出血性脑梗死30例临床和影像分析

目的 研究出血性脑梗死的病因、影像和临床特征。方法 回顾3年中341例住院非腔隙性脑梗死的临床资料。分析30例HI的病因、临床和影像改变。结果 HI发病率占同期脑梗死的8．8％。脑栓塞为其主要病因，占70％，并以心源性栓塞为主。HI最早发生在脑梗死后24h内。最长时间为30d。26例发生在MCA分布区。有血肿型和非血肿型之分（18例12 例）。结论 脑栓塞和大面积脑梗死患者症状加重或治疗后无明显好转者，建议发病后1到2周内进行影像学复查。     

出血性脑梗死23例CT与临床分析

目的 探讨出血性脑梗死(HI)的CT表现及临床特点。方法 通过CT和临床检查，对23例患者进行观察分析。结果 HI多见于病情加重或经治疗持续不缓解或癫痫发作者16例（69.6%），病后1-2周内HI发生率达91.35%，且均见于大面积脑梗死患者。CT表现分二型：血肿型和非血肿型。结论 脑栓塞和大面积脑梗死患者症状加重或治疗后无明显好转者，建议发病后1-2周内进行颅脑CT复查。治疗中应依据曩像及病情变化而进行分别治疗。     

出血性脑梗死临床与CT、MRI分析

１６例出血性脑梗死（ＨＩ）病人，均经二次ＣＴ或ＭＲＩ检查。１４例均在首次ＣＴ检查发现颅内单发或多发低密度灶，二次ＣＴ或ＭＲＩ检查均显示大面积脑梗死伴出血，按部位分类以大脑中动脉区为最多（１０例，）影学改变可分为血肿型（５例）及非血肿型（１１例），本组中报告ＨＩ患者率较国外为低，所有病例治疗结果表明非血肿型预后较好，治疗中依其病变没情况进行分别治疗是必要的。     

出血性脑梗死CT与临床分析

目的 探讨出血性脑梗死的病因、CT和临床表现。方法 回顾我院收治的35例HI的临床资料，分析其病因、CT及临床表现的改变。结果 出血性脑梗死最常见病因为心源性脑栓塞．以梗死后第2周发病率最高．血肿型症状重，有占位效应；非血肿型症状轻，但恢复慢。结论 对初诊为脑梗死的患者临床症状继续加重或出现新的症状体征以及按脑梗死治疗效果不明显时。应及时行头颅CT扫描，以相应调整治疗方案。     

出血性脑梗死的CT表现特点分析

目的通过对出血性脑梗死患者的CT检查结果进行回顾性分析,探讨CT诊断出血性脑梗死的临床价值,及CT扫描的表现特点。方法选取本院2005-03—2014-03收治的出血性脑梗死患者74例,均接受CT检查,将影像学资料进行回顾性分析,总结CT诊断的准确性,并观察患者的影像学表现特点,为临床检查提供指导性建议。结果 CT扫描后均确诊为脑梗死,经后期持续复检明确诊断为出血性脑梗死,诊断准确率为100.0%。病灶部位多为大脑中动脉主干、动脉供血区以及分支供血区。血肿型20例,非血肿型54例。血肿型患者CT检查的表现特点为低密度区存在明显可见的高密度团块状影,而非血肿型患者CT表现特点为各形态低密度影中存在不均匀的条索状或斑片状高密度影。且样本均存在不同程度的占位效应。结论出血性脑梗死的发病率与病死率较高,临床早期诊断措施可指导治疗的准确程度,进而降低不良预后事件的发生率。针对疑似患者采用CT检查与复查可有效提高出血性脑梗死的确诊率,具有良好的准确性,通过检查结果的不同表现特征也能够明确指出出血范围与部位,进一步为临床治疗提供方向与依据,值得推广应用。     

出血性脑梗死58例临床分析

目的 探讨出血性脑梗死的病因、发病机制及影像学特点.方法 对58例经颅脑CT/MRI证实的出血性脑梗死患者的临床和影像资料进行分析.结果 出血性脑梗死发生率为7.05%,好发于心房纤颤、大面积梗死、溶栓、降纤、抗凝患者;影像学上表现为非血肿型占86.21%,血肿型占13.79%.结论 脑栓塞、大面积脑梗死、溶栓、降纤、...     

