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.
