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S11-3. Neurophysiological basis of body-weight supported step training
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Society Proceedings / Clinical Neurophysiology 124 (2013) e19–e38
studies are limited: single photon emission tomography (SPECT), positron emission tomography (PET) and near-infrared spectroscopy (NIRS). These techniques allow us to measure blood perfusion or oxygenation information during actual walking, and have shown the roles of cortical motor areas (especially supplementary motor areas), basal ganglia and cerebellum in control of walking. Several studies have examined pathophysiological changes in gait-disturbed patients. However, they have limitations and drawbacks such as radiation exposure (SPECT/PET) and vulnerability to motion artifacts and contamination of non-brain signals (NIRS). An emerging neuroimaging protocol to study neural mechanisms of gait is functional magnetic resonance imaging (fMRI) using walking imagery as a behavioral paradigm. Interestingly, many fMRI studies with walking imagery paradigms reported activity in the dorsal brainstem, which might correspond to the midbrain locomotor centers and/or pedunculopontine nucleus known as important structure controlling walking in experimental animals. It is important to characterize those brainstem activities during walking imagery more precisely than now, and to explore their roles in actual walking or pathophysiology underlying walking difficulty. doi:10.1016/j.clinph.2013.02.047
S11-2. The effects of walking exercises on spinal cord injury— Masahiko Mukaino, Shoichi Tashiro, Masaya Nakamura, Hideyuki Okano (Keio University School of Medicine, Tokyo, Japan) The aim of this study was to compare the functional effects of early and delayed interventions involving walking exercises with treadmills, using animal subjects. Contusive spinal cord injury (SCI) was made at the Th10 level in adult Sprague–Dawley rats, which were then assigned to one of the following conditions: control, early training (days 7 to 20), and delayed training (days 21 to 34). A significant increase in step height and step length was observed in the early-training group, while the delayed-training group showed no significant improvement. In addition, a reduction in synergic contraction was observed in electromyographic activity of the hind limb muscles, as well as a reduction in spastic muscle activities, but this was observed only in the early-training group. Immunohistochemical analysis of the lumbar spinal cord using synaptic markers showed a significant decrease in the inhibitory synapses and an increase in the excitatory synapses which were caused by an earlier start to training. Further studies are necessary to determine underlying mechanisms involved the above process. doi:10.1016/j.clinph.2013.02.048
S11-3. Neurophysiological basis of body-weight supported step training—Kimitaka Nakazawa (The University of Tokyo, Tokyo, Japan) The body-weight supported step training (BWSS) has been originally applied to individuals with spinal cord injury (SCI) on the basis of numerous experimental evidences indicating that the central pattern generator (CPG) of quadruped animals can be reorganized and allows those animals walk independently after BWSS training. However, beside the fact that the CPG alone cannot provide full weightbearing force and stepping in human, it is not known whether the other factors such as central command and sensory afferent information are involved in restoration of bipedal walking especially after incomplete SCI. To address this issue we have conducted a series of experiments, which aimed to reveal effects of both sensory inputs and descending commands on excitability modulation of neural circuits involving human bipedal locomotion. By using the Lokomat
robotic gait trainer, we tested effects of sensory inputs on corticospinal (CS) excitabilities during assisted stepping. The results so far demonstrate that sensory inputs, especially body-weight related somatosensory input, have a facilitatory effect on CS pathway of an ankle flexor muscle, whereas those sensory inputs regardless of body-weight related or not have an inhibitory effect on spinal stretch reflex circuits of upper and lower limb muscles during the assisted stepping. doi:10.1016/j.clinph.2013.02.049
S11-4. Efficacy and its neural mechanisms of neurorehabilitation for ataxic gait—Ichiro Miyai a, Noriaki Hattori a, Masahito Mihara a,b, Megumi Hatakenaka a, Hiroaki Fujimoto a, Teiji Kawano a, Hajime Yagura a (a Neurorehabilitation Research Institute, Morinomiya Hospital, Osaka, Japan, b Department of Neurology, Osaka University Medical School, Osaka, Japan) In degenerative cerebellar diseases, it is unclear whether patients can relearn motor sequences required for activities of daily living (ADLs) after neurorehabilitation since the cerebellum plays a crucial role in motor learning. It is also unknown whether functional gain can be sustained for a long period because of the progressive nature of the diseases. Thus Cerebellar Ataxia Rehabilitation (CAR) trial tested if intensive rehabilitation improved ataxia, gait and ADLs in 42 patients with degenerative cerebellar diseases. Intensive rehabilitation comprising 1-h physical and 1-h occupational therapy for 4 weeks significantly improved ataxia, gait speed and ADLs than control. The improvements in ataxia and gait speed were sustained at 12 weeks and 24 weeks after the intervention, respectively (Miyai I et al. Neurorehabil Neural Repair 2012;26:515–22). Neural mechanisms underlying functional improvement remain to be elucidated. Functional near-infrared spectroscopy studies have implied that recruitment of the prefrontal cortex and supplementary motor area are involved in improvement of gait and balance function as well as motor learning in patients with cerebellar damage (Mihara M et al. NeuroImage 2007;37:1338–45, Mihara M et al. NeuroImage 2008:43:329–33, Mihara M et al. NeuroReport 2012;23:314–19, Hatakenaka H et al. Neurorehabil Neural Repair 2012;26:293–300). doi:10.1016/j.clinph.2013.02.050
