未发现压迫的创伤性非一过性脊髓损伤

未发现压迫原因的非一过性脊髓损伤在脊髓创伤中较为少见。作者1984年至1994年间对423例脊髓损伤中22例此类损伤作随访分析，对其诊断、治疗及可能发生的原因进行探讨。认为：（1）MRI能显示脊髓伤后的早期变化，对预后及治疗有重要的指导意义。（2）除了过伸损伤，其它损伤机制也能导致此类损害。（3）脊髓血管损伤、出血、髓内代谢产物沉积在这类损伤产生过程中占重要地位。（4）非手术治疗与单纯椎管减压术疗效比较无意义，而借助手术显微镜的髓内外联合减压术对该类损伤的恢复有一定帮助，即使完全性脊髓损伤亦不能轻易放弃积极治疗。     

高位颈髓压迫症的治疗策略

目的：探讨高位颈髓压迫症的外科治疗。方法：商位颈髓压迫症228例,其中齿突骨折58例（新鲜骨折38例,陈旧性骨折20例）,Hangman骨折45例（其中新鲜骨折28例,陈旧性骨折17例）,寰椎横韧带断裂24例,寰椎单侧后弓骨折19例,类风湿性天节炎17例,一侧关节突骨折9例,Jefferson骨折并慢性不稳3例,先天畸形48例,肿瘤4例。根据复位情况及脊髓受乐部何选择不同的术式,重建其稳定性。结果：平均随访4年11个月。JOA评分术前平均7．5分,随访时评分14．9分,改善率79．9％。结论：充分减压是最大限度恢复神经功能的有效方法,稳定性的重建非常必要。     

大鼠脊髓受压后的病理学变化

目的　观察脊髓受压后的病理学变化。方法　通过注射 1 0 6Walker 2 5 6癌细胞液到大鼠 T1 3椎体前 ,建立脊髓硬膜外压迫实验模型。大约 1 6天左右所有动物产生瘫痪 ,快速切取受压处的脊髓组织作透射电镜观察。结果　电镜发现脊髓白质细胞间隙扩大 ,含有外渗的血液细胞 ,并见髓鞘退变。结论　研究提示脊髓受压后的水肿在神经功能障碍的形成中起着重要作用。     

枕颈部发育畸形致脊髓压迫症与损伤的关系

旨在对75例上颈椎和枕部发育畸形的类型、临床特点及影像学表现进行研究。全组均有不同类型齿状突发育畸形,其中合并寰椎枕骨化17例,颅底凹陷畸形11例。根据畸形特点和稳定程度选择寰枢椎融合29例,枕颈减压融合术46例。结果73例获骨性愈合,随访26个月,优良者59例(81.9％)。     

罕见病因的胸椎管压迫症13例

１９８５年１月～１９９４年１２月收治罕见病因所致胸椎管压迫症１３例，其中胸椎间盘突出６例，硬膜外脓肿４例，硬膜下血肿１例，硬膜外脂肪血管瘤１例，硬膜下结核肉芽肿１例。１２例曾被误诊．１３例均有腰背痛和脊髓病症状，预后同术前脊髓病程度有关。作者分析各病临床特征，提出早期诊断方法，强调ＣＴＭ和ＭＲＩ的诊断价值，主张早期手术减压。     

Partial Tumor Resection Combined with Chemotherapy for Multiple Myeloma Spinal Cord Compression

Background

Some controversies about the optimal therapy for multiple myeloma (MM) spinal cord compression are still presented. This study was conducted to investigate the efficacy of partial tumor resection combined with chemotherapy for MM spinal cord compression.

Methods

Eleven patients were diagnosed with MM spinal cord compression. Radiological examinations manifested 12 spinal lesions on 11 patients. All patients were treated with partial tumor resection with adjuvant chemotherapy. The mean procedure time, the mean blood loss, visual analog scale score, Oswestry Disability Index (ODI) score, neurological status, complication, recurrence, and quality of life were evaluated.

