Spinal canal narrowing during simulated frontal impact

Between 23 and 70% of occupants involved in frontal impacts sustain cervical spine injuries, many with neurological involvement. It has been hypothesized that cervical spinal cord compression and injury may explain the variable neurological profile described by frontal impact victims. The goals of the present study, using a biofidelic whole cervical spine model with muscle force replication, were to quantify canal pinch diameter (CPD) narrowing during frontal impact and to evaluate the potential for cord compression. The biofidelic model and a sled apparatus were used to simulate frontal impacts at 4, 6, 8, and 10 g horizontal accelerations of the T1 vertebra. The CPD was measured in the intact specimen in the neutral posture (neutral posture CPD), under static sagittal pure moments of 1.5 Nm (pre-impact CPD), during dynamic frontal impact (dynamic impact CPD), and again under static pure moments following each impact (post-impact CPD). Frontal impact caused significant (P<0.05) dynamic CPD narrowing at C0-dens, C2-C3, and C6-C7. The narrowest dynamic CPD was observed at C0-dens during the 10 g impact and was 25.9% narrower than the corresponding neutral posture CPD. Interpretation of the present results indicate that the neurological symptomatology reported by frontal impact victims is most likely not due to cervical spinal cord compression. Cord compression due to residual spinal instability is also not likely.     

Idiopathic Spinal Cord Herniation as a Treatable Cause of Progressive Brown-Sequard Syndrome

Idiopathic spinal cord herniation is a rare spinal cord disorder caused by spinal cord prolapse through a adural defect. It is a curable disease, so early detection is of particular importance. We report a 38-year-old woman with Brown-Sequard syndrome which was caused by the thoracic spinal cord herniation. Her weakness was almost completely resolved after surgical management, which emphasizes the importance of early diagnosis and surgical management in this rare disease entity.     

Effect of the free radical scavenger MCI-186 on spinal cord reperfusion after transient ischemia in the rabbit

Objective: Paraplegia remains a serious complication of aortic operations. The production of free radicals during reperfusion after transient ischemia is believed to induce secondary spinal neuronal injury, resulting in paraplegia. The aim of the present study was to clarify the protective effect and method of administration of antioxidants on the neurological and histological outcome in the animal model for reperfusion injury after transient spinal cord ischemia. Methods: New Zealand white rabbits underwent surgical exposure of the abdominal aorta that was clamped for 15 minutes to achieve spinal cord ischemia. Group A animals received two 10 mg/kg doses of 3-methyl-l-phenyl-2-pyrazolin-5-one (MCI-186) at the time of release of the aortic clamp and 30 minutes later. In group B, MCI-186, 5 mg/kg, was given three times, at the time of aorta clamp release, 30 minutes and 12 hours later. In group C (control group), one dose of vehicle was administered. Neurological status was assessed using modified Tarlov’s score until 168 hours after operation. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Groups A and B animals had better neurological function than group C (p(0.001). In contrast, group C animals exhibited paraplegia or paraparesis with marked neuronal necrosis. The number of surviving neurons within examined sections of the spinal cord was significantly greater in group B than in group C (p(0.001). Conclusion: In a 15-minute ischemia-reperfusion model using rabbits, systemic repetitious administration of MCI-186, a free radical scavenger, was found to have a protective effect on the spinal cord neurons both neurologically and histologically. We postulate that the drug minimizes the delayed neuronal cell death for reperfusion injury after transient ischemia by reducing the free radical molecules. Moreover, it was thought that we could protect delayed neuronal cell death more effectively by administering MCI-18612 hours later.     

Mechanisms mediating the brain stem control of somatosensory transmission in the dorsal horn of the cat's spinal cord: an intracellular analysis

Summary The effect of brainstem stimulation was studied on neurones recorded intracellularly in the superficial and deeper laminae of the lumbosacral dorsal horn of the spinal cord in anaesthetised cats. Stimulation in the nucleus locus coeruleus (LC) produced a hyperpolarisation in 4/13 multireceptive neurones and produced a biphasic action consisting of a hyperpolarisation which was followed by a depolarisation in 3/13 neurones. These actions were produced irrespective of whether the multireceptive neurone was located in the superficial or deeper laminae of the dorsal horn. Stimulation failed to produce postsynaptic potentials in the remaining 6/13 multireceptive neurones. The amplitude of hyperpolarisation was increased by the passage of depolarising pulses through the recording microelectrode and decreased by hyperpolarising pulses. Stimulation in other brainstem areas such as, the lateral (FTL), paralemniscal (FTP) and central (FTC) divisions of the tegmental field and the nuclei raphe magnus (NRM) and reticularis magnocellularis (RMc) also hyperpolarised neurones in the dorsal horn. The polarity of hyperpolarisation evoked from some brainstem areas (FTP, FTC, RMc) could be reversed to depolarisation by the passive diffusion of ions from the recording microelectrode containing 3M-KCl. Brainstem (LC, NRM, FTP, FTL) stimulation generated long lasting (700 ms) hyperpolarisation on 4/4 selectively nocireceptive neurones of lamina I. There was, however, no effect on the activity of 5/5 neurones recorded in laminae I/II which in addition to receiving excitatory cutaneous inputs were inhibited by heat stimuli. Stimulation in LC also produced dorsal root potentials (DRPs) and reduced the amplitude of simultaneously recorded excitatory postsynaptic potentials (EPSPs) generated by the activation of primary afferent fibres in 3 multireceptive neurones. It is concluded that inhibition of nociceptive transmission in the spinal cord from LC and other brainstem areas may involve both pre- and postsynaptic mechanisms.     

