MR Findings of Intrathecal Chemotherapy-Related Myelopathy in Two Cases: Mimicker of Subacute Combined Degeneration

We report the findings of spinal magnetic resonance imaging (MRI) in 2 patients who had undergone intrathecal chemotherapy and presented with the subacute onset of ascending numbness and weakness. MRI revealed a symmetric hyperintensity at the posterior columns of the spinal cord from the lower cervical region down to the conus medullaris level on T2-weighted images, and no abnormal enhancement. The imaging findings are similar to those seen in subacute combined degeneration (SCD), but the serum vitamin B(12) levels were normal in these 2 cases.     

Neuroprotective effect of estrogen after chronic spinal cord injury in ovariectomized rats

BACKGROUND: At present, there is still lack of effective drugs for chronic spinal cord injury, whereas it is found recently that estrogen has a neuroprotective effect on brain and spinal cord injuries. OBJECTIVE: To observe the effect of estrogen on the apoptosis of nerve cells after gradual chronic spinal cord injury in ovariectomized rats. DESIGN: A randomized controlled animal trial. SETTING: Institute of Orthopaedics, the Second Hospital of Lanzhou University. MATERIALS: Sixty-five female Wistar rats of common degree, weighing 220–250 g, were provided by the experimental animal center of Lanzhou University. The rats were randomly divided into sham-operated group (n =5), estrogen-treated group (n =30) and saline control group (n =30), and the latter two groups were observed at 1, 3, 7, 14, 28 and 60 days respectively, and 5 rats for each time point. METHODS: All the rats were treated with bilateral oophorectomy 2 weeks before the experiment. T10 vertebral lamina was revolved into using plastic screw. The spinal canal impingement was not induced initially. After that, the original incision was opened to expose the screw every 7–10 days. MAIN OUTCOME MEASURES: The apoptosis and Caspase-3 positive cells in the damaged spinal cord were detected using terminal deoxynucleotidal transferase-mediated dUTP-biotin nick end labeling (TUNEL) method and Caspase-3 immunohistochemical staining at 1, 3, 7, 14, 28 and 60 days after chronic spinal cord injury respectively. RESULTS: Totally 65 rats were used, and the deleted ones during the experiment were supplemented by others. Changes of Caspase-3 expression after spinal cord injury: In the sham-operated group, only a small amount of Caspase-3 proteins were observed in the rat spinal cord, mainly located in motor neurons of spinal cord anterior horn. In the estrogen-treated group and saline control group, positive cells expressed occasionally at 1 day postoperatively, began to increase obviously at 7 days after injury, strongly expressed at 14 and 28 days, but decreased at 60 days, mainly located in the neurons of spinal cord gray matter anterior horn, and they expressed fewer in the motor neurons and white matter of ventral horn, and there were obvious differences between the estrogen-treated group and saline control group at 7, 14, 28 and 60 days (P < 0.05). CONCLUSION: Estrogen can reduce the apoptosis of nerve cells and promote the recovery of neurological function following gradual chronic spinal cord injury.     

Engineering angiogenesis following spinal cord injury: a coculture of neural progenitor and endothelial cells in a degradable polymer implant leads to an increase in vessel density and formation of the blood–spinal cord barrier

Angiogenesis precedes recovery following spinal cord injury and its extent correlates with neural regeneration, suggesting that angiogenesis may play a role in repair. An important precondition for studying the role of angiogenesis is the ability to induce it in a controlled manner. Previously, we showed that a coculture of endothelial cells (ECs) and neural progenitor cells (NPCs) promoted the formation of stable tubes in vitro and stable, functional vascular networks in vivo in a subcutaneous model. We sought to test whether a similar coculture would lead to the formation of stable functional vessels in the spinal cord following injury. We created microvascular networks in a biodegradable two-component implant system and tested the ability of the coculture or controls (lesion control, implant alone, implant + ECs or implant + NPCs) to promote angiogenesis in a rat hemisection model of spinal cord injury. The coculture implant led to a fourfold increase in functional vessels compared with the lesion control, implant alone or implant + NPCs groups and a twofold increase in functional vessels over the implant + ECs group. Furthermore, half of the vessels in the coculture implant exhibited positive staining for the endothelial barrier antigen, a marker for the formation of the blood–spinal cord barrier. No other groups have shown positive staining for the blood–spinal cord barrier in the injury epicenter. This work provides a novel method to induce angiogenesis following spinal cord injury and a foundation for studying its role in repair.     