出血性脑梗死58例临床分析及CT特点

目的探讨出血性脑梗死（HI）的临床表现与头颅CT特点。方法对58例出血性脑梗死患者的临床特点及头颅CT检查结果进行分析。结果发生HI时部分患者病情再度加重,且以头痛频度最高,也有部分患者临床症状无变化;根据头颅CT表现可分为非血肿型和血肿型。结论头颅CT是诊断HI的可靠手段。对脑梗死特别是大面积梗死及心源性栓塞,不论临床症状有无加重,均须定期头颅CT检查,以及时发现本病,争取合理治疗。     

出血性脑梗死CT与临床分析

目的　探讨出血性脑梗死的病因、CT和临床表现。方法　回顾我院收治的 35例HI的临床资料 ,分析其病因、CT及临床表现的改变。结果　出血性脑梗死最常见病因为心源性脑栓塞 ,以梗死后第 2周发病率最高 ,血肿型症状重 ,有占位效应 ;非血肿型症状轻 ,但恢复慢。结论　对初诊为脑梗死的患者临床症状继续加重或出现新的症状体征以及按脑梗死治疗效果不明显时 ,应及时行头颅CT扫描 ,以相应调整治疗方案。     

出血性脑梗死37例临床分析

目的提高对出血性脑梗死的发病规律、临床特点的认识和指导临床治疗。方法回顾分析37例出血性脑梗死病例,根据其临床表现、影像资料及预后进行分型。结果出血性脑梗死的临床表现取决于继发性出血的时间和出血量的多少,按发病时间及部位可分为早发型、迟发型及血肿型、不规则型。早发型及血肿型预后较差。结论出血性脑梗死分型不同,预后不同。治疗上应分型分治,个体化治疗。     

心源性脑梗死的影像表现

目的：评价CT和MRI-DWI在心源性脑梗死诊断中的临床应用价值。方法选择临床资料完整的89例心源性脑梗死患者的首次和治疗中复查影像表现进行回顾性分析。结果（1）首次影像学检查表现：单发47例,多发42例。C T检查57例,超急性期2例,急性期21例,亚急性期34例;M RI-DWI检查32例,超急性期15例,急性期10例,亚急性期7例。多呈片状、斑片状分布于皮质或（和）皮质下区,CT呈低密度灶,T2 WI呈高信号,DWI呈异常高信号,范围较 T2 WI大。大梗死灶（面积＞3 cm2）55个,小梗死灶（1.5～3.0 cm2）42个,腔隙性梗死灶（＜1.5 cm2）63个。（2）栓塞的血管分布：颈内动脉系统受累73例,其中大脑前动脉18例,大脑中动脉55例;椎基底动脉系受累11例,颈内动脉与椎基底动脉同时受累5例。（3）出血性脑梗死的影像表现：72例治疗中复查检出出血性脑梗死34例,1～3 d检出5例,3～7 d 9例,7～14 d 17例,14 d以上3例;影像表现为在片状梗死区内斑点、片状,血肿样出血灶或多处皮质区梗死灶内出血征象,斑点片状28例,血肿样6例,中心型10例,边缘型19例,混合型5例。结论 C T和M RI能够为心源性脑梗死的诊断、随访复查及判断预后提供更多直接可靠的影像学依据,DWI比CT与常规MRI在超急性期脑梗死治疗决策的确立中更具临床应用价值。     

Anticoagulation and hemorrhagic infarction in cerebral embolism secondary to rheumatic heart disease

