Characterization of Moyamoya and Middle Cerebral Artery Diseases by Carotid Canal Diameter and RNF213 p.R4810K Genotype

ObjectivesIt is sometimes difficult to differentiate middle cerebral artery disease from moyamoya disease because the two can present similarly yet have different treatment strategies. We investigated whether the presence of a narrow carotid canal and the RNF213 mutation can help differentiate between the two phenotypes.Population and MethodsWe analyzed 78 patients with moyamoya disease, 27 patients with middle cerebral artery disease, and 79 controls from 2 facilities. The carotid canal diameter was measured using computed tomography. The p.R4810K mutation was genotyped by TaqMan assay. A receiver operating characteristics analysis was performed to assess the significance of the carotid canal diameter for the accurate diagnosis of moyamoya disease.ResultsThe carotid canal diameter was significantly narrower in patients with moyamoya disease than in controls. The optimal cutoff values were 5.0 mm for adult males and 4.5 mm for adult females and children (sensitivity: 0.82; specificity: 0.92). Among the patients with middle cerebral artery disease, 18.5% and 25.0% of the affected hemispheres had the p.R4810K mutation and narrow canal (i.e., below the cutoff), respectively, whereas only 3.1% of those had both. Contrastingly, 68.8% of the affected hemispheres in patients with moyamoya disease had both these characteristics. Among the patients with moyamoya disease, those with the p.R4810K mutation tended to have narrower carotid canals.ConclusionsAlthough the presence of a narrow carotid canal or the p.R4810K mutation alone could not be used to distinguish those with moyamoya disease from those with middle cerebral artery disease, the combination of these factors could better characterize the two phenotypes.     

The Potential Role of Neuromodulation in Subarachnoid Hemorrhage

ObjectivesAneurysmal subarachnoid hemorrhage (SAH) continues to be a difficult cerebrovascular disease with limited pharmacologic treatment options. Cerebral vasospasm (CV) and delayed cerebral ischemia (DCI) are leading causes of morbidity and mortality after SAH. Despite the advances in the understanding of its pathophysiology and tremendous efforts to date, nimodipine is currently the sole Food and Drug Administration–approved treatment for patients with SAH, with benefits that are marginal at best. The neuromodulation therapies are promising, especially those that target CV and DCI to improve functional outcomes. The aim of this review is therefore to summarize the available evidence for each type of neuromodulation for CV and DCI, with a special focus on its pathophysiological mechanisms, in addition to their clinical utility and drawbacks, which we hope will lead to future translational therapy options after SAH.Materials and MethodsWe conducted a comprehensive review of preclinical and clinical studies demonstrating the use of neuromodulation for SAH. The literature search was performed using PubMed, Embase, and ClinicalTrials.gov. A total of 21 articles published from 1992 to 2021 and eight clinical trials were chosen.ResultsThe studies reviewed provide a compelling demonstration that neuromodulation is a potentially useful strategy to target multiple mechanisms of DCI and thus to potentially improve functional outcomes from SAH. There are several types of neuromodulation that have been tested to treat CV and DCI, including the trigeminal/vagus/facial nerve stimulation, sphenopalatine ganglion and spinal cord stimulation, transcranial direct electrical stimulation, transcutaneous electrical neurostimulation, and electroacupuncture. Most of them are in the preclinical or early phases of clinical application; however, they show promising results.ConclusionsDCI has a complex pathogenesis, making the unique anatomical distribution and pleiotropic capabilities of various types of neuromodulation a promising field of study. We may be at the cusp of a breakthrough in the use of these techniques for the treatment of this stubbornly difficult disease.     

颅内深静脉血栓形成的临床诊治

目的　探讨颅内深静脉血栓形成（deep cerebral venous thrombosis，DCVT）的临床诊断与治疗策略。 方法　回顾性分析10年来影像学诊断为DCVT的5例患者的临床表现、影像学特征、治疗及预后情况。 结果　DCVT最常累及Rosenthal基底静脉、大脑内静脉、Galen静脉和直窦，其临床表现不典型，常见有头痛、意识障碍、复视、偏瘫等，常见诱发因素有口服避孕药、产褥期、妊娠期等。丘脑水肿为DCVT患者最常见的影像学征象。肝素抗凝治疗简单有效，大脑深静脉可恢复再通，临床症状缓解。 结论　DCVT患者临床症状缺乏特异性，早期诊断困难，特殊成像技术和特定影像学特征有助于其明确诊断，及时正确的抗凝治疗可获得良好的预后。     

