有机磷中毒迟发性神经病单纤维肌电图分析

目的:探讨单纤维肌电图(SFEMG)在有机磷中毒迟发性神经病(OPIDN)的应用价值。方法:分别检测19例OPIDN患者和18例健康对照组指总伸肌、胫前肌的颤抖(Jitter)及纤维密度(FD)。结果:OPIDN患者指总伸肌和胫前肌的Jitter均增宽、部分患者伴有阻滞,FD均增大。结论:SFEMG有助于有机磷中毒神经病的早期诊断,是诊断OPIDN的敏感的电生理检测手段。     

有机磷中毒迟发性周围神经病临床及电生理分析

目的分析有机磷农药中毒迟发性周围神经病临床及电生理特点,为早期诊断及判断预后提供依据。方法 对确诊的32例患者行肌电图和神经传导速度检测。结果 32例均为急性有机磷农药中毒经治愈出院后发生迟发性周围神经病患者,平均潜伏期18d。肢体远端无力32例,肌萎缩31例。32例肌电图均呈神经源性损害。运动神经传导速度(MCV)减慢29例,感觉神经传导速度(SCV)减慢4例。结论有机磷农药中毒迟发性周围神经病是一种以轴索病变为主的周围运动神经病。中毒轻、中、重度均可发病,但中毒的程度越重,预后越差。     

三磷酸胞苷二钠在有机磷中毒后迟发性神经病中的应用

目的 探讨三磷酸胞苷二钠对有机磷中毒后迟发性神经病的治疗效果.方法 选择有机磷中毒后迟发性神经病患者30例,随机分为治疗组与对照组.治疗组给予三磷酸胞苷二钠治疗10～14 d,对照组不予治疗.观察2个月后肢体瘫痪肌肉萎缩缓解情况.结果 治疗组神经功能缺损较对照组明功能损害减少,治疗效果明显优于对照组.结论 三磷酸胞苷二钠能够改善有机磷中毒后迟发性神经病患者的预后.     

有机磷引起的迟发性神经病的临床与电生理研究

目的：依据迟发性神经病（ＯＰＩＤＮ）电生理异常特性，神经髓鞘与轴索共同受累现象，探讨ＯＰＩＤＮ发病机制学说。方法：对２８例有机磷引起的ＯＰＩＤＮ行运动神经传导速、速神经传导速度和肌电图检测。结果：６９．４％的被检肌肉出现失神经电位（正锐波及纤颤电位），运动神经传导速度与正常对照组比较显著减慢（Ｐ〈０．０１），感觉神经传导速度与正常对照组比较无显著差异（Ｐ〉０．０１）。     

有机磷中毒迟发性神经病42例临床与电生理检查

目的：探讨有机磷中毒迟发性神经病的临床与电生理检查的价值。方法：对2005年7月-2009年2月42例有机磷中毒迟发性神经病（OPIDP）患者的临床表现和神经电生理检查资料进行总结分析。结果：MCV表现为减慢共39例,3例未引出波型;SCV表现为减慢5例,其余37例正常。经临床随访观寨,分别于3～12个月症状、体征消失,肌力恢复正常,肌电图复查正常。结论：神经电生理检查有助于及早发现病变,值得临床医生予以重视。     

有机磷农药中毒迟发性神经病26例分析

自1982年～1995年，我院共收治急性有机磷中毒病人604例。其中26例患者在急性中毒症状消失后11～60天，出现迟发性神经病，占总数的43％，现报告如下。临床资料一、26例患者均有自服或误服有机磷农药史，其中男16例，女10例。年龄10岁～62岁。平均年龄26．8岁。二、26例均有昏迷史，昏迷时间半小时～68，J‘时，平均8．1／J‘时．眼原液药量20ml～250ml。抢救中全部采用综合措施，应用阿托品、解磷定。阿托品总用量55mg～186mg，解磷定总用量ag～og。神经精神症状出现的时间为11天～60天。本组病例均急性起病，大多数人在体力活动时诱发。…     

