Abstract
Central Vs. Peripheral Manifestations of Neuromuscular Force in Persons With Parkinson's Disease. Parkinson's disease (PD) is a central nervous system disorder that results in several symptoms including reduced neuromuscular strength and bradykinesia. PURPOSE: The purpose of this study was to quantify the neurological deficiencies in persons with PD and observe the sources of reduced strength and rate of force development in this population using superimposed electrical stimulation. METHODS: Seven men and seven women with idiopathic PD (age 65.4 ± 7.3y, disease duration 7.9 ± 5.Oy, Hoehn and Yahr 1.5-2) participated. Six neurologically healthy, age-matched men and women (age 60.5 ± 4.9) were recruited for the control group. The subjects were seated in a customized chair, and seatbelt restraints were placed across the subject's trunk and lap to minimize movement of the torso. Rubber stimulating electrodes were secured over the femoral triangle and just proximal to the superior border of the patella. The subject's right leg was inserted into a padded sleeve and then an ankle cuff, and attached to the load cell with enough tension to eliminate slack. The subject was instructed to cross their arms over their chest for each trial. The subject was instructed to relax and then was given a 200µ3 triplet pulse of 5OmA at 400V to the quadriceps femoris (QF). The amperage was increased in 5OmA increments until the peak force reached a plateau. An octet pulse was administered at the peak force parameters to identify maximal involuntary rate of force development (MIRFD). After adequate rest, the subject was instructed to perform a maximal voluntary contraction (MVC) of the QF of their restrained leg. Following familiarization, two MVCs were performed. The maximal voluntary rate of force development (MVRFD) was calculated as the maximum velocity of the signal (N/s) during the rise phase of the MVC Start of the action was defined as the point at which the first derivative of the filtered force signal crossed zero for the last time. The rate of force development ratio (RFDR) was calculated as RFDR = MVRFD/MIRFD. The subject was asked to perform an MVC where the predetermined triplet pulse was applied during the plateau phase. The MVC with stimulation trial was repeated twice. RESULTS: We found significant differences between groups in MVRFD (PD = 2544.7N/S ± 1183.6, CTRL = 4598.9 ± 1 076.8; ? = 0.008) and RFDR (PD = 0.45 ± 0.1 5, CTRL = 0.80 ± 0.20; ? = 0.004), with the PD group having reduced scores compared to controls. No other significant differences were found between groups. Large effect sizes were found for RFDR (d = 2.03) and MVRFD (d = 1.82). CONCLUSIONS: Because MIRFD was not different between PD and controls, the mechanisms responsible for the deficit in RFD must be purely central in nature early in the disease. The PESinduced activation of the QF demonstrates the peripheral ability of the muscles to function, but the individuals with PD were not able to actively replicate the voluntary rate of force development of healthy controls. Practical Applications: PES could enable quantitative measures of involuntary activation for the manipulation of numerous variables ranging from medication dose to the effects of exercise training programs in PD. Using PES for pre- and post-testing in training interventions would provide quantifiable assessments for evaluating training protocols for persons with PD. [PUBLICATION ABSTRACT]