DTI态观察脑梗死后颈髓皮质脊髓束继发性损害

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。     

颈髓弥散张量成像在肌萎缩性侧索硬化诊断中的应用

目的 初步探讨颈髓弥散张量成像(DTI)在肌萎缩性侧索硬化(ALS)诊断中的应用价值. 方法 选择自2000年1月至2007年1月中山大学附属第二医院骨科收治的28例ALS患者为患者组,20例同期门诊查体健康成年人为对照组,对2组成员进行常规MRI扫描及DTI检查,获取颈髓MD值及FA值的直方图,并对ALS患者颈髓DTI弥散张量值与患者ALS残损功能评分量表(ALSFRS)评分进行相关性分析. 结果 与对照组相比,患者组颈髓FA值和颈髓横断面积明显降低,差异有统计学意义(P<0.05);MD值轻微增加,差异无统计学意义(P>0.05).患者颈髓FA值与ALSFRS评分高度相关(r=0.730,P=0.000),与MD值等指标无相关关系. 结论 ALS患者颈髓DTI显像FA值显著降低,FA值可能成为ALS诊断中的神经影像学阳性支持指标:颈髓的弥散张量值与ALSFRS结合,可以更伞面反映ALS患者的病情进展.     

肌萎缩侧索硬化症的磁共振弥散张量成像研究

目的初步探讨磁共振弥散张量成像(DTI)在肌萎缩侧索硬化(ALS)诊断中的应用价值。方法选取54例具有不同诊断级别的ALS患者,包括确诊(21例)、很可能(22例)、可能(11例)的患者,同时选取23名健康体检的志愿者作为健康对照。分别行DTI扫描,测量各感兴趣区(ROI)的平均扩散系数(ADC)和各向异性系数(FA),分析两组间ADC和FA的差异,并对ALS组患者ADC值及FA值与临床资料的相关性进行分析。结果与健康对照组比较,ALS患者大脑脚、内囊后肢区的ADC值升高(P0.01),大脑脚、内囊后肢及中央前回区的FA值降低(P0.01);相关分析显示ALS患者内囊后肢的ADC值与诊断级别呈负相关(r=-0.289,P0.05),与上运动神经元损伤评分呈正相关(r=0.304,P0.05);大脑脚及内囊后肢的FA值与诊断级别呈正相关(r=0.394,P0.01;r=0.547,P0.01),与上运动神经元损伤评分呈负相关(r=-0.301,P0.05;r=-0.653,P0.01).结论 DTI可客观定量评估ALS患者锥体束的损伤情况,在ALS的诊断中具有重要的辅助价值。     

磁共振弥散张量成像对脑出血致皮质脊髓束损害的诊断价值

目的 研究磁共振弥散张量成像(DTI)对脑出血致皮质脊髓束(CST)损害的诊断价值.方法 对20例基底节区脑出血患者(急性期14例,亚急性期6例,均有偏瘫)进行DTI检查,分别测量患侧CST损害区及健侧相应区域的各向异性分数(FA)值、表观弥散系数(ADC)值.结果 DTI显示20例脑出血患者患侧CST受压、移位、变薄或显示不清,患侧CST受损区FA值(0.43±0.16)均较健侧(0.70±0.06)明显降低(t=9.11,P<0.01);14例急性期患者患侧受损CST区ADC值(0.60±0.11)较健侧(0.76±0.10)明显降低(t=7.03,P<0.01).6例亚急性期患者两侧CST区ADC值的差异无统计学意义.结论 DTI可以清楚地显示脑出血患者CST的损害状况,这对判断脑出血患者的病情和预后有参考价值.     

视神经脊髓炎和多发性硬化患者颈髓扩散张量成像研究

目的通过扩散张量成像(DTI)比较视神经脊髓炎和多发性硬化患者与正常对照者常规MRI表现正常脊髓的扩散性差异,并探讨其临床应用价值。方法采用平面回波成像技术对10例视神经脊髓炎、14例多发性硬化患者和13例正常对照者进行颈髓DTI检查,分别测量颈椎C2~5水平前索、侧索、后索和灰质兴趣区的部分各向异性(FA)和平均扩散率(MD)。结果与正常对照组相比,视神经脊髓炎组患者前索、侧索、后索FA值降低(均P0.05),左侧侧索、后索、灰质MD值升高(均P≤0.05);多发性硬化组患者右侧侧索、后索FA值降低(均P0.05)。与多发性硬化患者相比,视神经脊髓炎患者侧索FA值更低,左侧侧索和右侧后索MD值更高(均P0.05)。结论 DTI可以检出视神经脊髓炎和多发性硬化患者常规MRI表现正常脊髓的水分子扩散异常,进而发现二者脊髓扩散指标的差异性,为早期诊断与鉴别诊断提供重要信息。     

