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1.
局灶性脑梗死继发逆行性神经纤维变性及其临床意义   总被引:4,自引:3,他引:1  
目的应用磁共振弥散张量成像(diffusion tensorimaging,DTI)技术前瞻性动态观察皮质下或脑干局灶性脑梗死后,病灶上方继发的神经纤维逆行性变性的过程,探讨其对神经功能恢复的影响。方法选择具有单侧内囊区或脑干的独立病灶的脑梗死患者16例,选择年龄及性别相匹配的健康志愿者16名作为对照组。患者分别在发病的第1周(W1)、第4周(W4)、第12周(W12)进行DTI检测和美国国立卫生研究院卒中评分(national institutes of health stroke scale,NIHSS)、简式Fugl-Meyer运动功能评分法(FM)和Barthel生活指数(Barthel Index,BI)评分。计算半卵园中心的DTI参数和各临床评分在观察期内变化的百分数绝对值,分析两者之间的相关关系。结果与对照组比较,病灶上方半卵园中心的部分弥散各向异性(fractional anisotropy,FA)值在各个时间点均明显减少(患者组W1:(0.43±0.02),W4:(0.39±0.01),W12:(0.33±0.02),分别与对照组比较:(0.46±0.01),P<0.01),而平均弥散量(mean diffusivity,MD)无统计学差异(P>0.05)。患者从W1至W12,半卵园中心FA值减少的百分数的绝对值与NIHSS评分减少百分数的绝对值之间(r=-0.49,P<0.05)及与FM增加百分数的绝对值之间(r=-0.56,P<0.05)呈负相关,与BI变化的百分数的绝对值之间无明显相关(P>0.05)。结论局灶性皮质下脑梗死可引起神经纤维逆行性的继发性变性,而且这种逆行性的神经纤维继发性变性会持续存在并可能阻碍患者神经功能的恢复。  相似文献   

2.
DTI态观察脑梗死后颈髓皮质脊髓束继发性损害   总被引:1,自引:0,他引:1  
目的应用磁共振弥散张量成像(diffusion tensori maging,DTI)动态观察脑梗死后颈髓皮质脊髓束的弥散变化,及其与患者神经功能恢复之间的关系,探讨脑梗死后颈髓皮质脊髓束纤维继发性损害及其意义。方法患者分别在的第1周,第4周以及第12周进行DTI检测,每次MRI检测之前采用NIHSS、简式Fugl-Meyer运动功能评分法(FM)和Barthel生活指数(Barthel Index,BI)评定。分别测量颈髓皮质脊髓束的部分弥散各向异性(fractional anisotropy,FA)值与平均弥散量(mean diffusivity,MD)。结果与对照组比较,患者组病灶对侧颈髓皮质脊髓束FA值在各个时间点都明显低于健康对照组第1周:(0.66±0.01,vs,0.71±0.01,P0.01),第4周(0.61±0.02,vs,0.69±0.01,P0.01),第12周(0.53±0.02,vs,0.69±0.01,P0.01),MD值则无明显差异。患者病灶对侧颈髓皮质脊髓束FA值在观察期内变化的百分数与NIHSS、Fugl-Meyer运动评分变化的百分数呈负相关(P0.05)。结论局灶性脑梗死引起的皮质脊髓束纤维的继发性损害可以延续到颈髓水平,颈髓皮质脊髓束的继发性损害可能延缓患者神经功能的恢复。  相似文献   