电针对SNI大鼠痛敏及脊髓相应节段谷氨酸和P物质的影响

目的:探讨电针对神经病理性痛大鼠痛觉过敏以及脊髓谷氨酸和P物质含量的影响。方法:40只SD大鼠,随机分为空白组、假手术组、手术组和电针组(n=10)。采用坐骨神经分支选择性损伤模型,电针"委中"和"环跳"穴,观察其对大鼠机械痛阈和热痛阈的影响,以OPA柱前衍生+HPLC荧光检测和放射免疫分析法测定脊髓相应节段谷氨酸和P物质含量的变化。结果:SNI手术可明显降低大鼠机械痛阈,并且其脊髓相应节段谷氨酸含量明显升高,P物质含量则明显降低;而电针干预后可显著降低大鼠脊髓相应节段谷氨酸的含量,升高P物质含量,并减轻SNI大鼠的机械痛敏状态,进而改善其痛行为。结论:电针干预神经病理性痛的脊髓机制之一可能与其有效的减少大鼠脊髓相应节段谷氨酸和P物质的释放有关。     

血管内皮生长因子在高原脑水肿形成中作用的实验研究

目的:探讨血管内皮生长因子(VEGF)在高原脑水肿形成中的作用。方法:建立大鼠模拟高原模型,应用脑干湿重比率法定量脑水肿情况、应用荧光素钠透过率测定BBB通透性、应用实时荧光定量RT-PCR法检测脑组织VEGF mRNA含量以及应用蛋白印迹法半定量脑组织VEGF含量。结果:大鼠在高原24 h后脑组织含水率明显增高(P<0.05),荧光素钠透过率显著增加(P<0.01);VEGF mRNA转录及其表达显著增高(P<0.001)。结论:VEGF表达在高原脑水肿形成中起重要作用。     

丹参注射液椎管内局部灌注对急性脊髓损伤的保护作用

目的 探讨丹参对急性脊髓损伤的防治作用。方法 以改良Allen's法造成兔不完全性脊髓损伤的模型,硬膜下插管。随机分成丹参治疗组和对照组。术后按每天0.3ml/kg体重的总量分4次从硬膜下导管推入丹参注射液,对照组推入生理盐水。损伤后8、72h对脊髓损伤区进行过氧化物歧化酶(SOD)、丙二醛(MDA)、组织形态学观察、神经元凋亡、bcl-2等进行评价。结果 丹参组SOD含量高于对照组(P<0.01),MDA含量低于对照组(P<0.01)。细胞凋亡数目TUNEL法丹参组低于对照组(P<0.01),流式细胞术检测凋亡丹参组低于对照组(P<0.05)。bcl-2的表达丹参组高于对照组(P<0.05)。神经元及神经纤维变性、坏死轻于对照组。结论 丹参能改善损伤脊髓微循环,抑制和减轻脊髓损伤后的两种死亡方式坏死和凋亡。     

胸椎骨折合并胸外伤的外科治疗

目的　总结 17例胸椎骨折患者的特点与诊疗情况 ,为提高此类合并胸外伤患者的疗效提供有效的治疗方案。方法　分析了 17例胸椎骨折患者的临床特点、诊疗经过、近远期随访结果。结果　 14例 (82 .4 % )合并肋骨骨折 ,11例 (6 4 .7% )合并血气胸 ,10例 (5 8.8% )合并严重脊髓伤 ,3例 (30 % )远期脊髓伤为有用恢复。结论　胸椎骨折常合并肋骨骨折、血气胸、严重脊髓损伤 ,预后较差 ,为此应重视合并胸外伤的胸椎骨折的围手术期处理     

小干扰RNA干扰大鼠神经元Nogo受体mRNA表达的实验研究

目的观察大鼠Nogo受体(NgR)特异性小干扰RNA(small interfering RNA,siRNA)在原代神经元干扰其mRNA表达的效果。方法体外培养大鼠原代皮层和海马细胞,应用阳离子脂质体转染试剂转染4对化学合成的大鼠NgR特异性siRNA,72h后提取细胞总RNA,实时荧光定量RT-PCR检测NgR mRNA表达情况。结果4对siRNA均能够下调靶基因NgR的mRNA表达水平,siNgR199、siNgR562、siNgR772和siNgR964等干扰后,NgR mRNA的表达分别为对照siRNA干扰组的6.5%、62.4%、15.2%和6.86%,与对照siRNA干扰组比较有统计学意义(P<0.05)。结论化学合成的NgR特异性siRNA能够有效的干扰大鼠原代皮层和海马细胞内NgR基因mRNA的表达水平。