Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy
Comparative analysis of gait in Parkinson's disease, cerebellar ataxia and subcortical arteriosclerotic encephalopathy
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DOI：
10.1093/brain/122.7.1349
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发表时间：
1999-07-01
期刊：
影响因子：
14.5
通讯作者：
Poewe, W
中科院分区：
文献类型：
--
作者：
Ebersbach, G;Sojer, M;Poewe, W
定量步态分析已被用来阐明神经步态障碍的特征。尽管许多研究比较了单个患者组与对照组，但只有少数研究比较了影响步态的不同神经系统疾病患者之间的步态参数。在本研究中，步态参数之间进行了比较，对照组，帕金森病患者的帕金森步态由于特发性帕金森病，受试者患有小脑共济失调和步态障碍由于皮质下动脉硬化性脑病，除了记录基线参数在首选的步行速度，受试者被要求改变速度从非常慢到非常快。然后将每个受试者的速度和步长值用于线性回归分析。尽管所有患者组在首选行走期间进行评估时，与健康对照组相比，行走速度较慢，步长减少，但共济失调和皮质下动脉硬化性脑病患者的振幅和步长变异性增加。回归分析表明，随着速度的变化，帕金森病患者的步幅变化与对照组相同。与此相反，共济失调和皮质下动脉硬化性脑病的患者在速度增加时步幅的贡献不成比例。而帕金森病患者的研究结果可以解释为力增益的减少，共济失调和皮质下动脉脑病患者的观察结果反映了时空步态策略的改变，以补偿不稳定性。皮质下动脉硬化性脑病和小脑性共济失调步态障碍的相似性提示了共同的机制。
Quantitative gait analysis has been used to elucidate characteristic features of neurological gait disturbances. Although a number of studies compared single patient groups with controls, there are only a few studies comparing gait parameters between patients with different neurological disorders affecting gait. In the present study, gait parameters were compared between control subjects, patients with parkinsonian gait due to idiopathic Parkinson's disease, subjects suffering from cerebellar ataxia and patients with gait disturbance due to subcortical arteriosclerotic encephalopathy, In addition to recording of baseline parameters during preferred walking velocity, subjects were required to vary velocity from very slow to very fast. Values of velocity and stride length from each subject were then used for linear regression analysis. Whereas all patient groups showed slower walking velocity and reduced step length compared with healthy controls when assessed during preferred walking, patients with ataxia and subcortical arteriosclerotic encephalopathy had, in addition, increased variability of amplitude and timing of steps. Regression analysis showed that with changing velocity, subjects with Parkinson's disease changed their stride length in the same proportion as that measured in controls. In contrast, patients with ataxia and subcortical arteriosclerotic encephalopathy bad a disproportionate contribution of stride length when velocity was increased. Whereas the findings in patients with Parkinson's disease can be explained as a reduction of force gain, the observations for patients with ataxia and subcortical arteriosclerotic encephalolpathy reflect an altered spatiotemporal gait strategy in order to compensate for instability. The similarity of gait disturbance in subcortical arteriosclerotic encephalopathy and cerebellar ataxia suggests common mechanisms.