Therapeutic imaging window of cerebral infarction revealed by multisequence magnetic resonance imaging An animal and clinical study

In this study, we established a Wistar rat model of right middle cerebral artery occlusion and observed pathological imaging changes (T2-weighted imaging [T2WI], T2FLAIR, and diffusion-weighted imaging [DWI]) following cerebral infarction. The pathological changes were divided into three phases: early cerebral infarction, middle cerebral infarction, and late cerebral infarction. In the early cerebral infarction phase (less than 2 hours post-infarction), there was evidence of intracellular edema, which improved after reperfusion. This improvement was defined as the ischemic penumbra. In this phase, a high DWI signal and a low apparent diffusion coefficient were observed in the right basal ganglia region. By contrast, there were no abnormal T2WI and T2FLAIR signals. For the middle cerebral infarction phase (2-4 hours post-infarction), a mixed edema was observed. After reperfusion, there was a mild improvement in cell edema, while the angioedema became more serious. A high DWI signal and a low apparent diffusion coefficient signal were observed, and some rats showed high T2WI and T2FLAIR signals. For the late cerebral infarction phase (4-6 hours post-infarction), significant angioedema was visible in the infarction site. After reperfusion, there was a significant increase in angioedema, while there was evidence of hemorrhage and necrosis. A mixed signal was observed on DWI, while a high apparent diffusion coefficient signal, a high T2WI signal, and a high T2FLAIR signal were also observed. All 86 cerebral infarction patients were subjected to T2WI, T2FLAIR, and DWI. MRI results of clinic data similar to the early infarction phase of animal experiments were found in 51 patients, for which 10 patients (10/51) had an onset time greater than 6 hours. A total of 35 patients had MRI results similar to the middle and late infarction phase of animal experiments, of which eight patients (8/35) had an onset time less than 6 hours. These data suggest that defining the "therapeutic time window" as the time 6 hours after infarction may not be suitable for all patients. Integrated application of MRI sequences including T2WI, T2FLAIR, DW-MRI, and apparent diffusion coefficient mapping should be used to examine the ischemic penumbra, which may provide valuable information for identifying the "therapeutic time window".     

急性缺血性脑血管病合并脑微出血的临床特征研究

目的 研究不同类型急性缺血性脑血管病患者合并脑微出血(CMB)的患病率及分级,并探讨其临床意义.方法 选择南方医科大学附属南方医院及广州中医药大学附属中山医院神经内科自2009年9月至2010年7月收治的急性缺血性脑血管病患者259例,其中动脉粥样硬化性血栓形成146例、心源性脑栓塞28例、小动脉性脑梗死50例、不明原因脑梗死19例,短暂性脑缺血发作(TIA)16例,同期体检者96例作为对照.常规行核磁共振T2梯度回波加权扫描(GRE-T2*WI),比较不同类型脑血管病患者CMB的患病率、分级以及初发性和复发性各亚型脑梗死患者CMB的患病率.结果 不同类型缺血性脑血管病患者CMB的患病率、分级均不同,差异有统计学意义(P＜0.05),除TIA外,脑梗死患者CMB的患病率均高于对照组,差异有统计学意义(P＜0.05),其中小动脉性脑梗死组最高(68.0%);复发性动脉粥样硬化性血栓形成患者CMB的患病率高于初发性患者,差异有统计学意义(P＜0.05).结论 CMB在各亚型脑梗死患者中患病率较高,其中在小血管性脑梗死中最高且严重;复发性动脉粥样硬化性血栓形成患者较初发性患者CMB的患病率高,提示CMB可能与缺血性卒中的复发有关.

