肉毒素注射后中毒患者的护理

正肉毒素的全称是肉毒杆菌毒素,是由肉毒杆菌分泌的细菌内毒素,最早发现于变质的肉罐头内,是一种神经麻醉毒素,是革兰阳性厌氧肉毒梭菌在繁殖过程中产生的一种细菌外毒素。局部注射后可以阻断神经对肌肉的传导,作用于胆碱能运动神经的末梢,以某种方式拮抗钙离子的作用,干扰乙酰胆碱从运动神经末梢的释放,使肌肉暂时发生麻痹而失去收缩功能,从而达到除皱美容塑造线条的目的~([1])。它是生物毒素中毒性最强的一种神经毒素,仅     

注射A型肉毒素美容致中毒一例

<正>肉毒杆菌毒素中毒是肉毒梭状芽孢菌外毒素所致的中毒性疾病。肉毒杆菌毒素有极强的嗜神经毒性,肉毒杆菌毒素中毒以不同程度和不同部位的肌肉麻痹或瘫痪为主要临床表现。肉毒杆菌毒素中毒的常见病因是摄入被肉毒杆菌及毒素污染的食物,多系家庭自制的豆瓣酱、发酵的臭豆腐等,此类中毒     

肉毒杆菌食物中毒急诊救治一例

肉毒杆菌食物中毒是由肉毒杆菌释放的肉毒毒素引起严重的神经肌肉中毒症状。该病初期常因临床表现为急性胃肠道中毒症状引起误诊而耽误治疗,严重者导致患者死亡。及早明确诊断和临床对症治疗是成功救治该病的关键。该文总结分析1例肉毒杆菌食物中毒患者的急诊救治过程。经过详细询问该患者的发病史和进食史,进行全面的体格检查、常规检验、影像辅助检查和实验室血浆肉毒毒素检测分析并结合临床症状,该患者确诊为肉毒毒素中毒。在未明确肉毒毒素亚型情况下,对患者大剂量注射A、B型抗肉毒毒素,辅助抗感染和营养恢复神经功能的综合治疗取得较好的治疗效果。患者发病第7日症状好转,救治26 d后康复出院。     

7例食用自制臭豆腐中毒病人的护理

肉毒毒素是目前已知毒性最强的物质,也是一种重要的毒素战剂和生物恐怖剂。肉毒毒素中毒是属于神经型食物中毒,常因进食被肉毒杆菌污染的腌肉,制作不良的罐头食品以及食用豆瓣酱,臭豆腐及不新鲜的鱼、猪肉、猪肝等而发病[1]。我院     

A型肉毒毒素在整形美容方面及其临床拓展应用的进展

近年来,随着对A型肉毒毒素基础研究和临床研究的深入,其在临床上应用范围也越来越广泛。A型肉毒毒素在医学美容整形方面应用最为广泛,此外,国内外还将A型肉毒毒素用于涉及皮肤科疾病、雷诺现象、疼痛性疾病、泌尿系统疾病、眼科疾病以及脑血管系统疾病等50余种病症的治疗,被誉为"20世纪90年代神经药物的一大进展"。     

肉毒毒素临床应用进展及适应症审批的意义

肉毒毒素是肉毒梭菌增殖过程中产生的一种细菌外毒素,其可作用于周围神经末梢的神经肌肉接头处抑制突触前神经递质乙酰胆碱的释放,实现肌肉化学性去神经支配、镇痛、调节自主神经紊乱等效应。本文重点概述肉毒毒素的治疗效应,以及肉毒毒素临床应用进展和肉毒毒素适应症开发的临床价值。     

食用自制茄子酱致肉毒毒素中毒2例报告

肉毒毒素是肉毒杆菌产生的外毒素,最早在变质的火腿中被发现,少量食用即可致死,主要累及神经肌肉接头的突触前膜。近年来人们生活水平的提高,多食用新鲜食物,肉毒毒素中毒患者罕见。但是由于一些地区特殊的饮食习惯,喜食腌制食物,存在肉毒毒素中毒的潜在风险。本文报道的两例患者来自内蒙古,因食用肉沫茄子酱,造成中毒。由于诊断治疗及时,预后良好。     