The immediate clinical course of 42 patients with cerebral embolism secondary to rheumatic heart disease (RHD) was analyzed retrospectively. All the cases included cranial computed tomographic (CT) findings. Twenty-five patients received early anticoagulant therapy (AT) and 17 did not. Recurrent embolic events occurred in only one case. Seven instances of hemorrhagic infarction (HI) were found. In five cases, the development of HI correlated with a recurrent stroke, which occurred in each case within 48 hours after the initial cerebral embolism. Three of the patients with HI died (all of them were receiving AT). We believe that HI is a frequent cause of recurrent stroke after a cerebral embolic event, that it generally occurs in the first 48 hours, and that its outcome is possibly worsened by AT. Anticoagulant therapy should be delayed for three days after a cerebral embolic event secondary to RHD.     

出血性脑梗死的MRI特征性表现及临床分析

目的探讨出血性脑梗死(HI)的MRI特征性表现及与临床关系。方法分析30例HI患者的MRI表现和临床资料。结果HI以发病2周内常见,约占76.7%。不同部位脑梗死HI的出血形态、位置不同:脑叶HI15例(50.0%),脑回状、斑片状出血位于皮层和/或皮层下白质;脑深部HI(基底节及丘脑)10例(33.3%);小脑HI4例(13.3%),斑片状、线状出血位于梗塞区内、边缘;混合型2例(6.7%)。T2*WI呈低信号。结论HI的MRI表现与脑梗死部位、面积有密切关系。T2*WI有助于HI的检出。脑梗死患者病情加重或考虑大面积脑梗死应在2周内进行影像学复查,以利于HI的早期诊断和治疗。     

大块脑梗塞中出血性梗塞的病理特点

报告２４例大块脑梗塞的脑局解病例，对其中１６例ＨＩ的病理特点及发生机制进行探讨。结果证实：ＨＩ占本组大块脑梗塞的发生率为７１．４％，脑血栓ＨＩ的发生率为６０％。ＨＩ多发生在梗塞灶的边缘区及皮质区，以小静脉和毛细血管出血为主。ＨＩ的发生与梗塞的体积及动脉血压增高有关。其发生机制可能是周边区或皮质区侧枝循环建立和脑水肿导致静脉回流障碍，血液淤滞所致。本文还证实溶栓治疗与其它治疗比较并未见出血扩大。     

非大动脉粥样硬化型脑梗死130例临床分析

目的探讨非大动脉粥样硬化型脑梗死病因、神经功能缺损情况、影像学检查及治疗。方法连续收集非大动脉粥样硬化型脑梗死患者130例,按照TOAST分型标准进行病因分型并分析其临床特点。结果本组患者TOAST分型的结果是:不明原因型53例(40.8%),小动脉闭塞型39例(30.0%),心源性栓塞型28例(21.5%)、其他明确病因型10例(7.7%)。心源性栓塞型平均年龄最大,其他明确病因型最小(χ~2=16.211,P<0.05)。小动脉闭塞型入院时神经功能缺损最轻,其他明确病因型病情最重(χ~2=4.347,P<0.05)。结论非大动脉粥样硬化型脑梗死病因复杂,各亚型的临床特点存在较大差异,临床上需要根据不同病因予以个体化医疗支持及评估预后。     

116例大脑中动脉病变患者脑梗死类型分布和脑灌注异常分析

目的 应用神经影像检查,分析大脑中动脉闭塞性疾病(MCAOD)患者梗死类型分布和脑灌注异常. 方法 对经CT血管造影(CTA)证实的116例MCAOD患者的CT平扫、CT灌注成像(CTP)和CTA的影像资料进行回顾性分析,确定其脑梗死类型分布和脑灌注改变. 结果 116例患者中,CTA共检出133条大脑中动脉(MCA)狭窄或闭塞,其中单侧者99例,双侧者17例.其中MCA闭塞25条,重度狭窄39条,中、轻度狭窄69条.CT或MRI显示腔隙性脑梗死(LIS)45例,各型分水岭脑梗死(CWSI)38例,流域性脑梗死26例,纹状体内囊梗死(SCI)10例,未检出梗死病灶14例.CTP显示MCA供血区内脑血流灌注异常96例,其中58例有MCA供血区的大范围血流灌注减低.未检出血流灌注异常者37例. 结论 由于MCA狭窄的部位、程度和发病机制的不同以及侧支循环的建立,MCAOD可造成不同类型的脑梗死和血流灌注异常.     