3.
目的 采用磁共振弥散张量成像(diffusion tensor imanging,DTI)动态观察脑桥梗死后,远离梗死灶的延髓及小脑中脚神经纤维华勒变性及其对患者神经功能恢复的影响.方法 选择单侧脑桥梗死患者14例,以及年龄性别相匹配的健康志愿者14名作对照组.分别在发病第1、4、12周进行DTI检测,并行美国国立卫生研究院卒中评分(National Institutes of Health stroke scale,NIHSS)、简式Fugl-Meyer运动功能评分(Fugl-Meyer motor scale,FM)、共济失调评分(ataxia rating scale,ARS)和Barthel生活指数(Barthel index,BI)评分.结果 与对照组比较,患者梗死灶同侧延髓及双侧小脑中脚的部分弥散各向异性值(fractional anisotropy,FA)从第1周至第12周逐渐减少(延髓梗死同侧FA值:第1周0.43±0.01;第4周0.37±0.02;第12周0.30±0.02,小脑中脚梗死同侧FA值:第1周0.50±0.02;第4周0.43±0.02;第12周0.35±0.04,小脑中脚梗死对侧FA值:第1周0.54±0.02;第4周0.52±0.03;第12周0.47±0.04,t=1.92~28.56,均P<0.05),而平均弥散量(mean diffusivity,MD)的变化差异却无统计学意义(P>0.05).在观察期间,患者梗死灶同侧延髓及双侧小脑中脚的FA值减少的百分数绝对值与同期NIHSS及BI变化的百分数绝对值呈负相关(P<0.05).结论 局灶性脑桥梗死后,同侧延髓及双侧小脑中脚神经纤维的华勒变性持续存在,并且可能阻碍患者神经功能的恢复.  相似文献   

4.
磁共振弥散张量成像动态观察脑梗死后继发锥体束损害   总被引:7,自引:4,他引:3  
目的动态观察脑梗死后,远离梗死灶的锥体束纤维继发性损害的过程,并探讨其对神经功能恢复的影响。方法选择具单侧大脑中动脉(middle cerebral artery,MCA)供血区、累及内囊的单一病灶的脑梗死患者18例,选择年龄性别相匹配的健康志愿者18人作对照组。分别在发病的第1周、4周和第12周进行磁共振弥散张量成像(diffusion tensor imanging,DTI)检测,并行美国国立卫生研究院卒中评分(National Institutes of Health Stroke Scale,NIHSS)、简式Fugl-Meyer运动功能评分(FM)和Barthel生活指数(Barthel index,BI)评定。结果患者远离梗死灶的脑干(大脑脚、脑桥和延髓等部位的均数)部分弥散各向异性(fractional anisotropy,FA)值在第1周、4周和第12周各时间点逐渐减少(P<0.01),而平均弥散量(mean diffusivity,MD)却无明显变化(P>0.05)。脑干FA值减少的百分数与NIHSS减少的百分数(r=-0.46,P<0.05)及FM增加的百分数(r=-0.61,P<0.05)相关,与BI变化的百分数无明显相关(P>0.05)。结论局灶性脑梗死后,锥体束纤维继发性损害会随时间延长而逐渐加重,并可能会阻碍患者神经功能的恢复。  相似文献   

5.
阿尔茨海默病患者脑白质损害与认知功能的关系   总被引:4,自引:0,他引:4  
目的用磁共振扩散张量成像(DTI)研究阿尔茨海默病(AD)患者脑白质损害的特点及其与认知功能改变的相关性。方法对16例AD患者和12名年龄及性别相当的健康老年人行DTI、T1液体衰减反转恢复序列(FLAIR)及T2-FLAIR检查,测量胼胝体膝部和压部、内囊前肢和后肢、额颞顶枕叶白质的部分各向异性分数值(FA)和平均弥散度(MD),分析FA、MD值与简易精神状态量表(MMSE)评分之间的相关关系。结果AD患者胼胝体压部、额叶、顶叶、颞叶FA值分别为0.602±0.043、0.270±0.034、0.294±0.043、0.302±0.032,与健康老人组相比显著下降(P<0.05),且与MMSE评分呈正相关关系,而内囊前后肢、枕叶、胼胝体膝部的FA值则无明显变化(P>0.05);胼胝体压部、顶叶白质的MD值分别为(0.918±0.029)、(0.826±0.015)×10-9m2/s,与健康老人组相比显著升高(P<0.01),且与MMSE评分呈负相关,而内囊前后肢、额叶、颞叶、枕叶和胼胝体膝部的MD值则无明显变化(P>0.05)。结论AD患者表现为脑白质的选择性损害,且损害程度与认知功能密切相关;这种选择性损害反映了AD病理机制中皮质-皮质及皮质-皮质下联系的丢失;DTI技术可以用来监测疾病的进展情况及评价AD治疗药物的临床疗效。  相似文献   