注射用肉毒毒素制剂及其研发进展

肉毒毒素(Botulinum Toxin,BoNT)已成为现代医学最具多用途的治疗药物之一。通过将肉毒毒素注射到特定过度活动的肌肉中,可以阻断神经和肌肉之间的信号传导,引起肌肉的松弛性麻痹,从而达到治疗的功效。从业者应熟悉各类产品的特性,以实现安全有效地使用。除了已经上市的众多肉毒毒素产品外,目前还在开发其他新型制剂,这些产品将会进一步扩大肉毒毒素的适用范围,以及给患者提供更多的选择。     

眼科患者对A型肉毒毒素注射认知情况调查及护理对策

目的：了解眼科患者对A型肉毒毒素眼部注射的认知情况,探讨更有利于患者需求的护理对策。方法：2011年8月-2012年1月,采用白行设计调查问卷,对i00例在我院眼科门诊接受A型肉毒毒素眼部注射的患者进行调查。结果：70％的患者对A型肉毒毒索治疗眼睑及面肌痉挛相关知识为部分了解;82％的患者表示非常希望了解关于A型肉毒毒索眼部注射的相关医学及护理知识。患者不能坚持治疗的主要原因是担忧A型肉毒毒素眼部注射后出现的副作用。结论：眼科患者对A型肉毒毒素眼部注射认知情况较低,我们应将护理工作的重点放在让患者知晓A型肉毒毒素治疗眼睑及面肌痉挛的目的、方法,让其充分了解眼部注射后的局部表现,掌握注射部位的护理方法。满足患者对医护人员健康宣教的需求。     

肉毒杆菌中毒21例临床分析

肉毒中毒是由肉毒梭状芽孢杆菌外毒素所引起的中毒性疾病。其特点为毒素作用于颅脑神经核和外周神经肌肉接头以及植物神经末稍，阻碍乙酰胆碱释放影响神经冲动传递，导致肌肉的松弛性麻痹。现将我院2000年1月～2003年11月收治的来自四个家族，因食用自制臭豆腐致肉毒中毒21例（有两例在外院及转诊途中死亡）分析总结如下：     

Evidence for Antinociceptive Activity of Botulinum Toxin Type A in Pain Management

The neurotoxin, botulinum toxin type A, has been used successfully, in some patients, as an analgesic for myofascial pain syndromes, migraine, and other headache types. The toxin inhibits the release of the neurotransmitter, acetylcholine, at the neuromuscular junction thereby inhibiting striated muscle contractions. In the majority of pain syndromes where botulinum toxin type A is effective, inhibiting muscle spasms is an important component of its activity. Even so, the reduction of pain often occurs before the decrease in muscle contractions suggesting that botulinum toxin type A has a more complex mechanism of action than initially hypothesized. Current data points to an antinociceptive effect of botulinum toxin type A that is separate from its neuromuscular activity. The common biochemical mechanism, however, remains the same between botulinum toxin type A's effect on the motor nerve or the sensory nerve: enzymatic blockade of neurotransmitter release. The antinociceptive effect of the toxin was reported to block substance P release using in vitro culture systems. ¹
The current investigation evaluated the in vivo mechanism of action for the antinociceptive action of botulinum toxin type A. In these studies, botulinum toxin type A was found to block the release of glutamate. Furthermore, Fos, a product of the immediate early gene, c- fos , expressed with neuronal stimuli was prevented upon peripheral exposure to the toxin.
These findings suggest that botulinum toxin type A blocks peripheral sensitization and, indirectly, reduces central sensitization. The recent hypothesis that migraine involves both peripheral and central sensitization may help explain how botulinum toxin type A inhibits migraine pain by acting on these two pathways. Further research is needed to determine whether the antinociceptive mechanism mediated by botulinum toxin type A affects the neuronal signaling pathways that are activated during migraine.     