磁共振弥散张量成像在脑梗死中的应用

目的应用磁共振弥散张量成像(DTI)技术分析缺血性脑梗死不同时期的表观弥散系数(ADC)、各向异性分数(FA)变化,并通过弥散张量纤维束成像(DTT)观察梗死灶与皮质脊髓束(CST)位置关系,以评估预后。方法 45例由于皮质脊髓束受损所致运动功能障碍的不同时期脑梗死患者作为研究组,分为超急性期(<6h)、急性期(6h～3d)、亚急性期(4d～8w)和慢性期(>8w),分析其DTI参数的变化特点,并与正常组进行比较。结果患侧FA值在超急性期无明显变化,在急性期、亚急性期及慢性期逐渐降低,与健侧和对照组比较有显著性差异(P值均<0.05);患侧ADC值在超急性期、急性期明显减低,亚急性期逐渐恢复接近于健侧,慢性期再度增高;DTT成像显示CST受损严重其预后较差。结论不同时期脑梗死病灶其FA、ADC值有一定规律变化,DTT图像可无创性的显示梗死灶与皮质脊髓束的空间位置关系,可作为评估预后的客观依据。     

磁共振弥散张量成像与急性脑梗死患者认知功能的关系

目的 利用磁共振弥散张量成像(DTI)评估急性脑梗死患者的认知功能.方法 分别对30例急性脑梗死患者及30名健康志愿者进行DTI检查,观察兴趣区(ROIs)表观扩散系数(ADC)及部分各向异性(FA)的变化,同时评定患者的认知功能及神经功能缺损评分,分析内在的相关性.结果 脑梗死患者组梗死区FA值、ADC值(×10-3 mm2/s)明显下降,平均FA值、ADC值分别为0.12±0.01、1.08±0.11,其对侧相应部位平均FA值、ADC值为0.35±0.08、3.46±0.26,两者相比差异有统计学意义(P＜0.05);脑梗死患者健侧ADC、FA值与对照组相应部位对比差异无统计学意义.脑梗死同侧内囊后肢、大脑脚、皮质脊髓束与健侧相应部位相比,平均FA值明显下降(P＜0.05).脑梗死患者梗死区FA值、ADC值与认知功能呈正相关,与EDSS评分具有负相关性.结论 DTI与急性脑梗死患者认知功能具有一定的相关性,可为脑梗死患者认知功能障碍的早期诊断及早期治疗提供一些依据.     

弥散张量成像在高血压性脑出血中的临床应用初探

目的 应用磁共振弥散张量成像技术观察基底节区高血压性脑出血皮质脊髓束的受损情况,为临床干预治疗提供可靠依据.方法 对9例基底节区HICH患者进行磁共振弥散张量成像检查,分别测量患侧皮质脊髓束受压区及健侧皮质脊髓束相应区域的FA值,并重建一名患者的FA图、方向编码彩色图、双侧皮质脊髓束3D纤维束图.结果 患侧皮质脊髓束的FA值均较对侧降低,两侧相比差异有显著性意义(t=4.9041,P<0.05);患侧皮质脊髓束区FA值下降百分比和NIHSS评分有明显相关性(r=0.8336,P<0.05);皮质脊髓束3D纤维束图可显示病变侧皮质脊髓束受损情况.结论 通过弥散张量成像可以了解基底节区HICH患者的皮质脊髓束的损伤情况,这有助于临床医生全面掌握病情,开展干预性治疗.     