6.
磁共振弥散张量及纤维束成像在急性脑梗死的临床应用   总被引:1,自引:0,他引:1  
目的探讨急性脑梗死病人梗死灶弥散张量的参数变化及对皮质脊髓束的影响,以早期判断病情、评估预后。方法急性脑梗死患者45例,入院及治疗后分别行NIHSS评分记为NIHSS1、NIHSS2,常规MRI、DWI、DTI/DTT检查,分析病灶FA值的变化及与皮质脊髓束的关系。结果①梗死灶FA值降低百分比和NIHSS1相关(r=0.411,P<0.01)。②45例患者中,皮质脊髓束完整(1级)者15例,病灶致使皮质脊髓束受压、移位(2级)者20例,皮质脊髓束中断(3级)者10例。皮质脊髓束的损伤程度与NIHSS2相关(r=0.894,P<0.01)。结论病灶FA值下降越明显,患者病情越重;皮质脊髓束破坏越严重,患者运动功能受损越重,预后越差。  相似文献   

7.
目的 通过弥散张量成像(DTI)白质神经纤维示踪方法观察立体定向微创技术治疗丘脑出血对患者内囊神经纤维及运动功能的影响.方法 将贵阳医学院附属医院自2010年12月至2011年8月收治的22例丘脑出血患者按随机数字表法分为微创手术组(MI组)和药物治疗组(MT组).MT组采用常规药物治疗,MI组在入院后24 h内行立体定向微创手术清除颅内血肿,同时给予药物治疗.分别在入院时、入院后2周对2组患者进行DTI扫描,观察病灶侧及病灶对侧内囊皮质脊髓束(CST)的完整性并测定其部分各向异性值(FA值),在人院时、入院后2周及1月进行改良的美国国立卫生研究院卒中量表(mNIHSS)评分.结果 入院时2组患者DTI均显示病灶侧内囊CST数量减少或中断,其FA值与正常相比明显降低(MI组和MT组分别为0.432±0.022和0.410±0.028).MI组患者血肿清除后2周,病灶侧内囊CST的FA值与人院时相比均明显增加,与MT组比较差异有统计学意义(P<0.05).随着术后病灶侧内囊CST的FA值增加,mNIHSS评分减少,患者运动功能明显好转.结论 立体定向微创技术治疗丘脑出血能有效地减少患者运动功能的损害程度,应用DTI技术可直观地观察到丘脑出血患者微创清除血肿后内囊CST变化情况.  相似文献   

8.
多发性硬化患者的磁化传递及弥散张量成像特点   总被引:2,自引:0,他引:2  
目的比较多发性硬化(MS)患者脑内病灶、表现正常脑白质(NAWM)及健康志愿者脑白质的磁化传递及弥散特性的差异,探讨MS患者的磁化传递率(MTR)与平均弥散率(MD)的相关性。方法分别对24例复发缓解型MS患者和24名健康志愿者行常规MRI、磁化传递成像(MTI)及弥散张量成像(DTI),经处理后得到相应的MTR、MD及各向异性分数(FA)图。测量MS病灶、对侧NAWM及健康志愿者相应脑白质区域的MTR、MD及FA值。结果MS患者病灶的平均MTR值(23.49%±5.16%)明显低于NAWM组(29.49%±3.38%)及健康对照组(32.78%±3.42%,F=101.44,P<0.01);病灶的平均FA值(0.32±0.09)也明显低于NAWM组(0.42±0.09)及对照组(0.51±0.09,F=95.41,P<0.01);而病灶的平均MD值[(1.10±0.17)×10-3mm2/s]明显高于NAWM组[(0.92±0.13)×10-3mm2/s]及对照组[(0.76±0.04)×10-3mm2/s,F=144.89,P<0.01]。与MS患者T1WI等信号病灶相比,低信号病灶的MTR值及FA值降低,而MD值升高。MS患者病灶的MTR值与MD值显著相关,而NAWM的MTR与MD值无明显相关性。结论MTI和DTI的指标可以反映MS患者脑内不同部位病理变化的不同,为常规MRI提供补充信息。  相似文献   

