Altered patterns of reflex excitability, balance, and locomotion following spinal cord injury and locomotor training.
Altered patterns of reflex excitability, balance, and locomotion following spinal cord injury and locomotor training.
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DOI：
10.3389/fphys.2012.00258
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发表时间：
2012
影响因子：
4
通讯作者：
Thompson FJ
中科院分区：
文献类型：
--
作者：
Bose PK;Hou J;Parmer R;Reier PJ;Thompson FJ
痉挛是许多脊髓损伤(SCI)患者日常生活中的一个重要问题。虽然之前对人类和动物的研究表明，跑步机运动训练显著改善了运动能力，但运动训练对痉挛的影响程度尚不清楚。此外，了解更符合人体工程学的周期训练与跑步机训练相比如何在治疗脊髓损伤诱发的痉挛和改善运动功能方面具有相当大的实际意义。因此，我们目前研究的主要目的是评估不同类型的运动训练对肢体痉挛、步态和影响运动的反射成分的测量的影响。在这些研究中，30只动物接受了标准的多中心动物脊髓损伤研究(MASSCIS)方案的中胸脊髓损伤(10 g 2.5 cm体重下降)。将受试者随机分为三组：对照组(非训练组)、跑步机训练组和自行车训练组。在伤后第8天开始进行跑步机和自行车训练。测试不同速度范围(612°-49°/S)的踝关节速度相关扭矩，以量化强直(低速)和动态(高速)对肢体痉挛的贡献。在损伤后第4周和第6周，与手术前控制值相比，未训练组显示出显著的速度依赖性踝伸肌痉挛。在受伤后的这些时间点，两个训练组中的任何一个都没有观察到痉挛。相反，在4个最快的踝关节旋转速度(350~612°/S)下，跑步机训练组和自行车训练组在挫伤后8~12周检测到明显较轻的速度依赖性痉挛。与未接受训练的对照组相比，使用跑步机或自行车进行运动训练还显著提高了肢体放置措施(肢体轴线、支撑底座和开阔场地运动能力)和反射率抑制的恢复率，反射率抑制是对调节节段性反射兴奋性的神经生理过程的定量评估。对备用组织的光镜定性研究显示，在两种运动训练的动物中，髓鞘、轴突和胶原的形态都得到了更好的保存。两个运动训练组都显示病变体积减小(吻尾延伸)，病变部位有更多的备用组织。这些改善伴随着BDNF、GABA/GABAB和单胺类物质(如去甲肾上腺素和5-羟色胺)的显著上调，这可能是这些功能改善的原因。这些数据首次表明，在动物模型中，符合人体工程学的实用周期训练在减少脊髓损伤后痉挛和改善运动能力方面与更劳动密集型的跑步机训练的疗效相当。
Spasticity is an important problem that complicates daily living in many individuals with spinal cord injury (SCI). While previous studies in human and animals revealed significant improvements in locomotor ability with treadmill locomotor training, it is not known to what extent locomotor training influences spasticity. In addition, it would be of considerable practical interest to know how the more ergonomically feasible cycle training compares with treadmill training as therapy to manage SCI-induced spasticity and to improve locomotor function. Thus the main objective of our present studies was to evaluate the influence of different types of locomotor training on measures of limb spasticity, gait, and reflex components that contribute to locomotion. For these studies, 30 animals received midthoracic SCI using the standard Multicenter Animal Spinal cord Injury Studies (MASCIS) protocol (10 g 2.5 cm weight drop). They were divided randomly into three equal groups: control (contused untrained), contused treadmill trained, and contused cycle trained. Treadmill and cycle training were started on post-injury day 8. Velocity-dependent ankle torque was tested across a wide range of velocities (612–49°/s) to permit quantitation of tonic (low velocity) and dynamic (high velocity) contributions to lower limb spasticity. By post-injury weeks 4 and 6, the untrained group revealed significant velocity-dependent ankle extensor spasticity, compared to pre-surgical control values. At these post-injury time points, spasticity was not observed in either of the two training groups. Instead, a significantly milder form of velocity-dependent spasticity was detected at postcontusion weeks 8–12 in both treadmill and bicycle training groups at the four fastest ankle rotation velocities (350–612°/s). Locomotor training using treadmill or bicycle also produced significant increase in the rate of recovery of limb placement measures (limb axis, base of support, and open field locomotor ability) and reflex rate-depression, a quantitative assessment of neurophysiological processes that regulate segmental reflex excitability, compared with those of untrained injured controls. Light microscopic qualitative studies of spared tissue revealed better preservation of myelin, axons, and collagen morphology in both locomotor trained animals. Both locomotor trained groups revealed decreased lesion volume (rostro-caudal extension) and more spared tissue at the lesion site. These improvements were accompanied by marked upregulation of BDNF, GABA/GABAb, and monoamines (e.g., norepinephrine and serotonin) which might account for these improved functions. These data are the first to indicate that the therapeutic efficacy of ergonomically practical cycle training is equal to that of the more labor-intensive treadmill training in reducing spasticity and improving locomotion following SCI in an animal model.
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影响因子：
168.9
作者：
DIETZ, V;COLOMBO, G;JENSEN, L
通讯作者：
JENSEN, L
DOI：
10.1016/0168-5597(93)90131-8
发表时间：
1993-06-01
期刊：
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY
影响因子：
--
作者：
CALANCIE, B;BROTON, JG;AYYAR, DR
通讯作者：
AYYAR, DR
影响因子：
5.3
作者：
Bose, P;Parmer, R;Thompson, FJ
通讯作者：
Thompson, FJ
影响因子：
2.5
作者：
de Leon, RD;Hodgson, JA;Edgerton, VR
通讯作者：
Edgerton, VR
影响因子：
3.2
作者：
Behmran, AL;Harkema, SJ
通讯作者：
Harkema, SJ