Motor nerve dysfunction in delayed DFP neuropathy

A localized neuropathy was produced in cats by an intra-arterial injection of diisopropyl fluorophosphate (DFP). The soleus nerve-muscle system, and especially the motor nerve endings, were functionally evaluated during the following 1–56 days. Nerve conduction velocities remained unchanged. At 24–72 hr after DFP, the indirectly evoked but not directly evoked contractile strength of muscle fell to about 20% of normal; recovery had commenced by the 7th day. Motor nerve ending function was assessed by measurement of the neurogenic post-tetanic potentiation (PTP) of soleus muscle. PTP was initially unaffected, even though indirectly evoked contractile strength was severely attenuated. However, at day 7, a PTP reduction was evident and reached a loss of 62% on day 21. The underlying post-tetanic repetition (PTR) was lost at this time. Recovery of PTP and PTR occured over the next 5 weeks. These findings indicate that there is an initial functional damage of nerve endings in delayed organophosphate neuropathy. The pattern of nerve ending impairment suggests a trophic deprivation.     

Studies on drug-induced neuropathies. III. Motor nerve deficit in cats with experimental acrylamide neuropathy.

To assess motor nerve and motor nerve terminal function in acrylamide neuropathy, cats were given i.m. injections of acrylamide (15 mg/kg) daily for 10 days to induce a peripheral neuropathy. Tests of function were performed on the day of the 10th injection (day 0) and 7, 21 and 35 days thereafter. In untreated animals tetanic conditioning evoked stimulus-bound repetition (SBR) in 85% of soleus alpha-motoneurones. Following administration of acrylamide, the percent of axons elaborating SBR were: day 0 -- 79%, day 7 -- 71%, day 21 -- 31%, day 35 -- 22%. The response of soleus muscle to SBR is normally a post-tetanic potentiation (PTP) of contractile tension which is proportional to the tetanic conditioning frequency; during the development of the neuropathy, PTP in response to all tetanic frequencies progressively declined, concomitant with and as a result of the declining incidence of SBR. These data indicate that initial functional alterations in motor nerves during acrylamide neuropathy occurs at the level of the nerve terminal, preceding alterations in conduction velocities in the axons. However, the motor nerve deficit is not adequate, in either time to onset or severity, to account for the clinical manifestations of the neuropathy. The possible contribution to clinical signs of the neuropathy made by lesions to other peripheral nerves is discussed.     

同种异体神经与自体神经瘤联合修复周围神经缺损的运动功能研究

目的探讨通过以优化法处理后的脱细胞同种异体神经和自体神经瘤组成的联合体修复大鼠长段坐骨神经缺损,观察大鼠运动功能恢复情况。方法30只SD大鼠随机分为2组,A组实验组为异体神经与自体神经瘤联合移植组;B组对照组为自体神经移植组。Wistar大鼠作为神经供体,取单侧坐骨神经,制备脱细胞同种异体神经。在术后的不同时间段进行坐骨神经功能指数评价、神经电生理检查。结果A组术后8周电生理检测再生神经的传导速度明显慢于B组(P<0.05),术后16周两组差异无统计学意义(P>0.05)。A组和B组动物的坐骨神经功能指数差异无统计学意义(P>0.05)。结论同种异体神经与自体神经瘤的联合体可以修复周围神经缺损,是神经移植的一种良好替代体。     

对于糖尿病周围神经病变应用神经生长因子辅助治疗的效果分析

目的：分析和研究神经生长因子应用于糖尿病周围神经病变的临床效果及意义。方法：收集糖尿病周围神经病变患者80例并随机分为对照组和治疗组,对照组给予常规胰岛素及对症治疗,治疗组在常规治疗基础上予以神经生长因子治疗2个疗程,对比两组治疗后的神经传导速度和血流变学等指标。结果：治疗组总有效率为90.0%,明显高于对照组的67.5%（P〈0.05）,而且治疗组血流变学及神经传导速度各项数据明显优于对照组（P     