9.
目的 探讨磁共振弥散张量成像(DTI)在急性脑卒中患者运动神经损伤康复疗效预测中的价值.方法 采用美国国立卫生研究院卒中量表(NIHSS)、日常生活能力(ADL)量表、缺血性脑卒中/短暂性脑缺血发作(TIA)风险评估(ESSEN)量表、缺血性脑卒中/TIA风险评估(ABCD2)评分量表挑选我院2009年3月~2011年12月中重度急性脑卒中住院患者17例,发病1周内完成头颅磁共振血管显影(MRI)、弥散加权成像(DWI)、磁共振血管造影(MRA)和DTI检查、简化Fugl-Meyer运动功能(F-M量表)评分,发病2周后开始行物理康复治疗,发病10~12周复查头颅MRI和DTI、简化F-M量表评分.结果 急性脑卒中患者发病1周内病灶区平均各向异性分数(FA)值(0.39±0.10)较健侧相应部位(0.57±0.11)降低,差异有统计学意义(P<0.01);康复治疗前、后DTI中病灶部位不同兴趣区(ROI)对应的FA差值变化和F-M量表评分差值变化均有统计学意义(P<0.01);入院1周内DTI中ROI对应的健患侧FA差值同康复治疗前后F-M量表评分差值变化呈线性正相关关系(rs=0.497,P<0.05).结论 DTI中FA值改变与运动神经损伤程度、康复疗效存在关联性,急性期DTI对肢体功能障碍康复治疗疗效预测有一定的价值.  相似文献   

10.
目的 应用磁共振弥散张量(diffusion tensor imaging,DTI)技术动态观察局灶性丘脑梗死后丘脑放射纤维的弥散变化,探讨丘脑梗死后,病灶上方的丘脑放射纤维继发性损害的发生发展规律.方法 连续收录首次发病、单侧丘脑梗死患者17例为实验组,选择健康志愿者17例作对照研究.患者分别在发病的第1周(W1)、第4周(W4)和第12周(W12)进行1次DTI检测,对照组进行1次DTI检测.每次DTI检测之前进行美国国立卫生研究院卒中评分(national institute health stroke scale,NIHSS)和Barthel生活指数(BI)以及自订的感觉障碍分级评分(Sensory disturbance rating,SDR)评定.结果梗死灶上方的半卵圆中心部分异向(fractional anisotropy,FA)值随时间延长逐渐减少(W1:0.42±0.02,W2:0.38±0.02,W12:0.34± 0.03,P<0.01),而平均弥散量(mean diffusion,MD)却无明显变化.梗死灶上方的半卵圆中心FA值的变化百分数与NIHSS、和BI的变化百分数无明显相关(P>0.05),与SDR变化的百分数呈负相关(r=-0.246,P<0.05).结论 局灶性丘脑梗死可以引起丘脑放射纤维继发性损害,在12周内这种继发性损害逐渐加重,而且还可能阻碍患者感觉功能的恢复.  相似文献   

11.
B. J. Wilder 《Epilepsia》1987,28(S2):S1-S7
Summary: The long-standing practice of polypharmacy in treating epilepsy is giving way to use of monotherapy. Monotherapy can improve seizure control as well as reduce the risk of serious idiosyncratic reactions, dose-related side effects, and complex drug interactions. Monotherapy also offers improved compliance and cost-effectiveness. The basis of monotherapy is accurate diagnosis and assessment of the patient's seizure type(s), followed by selection of a single appropriate anticonvulsant drug. Many patients currently treated with multiple anticonvulsants can be successfully converted to monotherapy with a carefully monitored program in which troublesome and redundant drugs are gradually withdrawn from the therapeutic regimen.  相似文献   

