刺络闪火法治疗腰棘间韧带损伤

作者自1986年5月以来应用刺络闪火法治疗腰棘间韧带损伤取得满意效果。该法融按摩、刺络、闪火及复位于一体。结果表明该法不仅能消除棘间韧带的水肿,而且较好地调整损伤节段腰椎珠应和结构,从根本上促进损伤韧带的修复。     

部分背根切断对备用背根节NT-3表达的影响

目的　探讨部分去背根后备用背根节 (L6 )各类细胞NT 3及其mRNA的含量变化。　方法　对成年雄性猫行单侧部分背根切断术 (切除一侧L1 ～L5,L7～S2 DRG ,保留L6 为备用根 )。取正常组一侧和术后 3d及 7d组手术侧的L6 DRG制作 2 0 μm厚冰冻切片 ,分别用NT 3抗体及NT 3cRNA探针行免疫组织化学及原位杂交染色。观察NT 3及其mRNA在DRG各类细胞的分布 ,测定NT 3及其mRNA在神经元和卫星细胞的光密度值 ,所得数据用q检验进行统计分析。　结果　部分去背根后 ,各时相备用背根节大神经元内NT 3的光密度值较正常者进行性减少 ,(P <0 0 5 ) ,而NT 3mRNA的光密度值术后 3d减少 ,7d回升至近正常者水平。比较之 ,小神经元和卫星细胞NT 3及其mRNA的光密度值进行性增多 (P <0 0 5 )。　结论　部分背根切断对备用背根节各类细胞NT 3表达的影响不同 ,其功能意义可能与NT 3参与脊髓Ⅱ板层可塑性有关     

吗啡增强备用根大鼠脊髓后角组织提取液对培养鸡胚背根节的促神经突起生长的作用

用组织培养方法，探讨备用很大鼠手术侧和非手术侧脊髓后角组织提取液对鸡胚背根节（ＤＲＧ）神经突起的促生长作用，以及应用吗啡对此作用的影响。结果显示：备用根大鼠手术侧脊髓后角组织提取液作用的ＤＲＧ神经突起密度（３６．４２±４．６９），比非手术侧的（２３．９６±３．４７）明显增大。提示去初级传入纤维的脊髓后角组织具有促进ＤＲＧ神经突起生长的神经营养活性作用。应用吗啡的备用根大鼠手术侧脊髓后角组织提取液作用的ＤＲＧ神经突起密度（６４．１９±９．２４），又比备用根大鼠手术侧的大。这表明，吗啡具有进一步增强去初级传入纤维支配的脊髓后角组织提取液促进培养的ＤＲＧ神经突起生长的效应。     

黄韧带骨化的病理组织学研究

目的 :探讨黄韧带骨化的病理变化特点和发生机理。方法 :利用组织病理学和组织化学方法对比研究正常黄韧带和 5例病变黄韧带的病理形态学特点、胶原纤维、网状纤维、弹力纤维以及粘液物质的改变。结果 :根据大体形态特点可将黄韧带骨化分为结节型 (增生性 )骨化、周围型骨化和弥漫型骨化 3种类型。组织学上可见病变早期出现胶原纤维肿胀、融合 ,进一步发生软骨化生 ,最终出现钙化和骨化。在肿胀融合的胶原纤维和软骨化生处可见阿新蓝 (pH 2 5 )阳性的粘液性物质。结论 :黄韧带骨化的大体类型代表着同一病变发展的不同阶段 ;韧带的退行性改变是黄韧带骨化的基本原因 ;胶原纤维的肿胀融合及其粘液样变性是黄韧带骨化的起始病变。     

低频电针对选择性神经损伤大鼠神经痛维持期脊髓背角PKA-TRPV1通路及痛敏递质的干预作用

目的 探讨低频电针干预神经病理痛维持期脊髓背角（SCDH）蛋白激酶A（PKA）、辣椒素受体（TRPV1）通路的调控机制。 方法 将大鼠随机分为空白对照组、假手术组、模型对照组、电针干预组4组。采用坐骨神经分支选择性神经损伤（SNI）方法建立神经病理痛模型。电针干预取术侧足三里、昆仑穴,频率2Hz,每日1次,连续干预14d。检测大鼠术侧后足缩足阈值（PWT）、SCDH PKA和TRPV1以及降钙素基因相关肽（CGRP）和P物质（SP）水平。 结果 SNI模型大鼠术侧PWT下降（P<0.01）,术侧SCDH PKA、TRPV1、CGRP、SP水平均上调（P<0.05）;2Hz电针可提高SNI模型大鼠PWT（P<0.01）,降低术侧SCDH PKA、TRPV1、CGRP、SP水平（P<0.05）。 结论 低频电针能改善神经病理痛,可能与其下调SCDH PKA-TRPV1通路以及CGRP、SP痛敏递质水平有关。     

