替扎尼定治疗脑卒中后肩关节疼痛患者的不良反应

目的观察替扎尼定治疗脑卒中后肩关节疼痛患者过程中的不良反应。方法将脑卒中后肩关节疼痛患者172例随机分为试验组91例和对照组81例。2组患者均予以常规治疗,试验组同时给予替扎尼定口服,比较2组患者在治疗前后的肝肾功能、血压变化,并询问不良反应。结果治疗过程中,2组患者均出现胃肠道反应、嗜睡、口干、乏力、头晕、肝功能异常、体位性低血压等不良反应。其中试验组的嗜睡、头晕发生率显著高于对照组,而胃肠道反应发生率显著低于对照组,差异均有统计学意义（P〈0.05）。结论替扎尼定作为一种新型抗痉挛药,在有效缓解脑卒中后肩关节疼痛的同时,具有不良反应少的特点,值得临床推广。     

替扎尼定联合尼美舒利治疗纤维织炎的临床疗效

目的观察盐酸替扎尼定治疗腰背肌纤维织炎的临床疗效。方法2011年8月-2013年1月门诊就诊腰背肌纤维织炎患者,共166例,随机分为对照组与试验组,每组各83例。实际完成试验者145例,其中试验组74例,对照组78例。对照组采用尼美舒利进行治疗,试验组采用尼美舒利与盐酸替扎尼定联合治疗,治疗周期均为2周。分别对治疗前与治疗后心理测评（采用症状自评量表检测）、视觉疼痛模拟和日常生活能力进行测评,并进行组间比较,观察其疗效,治疗期间随访平均为3个月。结果治疗后与治疗前比较,各组均有所改善,且组间比较,试验组疗效优于对照组,试验组胃肠道疾病发生情况少于对照组。结论盐酸替扎尼定联合尼美舒利治疗腰背肌纤维织炎具有较好的临床疗效,且盐酸替扎尼定对胃肠道功能起到一定的保护作用。     

盐酸替扎尼定片溶出度方法的研究与改进

目的 改进盐酸替扎尼定片溶出度方法 .方法 统一溶出度方法 为桨法,以盐酸溶液900 ml为溶出介质,转速为50 r/min;检测方法 由原来的紫外分光光度法改为高效液相色谱法,色谱柱为C18(5μm,4.6 mm×250 mm),流动相为1-戊烷磺酸钠缓冲溶液(取1-戊烷磺酸钠3.5 g,溶于1000 ml水中,用12%磷酸溶液或氢氧化钠试液调节pH至3.0±0.05)-乙腈(80:20),流速为1.0 ml/min,检测波长为230 nm,35℃,进样量为20μl.比较两种方法 测定的样品累积溶出度.结果 盐酸替扎尼定检测质量浓度线性范围为0.5022~5.0225μg/ml(r=1.0000),平均回收率为99.4%,相对标准偏差为0.3%;样品的溶出时间由原来的30 min缩短至15 min.改进方法 测定的盐酸替扎尼定片的累积溶出率高于原方法 .结论 改进方法 提高了盐酸替扎尼定片溶出度检测的专属性和准确性,较好地体现了片剂间的差异.     

温胆汤加减治疗内科疾病体会

目的观察替扎尼定治疗卒中后肩关节疼痛的疗效,探讨其可能的作用机制。方法将卒中后肩关节疼痛患者103例随机分为实验组51例和对照组52例。两组患者均予以常规治疗。实验组同时给予患者口服替扎尼定。比较两组患者在实验前及实验开始第1、4、8、12周时肩关节疼痛程度、肩关节肌张力改善程度,并询问不良反应及监测肝肾功能、血压变化。结果治疗4周时,实验组患者肩关节疼痛与治疗前比较,有显著缓解(20.61±12.95VS 47.15±13.01,P<0.05)。治疗12周时,实验组患者肩关节疼痛与对照组比较,有显著性缓解(8.23±2.52VS 15.73±4.51,P<0.05)。治疗8周时,实验组患者肩关节肌张力与治疗前比较,有显著缓解(1.6±0.5VS 2.6±0.4,P<0.05)。治疗12周时,实验组患者肩关节肌张力与对照组比较,有显著缓解(1.2±0.2VS 1.7±0.3,P<0.05)。结论替扎尼定可以缓解卒中后肩关节疼痛,肩关节外展肌张力也可以得到改善,具有较好的临床疗效。但是,肩关节疼痛的缓解发生在肩关节肌张力缓解之前。因此,局部肌张力改善并非卒中后肩关节疼痛好转的唯一机制。     

肌筋膜疼痛触发点治疗技术治疗腰背肌筋膜疼痛综合征疗效分析

目的:评价利用肌筋膜疼痛触发点治疗腰背肌筋膜疼痛综合征临床疗效的优越性。方法:将500例符合诊断标准的患者随机分为治疗组和对照组,每组250例,治疗组采用肌筋膜疼痛触发点治疗技术(针刺和推拿疗法)进行治疗,对照组采用替扎尼定进行治疗;2组治疗均隔日1次,7d为1个疗程;治疗8个疗程后,进行2组自身治疗前后对照,以及2组间疗效的比较。结果:2组自身治疗前后对照,各组疼痛指数、功能状态指数和硬结条索状物指数均降低(P<0.05);治疗组总有效率为95.60%;对照组总有效率为85.20%;2组疗效比较差异有统计学意义(P<0.05)。结论:采用肌筋膜疼痛触发点治疗技术治疗腰背肌筋膜疼痛综合征疗效明显,且优于替扎尼定的治疗效果,值得临床进一步研究和推广。     

Effects of gender and moderate smoking on the pharmacokinetics and effects of the CYP1A2 substrate tizanidine

