目的:探讨健步强督方联合系统宣教法对腰椎间盘突出症患者症状复发的影响.方法:将80 例腰椎间盘突出症患者随机分为治疗组和对照组,每组 40 例.治疗组使用健步强督方联合系统宣教法治疗,对照组予传统宣教方式联合甲钴胺注射液、塞来昔布胶囊治疗.研究分为 2 步进行,①观察患者出院时临床疗效指标和视觉模拟评分法(VAS)评分,对 2 组在院治疗效果进行评估;②对在院治疗评估为有效的患者,进行出院后 16 周的连续随访,分析健步强督方联合系统宣教法是否对患者腰椎间盘突出症的疾病复发产生影响.结果:①经住院治疗后,治疗组和对照组中各有 1 例患者症状加重,分别选择转院或手术治疗,治疗组显效率为 65.00％,优于对照组的 40.00％(P<0.05);2 组总有效率均为 97.50％,差异无统计学意义(P>0.05);2 组VAS评分均≤3 分,差异无统计学意义(P>0.05).②随访后,治疗组复发人数、首次复发时间、复发次数和复发后治疗天数低于对照组(P<0.05).结论:采用健步强督方的温养督脉法治疗联合系统宣教法指导患者日常行为、康复锻炼和结合心理疏导可以减少腰椎间盘突出症患者症状复发.

目的:探讨健步强督方对腰椎间盘突出症疼痛-负性情绪患者的临床疗效.方法:选取2020年1-12月在山西中医药大学附属中西医结合医院住院治疗的腰椎间盘突出症60例患者,分为治疗组和对照组.治疗组口服健步强督方,对照组治疗方式:口服甲钴胺片、塞来昔布胶囊,两组患者均口服药物2个疗程.对照组和治疗组都配合中药热奄包、中频电疗.评估两组患者治疗前后视觉模拟评分法(Visual Analogue Scale,VAS)评分、抑郁自评量表(Self-rating Depression Scale,SDS)评分、焦虑自评量表(Self-rating Anxiety Scale,SAS)评分;血清学指标神经肽物质P物质、神经肽Y的水平;炎性应激指标白细胞介素-1β、肿瘤坏死因子-α的水平.结果:治疗2个疗程后,两组患者的SDS、SAS评分差异存在统计学意义(P<0.05),治疗组优于对照组.治疗后两组患者的VAS评分均优于治疗前(P<0.05),且治疗组VAS评分改善情况优于对照组.治疗前两组患者P物质、神经肽Y、白细胞介素-1β、肿瘤坏死因子-α水平比较差异无统计学意义,P>0.05.两组治疗方法对这4项指标均是有效的,治疗后两组P物质、神经肽Y进行组间比较,治疗组改善程度优于对照组(P<0.05).治疗后两组白细胞介素-1β、肿瘤坏死因子-α的改善程度差异无统计学意义(P>0.05).结论:使用健步强督方与甲钴胺联合塞来昔布相比可有效改善VAS评分,改善炎性指标白细胞介素-1β、肿瘤坏死因子-α,降低血清神经肽物质P物质、神经肽Y浓度,且SAS、SDS评分显示其在改善腰椎间盘突出症疼痛-负性情绪中焦虑、抑郁情绪上效果更佳.

腰椎退行性疾病包括腰椎间盘突出症、腰椎椎管狭窄症、腰椎不稳症等疾病,是骨科临床常见的一类疾病.林一峰教授认为,腰椎退行性疾病的病机是督脉阳气虚衰,治疗应以温养督脉为主,研制创立了补肾壮督方,并根据临床表现分为督脉虚弱型、风邪犯督型、湿滞督脉型、寒凝督脉型、瘀血阻督型、痰瘀聚督型6种证型辨证治疗,效果显著.

神经根型颈椎病为颈椎椎间盘及小关节退变刺激或压迫神经根引起上肢麻木疼痛等根性症状的疾病[1],在中医可归为"项痹"范畴.目前的治疗手段以保守为主[2],中医药在保守治疗方面有其特色和优势.广东省名老中医师承指导老师、广州中医药大学博士生导师林一峰教授长期致力于中医药防治退行性脊柱病的研究,曾在国内率先提出"从督脉论治脊柱退行性疾病"的学术思想[3-4],在此学术思想的指导下,其认为神经型颈椎病的根本病机在于督脉阳虚.基于此病机,在治疗上以温养督脉为法[5-7],创制"颈痛方"作为基础方药随证加减,临床上运用纯中药治疗神经根型颈椎病即可取得满意的疗效,且复发率低,不良反应少,值得临床推广.现将其治疗神经根型颈椎病的经验介绍如下.

