HAVE评分对非溶栓性脑梗死出血性转换的预测研究

目的制定简便易行的HAVE评分对非溶栓性脑梗死出血性转化(HT)预测研究。方法回顾性分析深圳市人民医院2008年~2010年间发病48 h内NIHSS评分≥5分的95例急性脑梗死患者,通过头部CT或MRI监测2 w内非溶栓治疗HT的发生,对HT危险因素进行综合分析,并对危险因素进行量化评分。结果模型(HAVE)中共纳入4个危险因素:3级高血压(Hypertension)、心房颤动(Atrial fibrillation)、梗死体积(Volume)及高龄(Elderly),总分共8分,其中评分大于等于4分即为出血性转化极高危人群,该评分对发生脑梗死出血性转化预测的灵敏度为0.73,特异度为0.84。结论 HAVE评分能够快速识别脑梗死出血性转化高危人群,具有良好的敏感性及特异性。     

同型半胱氨酸与脑卒中及相关因素分析

目的:研究同型半胱氨酸和脑梗死、短暂性脑缺血发作(TIA)及脑出血的关系。方法 对450例脑卒中(包括短暂性脑缺血发作、脑梗死、脑出血)患者及149例对照组进行血清同型半胱氨酸(Hcy)水平的测定,经颅超声多普勒(TCD)检测颅内外血管。结果 发现脑梗死、TIA组和脑出血组血浆Hcy水平(分别为20.82±11.86,20.61±13.73,24.78±12.75umol/L)非常显著高于对照组(9.84±2.25umol/L,p<0.01);脑梗死组与脑出血组HCY水平有显著差异,P=0.041,高同型半脱氨酸血症在脑出血组的比例(75.5％)明显高于脑梗死组(56.5％)和TIA组(48.6％),p<0.05,高同型半胱氨酸血症对脑梗死、TIA、脑出血的相对危险度分别为1.670(95％的可信区间为1.089,2.562)、1.654(95％的可信区间0.828,3.302)、2.454(95％的可信区间1.479,4.071)。未发现缺血性脑卒中血管狭窄与高同型半胱氨酸血症比例间的统计学上的显著差异。病例组中有糖尿病的患者HCY的水平16.14±7.82(umol/l)明显低于无糖尿病者22.55±12.66(umol/L),p<0.01。结论 血浆Hcy水平不但与缺血性脑卒中有关,而且对脑出血也有显著影响,高同型半胱氨酸血症与脑出血的关系更密切。血管狭窄和同型半胱氨酸水平及比例间无显著差异,无糖尿病的脑卒中患者中,同型半胱氨酸水平对脑卒中有重要影响?     

无症状性脑梗死46例临床分析

无症状性脑梗死(SBI)是指既往没有脑卒中病史,神经系统检查没有定位体征,而同时在CT或MRI检查中发现脑实质内有梗死灶的存在;或有脑卒中,但影像学发现非责任病灶,又称为静止脑梗死(SCI)。本文就我院近两年来收治的318例脑血管病人中发现SBI和SCI共46例,从危险因素、影像学特征等情况予以分析。1临床资料1.1一般资料本组318例,均经头颅CT或MRI检查,发现SBI及SCI46例,其中男31例,女15例,男女=2.071。年龄49～88岁,>60岁者38例,占82.6%。1.2影像学检查46例中,经头颅CT发现病灶42例,经MRI发现4例,其中单发脑梗死33例,多发性脑梗死…     

出血性脑梗死的临床分析

目的：研究出血性脑梗死的原因、影像学及临床特征。方法：分析116例出血性脑梗死的原因、影像学及临床特征（出自1990-2001年治疗的2050例脑梗死病例）。结果：2050例脑梗死中出血性脑梗死占5.66％，最常见的原因是脑梗死（62.06%），特别是心源性。最早出现的出血性脑梗死为脑梗死后17小时。78例为血肿型，38例非血肿型。结论：出血性脑梗死应严格控制血压、血糖。临床症状及体征不变或加重，特别是脑梗死或大面积脑梗死，应检查或复查CT和（或）MRI。发现出血性脑梗死，应立即停用抗凝、溶栓治疗。     