有机磷中毒致迟发性神经病变

急性有机磷(DDV)中毒常可并发精神障碍，而引起神经病变者罕见。现就我院所见1例报道如下：     

黄芪注射液治疗有机磷杀虫剂中毒致迟发性神经病

目的:观察黄芪注射液对急性有机磷杀虫剂中毒所致的迟发性神经病的治疗作用.方法:采用Doll法将有机磷杀虫剂中毒患者34例随机分为两组.对照组18例,采用常规方法治疗(维生素B12 500 μg,im,每周2次;维生素B6、维生素B1、三磷腺苷各20 mg,复方丹参片3片,均口服,tid;并给予对症、支持治疗等).治疗组16例,则在常规方法基础上加用黄芪注射液30 mL加入0.9%氯化钠注射液200 mL中静脉滴注,bid,用6 d,停1 d,3个月为1个疗程.观察其迟发性神经病患者肌力恢复的情况,并采用肌电图测试正中神经和腓总神经的传导速度.结果:治疗组显效率43.7%,对照组显效率5.6%(P＜0.01);治疗组肌力及神经传导速度恢复情况明显优于对照组,差异有极显著性(P＜0.01).结论:黄芪注射液对急性有机磷杀虫剂中毒所致的迟发性神经病有较好的治疗作用.     

有机磷农药中毒迟发性周围神经病25例报告

有机磷农药中毒后致迟发性周围神经病临床并非罕见 ,我科近 4年来收治 2 5例 ,现报告如下。1　临床资料1.1　一般资料 :2 5例中 ,男 5例 ,女 2 0例 ;年龄 13～ 38岁。均为一次口服有机磷农药 ,其中乐果 10例 ,敌百虫 10例 ,甲胺磷 5例 ,量 2 0～ 40 ml。根据临床表现诊断为轻度中毒 15例 ,中度中毒 5例 ,重度中毒 5例。于中毒后 10～ 5 0天发病 ,平均17天。1.2　临床特征 :2 5例患者首发症状均表现双下肢远端麻木、疼痛、乏力 ;其中 15例仅表现双下肢远端麻木、疼痛、乏力 ,10例首先表现双下肢远端麻木、疼痛、乏力 ,渐向近端发展 ,累及上肢…     

有机磷中毒后迟发性神经系统损伤3例报告

有机磷中毒较为多见,但中毒后迟发性神经系统损伤的临床病例报告较少,现报告3例如下.     

Delayed neuropathy by the organophosphorus nerve agents soman and tabun

The organophosphorus nerve agents soman and tabun were tested in the hen at doses 120–150 times higher than their acute LD₅₀, as it was assumed that these doses would produce delayed neuropathy. The animals were protected against the acute lethal effect of these agents by pretreatment with atropine, physostigmine, diazepam, and the oxime HI-6 or obidoxime.The surviving animals were followed for 30 days and the occurrence of delayed neuropathy was clinically diagnosed. Soman produced severe delayed neuropathy at a dose of 1.5 mg/kg, a dose which produced acute lethality in five animals out of six. Tabun elicited very mild neuropathic symptoms in one animal out of two at a dose of 6 mg/kg given on 2 consecutive days. Delayed neuropathy was not seen in the hens that survived the acute toxicity of a single dose of tabun, 12 mg/kg (three out of six) or 15 mg/kg (two out of six).     

Changes in beclin-1 and micro-calpain expression in tri-ortho-cresyl phosphate-induced delayed neuropathy