Results

Eleven patients were followed up with a mean of 25.1 months. The mean procedure time was 152.6 ± 30.4 min, and the mean blood loss was 396.4 ± 82.7 ml. Overall pain control rate was 89 %, with complete pain relief in 64 %, and partial pain relief in 25 %. The median pre-ODI values of 85 % significantly improved to 12 % at the last follow-up. Neurological improvement of one to two grades was observed 6 months postoperatively. Complications included pleural effusion, titanium cage loose, and thrombocytopenia in three patients each. Local recurrence was 18.2 %. One patient died of pulmonary infection. Quality of life improved from 39 % before surgery to 81 % in ten survivors at the last follow-up.

Conclusions

Partial tumor resection combined with chemotherapy seems to be an effective treatment for MM spinal cord compression owing to the minor surgical trauma, fewer complications, and effective pain control. Total resection of the tumor is not necessary for MM of the spine.     

Extradural Giant Multiloculated Arachnoid Cyst Causing Spinal Cord Compression in a Child

Abstract

Background: Spinal extradural arachnoid cysts are rare expanding lesions in the spinal canal. Enlargement may cause progressive signs and symptoms caused by spinal cord compression. They are associated with trauma, surgery, arachnoiditis, and neural tube defects. Most nontraumatic spinal extradural arachnoid cysts are thought to be congenital.

Design: Case report and literature review.

Findings: A 9-year-old boy with mild paraparesis was found to have an extradural multiloculated arachnoid cyst with fibrous septa at T4-L3 levels and anterior compression and displacement of the spinal cord.

Conclusions: Definitive treatment of arachnoid cyst entails radical cyst removal and dura cleft repair. Formation of a postoperative cerebrospinal fluid fistula may require external lumbar drainage.     

大鼠脊髓受压后的平均刚度的变化

目的：观察脊髓刚度在脊髓压迫综合征发病机制中的作用及消炎痛的作用机制。方法：通过注射１０＾６Ｗａｌｋｅｒ２５６瘤细胞液到大鼠Ｔ１３椎体前,建立脊硬膜外压迫实验模型,对脊髓进行一次载荷下的压力－位移关系实验,利用增量法求出脊髓的平均刚度;分析实验数据,求出脊髓的拟合函数。结果：压迫对照组动物大ｄ左右,治疗组动物大约１７．５ｄ左右双后肢产生瘫痪;压迫对照组脊髓的平均刚度明显增高,治疗组脊髓的平均刚度明     

脊髓损伤大鼠脊髓组织的病理形态学观察

目的：研究脊髓损伤（SCI）用高压氧（HBO）处理后脊髓的病理学变化。方法：用SD大鼠复制SCI模型，0．1MPa和0．25MPaHBO处理后，取损伤脊髓作HE染色。结果：正常对照组脊髓结构完整，细胞形态正常，分布均匀，胞膜，胞核正常，组织间隙正常，单纯损伤组示组织出血，疏松水肿，细胞空泡变性，神经纤维溶解，消失；处理后，0．25MPaHBO组及0．25MPaHBO＋激素（L，M）组脊髓恢复最明显，组织水肿，细胞空泡变性减轻，细胞形态恢复，结构排列完整，结论：HBO治疗可明显阻止或减轻脊髓损伤的病理变化，有利于脊髓功能的恢复。     

Infection as a Cause of Spinal Cord Compression: A Review of 36 Spinal Epidural Abscess Cases

A retrospective survey of 36 cases treated in the Department of Neurosurgery, Hacettepe University Hospitals since 1970 was performed. Clinical presentation, aetiology and outcome of this rare disease compared to recently published series. All cases were admitted with signs of neural compression. Clinical and laboratory data suggesting an infectious origin were present only in 4 cases. Radiological investigation including magnetic resonance imaging in 10 patients, were not confirmative for an epidural abscess except for two cases. All cases underwent urgent surgical decompression and tuberculous abscess either in granulation or pus form was found in the majority. Overall mortality rate was 5.8%. Outcome was closely related to the neurological condition on admission rather than the underlying infectious origin. When compared with recently reported series, our cases demonstrated a significant divergence in terms of clinical presentation, pathogenesis and outcome. The most probable reason for this discrepancy is that risk factors for compromised immunity or systemic infection were much less than the other series and mycobacterium tuberculosis is the responsible agent in the majority which has a much more favourable outcome than non-spesific infections.     