Objective We studied the effects of gender and smoking on the pharmacokinetics and effects of the cytochrome P450 (CYP) 1A2 substrate tizanidine. Methods Seventy-one healthy young volunteers (male and female nonsmokers, male smokers) ingested 4 mg tizanidine. Plasma concentrations and pharmacodynamics of tizanidine were measured, and a caffeine test was performed. Results Among nonsmokers, the peak concentration (C_max) and area under concentration-time curve from 0 to infinity [AUC(0-∞)] of tizanidine did not differ significantly between females and males. However, the half-life (t_1/2) was 9% shorter in female nonsmokers than in male nonsmokers (P < 0.05). In male smokers, the t_1/2 was 10% shorter and the weight-adjusted AUC(0-∞) 33% smaller than in male nonsmokers (P < 0.05). The caffeine/paraxanthine ratio was 35–40% smaller (P = 0.001) in male smokers than in nonsmoking males or females, but did not differ between males and females. Tizanidine lowered blood pressure and caused drowsiness significantly (P < 0.05) more in females than in either male groups. The effects on blood pressure were smallest in male smokers (P < 0.05). Conclusions Gender by itself seems to have no clinically significant effect on the pharmacokinetics of tizanidine, whereas smoking reduces plasma concentrations and effects of tizanidine. Any possible effect of gender and smoking is largely outweighed by individual variability in CYP1A2 activity due to genetic and environmental factors and in body weight. Careful dosing of tizanidine is warranted in small females, whereas male smokers can require higher than average doses. This study was supported by grants from the Helsinki University Central Hospital Research Fund, the National Technology Agency, and the Sigrid Jusélius Foundation, Finland.     

A case of delirium, motor disturbances, and autonomic dysfunction due to baclofen and tizanidine withdrawal: a review of the literature

We report a case of delirium accompanied by extrapyramidal symptoms and autonomic dysfunction in a 59-year-old man following abrupt cessation of baclofen and tizanidine. An extensive search for the etiology was undertaken, but it was only after a careful history was taken that suspicion for baclofen and tizanidine withdrawal was raised. The delirium and motor disturbances resolved within 24 h of reintroduction of baclofen. Withdrawal from muscle relaxants requires a high index of suspicion but should be considered in patients who manifest signs and symptoms of withdrawal from the medications, particularly visual hallucinations, rigidity and autonomic dysfunction.     

The Effect of Tizanidine on Chronic Vasospasm in Rats

Summary ? Background. Cerebral vasospasm after subarachnoid hemorrhage (SAH) has remained a major cause of morbidity and mortality in patients with SAH. Excitatory neurotransmitters are gathered in the extracellular space during ischemia due to cerebral vasospasm and initiate or stimulate a series of pathophysiological biochemical processes which consequently lead to neuronal death. Tizanidine (Sandoz compound DS 103–282, 5-chloro-4,2 (2-imidazolin-2-yl-amino)-2,1,3-benzothiazol hydrochloride) is a centrally-acting muscle relaxant and a selective α 2 adrenoreceptor agonist which shows its effect by stimulating presynaptic α 2 adrenoreceptors in central ASPergic and GLUergic system by inhibiting aspartic acid and glutamic acid release. In this study, the effect of Tizanidine on vasospasm was evaluated.  Methods. We used a femoral artery vasospasm model in rats which has been described by Okada et al. 60 rats were examined in three groups. The first group was used as control group (Control) (n=20), in the second group subarachnoid hemorrhage was performed (SAH) (n=20), in the third group Tizanidine was administered in addition to SAH (SAH+Tizanidine administration) (n=20). Animals in SAH+Tizanidine administration group received 0,3 mg/kg/day intraperitoneally for 7 days. Seven days after the experiment, after perfusion-fixation, 10 mm segments of both femoral arteries were removed and the femoral artery was prepared for light microscope examination, scanning and transmission electron microscopy and for morphometric analysis.  Results. There was a statistically significant difference between the electron, scanning and light microscopic observations and morphometric analysis of SAH+Tizanidine administration group and SAH group, and no statistically significant difference between SAH+Tizanidine administration group and control group.  Conclusion. This study has disclosed that Tizanidine administration before the vasospasm reduces ultrastructural and morphometric vasospastic insult significantly. However, the clinical application of Tizanidine as a protective and therapeutic agent in cerebral vasospasm needs further studies including the employment of clinically more relevant SAH models.     

Tizanidine for the treatment of intention myoclonus: a case series

OBJECTIVE: To evaluate the effectiveness of tizanidine in treating intention myoclonus. DESIGN: Case series. SETTING: Inpatient rehabilitation center. PARTICIPANTS: Three subjects whose activities of daily living were impaired due to intention myoclonus related to mitochondrial encephalomyopathy, stroke, and multiple sclerosis (MS). INTERVENTION: Tizanidine. MAIN OUTCOME MEASURES: Reduction in intention myoclonus and change in score on the FIM instrument. RESULTS: The patient with mitochondrial encephalomyopathy had left upper- and lower-extremity intention myoclonus; the patient with stroke had left upper intention myoclonus; and the patient with MS had right upper- and left lower-intention myoclonus. In the patient with mitochondrial encephalomyopathy, the FIM score increased from 90 to 103 points over 2 days of tizanidine. The stroke patient's FIM score improved only from 74 to 79 after 4 weeks of tizanidine. The patient with MS improved from 83 to 101 after 6 days of tizanidine. All 3 patients had almost full resolution of the intention myoclonus. All continued on tizanidine except the patient with stroke, who had minimal gains and a low systolic blood pressure. None of the patients experienced significant sedation or hypotension. CONCLUSIONS: Tizanidine may be a safe and effective option for treating intention myoclonus that occurs in a variety of neurologic conditions.