"少阳主骨""肾主骨"是中医骨伤科学领域中的两个重要论点."少阳主骨"的观点和临床探讨多集中在痹证、筋伤、痿证上,较少有脊柱退行性疾病方面的论述.该文基于"从督脉论治""肾虚督滞"观点,探讨"少阳主骨"与脊柱退行性疾病的相关性.

目的 观察大鼠退变椎间盘髓核组织miR-155-5p及凋亡相关蛋白表达差异,及补肾壮督方对其的影响.方法 SD雄性大鼠,采用纤维环全层针刺造模,随机分为空白对照组,模型组,低剂量中药组、中剂量中药组及高剂量中药组.中药干预4周后,TUNEL法检测退变椎间盘中髓核细胞凋亡率,qRT-PCR检测miR-155-5p及Bax、Bcl-2、Cytc mRNA的表达;Western Blot检测髓核组织中active Caspase-3,Bcl-2、Cytc及Bax蛋白表达水平.结果 模型组大鼠髓核细胞凋亡率明显增加(P＜0.05),Cytc和Bax mRNA及其蛋白表达量均显著增加(P＜0.05),Bcl-2 mRNA及其蛋白表达量显著下降(P＜0.05),Bax/Bcl-2比值显著增加(P＜0.05).中药干预后检测,髓核细胞凋亡率明显减少(P＜0.05),Cytc和Bax mRNA及其蛋白表达量均明显下降(P＜0.05),Bcl-2 mRNA及其蛋白显著增加(P＜0.05),Bax/Bcl-2比值显著减小(P＜0.05).结论 补肾壮督方可能通过减少active Caspase-3、Cytc和Bax蛋白表达,增加Bcl-2蛋白表达,抑制线粒体凋亡通路,从而改善椎间盘退变;miR-155-5p可能参与髓核细胞凋亡的线粒体凋亡通路.

背景:线粒体凋亡通路是细胞凋亡中的重要通路,前期动物实验发现补肾壮督方可通过抑制线粒体凋亡通路改善椎间盘退变,但其作用机制还有待研究.目的:观察补肾壮督方含药血清对人髓核细胞线粒体凋亡通路关键蛋白的影响,探讨其改善椎间盘退变的机制.方法:①37只SD雄性大鼠,随机分为正常组、低剂量中药组[0.506 g/(kg·d)]、中剂量中药组[1.012 g/(kg·d)]及高剂量中药组[2.024 g/(kg·d)],连续灌胃2周,灌胃结束后制备含药血清;②人髓核细胞随机分为正常组、模型组、低剂量含药血清组、中剂量含药血清组、高剂量含药血清组,模型组用200 μmol/L H2O2处理6h,正常组不进行任何处理,低、中、高剂量含药血清组造模后用体积分数为2％含药血清干预48 h.透射电镜观察髓核细胞的超微结构,流式细胞术检测髓核细胞凋亡率和线粒体膜电位,qPCR和Western blot检测Apaf1、Bcl-2、Bax及Cytc的表达.结果 与结论:①与正常组相比,模型组出现明显的细胞凋亡形态特征,髓核细胞凋亡率显著增加(P＜0.05),Apaf1、Cytc、Bax mRNA及蛋白表达量均显著增加(P＜0.05),线粒体膜电位、Bcl-2 mRNA及其蛋白表达量显著下降(P＜0.05);②补肾壮督方含药血清干预后,髓核细胞凋亡率明显减少(P＜0.05),Apaf1、Cytc、Bax mRNA及蛋白表达量均明显下降(P＜0.05),线粒体膜电位、Bcl-2 mRNA及其蛋白表达量显著增加(P＜0.05);③补肾壮督方含药血清可有效抑制髓核细胞凋亡,并呈剂量依赖性,可能通过减少Apaf1、Cytc、Bax蛋白及mRNA表达,增加Bcl-2蛋白及mRNA表达,抑制线粒体凋亡通路,从而改善椎间盘退变.