鼠神经生长因子治疗糖尿病周围神经病变疗效观察

目的 分析鼠神经生长因子应用于糖尿病周围神经病变的治疗效果.方法 选择糖尿病周围神经病变患者62例.按照不同治疗方案分为观察组(31例)和对照组(31例).所有患者均接受糖尿病基础治疗,其中观察组加用鼠神经生长因子,对照组加用甲钴胺,1个疗程后比较两组治疗效果及不良反应发生情况.结果 观察组显效17例,有效12例,总有效率93.55％;对照组显效6例,有效10例,总有效率51.61％,观察组有效率明显高于对照组(x2 =37.917,P＜0.05).两组治疗后运动传导速度和感觉传导速度均较治疗前改善(t =31.681、19.370、25.409、12.084、21.692、11.308、17.295、9.064,均P＜0.05),但观察组改善情况明显优于对照组(t =11.075、8.376、9.086、7.319,均P＜0.05).结论 采用鼠神经生长因子治疗糖尿病周围神经病变对患者临床症状可起到明显缓解效果,能有效改善运动和感觉神经传导速度,且安全性好,值得临床推广.     

Peripheral neuropathy following intraneural injection of mercury compounds

Between 0.25–25 g of an aqueous solution of either mercuric chloride or methyl mercuric acetate was injected directly into the sciatic nerve of 28 adult Wistar rats. The resultant pathological changes in the nerve were examined by teasing individual fibres and by light and electron microscopy. In most respects mercuric chloride was more toxic than methyl mercuric acetate.The large doses of mercuric chloride produced a hind limb paresis within 24 h but no clinical signs followed injection of organic mercury. The predominant effect of mercuric chloride was on Schwann cells which showed cytoplasmic swelling and nercrosis, associated with extensive segmental demyelination. In contrast methyl mercuric acetate caused axonal degeneration in many of the large myelinated fibres but only minor alterations were observed in Schwann cells.     

神经生长因子对2,5-己二酮中毒大鼠周围神经损伤的治疗作用

目的　观察鼠源性神经生长因子 (mNGF)对2 ,5 己二酮中毒大鼠周围神经病的治疗效果。方法采用 2 ,5 己二酮 4 5 0mg·kg- 1·d- 1ig染毒 ,通过对姿势、步态、前后肢肌力的体征评分、坐骨神经运动神经传导速度 (MNCV)测定和神经病理检查 ,证实制成 2 ,5 己二酮中毒大鼠周围神经病模型 ,而后将相同周围神经体征评分的中毒大鼠 2 6只随机分为mNGF治疗组与染毒未治组进行疗效比较。结果染毒组大鼠于染毒 2 5d体征评分显示 ,中度与重度周围神经损伤者约占总数的 92 % ;坐骨神经MNCV比对照组明显减慢 ;神经病理检查发现 ,胫神经部分神经纤维轴索变性。经mNGF 30 μg·kg- 1·d- 1im治疗 2 1d后 ,治疗组大鼠的姿势、步态与前后肢肌力的恢复情况显著优于染毒未治组。结论　mNGF能显著加速 2 ,5 己二酮中毒性周围神经病的恢复 ,为临床应用mNGF治疗正己烷中毒性周围神经病提供了动物实验依据。     

Relative effects of streptomycin on motor nerve terminal and endplate

Using standard microphysiologic recording techniques, the effects of streptomycin on nerve terminal and endplates were evaluated using the isolated frog satorius muscle. Twitch tension studies were performed on the sciatic nerve sartorius muscle preparation. In low concentrations the agent increased mepp frequency and twitch strength and caused antidromic firing from the nerve terminal. In the concentration range causing inhibition of muscle twitch, nerve terminal activity remained elevated. In this range mepp amplitude and endplate sensitivity were markedly reduced. At high doses streptomycin finally inhibited nerve terminal function. The reduction in twitch height was explained by blockade of the post-junction membrane. It is postulated that streptomycin has three effects on the myoneural junction: (1) stimulation of the nerve terminal at low doses; (2) reduction of the endplate sensitivity to acetylcholine concomitant with a reduction in the twitch height at higher doses and (3) inhibition of nerve terminal function at the highest doses studied.     