The interaction between aminoquinolines and presynaptically acting neurotoxins

Chloroquine and hydroxychloroquine block neuromuscular transmission in isolated tissues from mouse, rat, guinea pig and chick. Blockade is associated with depressed muscle responses to potassium and abolished muscle responses to nicotinic cholinergic agonists. Within certain time and concentration limits, the blocking effects of chloroquine and hydroxychloroquine are reversible. Both drugs antagonize the onset of paralysis caused by botulinum neurotoxin types A and B, but neither drug antagonizes tetanus toxin or beta-bungarotoxin. The ability of chloroquine and hydroxychloroquine to antagonize botulinum toxin is not due to blockade of nicotinic cholinergic receptors. At concentrations that produce neuromuscular blockade, d-tubocurarine does not antagonize botulinum toxin types A and B. Chloroquine causes botulinum toxin to remain at an antitoxin sensitive site. These data could mean that chloroquine acts at the cell membrane to inhibit toxin binding or internalization, or that it acts in the cell interior to inhibit lysosomal processing of toxin. Whatever its action, chloroquine is the most effective antagonist of botulinum toxin yet described.     

Cost-effectiveness of botulinum toxin type a in the treatment of post-stroke spasticity.

OBJECTIVE: Treatment strategies for post-stroke spasticity include oral anti-spastic drugs, surgery, physiotherapy and botulinum toxin type A injection. The objective of this study was to compare the cost-effectiveness and outcomes of oral therapy vs. botulinum toxin type A treatment strategies in patients with flexed wrist/clenched fist spasticity. METHODS: Treatment outcome and resource use data were collected from an expert panel experienced in the treatment of post-stroke spasticity. A decision tree model was developed to analyse the data. RESULTS: Thirty-five percent of patients receiving oral therapy showed an improvement in pre-treatment functional targets which would warrant continuation of therapy, compared with 73% and 68% of patients treated with botulinum toxin type A first- and second-line therapy, respectively. Botulinum toxin type A treatment was also more cost-effective than oral therapy with the "cost-per-successfully-treated month" being 942 pounds, 1387 pounds and 1697 pounds for botulinum toxin type A first-line, botulinum toxin type A second-line and oral therapy, respectively. CONCLUSION: In conclusion, botulinum toxin type A is a cost-effective treatment for post-stroke spasticity.     

A型肉毒素在皮肤科疾病治疗中的进展

A型肉毒素是肉毒梭状芽孢杆菌在繁殖过程中分泌的A型毒性蛋白质,具有很强的神经毒性。其在皮肤美容方面的疗效显著而被熟知。除皮肤美容外,临床实践和前期研究均证实A型肉毒素在治疗皮肤病方面亦有明显疗效,且部分疾病经治疗预后明显优于传统治疗,如瘢痕与多汗症等。     

Effect of intramuscular botulinum toxin injection on upper limb spasticity in stroke patients

OBJECTIVE: To evaluate the therapeutic effect of intramuscular injection of botulinum toxin on spasticity of the upper limb, with emphasis on its influence over limb function. DESIGN: An open-label, noncontrolled trial with a duration of 12 wk was designed to determine the safety and efficacy of intramuscular botulinum toxin A injection in the treatment of 16 patients with stroke with spastic hemiparesis. Electromyographically guided intramuscular botulinum toxin A injections were applied to the spastic limbs. A detailed scale system was used for the evaluation of muscle tone and functional changes induced by botulinum toxin A treatment. RESULTS: No major side effect secondary to botulinum toxin A injection was reported. Statistically significant (P < 0.05) improvements of muscle tone, joint range of motion, hand muscle strength, and muscular pain were seen after the injection. The improvements lasted up to 8-12 wk after the treatment. However, there was no significant functional improvement except in two of the patients. CONCLUSIONS: Botulinum toxin A injection may help relieve upper limb spasticity and pain in patients with stroke. Its effect on function is probably determined by case selection.     

Is there a role for botulinum toxin in the treatment of migraine?