目的:观察鹿茸多肽对IL-1β诱导的大鼠椎间盘软骨终板细胞的增殖及基质蛋白(Ⅱ,X型胶原)、基质降解酶(金属蛋白酶-13)基因表达的影响.方法:选取1月龄的健康SD大鼠,对其椎间盘软骨终板细胞进行分离与培养,取第3代软骨终板细胞实验,空白对照组不做任何处置,诱导组单加入10 μg/L的IL-1β,药物处理组分三组,分别在培养基中加入10 μg/L的IL-1β和10 μg/mL,30μg/mL,50 μg/mL的鹿茸多肽.MTT比色法检测三个时间节点(24 h,48 h,72 h)各组椎间盘软骨终板细胞的增殖情况;qPCR检测法对软骨终板细胞中基质Ⅱ,X型胶原蛋白、基质金属蛋白酶-13基因的表达情况.结果:在24 h,48 h,72 h时间点,MTT法检测10 μg/mL鹿茸多肽组在各时间点软骨终板细胞增殖情况与IL-1β组比较,差异无统计学意义(P＞0.05);而30 μg/mL组和50 μ上g/mL组均能减轻IL-1β对软骨终板细胞增殖的抑制作用,差异有统计学意义(P＜0.05,P＜0.01).qPCR检测结果显示:IL-1β诱导组的Ⅱ型胶原蛋白基因的表达减弱,X型胶原蛋白、基质金属蛋白酶-13基因的表达增强,与空白组对比差异有统计学意义(P＜0.05);鹿茸多肽各浓度组均能上升Ⅱ型胶原蛋白基因的表达,下调X型胶原蛋白、基质金属蛋白酶-13基因的表达水平,差异有统计学意义(P＜0.05,P＜0.01),以50 μg/mL组效果显著,差异有统计学意义(P＜0.01).结论:一定浓度的鹿茸多肽(50 μg/mL组)能有效地拮抗IL-1β对软骨终板细胞增殖的抑制作用,上升Ⅱ型胶原蛋白基因的表达,下调X型胶原蛋白、基质金属蛋白酶-13基因的表达,改善了基质的代谢,起到延缓椎间盘软骨终板退变的作用.

大约80％o～90％的人在其一生中都或多或少的会受到颈腰痛的折磨,以颈腰痛为主要症状的退变性脊柱病,其病理基础责之于椎间盘的退变[1].受年龄、异常应力等诱发,椎间盘软骨终板细胞的凋亡呈线性增加[2],导致活性细胞密度降低[3],刺激促炎细胞因子(如白细胞介素-1、肿瘤坏死因子等)的上升,不仅抑制了蛋白聚糖、Ⅱ型胶原等细胞外基质的合成,还促进基质金属蛋白降解酶(MMP-1,-2,-3,-4,-13及-6等)的释放,水、离子等营养通道也随之改变[4,5],进一步降低软骨终板的生物物理学特性[6],加速整个椎间盘退变.因此研究影响软骨终板细胞凋亡的诱发因素和调控其凋亡的信号传导途径是维持细胞正常稳态和延缓椎间盘退变、预防脊椎病变的一种策略.

李济春教授幼承家学,精研岐黄,从医40余年医技精湛,师古而不泥于古,创新而不离其宗,擅长针药并用治疗腰腿疼痛、麻木等各种疑难疾病.根据其多年的临床经验和学术思想,本文总结其治疗腰椎间盘突出症的有效辨治思路和方法,其病机多为本虚标实,腰部受邪为发病之源,与肾虚和寒湿阻络密切相关.在家传的“乾坤针法”上,大胆提出腰部围刺法,同时结合补肾除湿方药及开合手法进行医治,疗效显著.

目的:观察不同浓度的鹿茸多肽对IL-1β诱导的大鼠椎间盘软骨终板细胞增殖和Ⅰ型胶原(type Ⅰ collagen,Collagen Ⅰ)、Collagen Ⅱ、白细胞介素(interleukin-6,IL-6) mRNA表达的影响.方法:选取健康SD大鼠(1个月龄),取其脊柱椎间盘软骨终板细胞,并培养至第3代软骨终板细胞进行实验.空白对照组不做任何处理,诱导组只加入10 μg·L-1的IL-1β,给药组在培养基中加入10 μg·L-1的IL-1β和不同质量浓度的鹿茸多肽(分别为10 mg·L-1、30 mg·L-1、50 mg·L-1).用MTT比色法检测3个时间点(24 h、48 h、72 h)各组椎间盘软骨终板细胞的增殖情况;qPCR法检测Collagen Ⅰ、Collagen Ⅱ及IL-6 mRNA的表达.结果:MTT法检测结果:鹿茸多肽10 mg·L-1组的软骨终板细胞增殖与诱导组比较,差异无统计学意义(P＞0.05);鹿茸多肽30 mg·L-1组和鹿茸多肽50 mg·L-1组能促进软骨终板细胞的增殖,与诱导组比较,差异有统计学意义(P＜0.05,P＜0.01).qPCR检测结果:IL-1β诱导组的CollagenⅡmRNA的表达降低,Collagen Ⅰ、Collagen Ⅱ、IL-6的mRNA的表达升高,与空白对照组比较,差异有统计学意义(P＜0.05);不同质量浓度的鹿茸多肽均能增强Collagen ⅡmRNA的表达,降低CollagenⅠ和IL-6 mRNA的表达,差异均有统计学意义(P ＜0.05,P＜0.01),30 mg·L-1、50 mg·L-1鹿茸多肽效果更加显著(P＜0.01).结论:一定浓度的鹿茸多肽能减轻IL-1β对软骨终板细胞增殖的抑制,升高Collagen ⅡmRNA的表达,降低Collaoen Ⅰ、IL-6 mRNA的表达,从而延缓椎间盘的退变.