Effects of trolox on nerve dysfunction, thermal hyperalgesia and oxidative stress in experimental diabetic neuropathy

1. Diabetic neuropathy is one of the most common complications of diabetes and oxidative stress has been implicated to play a major role in its pathophysiology. 2. In the present study, we targeted oxidative stress using trolox, an anti-oxidant, in streptozotocin-induced diabetic neuropathy in rats. 3. Compared with control rats, diabetic rats showed significant deficits in motor nerve conduction velocity (MNCV; 49.91 +/- 1.94 vs 42.77 +/- 1.39 m/s, respectively) and nerve blood flow (NBF; 107.98 +/- 8.22 vs 38.9 +/- 2.7 arbitarary perfusion units, respectively) after 8 weeks of diabetes. Tail flick latencies for cold and hot immersion tests were also significantly reduced in diabetic rats, indicating thermal hyperalgesia. These observations indicate development of diabetic neuropathy. 4. A significant decrease in the activity of anti-oxidant enzymes (superoxide dismutase and catalase) and an increase in lipid peroxidation were observed in sciatic nerves from diabetic rats compared with age-matched control rats. Alterations in the activity of anti-oxidant enzymes and lipid peroxidation in diabetic rats indicate oxidative stress in diabetic neuropathy. 5. Two weeks treatment with trolox (10 and 30 mg/kg, i.p.) started on completion of the 6th week of diabetes significantly improved MNCV, NBF and inhibited thermal hyperalgesia. Trolox treatment also improved the activity of anti-oxidant enzymes and inhibited lipid peroxidation in sciatic nerves of diabetic rats. 6. The results of the present study suggest the beneficial effects of trolox in experimental diabetic neuropathy.     

基于中国临床证据的前列地尔对DPN患者神经传导速度作用的Meta分析

目的 系统评价前列地尔(Alprostadil)防治糖尿病性周围神经病变(DPN)患者临床疗效的有效性,为临床应用该药防治DPN提供证据.方法 运用系统评价的方法,计算机全面检索Cochrane图书馆临床对照试验资料库、Pubme数据库、中国知网期刊全文数据库等相关资料,检索时限均为从建库至2013年12月.按照Cochrane系统评价的方法分析纳入试验的质量,提取本研究观察的有效资料,采用RevMan 5.2软件对纳入研究的资料进行Meta分析.结果 按照相关要求,共纳入11篇前列地尔对DPN患者神经传导速度作用随机对照试验,包括935例试验研究对象.结果数据表明,与研究中的对照组相比,Alprostadi组可提高腓总神经、正中神经的运动神经传导速度[MD=-5.87,95％ CI(-6.31,-5.43),P＜0.01],[MD=-5.63,95％ CI(-6.05,-5.20),P＜0.01];提高腓总神经、正中神经的感觉神经传导速度[MD=-4.91,95％ CI(-5.35,-4.48),P＜0.01],[MD=-5.51,95％ CI(-5.96,-5.06),P＜0.01].结论 现有证据表明,Alprostadi对DPN患者临床疗效是确定的,主要通过改善神经传导速度.     

注射用鼠神经生长因子多药联合治疗对缺血性视神经病变的作用

目的:探讨鼠神经生长因子多药联合治疗缺血性视神经病变的疗效。方法:选取2012年11月-2013年11月收治的120例(120眼)缺血性视神经病变患者作为研究对象,按收治时间顺序分为联合组和对照组,各60例,对照组给予常规药物治疗,联合组在常规药物治疗基础上,加用鼠神经生长因子,比较2组患者的疗效及不良反应。结果:联合组患者的治疗总有效率为96.7%,显著高于对照组的78.3%,P<0.05,差异具有统计学意义;治疗期间,联合组有13例发生注射不良事件,其中臀部疼痛1例,注射部位硬结、红肿、疼痛12例,实验室指标不良事件4例(6.7%)。结论:注射用鼠神经生长因子多药联合治疗缺血性视神经病变,具有确切的疗效,且不良反应少,是一种安全、有效的治疗方案。     

Effects of the facilitatory compounds catechol,guanidine, noradrenaline and phencyclidine on presynaptic currents of mouse motor nerve terminals