In this review, the studies and case reports that are available from reference systems and published congress contributions on the treatment of migraine with botulinum toxin are evaluated. The studies and reports were analyzed with respect to the study design, the efficacy parameters, and the significance of results. One double-blind, placebocontrolled, randomized study with negative (for a 75 U dose of botulinum toxin) and positive (for a 25 U dose of botulinum toxin) evidence of efficacy, one that was a partly positive controlled study (pain intensity, but not attack-frequency improved), and four positive open studies were available. For the acute treatment of migraine with botulinum toxin, only positive case reports were published. As a result of this analysis, there is no sufficient scientific evidence for a treatment recommendation of migraine with botulinum toxin. Further studies are needed for a definite evaluation of subgroups with probable benefit from such a treatment and for the comparison of botulinum toxin with other migraine prophylactic drugs.     

The role of botulinum toxin injections in the management of muscle overactivity of the lower limb

Muscle overactivity is common in patients with adult onset central nervous system damage. It can produce significant disablement in conjunction with other impairments such as adaptive soft tissue shortening and loss of muscle strength. Muscle overactivity is not evenly distributed throughout the body; across joints there is frequently imbalance between agonist and antagonist, producing abnormal joint postures and movement patterns. Due to the asymmetric nature of the abnormal activity across joints, in general we recommend local treatment targeting the more overactive of the two agonists, rather than systemic treatment. Considerable experience with the use of botulinum toxin, both serotypes A and B, in the treatment of muscle overactivity has been accumulated in the last two decades through pragmatic clinical practice and open label studies, supported by an increasing number of randomized controlled trials. In most cases, it is important to use botulinum toxin injection for treatment of muscle overactivity in the setting of wider rehabilitation goals and interventions. Focal and partial blocks with botulinum toxin should be used as a component of a general neurorehabilitation programme rather than as an alternative to other treatments. We review the evidence supporting the use of botulinum toxin to treat muscle overactivity in the lower limb, present practical guidelines on when and how to use botulinum toxin and provide direction for future research.     

The role of botulinum toxin injections in the management of muscle overactivity of the lower limb

Muscle overactivity is common in patients with adult onset central nervous system damage. It can produce significant disablement in conjunction with other impairments such as adaptive soft tissue shortening and loss of muscle strength. Muscle overactivity is not evenly distributed throughout the body; across joints there is frequently imbalance between agonist and antagonist, producing abnormal joint postures and movement patterns. Due to the asymmetric nature of the abnormal activity across joints, in general we recommend local treatment targeting the more overactive of the two agonists, rather than systemic treatment. Considerable experience with the use of botulinum toxin, both serotypes A and B, in the treatment of muscle overactivity has been accumulated in the last two decades through pragmatic clinical practice and open label studies, supported by an increasing number of randomized controlled trials. In most cases, it is important to use botulinum toxin injection for treatment of muscle overactivity in the setting of wider rehabilitation goals and interventions. Focal and partial blocks with botulinum toxin should be used as a component of a general neurorehabilitation programme rather than as an alternative to other treatments. We review the evidence supporting the use of botulinum toxin to treat muscle overactivity in the lower limb, present practical guidelines on when and how to use botulinum toxin and provide direction for future research.     

Effect of botulinum toxin A injections in the treatment of chronic tension-type headache: a double-blind, placebo-controlled trial

In addition to vascular and supraspinal influences, contraction of craniofacial muscles or central sensitization processes following continuous nociceptive input of craniofacial muscles may play an important role in the pathogenesis of tension-type headache. Chemodenervation induced by botulinum toxin injection is successfully used to decrease muscle tension. If muscle tension is important in this type of headache, then botulinum toxin could be helpful in its treatment. We conducted a randomized, placebo-controlled study to examine the effect of 20 U botulinum toxin injected into frontal and temporal muscles in patients with chronic tension-type headache. During a baseline of 4 weeks and a posttreatment period of 8 weeks, the effect was evaluated with daily records and the West Haven-Yale Multidimensional Pain Inventory. Some improvement in affective variables were demonstrated in the botulinum group, but important outcome variables, such as pain intensity, the number of pain-free days, and consumption of analgesics, were not statistically different between the groups. Reasons for these moderate effects may include the injection sites, dose of botulinum toxin, and duration of treatment.