急性脑梗死患者血浆CD147水平与神经功能缺损程度的关系

目的探讨急性脑梗死(acute cerebral infarction,ACI)患者血浆CD147的水平及其与神经功能缺损的关系。方法选择2015年6月至2016年6月期间作者医院住院治疗的ACI患者79例(ACI组),另设对照组37例,选自门诊体检者,入选者均无脑血管病证据和(或)头颅MRI/CT检测正常者。以ELISA法检测两组血浆CD147水平,并比较两组CD147水平;以美国国立卫生研究院脑卒中量表(NIHSS)评分评估ACI组神经功能缺损情况;并分析其与CD147水平的关系。结果ACI组血浆CD147水平明显高于对照组〔(635.80±187.63)pg/mL比(352.70±91.32)pg/mL;t=8.693,P=0.000〕。ACI组患者NIHSS评分<8分组明显低于≥8分组〔(526.48±143.02)pg/mL比(761.02±150.56)pg/mL;t=-7.103,P=0.000〕。相关分析显示CD147水平与NIHSS评分成正相关(r=0.749,P=0.000)。结论ACI组患者血浆CD147水平明显升高,并且与神经功能缺损程度成正相关。     

急性单发腔隙性脑梗死患者BG/CSO-VRS扩大严重程度的危险因素分析

目的 探讨急性单发腔隙性脑梗死患者基底节(basal ganglia,BG)/半卵圆中心(central semioval,CSO)-血管周围间隙(Virchow-Robin Spaces,VRS)扩大严重程度的危险因素。方法 回顾性分析本院2018年1月-2019年3月收治急性单发腔隙性脑梗死患者共476例的临床资料,其中基底节(BG)梗死262例,半卵圆中心(CSO)梗死214例,根据影像学手段评估BG/CSO-VRS扩大严重程度; 采用χ²检验和Logistic回归模型分析确定BG/CSO-VRS扩大严重程度的相关危险因素。结果 基底节和半卵圆中心梗死VRS评分比较无显著差异(P>0.05); BG-VRS轻度扩大和重度扩大患者性别、高血压病比例、收缩压及BMI水平比较有明显差异(P<0.05); CSO-VRS轻度和重度扩大患者高血压病、糖尿病比例及BMI水平比较有明显差异(P<0.05); 采用多因素Logistic回归模型分析显示,高血压病和BMI均是BG-VRS扩大严重程度的独立影响因素(P<0.05),而BMI也是CSO-VRS扩大严重程度的独立影响因素(P<0.05)。结论 高血压病和BMI与急性单发腔隙性脑梗死患者VRS扩大密切相关,其中合并高血压病和BMI降低是导致BG-VRS扩大的独立危险因素,而BMI降低也是CSO-VRS扩大的独立危险因素     

急性脑梗死合并阻塞性睡眠呼吸暂停综合症患者认知功能障碍发生现状及相关危险因素分析

目的 探讨急性脑梗死合并阻塞性睡眠呼吸暂停综合症(obstrucyive sleep apnea syndrome, OSAS)患者认知功能障碍发生现状及相关危险因素。方法 选择2016年1月-2017年10月于本院住院治疗的急性脑梗死合并OSAS患者130例作为研究对象,观察2组患者呼吸暂停低通气指数、最低血氧饱和度、平均血氧饱和度、低氧指数等; 评估患者的认知功能; 检测2组患者血清HIF-1和Ngb水平; 根据2组患者的临床资料,对影响认知功能的因素进行Logistic回归分析。结果 认知功能障碍组夜间睡眠期的呼吸暂停低通气指数和低氧指数显著高于认知正常组,而其最低血氧饱和度和平均血氧饱和度的指数显著高于认知正常组(P<0.05); 认知障碍组视空间技能、执行技能、定向力、语言能力、记忆力(延迟记忆)、注意力以及抽象思维7个不同的认知领域的得分以及总分均低于认知正常组(P<0.05); 认知功能障碍组HIF-1和Ngb高水平患者的比例显著高于认知正常组(P<0.05); 认知障碍组P300潜伏期显著高于认知正常组,但波幅较认知正常组显著降低(P<0.05)。单因素分析显示,体重指数(χ²=7.428,P=0.006)、血脂血糖水平异常(χ²=9.917,P =0.002)、AHI(χ²=5.489,P=0.019)、脑梗死面积(χ²=5.857,P=0.016)、脑梗死部位(χ²=6.207,P=0.013)、HIF-1水平(χ2=29.138,P=0.000)和Ngb水平(χ²=32.385,P=0.000)是急性脑梗死合并OSAS患者认知障碍的影响因素; 经Logistic多因素回归分析显示,AHI≥20次/h(OR=6.417,95% CI=2.774～14.848,P=0.000)、HIF-1高水平(OR=4.768,95% CI=2.009～11.318,P=0.000)、Ngb高水平(OR=4.477,95% CI=2.443～8.204,P=0.002)、血脂血糖水平异常(OR=3.622,95% CI=1.422～9.225,P=0.004)、脑梗死部位(OR=4.428,95% CI=1.801～10.888,P=0.027)为影响认知功能障碍预后的独立危险因素。结论 影响急性脑梗死合并OSAS患者认知功能障碍的危险因素主要是AHI≥20次/h、HIF-1高水平、Ngb高水平、血脂血糖水平异常、脑梗死部位     