应用ABCD^2评分法和纤维蛋白原预测TIA后短期脑卒中风险

目的探讨ABCD^2＋纤维蛋白原评分法对短暂性脑缺血发作后7d内发生脑梗死的预测价值。方法用ABCD^2评分法和ABCD^2＋纤维蛋白原评分法分别测定135例TIA患者的评分,并观察TIA后7d内脑梗死的发生率。结果ABCD^2＋纤维蛋白原评分法和ABCIY评分法的曲线下面积（95％CI）分别为0．755（0．668-0．842）和0．711（0．618-0．804）。135例TIA患者中42分者13例,脑梗死的发生率为零;评分为3分者12例,脑梗死的发生率为8％;评分为4分者30例,脑梗死的发生率为17％;评分为5分者40例,脑梗死的发生率为25％;评分为6分者28例,脑梗死的发生率54％;评分≥7分者12例,脑梗死的发生率为58％。低危（0～3分）、中危（4-5分）和高危（6～8分）组TIA后7d内发生脑梗死的比例分别为4％、21％和55％（P〈0．05）。结论ABCD^2＋纤维蛋白原评分法的预测价值高于ABCD^2评分法。ABCD^2＋纤维蛋白原评分标准是临床上预测TIA短期进展为脑梗死的一种比较有效的方法。     

无症状性脑梗死46例临床分析

无症状性脑梗死（SBI）是指既往没有脑卒中病史，神经系统检查没有定位体征，而同时在CT或MRI检查中发现脑实质内有梗死灶的存在；或有脑卒中，但影像学发现非责任病灶，叉称为静止脑梗死（SCI）。本文就我院近两年来收治的318例脑血管病人中发现SBI和SCI共46例，从危险因素、影像学特征等情况予以分析。     

无症状性脑梗死43例影像学及临床分析

目的;探讨无症状性脑梗死(ACI)患者的影像学改变与临床表现。方法:对1999～2002年有短暂性脑缺血发作(TIA)史或有眩晕、头痛而无明确脑卒中病史的180例60岁以上老年人进行CT或MRI检查.并对43例影像学检查为ACI者进行简易智能量表检查(MMSE)和认知功能测验。结果:行CT检查的110例老年人中ACI18例(16％),MRI检查的70例中ACI25例(36％)。43例ACI者中38例心理学测验得分均低于非ACI者。结论:ACI并非无临床症状,只是症状轻微、短暂,或者没有经过仔细、敏感的量化检测而被忽略,最终将演变成血管性痴呆。     

高血糖对急性脑梗死的预后影响

326例急性脑梗死患者分为3组：糖尿病组48例,非糖尿病高血糖组86例和非糖尿病正常血糖组192例。按照脑梗死病人临床神经功能缺损程度评分法和缺血性脑卒中CT扫描病灶范围评分法,对照分析了脑梗死后高血糖症与临床表现及脑缺血性损害程度与短期预后的关系。结果表明,急性脑梗死后高血糖不仅临床表现病情重（P＜0．01）和脑缺血性损害范围大（P＜0．05）,而且对卒中短期预后也有不良的影响。     

首发脑卒中的无症状性脑梗死的临床分析

目的探讨无症状性脑梗死在首发脑卒中患者中的发生率、临床特点、影像学分布特点及危险因素，提高对该病的认识及早期诊断的重要性。方法对520例首发脑卒中患者进行头颅CT和MRI检查，并对发现的143例无症状性脑梗死患者的影像学及临床资料进行回顾性分析。结果首发脑卒中病人无症状性脑梗死的发生率为27．5％，其中86．56％为腔隙性梗死。病灶部位以放射冠区为最多(48．58％)，其次为侧脑室旁(28．55％)及基底节区(9．17％)。结论无症状性脑梗死与症状性脑梗死一样，二者有共同的危险因素。     

小脑梗死52例临床分析

目的深入探讨小脑梗死的病因、临床表现、影像学改变、诊断及治疗。方法对1997年4月～2002年11月我院收治的52例小脑梗死患者的临床资料进行回顾性分析。结果该病51～60岁为高发年龄段，病因及危险因素主要为高血压病及心脏病。最主要的临床表现为眩晕、小脑性共济失调。此外．头痛重要又易被忽视．占本组患者的32．7％。头部CT48h内阳性率30．8％。头部MRI确诊率100％。46例经内科保守治疗．6例行外科于术治疗．总治愈率48．1％．死亡率5．8％．脑疝为主要死因。结论中老年人持续出现眩晕、共济失调要注意小脑梗死的可能．头部MRI确诊小脑梗死优于头部CT．一般采用内科保守治疗．病情严重者应外科手术，防治脑疝。     