应用弥散张量成像研究脑梗死后皮质脊髓束Wallerian变性与运动功能缺损的相关性

目的:应用弥散张量成像(DTI)研究脑梗死后皮质脊髓束Wallerian变性与神经运动功能缺损的相关性。方法:对11例单侧大脑中动脉供血区脑梗死的患儿进行了DTI研究。通过放置兴趣区(ROI)的方式获得定量部分各向异性(FA)和平均弥散量(MD)。ROI放置的部位包括:脑梗死区、脑梗死同侧内囊后支前部和大脑脚,以及上述部位对侧相应区域。根据手的运动情况将运动功能缺损分为轻、中和重3级。应用Mann-Whitney U检验确定差异有无显著性;应用Spearman相关检验确定皮质脊髓束DTI改变与神经运动功能缺损之间的相关性。结果:脑梗死同侧皮质脊髓束FA较对侧明显下降(P<0.05),但MD改变与对侧无明显差异(P>0.05)。FA下降与神经运动功能缺损之间存在明显相关性(r=-0.638,P=0.035)。结论:应用FA值的变化,DTI可以检测并定量分析儿童脑梗死后皮质脊髓束Wallerian变性,并可作为预测脑梗死后运动功能缺损的工具。     

磁共振扩散张量成像对肌萎缩侧索硬化症患者上运动神经元病变的定量评估意义

目的 初步探讨磁共振扩散张量成像（DTI）在肌萎缩侧索硬化症（ALS）诊断中的临床意义.方法 16例有明确上运动神经元（UMN）损害体征者作为A组,4例仅有下运动神经元（LMN）损害体征者作为B组,15名健康志愿者为对照组.行轴位DTI扫描,选取感兴趣区（ROI）测量各向异性分数（FA）和平均扩散系数（ADC）.结果 与对照组比较,A组内囊后肢水平FA值降低（t=3.452,P=0.002）,ADC值增大（t=2.670,P=0.012）;其他ROI的FA、ADC值差异无统计学意义.与对照组比较,B组内囊后肢水平FA值有下降趋势（U=11,P=0.057）;与A组比较差异无统计学意义（U=29,P=0.777）.A组内囊后肢水平FA值与ALS功能评分呈正相关（r=0.577,P=0.019）,与锥体束征评分呈负相关（r=-0.789,P=0.000）,与年龄、病程、病情进展速度无相关性;ADC值与以上指标间均无相关性.结论 DTI可以客观而定量地评价锥体束病变,为ALS的诊断提供有价值的信息.     

颈椎病磁共振扩散张量成像的研究

目的探讨颈椎病磁共振扩散张量成像（MRDTI）的特点。方法应用3．0TMRI仪对颈椎病患者进行M_RDTI检查,根据MRI显示的脊髓受压严重程度将颈椎病患者分为轻度组、中度组、重度组及严重度组。分析各组纤维示踪（FT）图的特征及各定量参数的变化。结果60例颈椎病患者FT显示纤维束狭窄、离断、稀疏,随着脊髓受压程度的加重而加重。FA值、Ez值、E3值、E⊥值、MD值在各组之间均存在差异（P〈0．05）。随着MRI评估的脊髓受压程度加重,E2值、E3值、E⊥值、MD值逐渐升高,FA值逐渐降低。结论MRDTI可以定量、直观显示颈椎病的脊髓受压程度。     

Leukoencephalopathy with vanishing white matter: serial MRI of the brain and spinal cord including diffusion tensor imaging

Vanishing white matter disease (VWM) is one of the most frequent inherited childhood white matter disorders. We present the brain and spinal cord disease progression on serial conventional magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI) in a 4-year-old boy. Consecutive MRI examinations demonstrated a progression of the signal abnormalities in the cerebral white matter. Globally, apparent diffusion coefficient (ADC) values as well as axial and radial diffusivity increased over time, while fractional anisotropy (FA) values decreased. Involvement of the cervical posterior spinal tracts and mild global spinal cord atrophy was found. In conclusion, serial MRI and DTI studies may help to better understand the selective injury of the myelin and axons in VWM disease. These data may help in monitoring disease progression. Our data also show that complete neuroimaging work-up in VWM should also include the spinal cord.     

Discrete mitochondrial aberrations in the spinal cord of sporadic ALS patients

Amyotrophic lateral sclerosis (ALS) is an adult onset neurodegenerative disease characterized by progressive motor neuron degeneration in the brain and spinal cord leading to muscle atrophy, paralysis, and death. Mitochondrial dysfunction is a major contributor to motor neuron degeneration associated with ALS progression. Mitochondrial abnormalities have been determined in spinal cords of animal disease models and ALS patients. However, molecular mechanisms leading to mitochondrial dysfunction in sporadic ALS (sALS) patients remain unclear. Also, segmental or regional variation in mitochondrial activity in the spinal cord has not been extensively examined in ALS. In our study, the activity of mitochondrial electron transport chain complex IV was examined in post‐mortem gray and white matter of the cervical and lumbar spinal cords from male and female sALS patients and controls. Mitochondrial distribution and density in spinal cord motor neurons, lateral funiculus, and capillaries in gray and white matter were analyzed by immunohistochemistry. Results showed that complex IV activity was significantly decreased only in gray matter in both cervical and lumbar spinal cords from ALS patients. In ALS cervical and lumbar spinal cords, significantly increased mitochondrial density and altered distribution were observed in motor neurons, lateral funiculus, and cervical white matter capillaries. Discrete decreased complex IV activity in addition to changes in mitochondria distribution and density determined in the spinal cord in sALS patients are novel findings. These explicit mitochondrial defects in the spinal cord may contribute to ALS pathogenesis and should be considered in development of therapeutic approaches for this disease.     