目的:观察补肾壮督方对大鼠退变椎间盘细胞凋亡的影响,探讨其改善椎间盘退变的机制.方法:100只SD雄性大鼠,采用纤维环全层针刺造模,随机分为空白组,模型组,补肾壮督方低、中、高剂量组(0.38,0.77,1.53 g·kg-1),连续中药灌胃4周后,苏木素-伊红(HE)染色观察大鼠椎间盘组织病理学变化;原位末端转移酶标记法(TUNEL)检测退变椎间盘中髓核细胞凋亡率,蛋白免疫印迹法(Western blot)检测椎间盘组织中活化半胱氨酸蛋白酶-3(active Caspase-3),B淋巴细胞瘤-2(Bel-2),细胞色素C(cytC)及Bel-2相关X蛋白(Bax)蛋白水平.结果:与空白组比较,模型组大鼠椎间盘组织病理学评分显著增加,髓核细胞凋亡率明显增加(P＜0.05),active Caspase-3,cytC和Bax表达量均明显增加(P＜0.05),Bel-2表达量明显下降(P＜0.05).与模型组比较,补肾壮督方低、中、高剂量组组织病理学评分明显降低(P＜0.05),髓核细胞凋亡率明显减少(P＜0.05),active Caspase-3,cytC及Bax表达量均明显下降(P＜0.05),Bcl-2表达量明显增加(P＜0.05).结论:补肾壮督方可能通过减少active Caspase-3,cytC和Bax蛋白表达,增加Bcl-2蛋白表达,抑制线粒体凋亡通路,并存在一定剂量依赖性,从而改善椎间盘退变.

目的:观察不同浓度的鹿茸多肽对IL-1β诱导的大鼠椎间盘终板软骨细胞的影响,分析其对终板软骨细胞保护的作用机制.方法:选取1月龄的健康SD大鼠,并对其椎间盘终板软骨细胞进行分离与培养,诱导组单加入10μg/L的IL-1β,药物处理组分3组,分别在培养基中加入10 μg/L的IL-1β和10、30、50μg/mL的鹿茸多肽,MTT比色法检测3个时间节点(24、48、72h)各组椎间盘终板软骨细胞的增殖情况;流式细胞仪检测大鼠椎间盘终板软骨细胞的凋亡;qPCR法检测Collagen Ⅱ、CollagenX、caspase-3、MMP-13、Bax、Bcl-2基因的表达水平.结果:在24、48、72 h时间点,MTT法检测10μg/mL鹿茸多肽组在各时间点终板软骨细胞增殖情况与IL-1β诱导组比较,差异不具有统计学意义(P＞0.(05);而30μg/mL组和50μg/mL组均能拮抗IL-1 β对软骨终板细胞增殖的抑制作用,差异具有统计学意义(P＜0.05,P＜0.01);流式分析结果表明,不同浓度的鹿茸多肽均能够降低IL-1 β诱导的大鼠椎间盘软骨终板细胞的凋亡比例(P＜0.05,P＜0.01);qPCR检测结果表明,IL-1 β诱导组的Cllagen Ⅱ、Bcl-2基因的表达减弱,CollagenX、caspase-3、Bax、MMP-13基因的表达增强,与空白对照组对比差异具有统计学意义(P＜0.05);各浓度鹿茸多肽组均能够上调Cllagen Ⅱ、Bcl-2基因的表达(P＜0.05,P＜0.01),下调Collagen X、caspase-3、Bax、MMP-13基因的表达(P＜0.05,P＜0.01),以50μg/mL组效果最为显著(P＜0.01).结论:一定浓度的鹿茸多肽通过抑制软骨终板细胞的凋亡,促进其增殖,调控其相关基质蛋白及基质降解酶、凋亡因子等基因的表达,起到了对退变的椎间盘终板软骨细胞的保护作用.