Summary Catechol, guanidine, noradrenaline, and phencyclidine can increase acetylcholine release at neuromuscular junctions. To determine if they act by affecting nerve terminal action potentials, the electrical activity of the terminal regions of motor nerves was recorded with an extracellular electrode inserted in the perineural sheaths of nerves in the mouse triangularis sterni preparation. Catechol (from 10 M) and guanidine (from 1 mM) produced a selective reduction in the component of the perineural waveform associated with voltage-dependent K⁺ currents, without significant effects on Na⁺, Ca⁺, or Ca²⁺-activated K⁺ currents. A selective block of K⁺ channels in nerve terminals would cause a prolonged depolarization and hence a large influx of Ca²⁺ to trigger acetylcholine release; this could explain the facilitatory effects of guanidine and catechol. Noradrenaline produced a slight increase in the amplitude of the. perineural waveform. This is consistent with hyperpolarization of the resting membrane potential of the nerve, which could lead to facilitation of acetylcholine release. Phencyclidine blocked Na⁺- and K⁺-related portions of the signal. Send offprint requests to A. L. Harvey at the above address     

苦碟子注射液联合依帕司他对糖尿病周围神经病变的疗效及对神经传导速度的影响

目的 研究苦碟子注射液联合依帕司他对糖尿病周围神经病变的疗效。方法 选择2017年1月-2018年12月喀什地区第二人民医院收治的100例糖尿病周围神经病变患者为研究对象,随机分为两组。对照组口服依帕司他片,50 mg/次,3次/d。观察组在对照组基础上联用苦碟子注射液,将40 mL苦碟子注射液加入250 mL生理盐水中静脉滴注,1次/d。两组均治疗14 d。比较两组患者的临床疗效,同时比较两组治疗前后的胫神经和正中神经的传导速度。结果 治疗后,观察组的有效率为86.00%,明显高于对照组的70.00%,差异有统计学意义（P<0.05）。治疗后,两组胫神经的传导速度明显加快,波幅明显升高,潜伏期明显缩短,同组治疗前后比较差异有统计学意义（P<0.05）;且观察组的胫神经传导速度明显优于对照组,差异有统计学意义（P<0.05）。两组治疗后的正中神经的潜伏期明显缩短,波幅明显升高,传导速度明显加快,同组治疗前后比较差异有统计学意义（P<0.05）;且观察组的正中神经传导速度明显优于对照组,差异有统计学意义（P<0.05）。结论 苦碟子注射液联合依帕司他对糖尿病周围神经病变的疗效较为理想,可明显改善神经传导速度。     

蝎龙酒治疗糖尿病周围神经病变32例临床疗效分析

目的 观察蝎龙酒治疗糖尿病周围神经病变的临床疗效.方法 64例确诊的糖尿病周围神经病变的患者随机分为治疗组32例和对照组32例,治疗组给予蝎龙酒治疗,对照组每天口服甲钴胺片治疗.结果 治疗组总的有效率为90.6%,高于对照组的71.9%,两组相比有统计学差异(P＜0.05).结论 蝎龙酒能改善糖尿病周围神经病变的微循环和神经传导速度,对糖尿病周围神经病变的治疗是有效的.     

糖痛方治疗糖尿病周围神经病变疗效分析

目的探讨糖痛方治疗糖尿病周围神经病变（DPN）的疗效。方法选择本院2010年1月-2012年1月收治的70例DPN患者为观察对象,随机将其分为对照组和实验组,两组患者均接受常规治疗,实验组患者同时接受糖痛方治疗,对比两组患者的临床治疗效果。结果实验组的总有效率、中医证候改善情况和下肢神经传导速度均显著优于对照组,两组间比较,差异有统计学意义（P〈0．05）。结论糖痛方治疗DPN具有较为满意的临床疗效,临床应用价值较高。     