Abstract：

Objective To study the prevalence and grade of cerebral microbleeds (CMB) among patients with different subtypes of acute ischemic cerebrovascular diseases, and investigate the clinical significance of CMB.Methods Consecutive 259 patients with acute ischemic cerebrovascular diseases, admitted to our hospitals from September 2009 to July 2010, were included; according to the stroke subtypes, these patients were classified into groups of atherothrombotic infarction (n=146),cardioembolic infarction (n=28), small artery infarction (n=50), infarction of unknown origin (n=19) and transient ischemia attack (TIA, n=16). The patients without cerebral vascular diseases were served as controls (n=96). The baseline data were registered and all patients were performed gradient echo-T2*weighted imaging (GRE-T2*WI); the prevalence and grade of CMB between each 2 different subtypes of acute ischemic cerebrovascular diseases were compared; the prevalence of CMB in patients with acute ischemic infarction for the first time and patients with recurrent cerebral infarction was compared.Results The prevalence and grade of CMB between each 2 different infarction subtypes varied with a statistical difference (P＜0.05). Apart from that of TIA group, the prevalence of all infarction groups was statistically higher than that of the controls (P＜0.05) with small artery infarction group being the highest (68.0%). The prevalence of CMB in patients with recurrent infarction was statistically higher than that in patients with primary infarction (P＜0.05).Conclusion The prevalence of CMB among different subtypes of infarction is high with the subtype of small artery infarction enjoying the highest rate; the prevalence of CMB in recurrent infarction goes higher as compared with that in primary infarction; the relapse of the cerebral infarction is possiblely related to the presence of CBMs.     

急性脑梗死合并2型糖尿病患者血清Caveolin-1的水平变化及其与早期神经功能恶化的关系

目的 探讨急性脑梗死合并2型糖尿病患者血清陷窝蛋白-1(Caveolin-1)的水平变化及其与早期神经功能恶化(END)的关系。方法 选择2018年1月-2019年12月本院收治的急性脑梗死合并2型糖尿病患者、急性脑梗死患者、2型糖尿病患者、健康志愿者,检测血清Caveolin-1的水平,评价急性脑梗死合并2型糖尿病患者的END,采用Logistic回归分析END的影响因素,采用ROC曲线分析Caveolin-1水平对END的预测价值。结果 急性脑梗死合并2型糖尿病组患者的血清Caveolin-1水平高于急性脑梗死组、2型糖尿病组、对照组(P<0.05); 急性脑梗死合并2型糖尿病组END患者的Caveolin-1水平、女性比例、入院时NIHSS评分、起病至入院时间、糖化血红蛋白、随机血糖、hs-CRP水平均高于非END患者(P<0.05); logistics回归分析显示,Caveolin-1水平增高、女性、糖化血红蛋白水平增高及入院时NIHSS评分增加是急性脑梗死合并2型糖尿病组患者END的危险因素(P<0.05); ROC曲线分析显示,血清Caveolin-1对急性脑梗死合并2型糖尿病患者的END具有预测价值,最佳截点为34.95 ng/mL。结论 血清Caveolin-1水平升高是急性脑梗死合并2型糖尿病患者END的危险因素,且对END具有预测价值。     

Recurrent lacunar infarction following a previous lacunar stroke: a clinical study of 122 patients

Objective

To determine clinical variables related to recurrent lacunar infarction following a previous lacunar stroke.

Methods

A total of 122 out of 733 consecutive patients with lacunar infarction collected from a hospital based registry between 1986 and 2004 were readmitted because of a recurrent lacunar infarction. In a subset of 59 patients, cognition was assessed using the Mini‐Mental State Examination (MMSE). Predictors of lacunar infarction recurrence were assessed by logistic regression analysis.

Results

First lacunar infarction recurrence occurred in 101 patients (83%) and multiple recurrences in 21. The mean time between first ever lacunar infarction and recurrent lacunes was 58.3 months (range 2–240). In the subset of 59 patients in whom cognition was studied, cognitive impairment, defined as an MMSE score <24, was detected in 16% (8/49) of patients with first lacunar infarction recurrence and in 40% (4/10) of those with multiple lacunar infarction recurrences. In the multivariate analysis, hypertension (odds ratio 2.01, 95% CI 1.23 to 3.30) and diabetes (odds ratio 1.62, 95% CI 1.07 to 2.46) were significant predictors of lacunar stroke recurrence, whereas hyperlipidaemia was inversely associated (odds ratio 0.52, 95% CI 0.30 to 0.90).

