Synnot Anneliese, Chau Marisa, Pitt Veronica, O'Connor Denise, Gruen Russell L, Wasiak Jason, Clavisi Ornella, Pattuwage Loyal, Phillips Kate
Cochrane Australia, School of Public Health and Preventive Medicine, Monash University, L4 551 St Kilda Rd, Melbourne, Victoria, Australia, 3004.
Cochrane Database Syst Rev. 2017 Nov 22;11(11):CD008929. doi: 10.1002/14651858.CD008929.pub2.
Skeletal muscle spasticity is a major physical complication resulting from traumatic brain injury (TBI), which can lead to muscle contracture, joint stiffness, reduced range of movement, broken skin and pain. Treatments for spasticity include a range of pharmacological and non-pharmacological interventions, often used in combination. Management of spasticity following TBI varies from other clinical populations because of the added complexity of behavioural and cognitive issues associated with TBI.
To assess the effects of interventions for managing skeletal muscle spasticity in people with TBI.
In June 2017, we searched key databases including the Cochrane Injuries Group Specialised Register, CENTRAL, MEDLINE (Ovid), Embase (Ovid) and others, in addition to clinical trials registries and the reference lists of included studies.
We included randomised controlled trials (RCTs) and cross-over RCTs evaluating any intervention for the management of spasticity in TBI. Only studies where at least 50% of participants had a TBI (or for whom separate data for participants with TBI were available) were included. The primary outcomes were spasticity and adverse effects. Secondary outcome measures were classified according to the World Health Organization International Classification of Functioning, Disability and Health including body functions (sensory, pain, neuromusculoskeletal and movement-related functions) and activities and participation (general tasks and demands; mobility; self-care; domestic life; major life areas; community, social and civic life).
We used standard methodological procedures expected by Cochrane. Data were synthesised narratively; meta-analysis was precluded due to the paucity and heterogeneity of data.
We included nine studies in this review which involved 134 participants with TBI. Only five studies reported between-group differences, yielding outcome data for 105 participants with TBI. These five studies assessed the effects of a range of pharmacological (baclofen, botulinum toxin A) and non-pharmacological (casting, physiotherapy, splints, tilt table standing and electrical stimulation) interventions, often in combination. The studies which tested the effect of baclofen and tizanidine did not report their results adequately. Where outcome data were available, spasticity and adverse events were reported, in addition to some secondary outcome measures.Of the five studies with results, three were funded by governments, charities or health services and two were funded by a pharmaceutical or medical technology company. The four studies without useable results were funded by pharmaceutical or medical technology companies.It was difficult to draw conclusions about the effectiveness of these interventions due to poor reporting, small study size and the fact that participants with TBI were usually only a proportion of the overall total. Meta-analysis was not feasible due to the paucity of data and heterogeneity of interventions and comparator groups. Some studies concluded that the intervention they tested had beneficial effects on spasticity, and others found no difference between certain treatments. The most common adverse event was minor skin damage in people who received casting. We believe it would be misleading to provide any further description of study results given the quality of the evidence was very low for all outcomes.
AUTHORS' CONCLUSIONS: The very low quality and limited amount of evidence about the management of spasticity in people with TBI means that we are uncertain about the effectiveness or harms of these interventions. Well-designed and adequately powered studies using functional outcome measures to test the interventions used in clinical practice are needed.
骨骼肌痉挛是创伤性脑损伤(TBI)导致的主要身体并发症,可导致肌肉挛缩、关节僵硬、活动范围减小、皮肤破损和疼痛。痉挛的治疗包括一系列药物和非药物干预措施,通常联合使用。由于TBI相关行为和认知问题的复杂性增加,TBI后痉挛的管理与其他临床人群不同。
评估干预措施对TBI患者骨骼肌痉挛的管理效果。
2017年6月,我们检索了主要数据库,包括Cochrane损伤组专业注册库、CENTRAL、MEDLINE(Ovid)、Embase(Ovid)等,此外还检索了临床试验注册库和纳入研究的参考文献列表。
我们纳入了评估TBI痉挛管理任何干预措施的随机对照试验(RCT)和交叉RCT。仅纳入至少50%参与者患有TBI(或可获得TBI参与者单独数据)的研究。主要结局是痉挛和不良反应。次要结局指标根据世界卫生组织《国际功能、残疾和健康分类》进行分类,包括身体功能(感觉、疼痛、神经肌肉骨骼和运动相关功能)以及活动和参与(一般任务和要求;移动性;自我护理;家庭生活;主要生活领域;社区、社会和公民生活)。
我们采用Cochrane预期的标准方法程序。数据进行叙述性综合;由于数据匮乏和异质性,无法进行荟萃分析。
本综述纳入了9项研究,涉及134名TBI患者。只有5项研究报告了组间差异,得出了105名TBI患者的结局数据。这5项研究评估了一系列药物(巴氯芬、肉毒杆菌毒素A)和非药物(石膏固定、物理治疗、夹板、倾斜台站立和电刺激)干预措施的效果,这些措施通常联合使用。测试巴氯芬和替扎尼定效果的研究未充分报告其结果。在可获得结局数据的情况下,除了一些次要结局指标外,还报告了痉挛和不良事件。
在有结果的5项研究中,3项由政府、慈善机构或卫生服务机构资助,2项由制药或医疗技术公司资助。4项没有可用结果的研究由制药或医疗技术公司资助。由于报告不佳、研究规模小以及TBI患者通常仅占总体总数的一部分,很难就这些干预措施的有效性得出结论。由于数据匮乏以及干预措施和对照人群的异质性,荟萃分析不可行。一些研究得出结论,他们测试的干预措施对痉挛有有益效果,而另一些研究发现某些治疗之间没有差异。最常见的不良事件是接受石膏固定者出现轻微皮肤损伤。鉴于所有结局的证据质量都非常低,我们认为对研究结果进行任何进一步描述都会产生误导。
关于TBI患者痉挛管理的证据质量极低且数量有限,这意味着我们不确定这些干预措施的有效性或危害。需要设计良好且有足够样本量的研究,使用功能结局指标来测试临床实践中使用的干预措施。