影响急性脑梗死出血性转化的危险因素

目的 探讨急性脑梗死的出血性转化的危险因素。方法 收集2012年1月～2015年1月在湖北省恩施州利川市人民医院神经内科住院的急性脑梗死患者的临床及实验室检查资料,并在入院后10 d内行头颅CT复查,采用多变量logistic回归分析确定出血性转化的独立危险因素。结果 共纳入345例急性脑梗死患者,其中男205例,女140例,101例发生出血性转化。出血性转化组的年龄、脑梗死体积、脑卒中史或TIA史、高血压病、糖尿病、抗凝药和房颤的比例均显著高于非出血性转化组(P<0.05),而2组抗血小板聚集药、他汀类、高脂血症史、吸烟或饮酒史无明显差异(P>0.05)。多变量logistic回归分析显示年龄(OR=1.168,95%,CI=1.059～3.412; P=0.021)、梗死体积(OR=3.461,95%C1=1.317～6.270; P=0.044)和房颤(OR=1.284,95%C1= 1.117～2.903; P=0.015)为出血性转化的独立危险因素。结论 急性脑梗死患者出血性转化的发生率为29.3%,年龄、脑梗死体积和房颤为出血性转化的独立危险因素,绝大多数出血性转化不会加重临床症状,临床症状加重的患者主要是脑实质血肿型。     

Prior antiplatelet use and infarct volume in ischemic stroke

BACKGROUND: Conflicting data exist on the role of antiplatelet agents in reducing incident ischemic stroke magnitude, but most prior studies used clinically-assessed neurologic deficit as the index of stroke extent rather than more precise volumetric measurements of infarct size. We assessed the relation of premorbid antiplatelet use to initial diffusion-weighted MRI (DWI) lesion volumes among acute ischemic stroke patients. METHODS: Consecutive patients presenting within 24 h of ischemic stroke over an 18-month period were studied. DWI lesions were outlined using a semi-automated threshold technique. Subjects were categorized into two groups: antiplatelet (AP) or no antithrombotic (NA). The relationship between prestroke antithrombotic status and DWI infarct volumes was examined using multivariate quantile regression. RESULTS: One hundred sixty-six individuals met study criteria: 75 AP and 91 NA patients. Median DWI volume was lower in the AP group than in the NA group (1.5 cc vs. 5.4 cc, p=0.031). A multivariable model (adjusting for age, history of transient ischemic attack, admission temperature, admission blood pressure, admission serum glucose, stroke onset to imaging interval, stroke mechanism, premorbid statin and antihypertensive use) demonstrated smaller infarcts in the AP vs. NA group (adjusted volume difference: -1.3 cc, 95% CI=-0.09, -2.5, p=0.037). Prior statin use, no history of TIA, large vessel atherosclerosis and microvascular ischemic disease stroke mechanism were also independently associated with reduced infarct volume. CONCLUSIONS: Prior antiplatelet treatment is independently associated with reduced cerebral infarct volume among acute ischemic stroke patients. Premorbid statin use, TIA history and stroke mechanism also predict infarct volume in ischemic stroke.     

Diffusion MRI in patients with transient ischemic attacks.

BACKGROUND AND PURPOSE: Diffusion MRI has established value in patients with ischemic stroke but has not been systematically investigated in patients with transient ischemic attack (TIA). METHODS: Clinical, conventional MRI, and diffusion MRI data were collected on 42 consecutive patients with symptoms of cerebral TIA. TIA imaging data were compared with those from a contemporaneous group of 23 completed stroke patients. RESULTS: Twenty of the 42 TIA patients (48%) demonstrated neuroanatomically relevant focal abnormalities on diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) imaging. When present, DWI/ADC signal changes in TIA patients were less pronounced and smaller in volume than those in completed stroke patients. TIA symptom duration was significantly longer for DWI-positive than for DWI-negative patients, 7.3 versus 3.2 hours. Diffusion MRI information changed the suspected anatomic and vascular TIA localization and the suspected etiologic mechanism in over one third of patients with diffusion MRI abnormalities. Of the 20 TIA patients with identifiable lesions on diffusion MRI, 9 had follow-up imaging studies; of these, 4 did not show a relevant infarct on follow-up imaging. CONCLUSIONS: Diffusion MRI demonstrates ischemic abnormalities in nearly half of clinically defined TIA patients. The percentage of patients with a DWI lesion increases with increasing total symptom duration. In nearly half, the diffusion MRI changes may be fully reversible, while in the remainder the diffusion MRI findings herald the development of a parenchymal infarct despite transient clinical symptoms. Finally, diffusion imaging results have significant clinical utility, frequently changing the presumed localization and etiologic mechanism.     

