Peter S Myers1, Marie E McNeely2, Kristen A Pickett3, Ryan P Duncan4, Gammon M Earhart5. 1. Program in Physical Therapy, Washington University in St. Louis School of Medicine, Campus Box 8502, 4444 Forest Park Blvd, Suite 11101, St. Louis, MO 63108, USA. Electronic address: petersmyers@wustl.edu. 2. Program in Physical Therapy, Washington University in St. Louis School of Medicine, Campus Box 8502, 4444 Forest Park Blvd, Suite 11101, St. Louis, MO 63108, USA; Department of Neurology, Washington University in St. Louis School of Medicine, Campus Box 8111, 660 S. Euclid, St. Louis, MO 63110, USA. Electronic address: mcneelym@wustl.edu. 3. Occupational Therapy Program, Department of Kinesiology, University of Wisconsin- Madison School of Education, Unit II Gym, 2000 Observatory Drive, Madison, WI 53706, USA. Electronic address: kristen.pickett@wisc.edu. 4. Program in Physical Therapy, Washington University in St. Louis School of Medicine, Campus Box 8502, 4444 Forest Park Blvd, Suite 11101, St. Louis, MO 63108, USA; Department of Neurology, Washington University in St. Louis School of Medicine, Campus Box 8111, 660 S. Euclid, St. Louis, MO 63110, USA. Electronic address: duncanr@wustl.edu. 5. Program in Physical Therapy, Washington University in St. Louis School of Medicine, Campus Box 8502, 4444 Forest Park Blvd, Suite 11101, St. Louis, MO 63108, USA; Department of Neurology, Washington University in St. Louis School of Medicine, Campus Box 8111, 660 S. Euclid, St. Louis, MO 63110, USA; Department of Neuroscience, Washington University in St. Louis School of Medicine, Campus Box 8108, 660 S. Euclid, St. Louis, MO 63110, USA. Electronic address: earhartg@wustl.edu.
Abstract
INTRODUCTION: Exercise improves gait in Parkinson disease (PD), but whether exercise differentially affects people with PD with (freezers) and without freezing of gait (non-freezers) remains unclear. This study examines exercise's effects on gait performance, neural correlates related to these effects, and potential neural activation differences between freezers and non-freezers during motor imagery (MI) of gait. METHODS: Thirty-seven participants from a larger exercise intervention completed behavioral assessments and functional magnetic resonance imaging (fMRI) scans before and after a 12-week exercise intervention. Gait performance was characterized using gait velocity and stride length, and a region of interest (ROI) fMRI analysis examined task-based blood oxygen-level dependent (BOLD) signal changes of the somatomotor network (SMN) during MI of forward (IMG-FWD) and backward (IMG-BWD) gait. RESULTS: Velocity (F(1,34) = 55.04, p < 0.001) and stride length (F(1,34) = 77.58, p < 0.001) were significantly lower for backward versus forward walking in all participants. The ROI analysis showed freezers had lower BOLD signal compared to non-freezers in the cerebellum (F(1,32) = 7.01, p = 0.01), primary motor (left: F(1,32) = 7.09, p = 0.01; right: F(1,32) = 7.45, p = 0.01), and primary sensory (left: F(1,32) = 9.59, p = 0.004; right: F(1,32) = 8.18, p = 0.007) cortices during IMG-BWD only. The evidence suggests the exercise intervention did not affect gait or BOLD signal during MI. CONCLUSION: While all participants had significantly slower and shorter backward velocity and stride length, respectively, the exercise intervention had no effect. Similarly, BOLD signal during MI did not change with exercise; however, freezers had significantly lower BOLD signal during IMG-BWD compared to non-freezers. This suggests potential decreased recruitment of the SMN during MI of gait in freezers.
INTRODUCTION: Exercise improves gait in Parkinson disease (PD), but whether exercise differentially affects people with PD with (freezers) and without freezing of gait (non-freezers) remains unclear. This study examines exercise's effects on gait performance, neural correlates related to these effects, and potential neural activation differences between freezers and non-freezers during motor imagery (MI) of gait. METHODS: Thirty-seven participants from a larger exercise intervention completed behavioral assessments and functional magnetic resonance imaging (fMRI) scans before and after a 12-week exercise intervention. Gait performance was characterized using gait velocity and stride length, and a region of interest (ROI) fMRI analysis examined task-based blood oxygen-level dependent (BOLD) signal changes of the somatomotor network (SMN) during MI of forward (IMG-FWD) and backward (IMG-BWD) gait. RESULTS: Velocity (F(1,34) = 55.04, p < 0.001) and stride length (F(1,34) = 77.58, p < 0.001) were significantly lower for backward versus forward walking in all participants. The ROI analysis showed freezers had lower BOLD signal compared to non-freezers in the cerebellum (F(1,32) = 7.01, p = 0.01), primary motor (left: F(1,32) = 7.09, p = 0.01; right: F(1,32) = 7.45, p = 0.01), and primary sensory (left: F(1,32) = 9.59, p = 0.004; right: F(1,32) = 8.18, p = 0.007) cortices during IMG-BWD only. The evidence suggests the exercise intervention did not affect gait or BOLD signal during MI. CONCLUSION: While all participants had significantly slower and shorter backward velocity and stride length, respectively, the exercise intervention had no effect. Similarly, BOLD signal during MI did not change with exercise; however, freezers had significantly lower BOLD signal during IMG-BWD compared to non-freezers. This suggests potential decreased recruitment of the SMN during MI of gait in freezers.
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