Dietz V
Swiss Paraplegic Centre, University Hospital Balgrist, Zurich, Switzerland.
Electroencephalogr Clin Neurophysiol. 1997 Sep;103(3):333-55. doi: 10.1016/s0013-4694(97)00047-7.
This article will review those electrophysiological investigations which have addressed the neuronal mechanisms underlying impaired gait. The aims of the review are to provide further insights to the underlying pathophysiology of impaired gait and also towards the selection of an appropriate treatment. From the patients' point of view the first indication of a central motor system lesion is an impairment of movement, most notably locomotion. These symptoms are characteristic in cases of spasticity, cerebellar lesion or Parkinson's disease. Clinical examination reveals typical changes in tendon tap reflexes and muscle tone which were believed to account for the movement disorder presented. However, we now know that there is only a weak relationship between the physical symptoms observed during clinical examination under passive motor conditions and the altered neuronal mechanisms underlying the impairment during active motion. By recording and analysing electrophysiological and biomechanical parameters during functional movements such as locomotion, the significance of impaired reflex behaviour or the pathophysiology of muscle tone and its contribution to the movement disorder can be reliably assessed. Consequently, the treatment should not be cosmetic, i.e. the correction of an isolated clinical parameter, but should be based on the pathophysiology and significance of those mechanisms underlying the impairment of the patients' movements. Data from electrophysiological and biomechanical investigations of locomotion of patients with spasticity, cerebellar disorder or Parkinson's disease are discussed in this review. The neuronal mechanisms, which are essentially central programs and afferent input, involved in disorders of gait are evaluated on the basis of their function in healthy subjects. The impact of this analysis in deciding an appropriate treatment are discussed with respect to the pathophysiology underlying the gait disorder (spasticity, cerebellar disorder or Parkinson's disease). At the present time we have only a basic understanding of the essential receptor systems, such as leg extensor load receptors, and their interaction with other systems involved in postural control. In the future, the knowledge gained from gait analysis may help in the selection of the appropriate pharmacological and physical treatment required even though the patient may only be at an early stage of motor impairment.
本文将回顾那些针对步态受损背后神经元机制的电生理研究。该综述的目的是进一步深入了解步态受损的潜在病理生理学，并为选择合适的治疗方法提供参考。从患者的角度来看，中枢运动系统病变的首个迹象是运动障碍，最明显的是行走能力受损。这些症状在痉挛、小脑病变或帕金森病病例中很典型。临床检查揭示了腱反射和肌张力的典型变化，人们曾认为这些变化可以解释所呈现的运动障碍。然而，我们现在知道，在被动运动条件下临床检查所观察到的身体症状与主动运动时受损背后改变的神经元机制之间只有微弱的关系。通过记录和分析诸如行走等功能性运动过程中的电生理和生物力学参数，可以可靠地评估反射行为受损的意义、肌张力的病理生理学及其对运动障碍的影响。因此，治疗不应只是表面的，即纠正单一的临床参数，而应基于患者运动受损背后那些机制的病理生理学和意义。本文综述了对痉挛、小脑疾病或帕金森病患者行走进行电生理和生物力学研究的数据。基于其在健康受试者中的功能，评估了参与步态障碍的神经元机制，这些机制主要是中枢程序和传入输入。针对步态障碍（痉挛、小脑疾病或帕金森病）背后的病理生理学，讨论了该分析在决定合适治疗方法方面的影响。目前，我们对诸如腿部伸肌负荷感受器等基本受体系统及其与参与姿势控制的其他系统的相互作用只有基本的了解。未来，即使患者可能仅处于运动障碍的早期阶段，从步态分析中获得的知识也可能有助于选择所需的合适药物和物理治疗方法。