Frequency and predictors of spontaneous hemorrhagic transformation in ischemic stroke and its association with prognosis

Few prospective studies have examined the frequency, predictors and long-term outcomes of spontaneous hemorrhagic transformation (HT) in patients with ischemic stroke not receiving thrombolytic treatment. We prospectively enrolled a consecutive cohort of 407 patients with ischemic stroke who were admitted within one month of stroke onset. In patients who developed spontaneous HT, the area of the infarct and HT were examined by computed tomography (CT) or magnetic resonance imaging (MRI). Univariate analysis was used to correlate clinical characteristics with appearance of HT, then multivariate logistical regression was used to identify independent predictors of spontaneous HT and factors that predict 3-month prognosis of ischemic stroke. Spontaneous HT was observed in 50 patients (12.3 %), comprising 33 cases (66 %) of hemorrhagic infarction, 17 (34 %) of parenchymal hematoma, 32 (64 %) of non-symptomatic HT, and 18 (36 %) of symptomatic HT. In 40 % of HT cases, the condition was detected by CT or MRI within 4–7 days of symptom onset. Multivariate logistic regression identified atrial fibrillation (OR 4.88, 95 % CI 1.83–13.00, P = 0.002) and infarct area (OR 4.48, 95 % CI 1.85–10.85, P = 0.001) as independent predictors of HT in ischemic stroke. Multivariate analysis also found that spontaneous HT was not independently associated with a worse 3-month prognosis for ischemic stroke (OR 1.59, 95 % CI 0.38–6.69, P = 0.527). Spontaneous HT occurred in 12.3 % of our patients with ischemic stroke, and atrial fibrillation and large infarct area were independent predictors. Spontaneous HT was not an independent predictor of a worse 3-month prognosis for ischemic stroke.     

Hemorrhagic lacunar stroke

A total of 17 patients with lacunar syndromes due to intracerebral hemorrhage or hemorrhagic lacunar stroke (pure motor hemiparesis 9, sensorimotor stroke 5, pure sensory stroke 3) are reported. Data from these patients were obtained from consecutive stroke patients included in the prospective Hospital Sagrat Cor-Alian?a Stroke Registry. Hemorrhagic lacunar stroke accounted for 3.8% of all cases of lacunar syndrome (n = 439) and 7.4% of all cases of intracerebral hemorrhage (n = 229) entered in the database. Demographic, anamnestic, clinical and neuroimaging variables in patients with hemorrhagic lacunar stroke, non-lacunar intracerebral hemorrhage and non-hemorrhagic lacunar stroke were compared. Predictors of hemorrhagic lacunar stroke were assessed by logistic regression analysis. Hypertension, cigarette smoking and involvement of the internal capsule were significantly more frequent in patients with hemorrhagic lacunar stroke than in those with non-lacunar intracerebral hemorrhage, whereas nausea and vomiting, altered consciousness, speech disturbances, hemianopia, and ventricular hemorrhage were significantly less frequent. As compared with non-hemorrhagic lacunar stroke, patients with hemorrhagic lacunar stroke were more likely to have hypertension, sudden stroke onset (minutes), head injury, headache, and basal ganglia involvement and less likely to have diabetes, gradual stroke onset (hours), and dysarthria. After multivariate analysis, only headache (OR 10.14), sudden onset (OR 9.89), and dysarthria (OR 0.10) were independent predictors of hemorrhagic lacunar stroke. Accordingly, the presence of headache and sudden onset of symptoms and absence of dysarthria may be useful signs for distinguishing hemorrhagic lacunar stroke from other causes of lacunar stroke.     

