William De Doncker1, Katlyn E Brown2, Annapoorna Kuppuswamy3. 1. Department of Clinical and Movement Neuroscience, Institute of Neurology, University College London, UK. Electronic address: william.doncker.11@ucl.ac.uk. 2. Department of Clinical and Movement Neuroscience, Institute of Neurology, University College London, UK; University of Waterloo, Department of Kinesiology, Faculty of Applied Health Sciences, Waterloo, ON, Canada. 3. Department of Clinical and Movement Neuroscience, Institute of Neurology, University College London, UK.
Abstract
OBJECTIVES: Reduced corticospinal excitability at rest is associated with post-stroke fatigue (PSF). However, it is not known if corticospinal excitability prior to a movement is also altered in fatigue which may then influence subsequent behaviour. We hypothesized that the levels of PSF can be explained by differences in modulation of corticospinal excitability during movement preparation. METHODS: 73 stroke survivors performed an auditory reaction time task. Corticospinal excitability was measured using transcranial magnetic stimulation. Fatigue was quantified using the fatigue severity scale. The effect of time and fatigue on corticospinal excitability and reaction time was analysed using a mixed effects model. RESULTS: Those with greater levels of PSF showed reduced suppression of corticospinal excitability during movement preparation and increased facilitation immediately prior to movement onset (β = -0.0066, t = -2.22, p = 0.0263). Greater the fatigue, slower the reaction times the closer the stimulation time to movement onset (β = 0.0024, t = 2.47, p = 0.0159). CONCLUSIONS: Lack of pre-movement modulation of corticospinal excitability in high fatigue may indicate poor sensory processing supporting the sensory attenuation model of fatigue. SIGNIFICANCE: We take a systems-based approach and investigate the motor system and its role in pathological fatigue allowing us to move towards gaining a mechanistic understanding of chronic pathological fatigue.
OBJECTIVES: Reduced corticospinal excitability at rest is associated with post-stroke fatigue (PSF). However, it is not known if corticospinal excitability prior to a movement is also altered in fatigue which may then influence subsequent behaviour. We hypothesized that the levels of PSF can be explained by differences in modulation of corticospinal excitability during movement preparation. METHODS: 73 stroke survivors performed an auditory reaction time task. Corticospinal excitability was measured using transcranial magnetic stimulation. Fatigue was quantified using the fatigue severity scale. The effect of time and fatigue on corticospinal excitability and reaction time was analysed using a mixed effects model. RESULTS: Those with greater levels of PSF showed reduced suppression of corticospinal excitability during movement preparation and increased facilitation immediately prior to movement onset (β = -0.0066, t = -2.22, p = 0.0263). Greater the fatigue, slower the reaction times the closer the stimulation time to movement onset (β = 0.0024, t = 2.47, p = 0.0159). CONCLUSIONS: Lack of pre-movement modulation of corticospinal excitability in high fatigue may indicate poor sensory processing supporting the sensory attenuation model of fatigue. SIGNIFICANCE: We take a systems-based approach and investigate the motor system and its role in pathological fatigue allowing us to move towards gaining a mechanistic understanding of chronic pathological fatigue.