Conclusions

Hypertension and diabetes were significant factors related to recurrent lacunar infarction. Hyperlipidaemia appeared to have a protective role. Cognitive impairment was a frequent finding in patients with multiple lacunar infarction recurrences.Lacunar stroke accounts for more than 25% of brain infarcts.¹ Despite the frequency of lacunar strokes, clinical data of patients presenting with a recurrent lacunar infarction are scarce, and differential features between recurrent and first ever lacunar infarctions have been poorly studied.² Neurological deficit related to a first lacunar infarction is usually mild. In contrast, recurrent lacunar infarctions may be associated with a more severe clinical picture, including lacunar state and vascular dementia.³A clinical study was performed to provide further information on the salient features of patients with recurrent lacunes and to identify factors influencing the recurrence of a lacunar infarction. The objectives of the study were: (a) to compare demographic data, vascular risk factors, clinical and topographic characteristics, and prognosis between patients with recurrent lacunar infarction and patients with first ever lacunar infarction and (b) to determine predictors of recurrent lacunes. Moreover, cognitive status was assessed in a subset of patients with recurrent lacunar infarction.     

老年2型糖尿病合并急性脑梗死患者血清IGF-1水平与神经功能及颈动脉斑块的关系

目的 探讨老年2型糖尿病合并急性脑梗死患者血清胰岛素生长因子-1(insulin-like growth factor-1,IGF-1)水平与神经功能及颈动脉斑块的关系。方法 选择2014年6月～2015年10月期间被我院神经内科收治的60例老年2型糖尿病并急性脑梗死患者为研究对象,60例老年2型糖尿病并急性脑梗死患者中,按照动脉粥样硬化严重程度不同分为:无斑块10例, 稳定斑块22例,不稳定斑块28例。选择40例老年急性脑梗死患者作为疾病对照组; 选老年健康者40名为健康对照组。采用双抗夹心法酶联免疫吸附试验(ELISA法)检测IGF-1水平。采用美国国立卫生院卒中量表(NIHSS)于发病1周、2周时行神经功能评估; 采用改良 Rankin 量表(MRS)于90 d时行神经功能评估。结果 糖尿病合并脑梗死组1周、2周时IGF-1水平均低于脑梗死组和对照组,而脑梗死组IGF-1水平高于对照组,差异有统计学意义(P<0.05)。1周、2周时糖尿病合并脑梗死患者NIHSS评分均高于脑梗死组患者(P<0.05); 糖尿病合并脑梗死组患者90 dMRS评分高于脑梗死组患者(P<0.05)。1周、2周时糖尿病合并脑梗死患者血清IGF-1水平与NIHSS评分均呈负相关(r=-0.561,P=0.006,r=-0.672,P=0.000); 1周、2周时糖尿病合并脑梗死患者血清IGF-1水平与MRS评分均呈负相关(r=-0.426,P=0.016,r=-0.445,P=0.009)。随着糖尿病合并脑梗死患者颈动脉斑块严重程度的加重,血清IGF-1水平呈下降趋势(P<0.05)。结论 IGF-1在老年2型糖尿病合并脑梗死患者外周血血清中呈现异常表达,IGF-1水平与老年2型糖尿病合并脑梗死的神经功能缺损及颈动脉斑块严重程度密切相关。     

Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage

Background

Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14.

Methods

We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both.

Results

Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH‐Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH‐PDS than patients with later cerebral infarction (p = 0.025).

Conclusions

: Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.Subarachnoid haemorrhage (SAH) is a common and serious disorder, affecting approximately 11 in every 100 000 people.¹ Cerebral infarction after SAH is a well‐described complication and is strongly associated with a poor outcome.² Strategies to improve outcome after SAH usually focus on preventing or treating vasospasm.Nimodipine reduces the risk of cerebral infarction after SAH due to vasospasm³; yet, cerebral infarction still occurs and remains a major predictor of poor outcome in multivariate models.⁴ Vasospasm is traditionally defined as arterial narrowing 3–14 days after SAH.⁵ Cerebral infarction after SAH is generally assumed to be due to vasospasm, but causality is difficult to prove in critically ill patients. Radiographic cerebral infarction allows different observers to independently review studies at leisure, but may not be symptomatic. Acute cerebral infarction may be due to the acute effects of haemorrhage and the spike in intracranial pressure, but there are few objectively defined risk factors. We sought to identify patients with cerebral infarction associated with SAH in whom the cerebral infarction was unlikely to be due to vasospasm and to describe novel risk factors for targeted intervention.     