12.
Diagnostic Difficulties and Treatment Implications   总被引:1,自引:0,他引:1  
Robert J. Gumnit 《Epilepsia》1987,28(S3):S9-S13
Summary: Differentiation between types of epileptic seizures has been aided in recent years by the introduction of intensive neurodiagnostic techniques and the development of increasingly detailed classification systems. Paradoxically, these developments have not simplified the task of matching the appropriate antiepileptic drug to a particular seizure type. It is reasonable to assume that anticonvulsant drugs will have different effects on different types of seizures, but faulty, circular reasoning can enter the picture if one also assumes that responses of seizures to different drugs signify different seizure types. There are several examples of differential diagnoses that can fall prey to this problem, including the diagnosis between partial seizures with secondary generalization and generalized tonic-clonic seizures, and the diagnosis between complex partial seizures and absence seizures with automatisms, among others. Considerations of etiology in future classification systems can further complicate the problem: should one then choose an anticonvulsant drug on the basis of individual seizure type or on the basis of the type of epilepsy? Ramifications of this issue extend even to the drug approval process. Official sanction is not given for use of a drug for a seizure type not included in the original efficacy studies, even if later scientific evidence shows that seizure type to be related to a type that is included. New trials must be undertaken. These problems arise from how we choose to classify seizures.  相似文献   

13.
Cognitive Dysfunction Associated with Antiepileptic Drug Therapy   总被引:7,自引:5,他引:2  
Eileen P.G. Vining 《Epilepsia》1987,28(S2):S18-S22
Summary: Epilepsy is frequently associated with cognitive dysfunction. However, the reasons for this correlation are unclear. Possible influential factors include patient age; duration, frequency, etiology, and type of seizures; hereditary factors; psychosocial issues; and antiepileptic drug (AED) therapy. Whereas many of these factors are beyond the physician's control, AED therapy is one element that can be addressed in treatment decisions by recognizing the potential cognitive effects of particular AEDs. For example, phenobarbital impairs memory and concentration; phenytoin affects attention, problem solving ability, and performance of visuomotor tasks. In contrast, carbamazepine may affect concentration, while valproate would appear to have minimal effects on cognition. Moreover, cognitive effects of AEDs are amplified with coadministration of multiple anticonvulsants (polytherapy). A review of studies on the cognitive effects of monotherapy with AEDs, as opposed to those of polytherapy, provides evidence that drug-related cognitive dysfunction can be reversed if patients are switched to a simpler therapeutic regimen. Future research should be directed toward developing reliable measures for assessing and monitoring cognition, and understanding the particular cognitive side effects of each AED. Physicians also need to revise their opinions about which side effects are "tolerable" for epileptic patients.  相似文献   

14.
Dextromethorphan: Cellular Effects Reducing Neuronal Hyperactivity   总被引:5,自引:1,他引:4  
G. Trube  R. Netzer 《Epilepsia》1994,35(S5):S62-S67
Summary: Dextromethorphan is a dextrorotary morphinan without affinity for opioid receptors, commonly used as an antitussive medication. During the past 5 years, interest in the compound and its demethylated derivative, dextrorphan, has been revived because additional neuroprotective and an-tiepileptic properties were found in in vitro studies, animal experiments, and a few clinical cases. Both morphinans are able to inhibit N -methyl-D-aspartate (NMDA) receptor channels and voltage-operated calcium and sodium channels with different potencies. The inhibition of the NMDA receptor is believed to be the predominant mechanism of action responsible for the anticonvulsant and neuroprotective properties of the compounds.  相似文献   

15.
Summary: Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment. Carbamazepine is judged a drug of choice in the treatment of these secondarily generalized tonic-clonic seizures, and the drug of choice in children, adolescents, and women susceptible to the dysmorphic side effects associated with other anticonvulsant agents.  相似文献   

16.
Summary: Four broad categories of basic phenomena are pertinent to developing ways to prevent epilepsy. These include mechanisms of epileptogenesis, ictal initiation and temporary entrainment by the seizure discharge of normally functioning brain, seizure propagation, and control mechanisms that function both to restrain the cascade of epileptic events culminating in a seizure and to arrest the epileptic event and restore the interictal state. In newborns and children, hypoxia-ischemia is a major factor leading to epileptogenesis, and several schemes are proposed to classify, quantify, and prevent hypoxic-ischemic encephalopathy. Control mechanisms must be better understood in order to develop prophylactic recommendations for epilepsy, and an experimental model of "kindling antagonism" may increase our understanding of these. Programs of prevention of seizures in children will evolve only if basic researchers and clinicians work productively together to develop an adequate understanding of factors important in epileptogenesis and antiepileptogenic control mechanisms.  相似文献   