BACKGROUND: Numerous studies focus on animal models of intervertebral disc degeneration (IDD), but criteria for establishing the animal models of IDD have not been confirmed, and there is a lack of systematic comparison among models. OBJECTIVE: To compare the rat models of IDD established by puncturing at annulus, endplate injection and their combination, thus providing reference for IDD model selection. METHODS: Eighty Sprague-Dawley rats were equivalently randomized into four groups: puncturing group (puncturing at the annulus), endplate injection group (endplate injected with ethyl alcohol), combination group (puncturing at the L5-6annulus and endplate injection at the same segment) and sham operation group. Three rats in each group were taken at postoperative 4, 8, and 12 weeks for X-ray examination to measure the disc height; and the discs were removed for histological observation and immunohistochemical staining. RESULTS AND CONCLUSION: The results of X-ray examination, hematoxylin-eosin staining and immunohistochemical staining all showed that the IDD degree was gradually aggravated in all groups except the sham operation group. At postoperative 4 weeks, compared with the sham operation group, in the endplate injection and combination groups, the percent disc height was significantly decreased, the pathological scores were significantly increased and the average gray value of collagen type I was significantly reduced (P ＜ 0.05). At postoperative 8 and 12 weeks, compared with the sham operation group, the percent disc height in the other three groups were all significantly decreased, the pathological score was significantly increased, and the average gray value of collagen type I was significantly decreased (P ＜ 0.05). Compared with the puncturing and endplate injection group, in the combination group, the percent disc height at postoperative 8 weeks was significantly decreased, and the average gray value of collagen type I at postoperative 12 weeks was significantly decreased (P ＜ 0.05). These results suggest that the rat IDD model can be successfully constructed by above three methods. Puncturing at the annulus is easy to operate and control IDD progression, which can be used to study different stages of IDD. Endplate injection is suitable for the etiological study of IDD, and induces IDD earlier than puncturing, but the final results are similar. The combination method can significantly accelerate IDD aggravation, and thus is not time consuming.

The clinical manifestation of lumbar disc herniation is not only low back pain and lower limb radiation pain,but also the characteristics of chronic disease and long course,seriously affecting the labor ability and the quality of life of the patients.Sixty-four cases of lumbar disc herniation patients in our hospital who recieved Bushen Zhuangdu Formula in the treatment of mental disorders characterised with depression and anxiety were studied.The treatment group were treated with Bushen Zhuangdu Formula and patients in control group were treated with fluoxetine hydrochloride capsule.The two groups were treated with conventional therapy.Two groups' HAMD-24 score comparison before and after treatment showed the two groups had no difference before treatment (P ＞ 0.05) and there was no statistical differences between two groups after 2 weeks treatment (P ＞ 0.05).The two groups' Oswestry Disability Index questionnaire (ODI) scores before and after treatment had no significant difference before treatment (P ＞ 0.05).After 1 week treatment,the ODI score in the treatment groupwas statistically significant (P ＜ 0.05).After 2 weeks treatment,the scores of the ODI in the two groups had no statistical significance (P ＞ 0.05).In general,Chinese medicine treatment group is superior to the control group in improving the symptoms of low back pain,for a short period of time is better than western medicine group.However,the side effects of traditional Chinese medicine are less,and the patients' compliance is good.

目的:观察葛根汤合半夏白术天麻汤治疗椎动脉型颈椎病的临床疗效.方法:选择60例符合纳入标准的椎动脉型颈椎病患者,随机分为对照组和治疗组,对照组予颈复康冲剂治疗,治疗组采用葛根汤合半夏白术天麻汤治疗,10d为1疗程,治疗2疗程后采用椎动脉型颈椎病临床疗效评定标准及中医证候积分比较两组的临床疗效.结果:对照组总有效率为83.33％,治疗组总有效率为93.33％,治疗组疗效明显优于对照组(P＜0.01),且治疗组中医证候积分改善优于对照组(P＜0.01).结论:葛根汤合半夏白术天麻汤能显著缓解椎动脉型颈椎病的临床症状,具有良好的临床疗效.