大鼠坐骨神经分支选择性损伤后脊髓背角毛细血管和星形胶质细胞的反应

目的探讨成年大鼠坐骨神经分支选择性结扎切断(SNI)后,腰段脊髓背角内毛细血管和星形胶质细胞的反应。方法成年雄性SD大鼠40只,随机分为光镜组(n=30)和电镜组(n=10)。光镜组又分为对照组、假手术组和SNI手术组。SNI手术为分别结扎切断左侧胫神经和腓总神经,保留腓肠神经,存活20d。部分动物在术后经尾静脉给予30g/L伊文思蓝,切取脊髓L4平面,荧光显微镜观察伊文思蓝的渗出;另一部分在术后进行常规固定取材,切片进行抗鼠IgG和GFAP的免疫组织化学反应。电镜组(对照组和SNI后20d组),脊髓切片进行常规抗大鼠IgG的免疫电镜处理。结果 1.SNI后20d,可见明显的伊文思蓝渗出红色光斑;2.SNI后GFAP阳性细胞变为反应型,数量明显增加,毛细血管壁及其周围的IgG颗粒也显著增加。3.电镜观察:SNI术后20d,IgG阳性颗粒增多,内皮细胞观察到下列变化:(1)内皮细胞向管腔内伸出许多微细的突起,有的含有IgG阳性颗粒。(2)内皮细胞的管腔侧胞膜上有许多"内吞"小凹,凹内可见IgG阳性颗粒,胞质内有含IgG阳性颗粒的小泡,在反管腔侧胞膜上有"胞吐"现象。(3)内皮细胞紧密连接出现间隙,间隙内有IgG颗粒。(4)胞质内出现囊泡,有的泡内显示IgG阳性颗粒。结论 SNI后脊髓背角内毛细血管内皮细胞发生明显的反应,大鼠IgG和伊文思蓝可经过血脊髓屏障渗出,星形胶质细胞被激活。     

The anticonvulsant retigabine attenuates nociceptive behaviours in rat models of persistent and neuropathic pain

We have tested for anti-nociceptive effects of the anticonvulsant KCNQ channel opener, N-(2-amino-4-(4-fluorobenzylamino)-phenyl)carbamic acid ethyl ester (retigabine), in rat models of experimental pain. In the chronic constriction injury and spared nerve models of neuropathic pain, injection of retigabine (5 and 20 mg/kg, p.o.) significantly attenuated (P<0.05) mechanical hypersensitivity in response to pin prick stimulation of the injured hindpaw. In contrast, retigabine had no effect on mechanical hypersensitivity to von Frey stimulation of the injured hindpaw in either model. Cold sensitivity in response to ethyl chloride was only attenuated (P<0.05) in the chronic constriction injury model. In the formalin test, retigabine (20 mg/kg, p.o.) attenuated flinching behaviour in the second phase compared with vehicle (P<0.05), and this effect was completely reversed by the KCNQ channel blocker 10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone (XE-991; 3 mg/kg, i.p.). Neither retigabine nor XE-991 administration affected the latency to respond to noxious thermal stimulation of the tail in control animals. These results suggest that retigabine may prove to be effective in the treatment of neuropathic pain.     

胸椎黄韧带骨化症临床研究

目的 探讨胸椎黄韧带骨化症的诊断特点及改良手术的疗效。方法 总结我院从1995～2005年收治的28例胸椎黄韧带骨化症的患者并对其手术疗效加以分析。结果28例患者全部获得随访，随访时间6～36个月，平均23个月。术后JOA评分为6～11分，平均9．3分，恢复率为73．6％，优良率为84．5％。结论临床表现结合CT及MRI检查是诊断胸椎黄韧带骨化症的有效手段，改良的外科手术方式安全可靠，手术疗效佳。     

Reversible attenuation of neuropathic-like manifestations in rats by lesions or local blocks of the intralaminar or the medial thalamic nuclei

BACKGROUND AND AIM: Thalamic somatosensory nuclei have been classified into medial and lateral systems based on their role in nociception. An imbalance between these two systems may result in abnormal somatic sensations and spontaneous pain. This study aims to investigate the effects of transient or permanent block of the medial and intralaminar nuclear groups on the neuropathic-like behavior in a rat model for mononeuropathy. METHODS: Neuropathy was induced on one hind paw in different groups of rats following the spared nerve injury model. When the resulting hyperalgesia and allodynia (tactile and cold) reached a maximum plateau, the rats received either chemical or electrolytic lesion or lidocaine (2%) microperfusion, placed in the various thalamic nuclear groups. RESULTS: All procedures produced transient but significant decrease of neuropathic manifestations. The magnitude and duration of decrease depended on the type and the site of the block. These effects can be ranked in increasing order as follows, electrolytic相似文献   

Neurons and satellite glial cells in adult rat lumbar dorsal root ganglia express connexin 36

Previous studies have shown that following peripheral nerve injury there was a downregulation of the gap junction protein connexin 36 (Cx36) in the spinal cord; however, it is not known whether Cx36 protein is expressed in the dorsal root ganglia (DRGs), nor if its levels are altered following peripheral nerve injuries. Here we address these aspects in the adult rat lumbar DRG. Cx36 mRNA was detected using qRT-PCR, and Cx36 protein was identified in DRG sections using immunohistochemistry (IHC) and immunofluorescence (IF). Double staining revealed that Cx36 co-localizes with both anti-β-III tubulin, a neuronal marker, and anti-glutamine synthetase, a satellite glial cell (SGC) marker. In neurons, Cx36 staining was mostly uniform in somata and fibers of all sizes and its intensity increased at the cell membranes. This labeling pattern was in contrast with Cx36 IF dots mainly found at junctional membranes in islet beta cells used as a control tissue. Co-staining with anti-Cx43 and anti-Cx36 showed that whereas mostly uniform staining of Cx36 was found throughout neurons and SGCs, Cx43 IF puncta were localized to SGCs. Cx36 mRNA was expressed in normal lumbar DRG, and it was significantly down-regulated in L4 DRG of rats that underwent sciatic nerve injury resulting in persistent hypersensitivity. Collectively, these findings demonstrated that neurons and SGCs express Cx36 protein in normal DRG, and suggested that perturbation of Cx36 levels may contribute to chronic neuropathic pain resulting from a peripheral nerve injury.