The Effects of Hypertonic Saline on Spinal Cord Blood Flow Following Compression Injury

Summary  7.5% hypertonic saline was administered following spinal cord injury to test its effect on spinal cord blood flow. Four different groups of rats underwent 10 minutes of spinal cord compression (45g) at the C3 to C5 levels. A fifth group was not injured, but received hypertonic saline (5 ml/kg) at 5, 15 and 60 minutes following injury. Somatosensory evoked potentials and spinal cord blood flow were measured prior to and for 4 hours following the injury. The administration of hypertonic saline caused a significant increase in flow when administered 5 minutes following injury. Topical nitroprusside administration did not cause any increase in spinal cord blood flow during this time period. Hypertonic saline administration at the later time periods did not increase spinal cord blood flow. The group of animals which were not injured, but received hypertonic saline also showed no significant change in flow. The somatosensory evoked response of the treated animals was maintained for 4 hours after the injury where as the untreated animals began to lose their evoked responses 3 hours after injury.     

经胸骨前路减压治疗颈胸段脊髓压迫症

观察经胸骨前路椎体扩大开窗减压,椎间植骨融合术治疗颈胸段脊髓压迫症的疗效。方法３例颈胸段脊髓压迫症中,２例为后纵韧带骨化,１例为胸椎骨折。手术取颈胸部联合切口,纵行劈开胸骨,显露颈胸段椎体,用切骨刀及气动球磨钻扩大开窗减压,去除椎体骨质,突出椎间盘或骨化的后纵韧带,取髂骨块行椎间植骨融合。     

Radiation Disrupts the Protective Function of the Spinal Meninges in a Mouse Model of Tumor-induced Spinal Cord Compression

