SENSORY AND MOTOR PROCESSING

感觉和运动处理。 衰老与运动功能的逐渐下降有关，这不仅影响老年人的生活质量，而且使他们容易发生导致住院时间延长的事故。 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）的标志之一，但尚不清楚是否有类似的机制导致两个人群的运动功能恶化。 中枢神经系统适当调节反射肌活动的能力改变与老年人和PD患者的强直、运动迟缓和运动精度丧失的发病机制有关。 特别是，施加关节位移（称为M2组件）引起的长潜伏期反射肌肉活动的初始段在两个人群中显着增强。 在上肢远端肌肉中诱发的M2反应部分由通过初级运动皮层的经皮层通路介导。 本研究的主要目的是检查：（1）机械感受性传入反馈的感觉运动皮层处理的改变是否有助于老年人和PD患者的运动控制受损，以及（2）介导这些损伤的病理生理机制在两个人群中是否相似。 我们将研究的完整性，经皮质通路的老年人（年龄大于65岁），中年PD患者（年龄小于50岁），对照组年龄匹配的PD患者，通过记录肌电图反应和脑电位引起的扭矩电机施加位移的手腕。 将使用偶极子源分析对头皮表面上记录的脑电位源的位置、定时和幅度进行建模。通过记录正中神经刺激的体感诱发电位和经颅磁刺激在初级运动皮层上诱发的肌肉收缩，进一步检查经皮层反馈回路时间。 我们假设，经皮质通路是完整的，但在老年人受到轴突和传导延迟，而感觉运动传导时间是正常的，在中年PD患者，但经皮质通路是功能障碍，由于在初级运动皮层内的神经元突触输入的改变。

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.