Silent intracerebral lesions identified on magnetic resonance imaging in patients presenting with initial stroke--comparative studies of the affected hemisphere and the contralateral one]

Among patients who had undergone MRI examinations with a clinical suspicion of stroke, we selected 82 patients with initial cerebral infarction being located only in a unilateral cerebral hemisphere. Seventeen (21%) subjects had wedge-shaped lesions including cerebral cortex (the cortical type), 65 (79%) had them predominantly in white matter and/or territory of the deep perforators (the subcortical type). Fifty nine cases out of total 82 (72%:9 in the cortical type, 50 in the subcortical type) had the silent cerebral infarction in the contralateral hemisphere to the affected side found on the 1.5 tesla superconductive system T2 weighted magnetic resonance imaging. Among them, 57 had the contralateral small cortical and/or subcortical (white matter) infarction, the other 2 cases had the contralateral lacunar infarction in the basal ganglia-internal capsule area as the silent lesion. The incidence of the cortical type was high in cases without the silent cerebral infarction in the contralateral hemisphere. It might be suspected that the cortical type had tendency to present clinical symptoms caused by initial stroke without prior silent cerebral infarction. The author proposed that the cerebral embolism might play an important role in showing the sudden onset clinical symptoms of the cortical type. And the author also proposed that there might be a difference in the development of clinical symptoms between the silent cerebral infarction located in the basal ganglia-internal capsule area and the cortical-subcortical (white matter) area.     

急性脑梗死的心电图改变

观察72例脑梗死患者,合并心电图（ECG）改变59例,占81．9％。腔隙性脑梗死及脑血栓ECG以窦性心动过速及占室肥厚劳损多见,脑栓塞以心房纤颤多见。CT与ECG对照发现,额顶叶大面积梗塞80?G正常,颞顶叶大面积梗塞灶ECG均提示心房纤颤。指出ECG改变与脑梗塞死型及部位相关。本级9例脑栓塞均由心房纤颤及心肌梗死引起,积极防治心脏病可减少脑血管病的发病率。     

Clinically overt and silent cerebral embolism in the course of infective endocarditis

The data on cerebral embolism prevalence in the course of infective endocarditis (IE) are most probably underestimated. Part of the cerebral embolism episodes are clinically silent. The objective of this study was to assess the prevalence of clinically silent cerebral embolism in the course of IE and to correlate hematological, inflammatory, and echocardiography parameters with the presence of clinically overt or silent cerebral embolisms. For this purpose, we examined 65 patients with IE by blood test, cultures, echocardiography, and MRI/CT imaging. Clinically overt cerebral embolism was found in 13 patients; 52 patients had no clinically overt cerebral embolism. MRI/CT examinations revealed that among patients with no clinically overt cerebral embolism, 24 had clinically silent cerebral embolism. Thus, 37 patients in all were diagnosed with a cerebral embolism episode (overt + clinically silent). Clinically silent cerebral embolism was diagnosed in 36.9% of all patients, being as high as 64.8% of cerebral embolism cases. Silent or overt embolism development did not depend on the localization of the inflammatory process in either native or artificial valves. The type of cerebral embolism was not found to be influenced by leukocytosis, platelet count, ESR, or hsCRP levels. Neither was the type of embolism found to be influenced by the etiologic factor. Nine patients died. In three patients, the cause of death was hemorrhage from a cerebral apoplectic focus. These results suggest that clinically silent central nervous system embolism is a common complication of infective endocarditis and each patient should undergo a neuroimaging examination.