急进性后极部早产儿视网膜病变的临床进程及疗效观察

目的 描述急进性后极部早产儿视网膜病变(AP-ROP)的临床进程及特征,评价视网膜光凝及冷凝对急进性后极部早产儿视网膜病变的治疗效果.方法 前瞻性、非对比性、连续性病例.2006年1月至2008年6月经检查确诊为急进性后极部ROP的患儿8例16只眼.确诊后24h内行间接眼底镜下行视网膜光凝治疗联合或不联合直视下冷凝治疗.结果 急进性后极部早产儿视网膜病变以病变大部分位于后极部1区,所有象限视网膜血管扩张迂曲,病程进展快,若不及时治疗,迅速发生视网膜漏斗状全脱离为临床特征.本组8例16只眼视网膜光凝和(或)冷凝治疗后,9只眼病变完全退化或控制,占56.2%.7只眼病情未能控制,最终发展为4b至5期视网膜病变.结论 AP-ROP进展快,预后不良,部分患儿虽经严密观察和治疗,病情仍进展.视网膜光凝和(或)冷凝治疗能控制大部分AP-ROP患儿视网膜病变的发展,挽救患儿视功能.临床上需要加强观察和随访,早发现、早诊断、早治疗是减低该病致盲率的惟一方法.     

猪腰段脊髓火器伤对肾脏及其功能的影响

[目的]建立猪腰段脊髓火器伤模型和改良Allen＇s打击伤后全瘫模型，观察伤后肾脏病理和肾功能的早期变化。[方法]动物随机分为两组，火器伤组（G）6只，在全麻状态下做L1-2脊髓火器伤模型；打击伤组（A）6只，L1节段脊髓行改良Allen＇s打击。两组动物分别于伤前（0h）、伤后0．5h、1h、2h、4h检测血肌酐和血尿素氮（BUN）。死亡动物行肾脏病理检查。[结果]A组BUN值在伤后4h升高，G组BUN值在伤后1h升高。两组肌酐在伤后0．5h升高，各点监测G组明显高于A组。G组动物伤后5．2h-7．5h死亡，死亡率为100％。病理检查示G组肾包膜及肾实质广泛充血、出血。[结论]G组火器伤较A组肾脏损伤及组织破坏严重，在伤后早期出现肾功能变化。脊髓火器伤后肾功能变化早期应给予积极处理，以降低早期死亡率。     

Role of proteasomes in the formation of neurofilamentous inclusions in spinal motor neurons of aluminum‐treated rabbits

We examined the role of the 20S proteasome in pathologic changes, including abnormal aggregation of phosphorylated neurofilaments, of spinal motor nerve cells from aluminum‐treated rabbits. Immunohistochemistry for the 20S proteasome revealed that many lumbar spinal motor neurons without intracytoplasmic neurofilamentous inclusions or with small inclusions were more intensely stained in aluminum‐treated rabbits than in controls, whereas the immunoreactivity was greatly decreased in some enlarged neurons containing large neurofilamentous inclusions. Proteasome activity in whole spinal cord extracts was significantly increased in aluminum‐treated rabbits compared with controls. Furthermore, Western blot analysis indicated that the 20S proteasome degraded non‐phosphorylated high molecular weight neurofilament (neurofilament‐H) protein in vitro. These results suggest that aluminum does not inhibit 20S proteasome activity, and the 20S proteasome degrades neurofilament‐H protein. We propose that abnormal aggregation of phosphorylated neurofilaments is induced directly by aluminum, and is not induced by the proteasome inhibition in the aluminum‐treated rabbits. Proteasome activation might be involved in intracellular proteolysis, especially in the earlier stages of motor neuron degeneration in aluminum‐treated rabbits.     