BackgroundRecent advances in multidisciplinary treatments for various cancers have extended the survival period of patients with spinal metastases. Radiotherapy has been widely used to treat spinal metastases; nevertheless, long-term survivors sometimes undergo more surgical intervention after radiotherapy because of local tumor relapse. Generally, intradural invasion of a spinal tumor seldom occurs because the dura mater serves as a tissue barrier against tumor infiltration. However, after radiation exposure, some spinal tumors invade the dura mater, resulting in leptomeningeal dissemination, intraoperative dural injury, or postoperative local recurrence. The mechanisms of how radiation might affect the dura have not been well-studied.Questions/purposesTo investigate how radiation affects the spinal meninges, we asked: (1) What is the effect of irradiation on the meningeal barrier’s ability to protect against carcinoma infiltration? (2) What is the effect of irradiation on the meningeal barrier’s ability to protect against sarcoma infiltration? (3) What is the effect of irradiation on dural microstructure observed by scanning electron microscopy (SEM)? (4) What is the effect of irradiation on dural microstructure observed by transmission electron microscopy (TEM)?MethodsEighty-four 10-week-old female ddY mice were randomly divided into eight groups: mouse mammary tumor (MMT) implantation 6 weeks after 0-Gy irradiation (nonirradiation) (n = 11), MMT implantation 6 weeks after 20-Gy irradiation (n = 10), MMT implantation 12 weeks after nonirradiation (n = 10), MMT implantation 12 weeks after 20-Gy irradiation (n = 11), mouse osteosarcoma (LM8) implantation 6 weeks after nonirradiation (n = 11), LM8 implantation 6 weeks after 20-Gy irradiation (n = 11), LM8 implantation 12 weeks after nonirradiation (n = 10), and LM8 implantation 12 weeks after 20-Gy irradiation (n = 10); female mice were used for a mammary tumor metastasis model and ddY mice, a closed-colony mice with genetic diversity, were selected to represent interhuman diversity. Mice in each group underwent surgery to generate a tumor-induced spinal cord compression model at either 6 weeks or 12 weeks after irradiation to assess changes in the meningeal barrier’s ability to protect against tumor infiltration. During surgery, the mice were implanted with MMT (representative of a carcinoma) or LM8 tumor. When the mice became paraplegic because of spinal cord compression by the growing implanted tumor, they were euthanized and evaluated histologically. Four mice died from anesthesia and 10 mice per group were euthanized (MMT-implanted groups: MMT implantation occurred 6 weeks after nonirradiation [n = 10], 6 weeks after irradiation [n = 10], 12 weeks after nonirradiation [n = 10], and 12 weeks after irradiation [n = 10]; LM8-implanted groups: LM8 implantation performed 6 weeks after nonirradiation [n = 10], 6 weeks after irradiation [n = 10], 12 weeks after nonirradiation [n = 10], and 12 weeks after irradiation [n = 10]); 80 mice were evaluated. The spines of the euthanized mice were harvested; hematoxylin and eosin staining and Masson’s trichrome staining slides were prepared for histologic assessment of each specimen. In the histologic assessment, intradural invasion of the implanted tumor was graded in each group by three observers blinded to the type of tumor, presence of irradiation, and the timing of the surgery. Grade 0 was defined as no intradural invasion with intact dura mater, Grade 1 was defined as intradural invasion with linear dural continuity, and Grade 2 was defined as intradural invasion with disruption of the dural continuity. Additionally, we euthanized 12 mice for a microstructural analysis of dura mater changes by two observers blinded to the presence of irradiation. Six mice (three mice in the 12 weeks after nonirradiation group and three mice in the 12 weeks after 20-Gy irradiation group) were quantitatively analyzed for defects on the dural surface with SEM. The other six mice (three mice in the 12 weeks after nonirradiation group and three mice in the 12 weeks after 20-Gy irradiation group) were analyzed for layer structure of collagen fibers constituting dura mater by TEM. In the SEM assessment, the number and size of defects on the dural surface on images (200 μm × 300 μm) at low magnification (× 2680) were evaluated. A total of 12 images (two per mouse) were evaluated for this assessment. The days from surgery to paraplegia were compared between each of the tumor groups using the Kruskal-Wallis test. The scores of intradural tumor invasion grades and the number of defects on dural surface per SEM image were compared between irradiation group and nonirradiation group using the Mann-Whitney U test. Interobserver reliabilities of assessing intradural tumor invasion grades and the number of dural defects on the dural surface were analyzed using Fleiss’κ coefficient. P values < 0.05 were considered statistically significant.ResultsThere was no difference in the median (range) time to paraplegia among the MMT implantation 6 weeks after nonirradiation group, the 6 weeks after irradiation group, the 12 weeks after nonirradiation group, and the 12 weeks after irradiation group (16 days [14 to 17] versus 14 days [12 to 18] versus 16 days [14 to 17] versus 14 days [12 to 15]; χ² = 4.7; p = 0.19). There was also no difference in the intradural invasion score between the MMT implantation 6 weeks after irradiation group and the 6 weeks after nonirradiation group (8 of 10 Grade 0 and 2 of 10 Grade 1 versus 10 of 10 Grade 0; p = 0.17). On the other hand, there was a higher intradural invasion score in the MMT implantation 12 weeks after irradiation group than the 12 weeks after nonirradiation group (5 of 10 Grade 0, 3 of 10 Grade 1 and 2 of 10 Grade 2 versus 10 of 10 Grade 0; p = 0.02). Interobserver reliability of assessing intradural tumor invasion grades in the MMT-implanted group was 0.94. There was no difference in the median (range) time to paraplegia among in the LM8 implantation 6 weeks after nonirradiation group, the 6 weeks after irradiation group, the 12 weeks after nonirradiation group, and the 12 weeks after irradiation group (12 days [9 to 13] versus 10 days [8 to 13] versus 11 days [8 to 13] versus 9 days [6 to 12]; χ² = 2.4; p = 0.50). There was also no difference in the intradural invasion score between the LM8 implantation 6 weeks after irradiation group and the 6 weeks after nonirradiation group (7 of 10 Grade 0, 1 of 10 Grade 1 and 2 of 10 Grade 2 versus 8 of 10 Grade 0 and 2 of 10 Grade 1; p = 0.51), whereas there was a higher intradural invasion score in the LM8 implantation 12 weeks after irradiation group than the 12 weeks after nonirradiation group (3 of 10 Grade 0, 3 of 10 Grade 1 and 4 of 10 Grade 2 versus 8 of 10 Grade 0 and 2 of 10 Grade 1; p = 0.04). Interobserver reliability of assessing intradural tumor invasion grades in the LM8-implanted group was 0.93. In the microstructural analysis of the dura mater using SEM, irradiated mice had small defects on the dural surface at low magnification and degeneration of collagen fibers at high magnification. The median (range) number of defects on the dural surface per image in the irradiated mice was larger than that of nonirradiated mice (2 [1 to 3] versus 0; difference of medians, 2/image; p = 0.002) and the median size of defects was 60 μm (30 to 80). Interobserver reliability of assessing number of defects on the dural surface was 1.00. TEM revealed that nonirradiated mice demonstrated well-organized, multilayer structures, while irradiated mice demonstrated irregularly layered structures at low magnification. At high magnification, well-ordered cross-sections of collagen fibers were observed in the nonirradiated mice. However, disordered alignment of collagen fibers was observed in irradiated mice.ConclusionIntradural tumor invasion and disruptions of the dural microstructure were observed in the meninges of mice after irradiation, indicating radiation-induced disruption of the meningeal barrier.Clinical RelevanceWe conclude that in this form of delivery, radiation is associated with disruption of the dural meningeal barrier, indicating a need to consider methods to avoid or limit Postradiation tumor relapse and spinal cord compression when treating spinal metastases so that patients do not experience intradural tumor invasion. Surgeons should be aware of the potential for intradural tumor invasion when they perform post-irradiation spinal surgery to minimize the risks for intraoperative dural injury and spinal cord injury. Further research in patients with irradiated spinal metastases is necessary to confirm that the same findings are observed in humans and to seek irradiation methods that prevent or minimize the disruption of meningeal barrier function.     

