Background: This study investigated the cortical activation mechanism underlying locomotor control during healthy and hemiplegic walking.
Methods: A total of eight healthy individuals with right leg dominance (male patients, 75%; mean age, 40.06 ± 4.53 years) and six post-stroke patients with right hemiplegia (male patients, 86%; mean age, 44.41 ± 7.23 years; disease course, 5.21 ± 2.63 months) completed a walking task at a treadmill speed of 2 km/h and a functional electrical stimulation (FES)-assisted walking task, respectively. Functional near-infrared spectroscopy (fNIRS) was used to detect hemodynamic changes in neuronal activity in the bilateral sensorimotor cortex (SMC), supplementary motor area (SMA), and premotor cortex (PMC).
Results: fNIRS cortical mapping showed more SMC-PMC-SMA locomotor network activation during hemiplegic walking than during healthy gait. Furthermore, more SMA and PMC activation in the affected hemisphere was observed during the FES-assisted hemiplegic walking task than during the non-FES-assisted task. The laterality index indicated asymmetric cortical activation during hemiplegic gait, with relatively greater activation in the unaffected (right) hemisphere during hemiplegic gait than during healthy walking. During hemiplegic walking, the SMC and SMA were predominantly activated in the unaffected hemisphere, whereas the PMC was predominantly activated in the affected hemisphere. No significant differences in the laterality index were noted between the other groups and regions ( > 0.05).
Conclusion: An important feature of asymmetric cortical activation was found in patients with post-stroke during the walking process, which was the recruitment of more SMC-SMA-PMC activation than in healthy individuals. Interestingly, there was no significant lateralized activation during hemiplegic walking with FES assistance, which would seem to indicate that FES may help hemiplegic walking recover the balance in cortical activation. These results, which are worth verifying through additional research, suggest that FES used as a potential therapeutic strategy may play an important role in motor recovery after stroke.
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http://dx.doi.org/10.3389/fneur.2022.1044982 | DOI Listing |
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Institute for Human Neuroscience, Boys Town National Research Hospital, Boys Town, NE, USA; Department of Pharmacology & Neuroscience, Creighton University, Omaha, NE, USA; College of Medicine, University of Nebraska Medical Center (UNMC), Omaha, NE, USA. Electronic address:
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School of Biomedical Engineering, Tsinghua University, Beijing, China; School of Medicine, Shanghai University, Shanghai, China. Electronic address:
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Department of Pharmacology, Vanderbilt Brain Institute, Vanderbilt Center for Addiction Research, Vanderbilt University, Nashville, TN 37232, USA; Department of Anatomy, Cell Biology, & Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address:
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Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, Bronx, NY 10461, USA. Electronic address:
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Department of Psychology, University of Nevada, Reno, NV 89557, United States.
A neural theory of human lightness computation is described and computer-simulated. The theory proposes that lightness is derived from transient ON and OFF cell responses in the early visual pathways that have different characteristic neural gains and that are generated by fixational eye movements (FEMs) as the eyes transit luminance edges in the image. The ON and OFF responses are combined with corollary discharge signals that encode the eye movement direction to create directionally selective ON and OFF responses.
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