初诊2型糖尿病合并颈动脉斑块患者颈动脉斑块灰阶中位数值预测脑梗死的临床研究

目的 探讨三维超声颈动脉斑块灰阶中位数值(Grayscale median,GSM)对初诊2型糖尿病(Type 2 diabetes mellitus,T2DM)合并颈动脉斑块患者发生脑梗死的预测价值。方法 回顾性分析2017年6月-2020年6月在本院住院治疗的初诊T2DM合并颈动脉斑块患者,根据随访中是否发生脑梗死分为脑梗死组(n=28)和非脑梗死组(n=199); 收集首次住院的临床资料及三维超声颈动脉斑块指标灰阶中位数值(Grayscale median,GSM)、斑块体积(Plaque volume,PV)、斑块厚度(Plaque thickness,PT); 比较2组临床资料及超声指标水平的差异,进一步采用logistic回归分析初诊T2DM患者发生脑梗死的影响因素,采用受试者工作特征(Receiver operating characteristic,ROC)曲线分析不同指标对初诊T2DM患者发生脑梗死的预测效能。结果 脑梗死组合并冠心病的比例(35.71% vs 19.09%)及空腹血糖[(7.37±1.32)vs(6.82±0.85)mmol/L]、餐后2 h血糖[(13.16±3.52)vs(11.97±2.14)mmol/L]、糖化血红蛋白(Glycosylated Hemoglobin, Type A1C,HbA1c)[(7.03±0.98)vs(6.55±0.33)%]、总胆固醇[(5.98±1.13)vs(5.41±0.94)mmol/L]、低密度脂蛋白胆固醇(Low density lipoprotein cholesterol,LDLC)[(3.42±0.65)vs(3.05±0.40)mmol/L]、尿酸[(360.01±76.87)vs(320.15±80.55)mmol/L]水平高于非脑梗死组(P<0.05),颈动脉斑块的GSM[(35.24±6.92)vs(41.93±11.82)]均低于非脑梗死组(P<0.05),颈动脉斑块PT,PV与非脑梗死组比较无明显差异(P>0.05)。LDLC,HbA1c、颈动脉斑块GSM是初诊T2DM患者发生脑梗死的影响因素,比值比分别为36.073、4.205、0.852(P<0.05)且四项指标单独或联合均对初诊T2DM患者发生脑梗死具有预测价值,联合指标的预测效能优于单一指标。结论 初诊T2DM患者颈动脉斑块GSM降低与脑梗死的发病有关,GSM联合实验室指标LDL-C,HbA1c能够进行脑梗死发病的预测。     

脂肪因子CTRP1与2型糖尿病合并脑梗死患者脂代谢异常的相关性研究

目的 探讨脂肪因子CTRP1与脂肪三酰甘油脂酶(ATGL)、内皮脂肪酶(EL)和脂蛋白相关磷脂酶A2(Lp-PLA2)与2型糖尿病合并脑梗死发病的关系.方法 选取2018-12—2020-10郑州大学第二附属医院确诊的2型糖尿病患者36例、合并脑梗死患者36例及健康体检者34例为研究对象.采用酶联免疫吸附法检测血清CT...     

Opalski syndrome detected on DWI MRI: A rare lateral medullary infarction. Case report and review

Introduction

Wallenberg's syndrome and ipsilateral paresis due to combined infarction of the lateral medullary and cervical spinal infarction is known as Opalski syndrome. This rarely described syndrome was reported, to our knowledge, with DWI MRI, only once.

Case report

We report the case of a 43-year-old man with autosomal dominant polycystic kidney disease who, after a brief episode of coma, developed Wallenberg syndrome and ipsilateral hemiparesis. Initial diffusion weighted-imaging MRI showed a high-intensity signal involving the lateral medulla oblongata and the spinal cord; but FLAIR MRI sequences showed bilateral high-intensity signals in the lateral medulla oblongata and spinal cord and high-intensity signals in the right and left cerebellar hemisphere in the PICA territories. MRI performed one year later showed an infarction involving the left medullary area and adjacent spinal segments alone.

Conclusion

This observation illustrates a rare syndrome of lateral medullary infarction, associated with spinal cord infarction related to a possible transient basilar occlusion.     