转化生长因子1和Toll样受体4与急性脑梗死患者静脉rt-PA溶栓后侧支循环代偿的相关性研究

目的 探讨急性脑梗死患者静脉rt-PA溶栓后侧支循环的影响因素及侧支循环代偿与转化生长因子1(TAK1)、Toll样受体4(TLR4)水平的相关性。方法 采用回顾性分析方法,收集急性脑梗死且接受重组组织型纤溶酶原激活剂(rt-PA)治疗的72例患者,根据软脑膜评分方法(rLMC)评分将患者分为侧支循环较好组(39例)和侧支循环较差组(33例); 收集患者一般的临床数据和血清,用ELISA实验检测患者血清TLR4和TAK1水平。结果 侧支循环较好组糖尿病和高血压患者的比例均少于侧支循环较差组(P<0.05); 侧支循环较好组与侧支循环较差组比较rLMC评分较高,NIHSS评分较低(P<0.05); 侧支循环较好组TLR4和TAK1水平均低于侧支循环较差组(P<0.05); 侧支循环较好组溶栓后24 h后NIHSS评分、30d后NIHSS评分和90d后MRS评分均低于侧支循环较差组(P<0.05)且侧支循环较好组预后良好患者的比例高于侧支循环较差组(P<0.05); rLMC评分与患者血清TLR4和TAK1水平呈负相关(r=-0.819,-0.701,P<0.01); 多因素二分类logistic回归分析显示,糖尿病、高血压病、TLR4和TAK1水平增加均为影响侧支循环建立的危险因素。结论 rLMC评分与TLR4和TAK1的水平呈负相关,急性脑梗死患者糖尿病、高血压病、TLR4和TAK1的水平增加均为静脉rt-PA溶栓后侧支循环代偿不良的影响因素     

血糖变异性与重症脑出血患者神经功能恢复的相关性

目的 探讨血糖变异性对重症急性脑出血患者神经功能恢复的影响及血糖变异性在重症脑出血患者发病时间轴上的表现特点。方法 选取2018年1月1日-2019年7月1日收入河南科技大学第一附属医院重症外科的脑出血患者,根据患者入院30 d后改良Rankin(Modified Rankin scale,mRS)评分将患者分为神经功能恢复良好组(mRS≤2分),和神经功能恢复不良组(mRS>2分)(残疾/死亡),比较2组入院时高血糖、平均血糖、血糖标准差、入院24 h内血糖变异性(CV1)、入院1～3 d血糖变异性(CV2)、入院3～7 d血糖变异性(CV3)、入院7 d内血糖平均变异性(CV7)、最低血糖水平以及其他临床资料,应用多变量logistic回归分析确定入院30 d后神经功能恢复的独立预测因素。结果 单因素分析显示年龄、CV1、CV3、CV7、最低血糖水平、血糖标准差是影响重症脑出血患者神经功能恢复的相关因素(P<0.05); 多因素logistic逐步回归模型分析显示血糖标准差、CV1、CV3、CV7、最低血糖水平能独立预测重症脑出血患者神经功能的恢复情况; 神经功能恢复良好组和神经功能恢复不良组患者的血糖变异性在入院24 h内、入院1～3 d和入院3～7 d时间轴上的变化特点不同(F=5.000,P=0.029),进一步分析可以看出神经功能恢复不良组的血糖变异性平均幅度较神经功能恢复良好组高,但2组在时间轴上的变化趋势基本相同,均在急性期(入院1～3 d)呈线性上升趋势,之后趋于下降; 组内效应显示患者的血糖变异性在3个时间段上的变化具有显著差异(F=11.663,P<0.001)。结论 血糖标准差、CV1、CV3、CV7、最低血糖水平是影响重症脑出血患者神经功能恢复的独立危险因素; 在重症脑出血患者超急性期、急性期、亚急性期过程中血糖变异性的变化具有显著差异,临床工作中重症脑出血患者应在入院早期密切监测血糖,并积极干预,减小血糖波动范围,以期减少不良预后的发生。