SENSORY AND MOTOR PROCESSING

感觉和运动加工。衰老与运动功能的进行性下降有关，这不仅会损害老年人的生活质量，还会使他们容易发生导致长期住院的事故。运动功能障碍包括运动减慢(运动迟缓)、肌肉僵硬(僵硬)以及步态和姿势控制障碍。类似的运动障碍是帕金森病(PD)的特征之一，但目前尚不清楚是否相似的机制导致两个人群的运动功能恶化。在老年人和帕金森病患者中，中枢神经系统适当调节反射肌肉活动的能力改变与僵直、运动迟缓和运动精确度丧失的发病机制有关。特别是，由关节移位引起的长潜伏期反射肌肉活动的起始段(称为M2成分)在两个人群中都显著增强。在上肢远端肌肉中诱发的M2反应，部分是通过初级运动皮质的跨皮质通路来调节的。本研究的主要目的是检验：(1)机械感受性传入反馈的感觉运动皮质处理的改变是否有助于老年人和帕金森病患者的运动控制受损，以及(2)在这两个人群中，调节这些损害的病理生理学机制是否相似。我们将通过记录腕部扭矩运动施加的位移引起的肌电反应和脑电位，在一组老年受试者(年龄大于65岁)、中年帕金森病患者(年龄小于50岁)和与帕金森病患者年龄匹配的对照组受试者中检查经皮质通路的完整性。记录在头皮表面上的大脑电位的来源的位置、时间和大小将使用偶极子来源分析来建模。通过记录正中神经刺激的体感诱发电位，以及经颅磁刺激在初级运动皮质上诱发的肌肉收缩，将进一步检查跨皮质反馈回路时间。我们假设，老年人的跨皮质通路是完整的，但受到轴突和传导延迟的影响，而中年帕金森病患者的感觉运动传导时间是正常的，但由于初级运动皮质内神经元的突触输入改变，跨皮质通路功能障碍。

Sensory and Motor Processing. Aging is associated with a progressive decline in motor function that not only compromises the quality of life in the elderly, but also predisposes them to accidents that result in prolonged hospitalization. Impairments in motor function include slowing of movement (bradykinesia), muscle stiffness (rigidity), and impairments in gait and postural control. Comparable motor impairments are among the hallmarks of Parkinson disease (PD), yet it is not known if similar mechanisms contribute to the deterioration of motor function in both populations. Alterations in the ability of the central nervous system to appropriately modulate reflex muscle activity have been implicated in the pathogenesis of rigidity, bradykinesia, and loss of movement precision in both the elderly and patients with PD. In particular, the initial segment of the long-latency reflex muscle activity evoked by imposed joint displacements (termed the M2 component) is markedly enhanced in both populations. The M2 response evoked in distal muscles of the upper limb is mediated, in part, by a transcortical pathway through the primary motor cortex. The primary objectives of this study are to examine: (1) if alterations in sensorimotor cortical processing of mechanoreceptive afferent feedback contribute to impaired movement control in the elderly and patients with PD, and (2) if the pathophysiological mechanisms mediating these impairments are similar in both populations. We will examine the integrity of the transcortical pathway in a population of elderly subjects (age greater than 65 years), middle-aged patients with PD (age less than 50 years), and control subjects age-matched to the PD patients, by recording the EMG responses and cerebral potentials evoked by torque motor-imposed displacements of the wrist. The location, timing, and magnitude of sources contributing to the cerebral potentials recorded on the scalp surface will be modeled using dipole source analysis. Transcortical feedback loop times will be further examined by recording somatosensory evoked potentials to median nerve stimulation, and muscle contractions evoked by transcranial magnetic stimulation over the primary motor cortex. We hypothesize that the transcortical pathway is intact in the elderly but compromised by axonal and conduction delays, whereas sensorimotor conduction times are normal in middle-aged patients with PD, but the transcortical pathway is dysfunctional due to alterations in synaptic input to neurons within the primary motor cortex.