MSCTA联合ABCD2评分对短暂性脑缺血发作早期进展为脑梗死的预测价值

目的 探究MSCTA联合ABCD2评分对短暂性脑缺血发作早期进展为脑梗死的预测价值。方法 选取2016年6月-2017年6月本院收治的短暂性脑缺血发作(TIA)患者共92例,对所有患者行MSCTA检查以及采用ABCD2评分进行危险分层与评估,观察不同动脉狭窄程度与不同ABCD2评分下TIA患者脑梗死的发生率以及MSCTA联合ABCD2评分对TIA患者早期进展为脑梗死的预测价值。结果 轻度、中度动脉狭窄患者在1周内脑梗死的发生率明显低于重度狭窄患者(P<0.05); ABCD2评分低危组与中危组患者在1周内脑梗死的发生率显著低于高危组(P<0.05); MSCTA联合ABCD2评分预测脑梗死的特异度、灵敏度、准确度、阳性预测值和阴性预测值均明显高于单独MSCTA与ABCD2评分(P<0.05)。结论 MSCTA联合ABCD2评分对短暂性脑缺血发作患者早期进展为脑梗死具有较高的预测价值。     

ABCD2评分对短暂性脑缺血后的中期脑梗死事件和死亡的预测能力

目的探讨ABCI2评分对中国人群短暂性脑缺血(TIA)后的中期脑梗死事件及死亡的预测能力,以便利用其识别高危TIA患者。 方法采用前瞻性设计,以广州医学院第二附属医院神经内科自2008年1月开始收治的TIA患者为研究对象,共收集到179例病例资料完整的患者。对就诊的TIA患者行ABCD2评分,追踪记录其TIA发作后18月内是否发生脑梗死事件,并根据是否发生脑梗死分为无脑梗死组和脑梗死组。以病程第18月为终点事件观察时间点,统计各种疾病导致的死亡情况,并根据是否临床死亡分为生存组和死亡组。采用统计学方法分析组间年龄、血压、临床特征、症状持续时间和糖尿病史等各指标的差异性,绘制ROC曲线。 结果179例TIA患者中无脑梗死组127例,脑梗死组52例。脑梗死组就诊时血压≥140/90 mm Hg(86.5％)、肢体无力(42.3％)、症状持续时间≥60 min(55.8％)、症状持续时间10～59 min(40.4％)和患糖尿病(80.8％)比例较无脑梗死组均明显增多,差异均有统计学意义(P＜0.05)。脑梗死组ABCD2评分比无脑梗死组高,差异有统计学意义(P＜0.05)。利用ROC曲线,以ABCD2评分来预测患者患脑梗死情况,其曲线下面积为0.874,P=0.000,95％可信区间为0.817～0.931,Cutoff值为4.5分。179例TIA患者中生存组144例,死亡组35例。死亡组ABCI2评分与生存组比较差异无统计学意义(P＞0.0.5)。利用ROC曲线,以ABCD2评分来预测患者死亡情况,其曲线下面积为0.492,P=0.889,95％可信区间为0.389～0.596。 结论ABCD2评分系统在判断TIA后中期脑梗死风险方面有一定预测价值,对TIA后中期死亡危险度无预测作用。     

Sustained enhancement of residual platelet reactivity after coronary stenting in patients with myocardial infarction compared to elective patients

Introduction

Elevated platelet reactivity despite antiplatelet therapy is associated with an increased cardiovascular risk after percutaneous coronary interventions. Current guidelines recommend uniform antiplatelet maintenance regimen after percutaneous coronary interventions for patients with myocardial infarction and elective patients. We sought to demonstrate that there is a persistent enhancement of residual platelet reactivity after myocardial infarction, requiring an intensified antiplatelet maintenance therapy.

Materials and Methods

A total of 66 patients after coronary stenting for myocardial infarction (n = 36) or elective coronary stenting (n = 30) were included in this prospective, controlled study. Platelet reactivity to adenosine-5-diphosphate and arachidonic acid under treatment with clopidogrel (75 mg) and acetyl salicylic acid (100 mg) were assessed 48 hours and 30 days after coronary stenting using light transmission aggregometry and multiple electrode platelet aggregometry (Multiplate analyzer) simultaneously.