17.
Pediatric Epilepsy Surgery   总被引:4,自引:3,他引:1  
Sidney Goldring 《Epilepsia》1987,28(S1):S82-S100
Summary: The use of implantable arrays of epidural electrodes has made it possible to carry out extraoperative electrocorticography (ECoG) and functional localization in the awake child. This has permitted cortical excisions that are determined by criteria similar to those obtained during surgical procedures performed under local anesthesia in adults. In addition, the method also permits simultaneous ECoG and video monitoring during the child's symptomatic seizures, providing additional important localizing information that is impractical to obtain in operations under local anesthesia. We report our experience with 75 children, ages 5 months to 15 years, whom we have managed with epidural electrode arrays. The method of extraoperative ECoG is described and illustrative cases are presented to demonstrate its feasibility and utility in children. In addition, we call attention to gliomas as a common cause of chronic focal seizures in children. Of 49 children undergoing resection and followed for from 1 to 14 years (mean of 5.8 years), 32 (65%) are either seizure free or have had a significant reduction in seizure frequency that has unambiguously improved their quality of life. The results are analyzed further by relating the surgical outcome to each of the pathologic entities that caused the seizures. This analysis reveals the variety of neurological conditions that commonly cause intractable focal seizure disorder in children and distinguishes those pathologic entities in which the seizure disorder is apt to respond to surgical intervention from those that will not.  相似文献   

18.
19.
Predisposing and Causative Factors in Childhood Epilepsy   总被引:6,自引:2,他引:4  
Summary: We review information from large studies of defined populations, examining the role of known factors and especially of prenatal and perinatal factors in contributing to nonfebrile seizure disorders of early childhood. We depend especially, but not exclusively, on the recently completed analyses from the Collaborative Perinatal Project of the National Institute of Neurological and Communicative Disorders and Stroke, the NCPP. About 4% of children in the NCPP who had at least one non-febrile nonsymptomatic seizure by the age of 7 years had a previous seizure during acute neurologic illness, such as meningitis or during the acute illness after trauma. Many such seizures should potentially be preventable. Of children with seizures, 10% had had a neonatal seizure and 13% had had a febrile seizure. Among the hundreds of prenatal and perinatal factors explored as predictors of childhood seizure disorders, the principal predictors identified were congenital malformations of the fetus, cerebral and noncerebral; family history of certain neurologic disorders; and neonatal seizures. In agreement with the British National Child Development Study, labor and delivery factors in the NCPP appeared to contribute very little to childhood seizure disorders. Maldevelopment, rather than damage at birth to an initially intact nervous system, appeared to be the more common mechanism. Most seizure disorders of early childhood remained unexplained by the large set of prenatal and perinatal characteristics examined.  相似文献   

20.
Anticonvulsant Drugs and Cognitive Function: A Review of the Literature   总被引:14,自引:12,他引:2  
Michael R. Trimble 《Epilepsia》1987,28(S3):S37-S45
Summary: Alterations of cognitive function are separate from disturbances of behavior seen in association with epilepsy. The nature of the cognitive disability may to a certain extent depend on the seizure type. Partial seizures, mainly derived from a temporal lobe focus, impair memory tasks, while generalized seizures seem to have more effect on attentional abilities. A number of studies, reviewed in this paper, suggest that anticonvulsant drugs further impair cognitive function. Maximal impairments are seen in patients receiving polytherapy: rationalization of polytherapy improves cognitive abilities. Studies in children and adults have allowed differentiation of the effects of various commonly used antiepileptic agents. Maximal cognitive deficits are seen with. phenytoin, while phenobarbital and sodium valproate induce moderate disturbances, and carbamazepine seems relatively free from such toxicity. Further research is needed on the interrelationship between types of seizure disorders, types of anticonvulsant medications, and cognitive function.  相似文献   

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