Widespread spinal cord involvement in progressive supranuclear palsy

We describe the histopathologic features of spinal cord lesions in 10 cases of progressive supranuclear palsy (PSP) and review the literature. Histologic examination revealed atrophy with myelin pallor in the anterior funiculus and anterolateral funiculus in the cervical and thoracic segments in eight of the 10 cases, whereas the posterior funiculus was well preserved. The degrees of atrophy of the anterior funiculus and the anterolateral funiculus correlated with that of the tegmentum of the medulla oblongata. Myelin pallor of the lateral corticospinal tract was observed in two of the 10 cases. Microscopic observation of the spinal white matter, particularly the cervical segment, revealed a few to several neuropil threads, particularly in the white matter surrounding the anterior horn after Gallyas‐Braak (GB) staining or AT‐8 tau immunostaining. However, the posterior funiculus was completely preserved from the presence of argyrophilic or tau‐positive structures. In the spinal gray matter, widespread distribution of neurons with cytoplasmic inclusions and neuropil threads was observed, particularly in the medial division of the anterior horn and intermediate gray matter, especially in the cervical segment. Globose‐type neurofibrillary tangles and pretangles were found. The distribution of GB‐ or AT‐8 tau‐positive small neurons and neuropil threads resembled that of the spinal interneurons. In conclusion, the spinal cord, especially the cervical segment, is constantly involved in the pathologic process of PSP. We speculate that spinal interneurons and their neuronal processes, particularly in the medial division of the anterior horn and intermediate gray matter of the cervical segment, are most severely damaged in the PSP spinal cord.     

Myelopathy patients studied with magnetic resonance for multiple sclerosis plaques

Seven patients with isolated spinal cord symptoms, and with evoked potential (EP) recordings and/or cerebrospinal fluid (CSF) findings supporting a demyelinating cause for their myelopathy, were examined with cervical and cranial magnetic resonance imaging (MRI). Lesions in the cervical spinal cord were detected in 6 of the patients, including 2 who also had disseminated lesions in the brain compatible with multiple sclerosis (MS). In one patient MRI of the cervical spinal cord was normal, while plaques were seen in the periventricular region of the brain and in the brain stem. Thus, in the 3 patients with cerebral plaques, MRI supported the diagnosis of MS by showing dissemination in space. In the remaining 4 patients MRI provided support for the diagnosis of MS by demonstrating the cervical spinal cord plaques while excluding other potential causes of myelopathy, such as spinal cord compression and intramedullary tumor.     

Spinal sources of noxious visceral and noxious deep somatic afferent drive onto the ventrolateral periaqueductal gray of the rat

Studies utilizing the expression of Fos protein as a marker of neuronal activation have revealed that pain of deep somatic or visceral origin selectively activates the ventrolateral periaqueductal gray (vlPAG). Previous anatomical tracing studies revealed that spinal afferents to the vlPAG arose from the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus at all spinal segmental levels, with approximately 50% of vlPAG-projecting spinal neurons found within the upper cervical spinal cord. This study utilized detection of Fos protein to determine the specific populations of vlPAG-projecting spinal neurons activated by noxious deep somatic or noxious visceral stimulation. Pain of cardiac or peritoneal (i.e., visceral) origin activated neurons in the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus of the thoracic cord, whereas pain of hindlimb (i.e., deep somatic) origin activated neurons in the same laminar regions but in the lumbosacral cord. Each of these deep noxious manipulations also activated neurons in the superficial and deep dorsal horn and nucleus of the dorsolateral funiculus of the upper cervical spinal cord. In a second set of experiments, the combination of retrograde tracing and Fos immunohistochemistry revealed that vlPAG-projecting spinal neurons activated by deep somatic pain were located in both the upper cervical and lumbosacral cord, whereas those activated by visceral pain were restricted to the thoracic spinal cord. Thus pain arising from visceral versus deep somatic body regions influences neural activity within the vlPAG via distinct spinal pathways. The findings also highlight the potential significance of the upper cervical cord in integrating pain arising from deep structures throughout the body.     

