Efficacy of radial extracorporeal shock wave therapy compared with botulinum toxin type A injection in treatment of lower extremity spasticity in subjects with cerebral palsy: A randomized, controlled, cross-over study.
桡动脉体外休克治疗与 a型肉毒毒素注射治疗脑瘫受试者下肢痉挛的疗效比较: 一项随机、对照、交叉研究。
- 作者列表："Vidal X","Martí-Fàbregas J","Canet O","Roqué M","Morral A","Tur M","Schmitz C","Sitjà-Rabert M
OBJECTIVES:To investigate whether botulinum toxin type A (BTX-A) injection is more effective than radial extracorporeal shock wave therapy in reducing plantar flexor muscle spasticity in subjects with cerebral palsy. METHODS:A total of 68 subjects with cerebral palsy were randomly allocated to BTX-A injection (Group 1) or radial extracorporeal shock wave therapy (Group 2) (first experiment; E1). Outcome was evaluated using the Tardieu V1 and V3 stretches, at 3 weeks, 2 months (M2) and M3 after baseline. At M6 subjects in Group 1 received radial extracorporeal shock wave therapy and subjects in Group 2 received BTX-A injection (second experiment; E2); outcome was evaluated as in E1. Treatment success was defined as improvement in foot dorsiflexion ≥10° when performing the V3 stretch at M2 in both experiments. RESULTS:In both experiments mean V1 and V3 significantly improved over time. In E1 both treatments resulted in similar treatment success. In E2 fewer subjects treated with BTX-A injection reached the criteria of treatment success than did subjects treated with radial extracorporeal shock wave therapy, which was due to a carry-over effect from E1. No significant complications were observed. CONCLUSION:BTX-A injection is not superior to radial extracorporeal shock wave therapy in the treatment of plantar flexor muscle spasticity in subjects with cerebral palsy.
目的: 探讨 a型肉毒毒素 (BTX-A) 注射在减少脑瘫患者足底屈肌痉挛方面是否比放射状体外休克疗法更有效。 方法: 68 例脑瘫患者随机分为 BTX-A 注射组 (1 组) 和放射状体外休克治疗组 (2 组) (首次实验; E1)。在基线后 3 周、 2 个月 (M2) 和 M3 时，使用 Tardieu V1 和 V3 延伸评价结局。在 M6，第 1 组受试者接受径向体外休克治疗，第 2 组受试者接受 BTX-A 注射 (第二次实验; E2); 按 e1 评价结局。治疗成功定义为在两个实验中在 M2 处进行 V3 拉伸时足部背屈 ≥ 10 ° 的改善。 结果: 在两个实验中，平均 V1 和 V3 随时间显著改善。在 E1 中，两种治疗均获得相似的治疗成功。在 E2 中，接受 BTX-A 注射治疗的受试者比接受放射状体外休克治疗的受试者少达到治疗成功的标准，这是由于 e1 的延续效应。未观察到明显的并发症。 结论: BTX-A 注射治疗脑瘫患者足底屈肌痉挛状态并不优于桡动脉休克治疗。
METHODS::Multiple sclerosis (MS) is a chronic neurodegenerative disorder with clinical symptoms of neuroinflammation and demyelination in the central nervous system. Recently, herbal medicines are clinically effective against MS as the current disease-modifying drugs have limited effectiveness. Hence, the present study evaluated the therapeutic potential of Ocimum basilicum essential oil (OB) in ethidium bromide (EB)-induced cognitive deficits in the male rats. Further, the effect of OB (50, 100 and 200 μL/kg) was evaluated on EB-induced neuroinflammation, astrogliosis and mitochondrial dysfunction in the pre-frontal cortex (PFC) of the animals. The EB was injected through bilateral intracerebroventricular route into hippocampus to induce MS-like manifestations in the rats. OB (100 and 200 μL/kg) and Ursolic acid (UA) significantly reduced the EB-induced cognitive deficits in Morris water maze and Y-maze test paradigms. OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced neuroinflammation in terms of increase in the levels of pro-inflammatory cytokines (TNF-alpha and IL-6) in the rat PFC. Further, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced astrogliosis in terms of increase in the levels of GFAP (Glial fibrillary acidic protein) and Iba-1 (Ionized calcium binding adaptor molecule-1) in the rat PFC. In addition, OB (100 and 200 μL/kg) and UA significantly attenuated the EB-induced decrease in the mitochondrial function, integrity, respiratory control rate and ADP/O in the PFC of the rodents. Moreover, OB (100 and 200 μL/kg) and UA significantly reduced the EB-induced mitochondria-dependent apoptosis in the PFC of the rat. Hence, it can be presumed that OB could be a potential alternative drug candidate in the pharmacotherapy of MS.
METHODS::Sleep fragmentation is an increase in sleep-wake transitions without an overall decrease in total sleep time. Sleep fragmentation is well documented during acute and chronic hospitalization and can result in delirium and memory problems in children. Sleep fragmentation is also often noted in neurodevelopmental disorders. However, it is unclear how sleep fragmentation independent of disease affects brain development and function. We hypothesized that acute sleep fragmentation during the neonatal period in otherwise healthy animals would result in neuroinflammation and would be associated with abnormalities in cognitive development. The orbital shaker method was used to fragment sleep for 72 h in postnatal day 3 New Zealand white rabbit kits (fragmentation group). To control for maternal separation, the sham group was separated from the dam and maintained in the same conditions without undergoing sleep fragmentation. A naïve control group remained with the dam. Kits underwent behavioral testing with novel object recognition and spontaneous alternation T-maze tests at 2-3 weeks post-fragmentation and were sacrificed 3-50 days after fragmentation. Sleep fragmentation resulted in acute and chronic changes in microglial morphology in the hippocampus and cortex, and regional differences in mRNA expression of pro- and anti-inflammatory cytokines at 3, 7 and 50 days post-fragmentation. Impaired novel object recognition and a longer latency in T-maze task completion were noted in the fragmented kits. This was in spite of normalization of sleep architecture noted at 2 months of age in these kits. The results indicate that transient neonatal sleep fragmentation results in short-term and long-term immune alterations in the brain, along with diminished performance in cognitive tasks long-term.
METHODS:BACKGROUND:Deep brain stimulation (DBS) of the anterior nucleus of the thalamus (ANT) is a recently approved therapy for patients with drug-resistant epilepsy. To date, there is a poor understanding of the mechanism of action and lack of in vivo biomarkers. We propose a method for investigating the in vivo stimulation effects using blood-oxygen-level dependent (BOLD) MRI and present the brain activation pattern associated with ANT DBS. METHODS:Two patients undergoing ANT DBS for epilepsy underwent BOLD MRI using a block design after the DBS was programmed to alternate ON/OFF in 30 second blocks. The scanner was triggered utilizing surface electrophysiological recording to detect the DBS cycle. Nine total runs were obtained and were analyzed using a general linear model. RESULTS:Active ANT stimulation produced activation within several areas of the brain, including the thalamus, bilateral anterior cingulate and posterior cingulate cortex, precuneus, medial prefrontal cortex, amygdala, ventral tegmental area, hippocampus, striatum, and right angular gyrus. CONCLUSIONS:Utilizing block-design BOLD MRI, we were able to show widespread activation resulting from ANT DBS. Overlap with multiple areas of both the default mode and limbic networks was shown suggesting that these nodes may modulate the effect of seizure control with ANT DBS.