供体神经的选择-周围神经端侧吻合的重要因素

目的探索周围神经端侧吻合时供体神经的选择。方法新西兰大白兔30只,随机分3组,每组10只。A组：端端吻合组,切断尺神经,端端吻合。B组：切断尺神经,与正中神经端侧吻合。C组：切断尺神经,与桡神经端侧吻合。各组分别于术后3月取材进行组织学、形态定量学和电生理检测。结果端端吻合组优于其他两组。余两组差异无统计学意义。结论原位端端吻合是神经损伤最佳修复方式。支配两组拮抗肌的神经行端侧吻合后有神经纤维再生。     

Motor nerve conduction velocity after carbon monoxide or m-dinitrobenzene poisoning following elimination of the poisons

24 hrs after acute carbon monoxide or m-dinitrobenzene poisoning (about 60% CO-Hb or Met-Hb) the sciatic motor conduction velocity of rats is significantly reduced by 33% and 16%, respectively. Whereas 48 hrs after methemoglobinemia the nerve conduction is normal, a retardation is detectable even 4 weeks following carboxyhemoglobinemia. Also, 4 weeks after single carbon monoxide intoxication producing a mean CO-Hb content of 19%, the motor conduction velocity is significantly decreased. This effect may be useful for detection of carbon monoxide intoxication after elimination of the poison. The results show that there are carbon monoxide effects independent of blockade of hemoglobin.     

振动感觉阈值测定对糖尿病周围神经病变诊断价值探讨

目的为早期诊断糖尿病周围神经病变,探讨感觉阈值检查的价值。方法对我院内分泌科住院的229例2型糖尿病患者进行感觉阈值检查中振动感觉阈值(VPT)测定,并在不同病程组间及年龄组间进行比较。结果 2型糖尿病VPT异常检出率占32.3%,病程小于1年的新诊断糖尿病占9.8%。2型糖尿病患者VPT值随病程的延长及年龄的增长而升高。结论 VPT测定方法简便、无创、患者顺应性好,有助于提高早期糖尿病周围神经病变的检出率,在糖尿病患者的诊疗中具有较高的应用价值。     

血清铁蛋白与老年糖尿病患者周围神经病变的相关性研究

目的 探讨老年糖尿病患者血清铁蛋白（SF）水平和糖尿病周围神经病变（DPN）的关系。方法 选取2011年1月至2017年8月在芜湖市第二人民医院就诊的548例老年2型糖尿病（T2DM）患者,根据双下肢肌电图检查结果,分为非DPN组（NDPN组）与DPN组,NDPN组304例,DPN组244例,另选取同期健康体检者220例为对照组（NC组）,分别检测3组研究对象体质指数（BMI）、血压（BP）、超氧化物岐化酶（SOD）、总胆固醇（TC）、三酰甘油（TG）、糖化血红蛋白（HbA1c）、内皮素（ET）、SF、一氧化氮（NO）等水平,DPN危险因素行logistic回归分析。结果 除HDL-C水平外,DNP组、NDNP组和NC组各指标的差异均有统计学意义（P<0.05）。DPN组HbA1c、ET、TC、TG、LDL-C、SF水平高于NDPN组及NC组,而SOD、NO水平低于NDPN组及NC组,差异有统计学意义（P<0.05）。SF与HbA1c、TC、TG、ET均成正相关（r=0.613、0.461、0.542、0.583,P<0.05）,与SOD、NO均成负相关（r=-0.432、-0.574,P<0.05）。logistic回归分析显示SF、ET是DPN的独立危险因素,而SOD、NO是DPN的保护性因素。结论 SF是老年T2DM患者DPN的独立危险因素,其可能通过氧化应激参与DPN的发展。     

凯时治疗糖尿病性周围神经病变50例疗效观察

目的 观察凯时注射液对糖尿病周围神经病变(DPN)的治疗效果。方法 对50例确诊为DPN的患者予凯时注射液10μg/d(加入莫菲氏管内滴入)共2周。结果 注射2周后症状和体征即改善,改善率分别为95.0％(下肢自发痛),94.1％(上肢自发痛),90.5％(感觉减退),94.5％(麻木),77.7％(发冷),57.1％(发热);患者治疗前MCV和SCV均明显下降,以下肢更为显著,经治疗后有一定改善(P<0.05)。结论 凯时是治疗DPN的一种安全、有效的药物。