Results

Fourty-eight hours after coronary stenting all measures of residual platelet reactivity were significantly elevated in the infarction group. After a mean follow up of 37 days, residual platelet reactivity to adenosine-5-diphosphate was still consistently elevated, albeit statistically not significant. Contrarily, residual platelet reactivity to arachidonic acid significantly decreased and returned to normal by the time of follow up. Regression analyses revealed myocardial infarction, C-reactive protein and fibrinogen as predictors of enhanced platelet reactivity 48 hours after coronary stenting.

Conclusions

Patients undergoing coronary stenting for acute myocardial infarction exhibit an enhancement of residual platelet reactivity sustaining for at least 48 hours following coronary stenting. This finding provides a rationale for a continued intensified antiplatelet therapy after myocardial infarction.     

Normobaric hyperoxia retards the evolution of ischemic brain tissue toward infarction in a rat model of transient focal cerebral ischemia

Objectives: Oxygen therapy has been long considered a logical therapy for ischemic stroke. Our previous studies showed that normobaric hyperoxia (normobaric hyperoxia (NBO), 95% O₂ with 5% CO₂) treatment during ischemia reduced ischemic neuronal death and cerebromicrovascular injury in animal stroke models. In this study, we studied the effects of NBO on the evolution of ischemic brain tissue to infarction in a rat model of transient focal cerebral ischemia.

Methods: Male Sprague-Dawley rats were given NBO (95% O₂) or normoxia (21% O₂) during 90-min filament occlusion of the middle cerebral artery (MCAO), followed by 3 or 22.5 h of reperfusion. 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to evaluate the longitudinal evolution of tissue infarction.

Results： In normoxic rats, MCA-supplied cortical and striatal tissue was infarcted after 90-min MCAO with 22.5 h of reperfusion. NBO-treated rats showed a 61.4% reduction in infarct size and tissue infarction mainly occurred in the ischemic striatum. When infarction was assessed at an earlier time point, i.e. at 3 h of reperfusion, normoxic rats showed significantly smaller but mature infarction (no TTC staining, white color), with the infarction mainly occurring in the striatum. Unexpectedly, NBO-treated rats only showed immature lesion (partially stained by TTC, light white color) in the ischemic striatum, indicating that NBO treatment also retarded the process of neuronal death in the ischemic core. Of note, NBO-preserved striatal tissue underwent infarction after prolonged reperfusion.

Conclusions： Our results demonstrate that NBO treatment given during cerebral ischemia retards the evolution of ischemic brain tissue toward infarction and NBO-preserved cortical tissue survives better than NBO-preserved striatal tissue during the phase of reperfusion.     

Tremor onset with acute frontal infarct and disappearance with the second stroke

Ischemic stroke associated movement disorders can be seen as the first sign of a stroke or as a delayed onset development. Tremor after a stroke is a rare finding among movement disorders. In addition to reports of tremor caused by cerebral infarction of varied locations, data on the disappearance of existing tremor following infarction is also available. In this report, we present a case with acute tremor in the contralateral hand following frontal cortical infarction, and disappearance of the tremor after the second infarction comprising large areas in the same hemisphere.Involuntary abnormal movements caused by strokes are relatively common. Chorea, tremor, dystonia, Parkinsonism, and myoclonus associated with both infarctions and cerebral hemorrhage may occur delayed or progressive as part of the symptomatology of acute stroke.1 Patients with hand tremor associated with cerebral infarct are not encountered frequently. In addition to reports of tremor caused by cerebral infarction of varied locations, data on the disappearance of existing tremor following infarction is also available.2-5 Kim2 reported hand tremor that developed 3-21 months after infarct of the caudate nucleus, internal capsule, and thalamus in 3 patients. Kim et al4 also reported a case with essential tremor, which improved 5 weeks after frontal infarct. There is a scarcity of reports in the literature on the development of, and improvement of hand tremor following a subsequent stroke. In this report, we present a case with acute tremor in the contralateral hand following frontal cortical infarction and disappearance of the tremor after the second infarction comprising large areas in the same hemisphere. Our objective in presenting this particular case is to report the interesting development and disappearance of tremor as a result of ischemic stroke.     

