Browsing by Author "Popa, Traian"

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    Multimodal neuroimaging of fatigability development
    (2025) Bedard, Patrick; Knutson, Kristine; McGurrin, Patrick; Vial Undurraga, Felipe; Popa, Traian; Horovitz, Silvina; Hallett, Mark; Nath, Avindra; Walitt, Brian
    Fatigability refers to the inability of the neuromuscular system to generate enough force to produce movements to meet task challenges. Fatigability has a central and a peripheral component linked via the neuromuscular system, but how these two components interact as fatigue develops lacks a complete understanding. The effects of fatigability are experienced in healthy humans but also accompany various disorders, often exacerbating their symptoms. We studied how fatigability develops in the neuromuscular system using multimodal neuroimaging. We recruited healthy participants to perform a fatiguing grip force task, while recording force, electromyography of forearm muscles (EMG), electroencephalography (EEG), and functional magnetic resonance imaging (fMRI) in 30-second blocks of grip task alternating with 30 seconds of rest. The task entailed maintaining 50% of the maximum force. We combined EMG and EEG to compute corticomuscular coherence and combined EEG and fMRI to compute EEG-informed fMRI. We selected eight task blocks specific to each participant to represent how the neuromuscular system adapted from pre-fatigability to actual fatigability. Those included five blocks for pre-fatigability in which participants could generate enough force to match the required 50% of maximum force and three blocks when the force fell below that limit. Across blocks of the grip force task, we observed changes in the neuromuscular system that preceded grip force changes. We found that electromyography of arm muscles shifted from high to low frequency, EEG in the channel covering the contralateral sensorimotor area increased steadily up to the fifth block and then plateaued, and fMRI signal also increased in the cerebellum. Corticomuscular coherence increased within each of the 30-second blocks of the grip task. EEG-informed fMRI revealed areas of the brain that the traditional regression did not, including the bilateral sensorimotor cortex, temporal-parietal junction, and supplementary motor area. Thus, as fatigability developed, the neuromuscular system experienced changes earlier than the actual behavior. While we found evidence for fatigability of central and peripheral origins, peripheral fatigue seems to occur first.
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    The role of the inferior parietal lobule in writer’s cramp
    (2020) Merchant, Shabbir Hussain I.; Frangos, Eleni; Parker, Jacob; Bradson, Megan; Wu, Tianxia; Vial-Undurraga, Felipe; Leodori, Giorgio; Bushnell, M.C.; Horovitz, Silvina G.; Hallett, Mark; Popa, Traian
    Humans have a distinguishing ability for fine motor control that is subserved by a highly evolved cortico-motor neuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. Task-specific dystonia can be viewed as a corruption or loss of motor control confined to a single motor skill. Using a multimodal experimental approach combining neuroimaging and non-invasive brain stimulation, we explored interactions between the principal nodes of the fine motor control network in patients with writer’s cramp and healthy matched controls. Patients and healthy volunteers underwent clinical assessment, diffusion-weighted MRI for tractography, and functional MRI during a finger tapping task. Activation maps from the task-functional MRI scans were used for target selection and neuronavigation of the transcranial magnetic stimulation. Single- and double-pulse TMS evaluation included measurement of the inputoutput recruitment curve, cortical silent period, and amplitude of the motor evoked potentials conditioned by cortico-cortical interactions between premotor ventral (PMv)-motor cortex (M1), anterior inferior parietal lobule (aIPL)-M1, and dorsal inferior parietal lobule (dIPL)-M1 before and after inducing a long term depression-like plastic change to dIPL node with continuous thetaburst transcranial magnetic stimulation in a randomized, sham-controlled design. Baseline dIPL-M1 and aIPL-M1 cortico-cortical interactions were facilitatory and inhibitory, respectively, in healthy volunteers, whereas the interactions were converse and significantly different in writer’s cramp. Baseline PMv-M1 interactions were inhibitory and similar between the groups. The dIPL-PMv resting state functional connectivity was increased in patients compared to controls, but no differences in structural connectivity between the nodes were observed. Cortical silent period was significantly prolonged in writer’s cramp. Making a long term depression- like plastic change to dIPL node transformed the aIPL-M1 interaction to inhibitory (similar to healthy volunteers) and cancelled the PMv-M1 inhibition only in the writer’s cramp group. These findings suggest that the parietal multimodal sensory association region could have an aberrant downstream influence on the fine motor control network in writer’s cramp, which could be artificially restored to its normal function.

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