根据林一峰教授多年的临床经验和学术思想,本文总结治疗颈性眩晕的有效辨治思路和方法,认为颈性眩晕病机为本虚标实,与督阳阳虚和风痰上扰密切相关.温养督脉联合熄风化痰法组方遣药,疗效显著.

目的 探讨补肾壮督散水煎液对大鼠腰椎间盘退变的影响及其可能机制.方法 将40只SD大鼠随机分为假手术组、模型组、补肾壮督散组、塞来昔布组,各10只.除假手术组外,其余各组均采用腰椎纤维环全层穿刺法制备腰椎间盘退变模型.造模第2天,补肾壮督散组和塞来昔布组分别给予补肾壮督散水煎液、塞来昔布胶囊水溶液灌胃,假手术组、模型组给予等量生理盐水灌胃,连续8周.各组处死后取出椎间盘组织,HE染色后观察病理变化,醋酸铀及枸橼酸铅双重染色后透射电镜观察超微结构,Western blotting法检测椎间盘组织基质金属蛋白酶3(MMP-3)蛋白表达.结果 假手术组椎间盘纤维环层次分明,与髓核界限分明;成纤维细胞呈梭条状,细胞质内细胞器较发达.模型组椎间盘胶原纤维排列紊乱,与髓核界限消失;成纤维细胞细胞质内细胞器不发达.补肾壮督散组椎间盘纤维环层次较分明,与髓核界限分明;成纤维细胞细胞质内细胞器稍不发达.塞来昔布组椎间盘纤维环层次较补肾壮督散组紊乱,与髓核界限欠分明;成纤维细胞细胞质内细胞器较不发达.假手术组椎间盘组织MMP-3蛋白相对表达量为0.198±0.028,补肾壮督散组为0.525±0.056,塞来昔布组为0.809±0.029,模型组为1.065±0.055;各组椎间盘组织MMP-3蛋白相对表达量依次升高,组间两两比较P均<0.05.结论 补肾壮督散水煎液灌胃可延缓大鼠腰椎间盘退变;抑制腰椎间盘组织MMP-3表达可能是其作用机制.

Objective: To investigate clinical effects of Bushen Zhuangdu San on ATP enzyme and TNF-α in rats with lumbar disc degeneration. Methods: The lumbar disc degeneration models were established by annulus puncture.The rats were divided into 4 groups randomly after successful modeling, namely: the blank control group, the model group, the Bushen Zhuangdu San group and the celecoxib capsules group. In 8 weeks, the content of ATP enzyme and TNF-α were detected; the changes of intervertebral disc collagen fibers and fibroblasts ultrastructure were scanned by electron microscopy. Results: ① Compared with the blank control group, lumbar degeneration disces in rats in others groups were obvious. Compared with the model group, the changes of lunbar degeneration disces in the Bushen Zhuangdu San group were slighter. ② Compared with the blank control group, the expression of ATP enzyme in the model group was reduced;the expression of TNF-α was increased in the model group; the differences were very significant (P<0.01). Compared with the model group, the expression of ATP enzyme was increased in the Bushen Zhuangdu San group; and the differences were very significant (P<0.05);the expression of TNF-α was reduced in the Bushen Zhuangdu San group; and the differences were very significant (P<0.01).Conclusion:Bushen Zhuangdu San can improve disc tissue ATP enzyme activity and reduce the expression of TNF-α,which may explain the mechanism of protective effect on intervertebral disc degeneration.

目的 观察温通督脉法治疗退行性腰椎管狭窄症的临床效果,评估对退行性腰椎管狭窄症以督脉阳虚为基本病机认识的临床意义.方法 选取确诊为退行性腰椎管狭窄症病例共70例,随机分为温通督脉治疗组及西药治疗对照组,最终纳入研究的病例共69例,治疗前后对比两组患者的十分制目测类比评分法(visual analogue scale,VAS)评分、日本骨外科学会腰痛疗效评价标准(JOA score) 29点法评分.结果 采用十分制目测类比评分法(visual analogue scale,VAS)评分评定患者治疗前后疼痛程度的变化情况,结果显示两组患者治疗后的VAS评分均较治疗前明显改善(P＜0.05),但治疗组改善优于对照组(P＜0.05).采用日本骨外科学会腰痛疗效评价标准(JOA score) 29点法评分评定患者治疗前后腰痛的变化情况.结果显示治疗组JOA评分改善优于对照组,组间差异有统计学意义(P＜0.05).结论 以“温通督脉法”治疗退行性腰椎管狭窄症可取得较好的临床效果.