Role of Associated Cortical Lesions in Motor Partial Seizures and Lenticulostriate Infarcts

Summary: In a population-based study, we evaluated seizures occurring in the first 15 days after strokes among 1,640 consecutive patients who had ischemic (814 infarcts with atheroma and 126 with cardiogenic embolism, 273 lacunar infarcts, 259 transient ischemic attacks) or hemorrhagic stroke (129 supratentorial hematomas and 24 subarachnoïd hemorrhage) on computed tomography (CT) scan. Ninety patients had an epileptic seizure in the first 15 days after stroke onset. Thirteen of the 90 had a lenticulostriate infarct, diagnosed on CT scan, without an apparent ipsilateral cortical ischemic lesion. No lenticulostriate hematoma was observed with seizures. To determine the possible existence of an ipsilateral cortical lesion, magnetic resonance imaging (MRI) with gadolinium perfusion, and HMPAO single photon emission CT (SPECT)were performed in the 13 patients with seizures. MRI showed an associated ipsilateral posterofrontal or anterotemporal cortical ischemic lesion in 11 cases, and SPECT showed decreased blood flow in the ipsilateral frontal area in all cases (superficial sylvian territory). Overall, 56 patients had a lenticulostriate infarct and clinical, CT, and MRI data from the 13 with seizures was compared with those of the 43 without seizures. Two criteria differentiated the two groups: the size of the lenticulostriate infarct was larger (8.3 vs. 3.9cm³) and ipsilateral cortical ischemic lesions were more frequent in the group with seizures (84 vs. 9%).     

Clinical diagnosis of ischemic versus hemorrhagic stroke: applicability of existing scores in the emergency situation and proposal of a new score.

Several scores exist to clinically differentiate between ischemic and hemorrhagic stroke, but none has been developed in the emergency situation in which transient ischemic attack (TIA) and cerebral infarction might not yet be clearly distinguished. Information on 540 patients with ischemia (including TIA) or hemorrhage was abstracted from medical charts. Of 540 patients hospitalized with stroke, 98 had a hemorrhage. Age, obesity, anamnestic stroke/TIA, peripheral arterial disease, onset during physical activity, headache, impaired consciousness, hemisyndrome, meningismus and systolic blood pressure contributed to the differential diagnosis and were included in our proposed score. The score performed well in comparison with existing scores. The inclusion of TIA and the explicit incorporation of incomplete information may enhance the applicability of differential diagnostic scores in the prehospital emergency situation.     

Headache associated with ischemic cerebrovascular disease

Headache often accompanies acute ischemic stroke. Observational studies indicate that 15 to 40% of patients with acute ischemic stroke report headache in close temporal relation to the event. The onset headache is more often seen in posterior circulation strokes than in strokes in other vascular territories. Transient ischemic attacks (TIA) can also lead to headache. The pathophysiology of headache associated with acute ischemic stroke includes edema, hemorrhagic transformation, and changes in the trigeminovascular system.     

The impact of delays in computed tomography of the brain on the accuracy of diagnosis and subsequent management in patients with minor stroke

OBJECTIVES: To determine the proportion of haemorrhagic strokes misdiagnosed as infarcts on computed tomography (CT) in patients with mild stroke, and the implications for health care. METHODS: Patients with mild stroke presenting as inpatients or outpatients four or more days after stroke to our stroke service (catchment population 500 000) were recruited prospectively. They underwent detailed clinical examination and brain imaging with CT and magnetic resonance imaging (MRI) on the day of presentation. CT and MR images were examined independently to identify infarct, primary intracerebral haemorrhage, haemorrhagic transformation, or non-vascular lesion. RESULTS: In 228 patients with mild stroke (median time from stroke to scan 20 days), primary intracerebral haemorrhage was identified by CT in two patients (0.9%; 95% confidence interval (CI), 0.1% to 3.1%) and MRI in eight (3.5%; 1.5% to 6.8%). Haemorrhagic transformation was identified by CT in three patients (1.3%; 0.1% to 5.6%) and MRI in 15 (6.6%; 3.7% to 10.6%). The earliest time primary intracerebral haemorrhage was not identified on CT was 11 days. CONCLUSIONS: CT failed to identify 75% of primary intracerebral haemorrhages, equivalent to 24 patients per 1000 (95% CI, 14 to 37) with mild strokes. To detect haemorrhages reliably, CT would need to have been performed within about eight days. Rapid access to neurovascular clinics with same day CT brain imaging is required to avoid inappropriate secondary prevention. Increased public awareness of the need to seek urgent medical attention after stroke should be encouraged. MRI should be considered in late presenting patients.     

Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.