）。两组PLT与MPV、PDW呈负相关（r=-0.181,r=-0.329,P均〈0.01）,PLT与PCT呈正相关（r=0.926,P〈0.01）。入院时LAA组NIHSS评分高于PAD组（P〈0.01）;出院时LAA组NIHSS评分高于PAD组,但差异无统计学意义（P〉0.05）。两组患者入院时NIHSS评分与PLT、MPV、PDW、PCT均无相关性（r=0.000,r=0.128,r=0.118,r=0.042,P均〉0.05）,出院时NIHSS评分与MPV、PDW呈正相关（r=0.160,r=0.146,P均〈0.05）,与PLT、PCT无相关性（r=-0.005,r=0.042,P均〉0.05）。结论血小板参数、NIHSS评分与CISS分型LAA及PAD关系密切,对疾病的疗效、预防及判断预后具有重要的参考价值。     

910例脑梗死患者治疗时间延迟原因的调查分析

目的：调查分析脑梗死患者治疗时间延误的原因,探讨开展脑梗死患者早期治疗的措施。方法：分别选取华北地区３ 家医院,组织专科医师,统一时间,统一标准,统一表格,调查脑梗死现症患者的发病时间,治疗时间及延迟治疗的各种原因。对有关资料进行汇总分析。结果：共调查患者９１０ 例,在起病６ 小时后治疗的６４４例,平均延误时间为１３３３ 小时,其中院前延误时间为１１８６ 小时（占８８９７％ ）,院后延迟时间为１４７ 小时（占１１０３％ ）。结论：脑梗死患者治疗延误时间的长短和患者的职业、文化程度密切相关;主要原因是重视不够,院前延迟是由患者的主、客观因素造成的,院后延迟是由医院和医务人员造成的。因此,对社区人群加强健康教育,对基层医务人员加强培训,是实施脑梗死患者早期治疗的一项根本措施。     

青壮年股骨颈骨折患者行闭合复位内固定手术后发生股骨头无菌性缺血坏死影响因素分析

目的探讨青壮年股骨颈骨折患者经闭合复位内固定手术治疗后发生股骨头无菌性缺血坏死的影响因素。方法回顾性分析自2015年1月至2020年1月北部战区总医院骨科收治的经闭合复位内固定手术治疗的62例青壮年股骨颈骨折患者临床资料,包括年龄、性别、体质量指数、骨折侧、Garden分型、损伤至手术前时间、术前是否牵引、内固定是否取出、股骨头后倾角度、是否有股骨颈皮质粉碎、术后负重活动时间、复位质量等,并分析上述指标对术后发生股骨头无菌性缺血坏死的影响。结果青壮年患者发生术后股骨头无菌性缺血坏死与Garden分型、内固定是否取出、股骨头后倾角度、股骨颈皮质粉碎情况、复位质量相关(P<0.05)。多因素Logistic分析显示,内固定是否取出、复位质量、股骨头后倾角度与术后发生股骨头无菌性缺血坏死关系密切(P<0.05)。结论青壮年股骨颈骨折闭合复位内固定术后发生股骨头坏死的影响因素较多,其中,内固定是否取出、复位质量、股骨头后倾角度与术后发生股骨头坏死密切关系。