Risk Factors for Cerebral Infarction in Duchenne Muscular Dystrophy: Review With our 2 Cases

Background: Although the incidence of cerebral infarction is higher in Duchenne muscular dystrophy (.75 per 100) than in the general population (7.5-11.4 per 100 000), only 18 cases have been reported, and prevention and management guidelines for infarction in this disorder remain lacking. Patients and Methods: We encountered 2 cases of Duchenne muscular dystrophy with cerebral infarction. To clarify risk factors for such infarction in Duchenne muscular dystrophy, we reviewed 20 cases, including our 2 patients. Results: Age at onset of infarction ranged from 4 to 31 years (n = 19). Most patients were 16-21 years old (14 of 19; 73.7%). Eighteen patients (90%) had dilated cardiomyopathy (DCM), showing a higher frequency than in the age-matched general Duchenne muscular dystrophy population. Left ventricular ejection fraction (LVEF) ranged from 10.2% to 42% (median, 20%; n = 9). Detectable cardiac thrombus and atrial fibrillation were rare (2 of 17; 11.8%, and 1 of 17; 5.9%, respectively). Conclusions: Presence of DCM with low LVEF seems to be the strongest risk factor for cerebral infarction in Duchenne muscular dystrophy.     

ABCD~2评分结合经颅多普勒和颈部血管超声对TIA患者近期预后的评价

目的分析ABCD2评分结合经颅多普勒和颈部血管超声对短暂性脑缺血发作(TIA)后7 d发生脑梗死的评估价值。方法以2010年1月～2011年1月住院治疗的126例TIA患者作为研究对象,收集其临床、TCD和颈部血管超声检查资料。按ABCD2评分法进行评分,计算TIA后7 d内脑梗死发生率。结果 126例TIA患者7 d内进展为脑梗死者26例,占20.6%。ABCD2评分越高,脑梗死的发生率越高(P<0.05)。TIA后7 d脑供血动脉狭窄≥50%的患者中脑梗死发生率较脑供血动脉狭窄<50%的患者明显升高(P<0.05)。ABCD2评分≥4分、脑供血动脉狭窄≥50%的TIA患者7 d脑梗死发生率为33.8%,与ABCD2评分≥4分、脑供血动脉狭窄<50%的TIA患者(7.7%)比较,其发生脑梗死的风险明显增加(P<0.05)。结论 ABCD2评分法预测7 d发生脑梗死风险的准确性较高,进一步结合经颅多普勒和颈部血管超声检查可提高预测的准确性。     

血清正五聚蛋白3、超敏C反应蛋白水平与急性脑梗死患者的病情严重程度及预后的关系

目的 探讨急性脑梗死患者血清正五聚蛋白3(PTX3)和超敏C反应蛋白(hs-CRP)水平与急性脑梗死患者的病情严重程度及预后的关系。方法 选择发病24 h内急性脑梗死患者151例为脑梗死组,同时选取同期于本院体检健康人群103例为对照组; 检测和比较2组血清PTX3、hs-CRP水平; 比较NIHSS≥5分和NIHSS<5分的患者血清PTX3、hs-CRP水平以及mRS≤2分和mRS>2分患者的血清PTX3、hs-CRP水平; 分析血清PTX3、hs-CRP水平与急性脑梗死患者NIHSS评分和mRS评分的关系以及两者对于脑梗死的严重程度和预后的预测价值。结果 与对照组比较,脑梗死组急性期血清PTX3、hs-CRP水平均明显升高(P<0.05); 与脑梗死组NIHSS<5分患者比较,NIHSS≥5分患者急性期血清PTX3、hs-CR水平升高(P<0.05); 脑梗死组mRS>2分患者急性期血清PTX3、hs-CRP水平亦均高于mRS≤2分的患者(P<0.05); 急性脑梗死患者血清PTX3、hs-CRP水平与其 NIHSS和mRS得分均呈正相关(PTX3:r_s=0.471,0.451; hs-CRP:r_s=0.381,0.320; P<0.05); ROC曲线分析显示急性脑梗死患者急性期血清PTX3、hs-CRP水平对于脑梗死的严重程度和预后的预测价值均良好,但以血清PTX3水平预测脑梗死严重程度及预后的价值最优。结论 急性脑梗死患者急性期血清PTX3、hs-CRP水平与脑梗死的严重程度和预后均相关,且均对其预后的预测价值良好,但以血清PTX3水平的预测价值更优。     