Tri-ortho-cresyl phosphate (TOCP) can cause toxic neuropathy known as organophosphate-induced delayed neuropathy (OPIDN), which is pathologically characterized by the swollen axon containing aggregations of neurofilaments, microtubules, and multivesicular vesicles. Autophagy is a self-degradative process which plays a housekeeping role in removing misfolded proteins and damaged organelles. The current study was designed to investigate the possible roles of autophagy in the pathogenesis of OPIDN. Adult hens were treated with a dose of 750mg/kg TOCP by gavage, or injected subcutaneously with 60mg/kg phenylmethanesulfonyl fluoride (PMSF) dissolved in DMSO 24h earlier and subsequently treated with TOCP, then sacrificed on the time-points of 0, 1, 5, 10, and 21 days after dosing of TOCP respectively. The levels of beclin-1 and μ-calpain in tibial nerves and spinal cords were determined by immunoblotting. The results showed that in both tissues TOCP increased the expression of μ-calpain while decreased that of beclin-1. When given before TOCP administration, PMSF pretreatment could protect hens against the delayed neuropathy. In the meantime, pretreatment with PMSF reduced calpain expression below basal and increased beclin-1 expression above basal in tibial nerve, whereas it simply returned calpain and beclin-1 expression to their basal levels in spinal cord. In conclusion, the intoxication of TOCP was associated with a significant change of beclin-1 in hen nervous tissues, which suggested that disruption of autophagy-regulated machinery in neurons might be involved in the pathogenesis of OPIDN.     

Phenylmethylsulfonyl fluoride protects against the degradation of neurofilaments in tri-ortho-cresyl phosphate (TOCP) induced delayed neuropathy

Tri-ortho-cresyl phosphate (TOCP) is an organophosphorus ester, which can cause a type of neurotoxicity known as organophosphate-induced delayed neuropathy (OPIDN). Our recent study has shown that the enhanced degradation of neurofilament (NF) in peripheral nerve of hens is an early event of TOCP-induced OPIDN (Song et al., 2009). The main objective of this investigation is to study the effect of TOCP administration on NF content and NF degradation when OPIDN is blocked by pretreatment with phenylmethylsulfonyl fluoride (PMSF). The hens were pretreated 24 h earlier with PMSF and subsequently treated with a single dosage of 750 mg/kg TOCP, then sacrificed on the corresponding time points of 0, 1, 5, 10, and 21 days after dosing TOCP, respectively. The tibial nerves were dissected, homogenized, and centrifuged at 100,000 × g. The level of NF triplet protein in both pellet and supernatant fractions of tibial nerves was determined. Western blotting analysis showed a significant increase of three NF subunits in hens treated with PMSF and TOCP compared with the control. These changes were observed within 24 h of PMSF administration and then followed by an obvious recovery. Furthermore, accompanied with the increase of NF content, a significant decline in NF-L degradation rate was observed in both fractions of tibial nerves. Taken together, these results demonstrated the pretreatment with PMSF could inhibit TOCP-induced NF degradation while it protected hens against the development of OPIDN, which suggested the inhibition of NF-associated protease in peripheral nerves might be an underlying protective mechanism of PMSF against OPIDN.     

Anomalous biochemical responses in tests of the delayed neuropathic potential of methamidophos (O,S-dimethyl phosphorothioamidate), its resolved isomers and of some higher O-alkyl homologues

The interaction with neural neuropathy target esterase (NTE) and acetylcholinesterase (AChE) in vivo of methamidophos (O,S-dimethyl phosphorothioamidate), its resolved stereoisomers and five higher O-alkyl homologues has been examined along with the ability of these compounds to cause organophosphorus-induced delayed polyneuropathy (OPIDP) in adult hens. For the lower homologues AChE was more sensitive than NTE and it was impossible to achieve high inhibition of NTE in vivo without both prophylaxis and therapy against acute anticholinesterase effects; for then-hexyl homologue high inhibition of NTE could be achieved without obvious anticholinesterase effects and spontaneous reactivation of inhibited AChE was seen as in vitro. The maximum tolerated dose ofl(–) methamidophos or of the ethyl oriso-propyl homologues did not inhibit NTE more than 60%, and surviving birds did not develop OPIDP. Then-propyl,n-butyl andn-hexyl compounds caused typical OPIDP at doses causing a peak of 70–95% inhibition of NTE in brain, spinal cord and sciatic nerve soon after dosing. Racemic methamidophos caused unusually mild OPIDP associated with very high inhibition of NTE at doses estimated to be >8 times the unprotected LD₅₀ and thed-(+) isomer caused OPIDP at about 5–7× LD₅₀. Clinical effects correlated with histopathology in 19 out of 20 examined birds. In contrast to results of many previous studies with organophosphates and phosphonates, all these cases of OPIDP were associated with formation of inhibited NTE which could be reactivated ex vivo by treatment of autopsy tissue with KF solution. It is not clear whether aging of inhibited NTE had occurred but with less associated stabilisation of the enzyme-phosphorus bond or whether, even without aging, the unusual N-unsubstituted phosphoramidate caused sufficient disturbance in or near the NTE target to initiate the same degenerative process as that caused typically by generation of aged organophosphorylated NTE.     