Axonal damage in the spinal cord of multiple sclerosis patients detected by magnetic resonance spectroscopy.

Axonal damage is a major factor contributing to permanent disability in patients with multiple sclerosis (MS); it has been extensively investigated in the brain using magnetic resonance spectroscopy (MRS). In this study, MRS was used to investigate the degree of neuronal damage in the cervical spinal cord in MS. Spectra were acquired from spinal cord and brain in 11 patients with MS (expanded disability status score [EDSS], range 2.5-7.0) and 11 controls. Brain lesion volume and spinal cord cross-sectional area were measured. Concentration of the neuronal metabolite N-acetyl-aspartate ([NAA]) was reduced in the spinal cord in MS patients relative to controls (reduced by 32%, P < 0.05), indicating significant neuronal damage. Additionally, the spinal cord was significantly atrophied in MS patients (15%, P < 0.001). No significant reduction in brain [NAA] was seen in the MS group. There were no correlations between clinical measures and cord atrophy or brain lesion volume on MRI; however, spinal cord [NAA] correlated with the cerebellar subscore of the neurological assessment (P < 0.005), while brain [NAA] correlated with disease duration (P < 0.05). MRS demonstrated cellular damage within the cord over and above the tissue atrophy seen by MRI. Combining MRI and MRS may therefore give a more complete picture of neurodegeneration in the spinal cord.     

退变性症状性腰椎侧凸的手术治疗

[目的]探讨后路椎管减压、椎弓根螺钉间断固定、椎间植骨融合、矢状位重建术式治疗退变性症状性腰椎侧凸的临床效果。[方法]1999年1月-2006年4月，采用经后路椎管减压、椎弓根螺钉间断固定、椎间植骨融合、矢状位重建术式治疗退变性症状性腰椎侧凸37例，男21例，女16例；年龄51—82岁，平均62．6岁。所有病例拍摄腰椎正侧位片及Bending片，常规备CT和MRI。根据患者下肢症状行全椎板或半椎板减压，神经根扩大，椎间植骨融合及椎弓根螺钉间断固定。[结果]本组病例均获随访（1—6年，平均2年零7个月），术后临床症状均明显缓解，按JOA评分，手术疗效优良率91．9％，侧凸平均矫正率54．8％。随访期间无明显矫正度数及椎间隙高度丢失，术后3个月、1年复查X片内置物无松动及断裂，植骨融合时间平均11．6周。[结论]对于退变性症状性腰椎侧凸患者：（1）采取个体化治疗，年龄不是绝对手术禁忌证，病程长短不是决定手术疗效的重要指标；（2）后路椎管减压、椎弓根螺钉间断固定、椎间植骨融合、矢状位重建术是安全有效的理想术式。     

肛门括约肌肌电图监测下双侧L2～S2选择性脊神经后根切断术治疗痉挛性脑瘫

目的为提高手术安全性,在L2～S2选择性脊神经后根切断(SPR)手术时,对肛门括约肌进行肌电图(EMG)监测,并评价其作用。方法在SPR手术监测中,当对S2后根小束进行电刺激时,采用针状电极记录双侧肛门括约肌的反应情况,有明显反应的后根小束予以保留。手术后随访患者踝痉挛改善情况和括约肌功能变化情况。结果所有患者手术后踝痉挛均有明显改善,无大小便功能障碍发生。结论SPR手术包括S2后根时,术中括约肌EMG监测对保证疗效,保护括约肌功能,提高手术安全,具有重要意义。