Reduced IL-2 but elevated IL-4, IL-6, and IgE serum levels in patients with cerebral infarction during the acute stage

Cytokines in the central nervous system (CNS) may play an important role in functioning as intercellular signals that orchestrate the response to injury. Whether this is a cause or result of the brain disease process is uncertain. We investigated IFN-γ, IL-2, IL-4, IL-6, and IgE in the sera of 38 patients with cerebral infarction during the acute stage and 10 normal controls using an originally devised sensitive sandwich enzyme-linked immunosorbent assay (ELISA). We found that serum levels of IL-2 derived from T helper 1 (Th1) cells were slightly reduced in patients with cerebral infarction, whereas serum levels of IL-4 and IL-6 derived from Th2 cells were elevated significantly. IL-4 induces synthesis of IgE in human B cells. Endogenous IL-6 plays an obligatory role in IL-4-dependent human IgE synthesis. We observed that serum IgE levels were elevated significantly in patients with cerebral infarction. However, serum IFN-γ levels were not elevated significantly in cerebral infarction patients. These findings suggest that elevated IL-4, IL-6, and IgE levels in the human serum may be an important factor in cerebral infarction during the acute stage. Decrease of IL-2 levels in the serum of patients with cerebral infarction may be a regulatory mechanism.     

基底节区进展性脑梗死侧支循环形成及其对近期神经功能缺失的影响

目的探讨基底节区进展性脑梗死脑侧支循环形成及其对近期神经功能缺失的影响。方法将该院收治的200例基底节区进展性脑梗死患者作为研究对象,在其入院后均采用头部CT血管造影(CTA)评估患者侧支循环建立情况,根据患者是否建立侧支循环将其分为侧支循环建立组和无侧支循环建立组,并以美国国立卫生研究院卒中量表(NIHSS)评估其入院时、卒中进展时和侧支循环建立后的神经功能缺损情况,探讨不同分级侧支循环、不同侧支循环开放类型的脑梗死患者神经功能缺失情况。结果 200例基底节区进展性脑梗死患者中有146例患者成功建立侧支循环,54例患者无侧支循环建立。侧支循环建立组在入院时和卒中进展时的NIHSS评分与无侧支循环建立组比较,差异均不显著(P 0.05);治疗2周时NIHSS评分低于无侧支循环建立组(P 0.05)。3～4级侧支循环患者在入院时和卒中进展时的NIHSS评分与1～2级侧支循环患者比较,差异均不显著(P 0.05);治疗2周时NIHSS评分低于1～2级侧支循环患者(P 0.05)。前循环脑梗死患者侧支循环建立数多于后循环脑梗死患者(P 0.05)。前循环脑梗死患者入院时和卒中进展时的NIHSS评分与后循环脑梗死患者比较,差异均不显著(P 0.05);治疗2周时NIHSS评分低于后循环脑梗死患者(P 0.05)。结论脑侧支循环形成可改善基底节区进展性脑梗死患者近期神经功能缺失情况。     

高血压脑梗死患者血管紧张素Ⅱ-1型受体基因多态性的研究

目的:探讨血管紧张素II-1型受体基因多态性与高血压脑梗死发病的关系。方法:采用聚合酶链反应技术(PCR)对48名40岁及以上人群(对照组)人和39例原发性高血压、63例高血压脑梗死患者血管紧张素Ⅱ-Ⅰ型受体基因多态性进行检测,并用非条件Logistic回归筛选出与高血压脑梗死发病相关的因素。结果:AC基因型、C等位基因频率高血压脑梗死组高于人群对照组(x2=3.92、4.53,P<0.05)和高血压组(x2=6.59、11.8,P<0.05)。高血压组与人群对照组则无差别(x2=0.026,0.023,P>0.05)。AC基因型、C等位基因是高血压脑梗死独立的危险因素。结论:血管紧张素Ⅱ。1型受体基因型AC者发生高血压脑梗死的危险性增高。