急性一氧化碳中毒迟发性脑病的MRI诊断及临床分析

目的:探讨急性一氧化碳中毒后迟发性脑病(DEACMP)患者的头颅磁共振成像特点和诊断价值。方法:分析32例DEACMP患者的临床表现、头颅MRI资料。结果:DEACMP患者的主要临床表现为智能、人格改变;头颅MRI表现可分为3型:(1)神经核团受累型;(2)脑白质受累型;(3)皮层受累型。MRI特征:苍白球为对称性的卵圆形长T1、长T2信号,皮层下白质为对称性的弥漫、模糊云雾状长T1、长T2信号,侧脑室周围、半卵圆中心白质亦为对称云絮状长T1、长T2信号,胼胝体常受累。MRI显示苍白球合并脑白质受累者及皮层受累者,临床表现较重。结论:本病的诊断主要依靠病史、临床表现和头颅磁共振改变。     

有机磷酸酯引起的迟发性神经病的“强化”机理

某些酯酶抑制剂可以强化创伤和中毒引起的轴突病 ,这可以从临床症状和组织病理学上加以证实。有机磷酸酯诱导的迟发性神经病是研究轴突病强化机制的良好模型 ,有机磷酸酯诱导的迟发性神经病的强化可能与神经系统的修复机理有关。强化剂的靶标位点还未清楚 ,但不是神经病靶标酯酶 ,而可能与一种类似于神经病靶标酯酶的特殊酯酶有关     

联合醒脑静治疗一氧化碳中毒迟发性脑病疗效观察

目的观察醒脑静注射液治疗急性一氧化碳中毒迟发性脑病临床疗效。方法将36例急性一氧化碳中毒迟发性脑病患者随机分为对照组和醒脑静组,两组均给予常规治疗,醒脑静组在常规治疗治疗的基础上联合使用醒脑静注射液,观察治疗效果。结果醒脑静组有效率为88.8%,对照组为72.2%,差异有统计学意义（P〈0.05）。结论醒脑静注射液可促进一氧化碳中毒迟发性脑病患者神经功能的恢复,改善其预后。     

一氧化碳中毒迟发性脑病的临床分析

目的分析探讨一氧化碳中毒后迟发性脑病的发病特征与机制,总结临床诊治经验。方法收集我院2007年1月至2011年1月期间因急性一氧化碳中毒迟发性脑病住院的患者共76例,对其临床资料进行回顾性调查分析。结果患者有众多临床表现:精神淡漠、痴呆、小便失禁、缄默、偏瘫、癫痫发作等;76例患者治疗后经疗效判定,其中治愈24例,显效26例,好转12例,无效14例,总有效率为81.6%。结论 DEACMP发病机制尚不明了,临床表现众多,影像学检查有助于提高对患者的诊断,减少误诊率,给予患者及时、足疗程的治疗可最大限度的促进患者预后。     

前列地尔和甲钴铵治疗糖尿病周围神经病变疗效观察

目的观察前列地尔和甲钴铵治疗糖尿病周围神经病变（DPN）疗效及成本比较。方法将120例2型糖尿病周围神经病变患者,在常规治疗的基础上,采用前列地尔注射液和甲钴铵注射液。观察两种药物治疗糖尿病周围神经病变的疗效及费用。结果两种药物均可改善血液循环,改善缺血、缺氧,促进神经细胞功能恢复,治疗糖尿病周围神经病变（DPN）疗效比较差异无统计学意义。结论前列地尔和甲钴铵治疗糖尿病周围神经病变效果明显,而甲钴铵比前列地尔更经济。