多种脊髓诱发电位测评高龄脊髓型颈椎病患者颈脊髓机能

目的调查高龄脊髓型颈椎病患者的颈脊髓机能状态,并结合磁共振影像学（MRI）及X线放射学探讨其病理生理形成机制.方法对23例MRI显示为多椎间脊髓压迫的高龄脊髓型颈椎病患者,采用经颅电刺激-脊髓硬膜外记录、经脊髓硬膜外刺激-脊髓硬膜外记录、经正中神经刺激-脊髓硬膜外记录的三种脊髓诱发电位进行颈脊髓机能测定.结果17例患者（73.9%）显示为颈脊髓单一椎间的障碍,其中10例位于C3-4、5例位于C4-5、2例位于C5-6.另外6例患者（26.1%）的正中神经刺激-脊髓硬膜外记录结果表现为多个或两个椎间的障碍.结论在MRI影像学上显示为多椎间脊髓压迫的高龄脊髓型颈椎病患者,其多数在脊髓电生理上：表现为单一颈椎椎间的脊髓白质损伤,特征是不仅脊髓后索的感觉传导束,而且侧索的皮质脊髓束也受到损伤.结合X线放射学结果分析,C3-4或C4-5颈椎椎间的过大活动度或不稳是导致高龄脊髓型颈椎病患者脊髓传导束损伤的一个重要原因.     

Collagen abnormalities in the spinal cord from patients with amyotrophic lateral sclerosis

During the last 10 years, we have demonstrated morphological and biochemical abnormalities of skin extracellular matrices in amyotrophic lateral sclerosis (ALS). However, currently little is known concerning collagen of the spinal cord in ALS. We measured the amount of collagen and characterized collagen at light and electron microscopic levels in posterior funiculus, posterior half of lateral funiculus and anterior horn of cervical enlargement of the spinal cord obtained from ten patients with ALS, 11 patients with other neurologic diseases (control group A), and ten patients without neurologic ones (control group B). In posterior half of lateral funiculus and anterior horn, (1) by light microscopy, there was no significant difference in vessel wall area between ALS patients and control groups A and B; (2) ultrastructurally, collagen bundles were more fragmented and widely separated, and the fibrils were randomly oriented in the perivascular space of capillaries in ALS patients, which were not observed in any areas of control groups or in posterior funiculus of ALS patients; and (3) the collagen contents in ALS were significantly lower (P<0.001 and P<0.001, respectively) than those in control groups A and B. Fragmented and widely separated collagen bundles in the interstitial tissue surrounding capillaries and markedly decreased amount of collagen in posterior half of lateral funiculus and in anterior horn of ALS could be related to the degeneration of the upper and lower motor neurons in the spinal cord in ALS, that is, selective neuronal vulnerability in ALS.     

Pursuit of the origin of the large myelinated fibers of the anterolateral funiculus in the spinal cord in humans in relation to the pathomechanism in amyotrophic lateral sclerosis

To determine the origin of the large myelinated fibers in the anterolateral funiculus (ALF) in the spinal cord of humans, myelinated fibers in the ALF of the mid-cervical spinal cord were examined quantitatively. Five groups of subjects were examined, consisting of control subjects, patients with cerebral lesions and showing complete degeneration of the unilateral/bilateral pyramis of the medulla oblongata, those with lesions of the pontine tegmentum, those with lesions of the lower cervical spinal cord, and those with thoracic/lumbar lesions. The results indicate that the large myelinated fibers in the ALF of the mid-cervical spinal cord of humans originate from the tegmentum of the brain stem and the lower cervical spinal cord, and not from the cerebrum, or the thoracic or lumbar spinal cord. Thus, they are descending fibers from the brain stem tegmentum and ascending fibers from the lower cervical cord, and not corticospinal tracts or long-ascending fibers from the thoracic or lumbar spinal cord. The origin of the large myelinated fibers in the ALF of the spinal cord in humans, the number of which was severely decreased in patients with amyotrophic lateral sclerosis, is considered to be the long-descending neurons in the brain stem tegmentum and the propriospinal neurons in the spinal cord. Received: 23 December 1998 / Revised, accepted: 29 March 1999