Spinal Myoclonus After Spinal Cord Injury

Abstract

Background/Objective: In the course of examining spinal motor function in many hundreds of people with traumatic spinal cord injury, we encountered 6 individuals who developed involuntary and rhythmic contractions in muscles of their legs. Although there are many reports of unusual muscle activation patterns associated with different forms of myoclonus, we believe that certain aspects of the patterns seen with these 6 subjects have not been previously reported. These patterns share many features with those associated with a spinal central pattern generator for walking.

Methods: Subjects in this case series had a history of chronic injury to the cervical spinal cord, resulting in either complete (ASIA A; n = 4) or incomplete (ASIA D; n = 2) quadriplegia. We used multi-channel electromyography recordings of trunk and leg muscles of each subject to document muscle activation patterns associated with different postures and as influenced by a variety of sensory stimuli.

Results: Involuntary contractions spanned multiple leg muscles bilaterally, sometimes including weak abdominal contractions. Contractions were smooth and graded and were highly reproducible in rate for a given subject (contraction rates were 0.3-0.5 Hz). These movements did not resemble the brief rapid contractions (ie, "jerks") ascribed to some forms of spinal myoclonus. For all subjects, the onset of involuntary muscle contraction was dependent upon hip angle; contractions did not occur unless the hips (and knees) were extended (ie, subjects were supine). In the 4 ASIA A subjects, contractions occurred simultaneously in all muscles (agonists and antagonists) bilaterally. In sharp contrast, contractions in the 2 ASIA D subjects were reciprocal between agonists and antagonists within a limb and alternated between limbs, such that movements in these 2 subjects looked just like repetitive stepping. Finally, each of the 6 subjects had a distinct pathology of their spinal cord, nerve roots, distal trunk, or thigh; in 4 of these subjects, treatment of the pathology eliminated the involuntary movements.

Conclusion: The timing, distribution, and reliance upon hip angle suggest that these movement patterns reflect some elements of a central pattern generator for stepping. Emergence of these movements in persons with chronic spinal cord injury is extremely rare and appears to depend upon a combination of the more rostrally placed injury and a pathologic process leading to a further enhancement of excitability in the caudal spinal cord.