S12-1. MMN in psychological research – A study of change in MMN peak latencies—Seiji Tamakoshi (Kwansei Gakuin University, Nishinomiya, Japan) In order to investigate how sound representations are compressed in sensory memory, we examined mismatch negativity (MMN), ERP component reflecting neural representations in sensory memory. Yabe et al. (2005) showed that the MMNm peak latencies by reversing standards to deviants from oddball sequences did not reflect physical time flow, and they suggested that the temporal information could be compressed in sensory memory. However, it is not clear that factors of the asymmetrical change in MMN peak latencies. The experiment 1 compared the conditions of the stimuli that included a silence gap and it replaced by a tone segment which was decreased intensity. As a result, duplicates as the finding of Yabe et al., and it indicates that the whole stimulus duration rather than only gap duration is compressed in sensory memory. The experiment 2 showed that the stimuli’s saliency affects the peak latency of MMN, examined by changing in sound intensity. The experiment 3 that examined to effect of stimuli’s duration, suggested that stimuli’s temporal element and saliency affect the asymmetrical change in MMN peak latencies. These findings suggest the temporal element
Society Proceedings / Clinical Neurophysiology 124 (2013) e19–e38
studies are limited: single photon emission tomography (SPECT), positron emission tomography (PET) and near-infrared spectroscopy (NIRS). These techniques allow us to measure blood perfusion or oxygenation information during actual walking, and have shown the roles of cortical motor areas (especially supplementary motor areas), basal ganglia and cerebellum in control of walking. Several studies have examined pathophysiological changes in gait-disturbed patients. However, they have limitations and drawbacks such as radiation exposure (SPECT/PET) and vulnerability to motion artifacts and contamination of non-brain signals (NIRS). An emerging neuroimaging protocol to study neural mechanisms of gait is functional magnetic resonance imaging (fMRI) using walking imagery as a behavioral paradigm. Interestingly, many fMRI studies with walking imagery paradigms reported activity in the dorsal brainstem, which might correspond to the midbrain locomotor centers and/or pedunculopontine nucleus known as important structure controlling walking in experimental animals. It is important to characterize those brainstem activities during walking imagery more precisely than now, and to explore their roles in actual walking or pathophysiology underlying walking difficulty. doi:10.1016/j.clinph.2013.02.047
S11-2. The effects of walking exercises on spinal cord injury— Masahiko Mukaino, Shoichi Tashiro, Masaya Nakamura, Hideyuki Okano (Keio University School of Medicine, Tokyo, Japan) The aim of this study was to compare the functional effects of early and delayed interventions involving walking exercises with treadmills, using animal subjects. Contusive spinal cord injury (SCI) was made at the Th10 level in adult Sprague–Dawley rats, which were then assigned to one of the following conditions: control, early training (days 7 to 20), and delayed training (days 21 to 34). A significant increase in step height and step length was observed in the early-training group, while the delayed-training group showed no significant improvement. In addition, a reduction in synergic contraction was observed in electromyographic activity of the hind limb muscles, as well as a reduction in spastic muscle activities, but this was observed only in the early-training group. Immunohistochemical analysis of the lumbar spinal cord using synaptic markers showed a significant decrease in the inhibitory synapses and an increase in the excitatory synapses which were caused by an earlier start to training. Further studies are necessary to determine underlying mechanisms involved the above process. doi:10.1016/j.clinph.2013.02.048
S11-3. Neurophysiological basis of body-weight supported step training—Kimitaka Nakazawa (The University of Tokyo, Tokyo, Japan) The body-weight supported step training (BWSS) has been originally applied to individuals with spinal cord injury (SCI) on the basis of numerous experimental evidences indicating that the central pattern generator (CPG) of quadruped animals can be reorganized and allows those animals walk independently after BWSS training. However, beside the fact that the CPG alone cannot provide full weightbearing force and stepping in human, it is not known whether the other factors such as central command and sensory afferent information are involved in restoration of bipedal walking especially after incomplete SCI. To address this issue we have conducted a series of experiments, which aimed to reveal effects of both sensory inputs and descending commands on excitability modulation of neural circuits involving human bipedal locomotion. By using the Lokomat
robotic gait trainer, we tested effects of sensory inputs on corticospinal (CS) excitabilities during assisted stepping. The results so far demonstrate that sensory inputs, especially body-weight related somatosensory input, have a facilitatory effect on CS pathway of an ankle flexor muscle, whereas those sensory inputs regardless of body-weight related or not have an inhibitory effect on spinal stretch reflex circuits of upper and lower limb muscles during the assisted stepping. doi:10.1016/j.clinph.2013.02.049
S11-4. Efficacy and its neural mechanisms of neurorehabilitation for ataxic gait—Ichiro Miyai a, Noriaki Hattori a, Masahito Mihara a,b, Megumi Hatakenaka a, Hiroaki Fujimoto a, Teiji Kawano a, Hajime Yagura a (a Neurorehabilitation Research Institute, Morinomiya Hospital, Osaka, Japan, b Department of Neurology, Osaka University Medical School, Osaka, Japan) In degenerative cerebellar diseases, it is unclear whether patients can relearn motor sequences required for activities of daily living (ADLs) after neurorehabilitation since the cerebellum plays a crucial role in motor learning. It is also unknown whether functional gain can be sustained for a long period because of the progressive nature of the diseases. Thus Cerebellar Ataxia Rehabilitation (CAR) trial tested if intensive rehabilitation improved ataxia, gait and ADLs in 42 patients with degenerative cerebellar diseases. Intensive rehabilitation comprising 1-h physical and 1-h occupational therapy for 4 weeks significantly improved ataxia, gait speed and ADLs than control. The improvements in ataxia and gait speed were sustained at 12 weeks and 24 weeks after the intervention, respectively (Miyai I et al. Neurorehabil Neural Repair 2012;26:515–22). Neural mechanisms underlying functional improvement remain to be elucidated. Functional near-infrared spectroscopy studies have implied that recruitment of the prefrontal cortex and supplementary motor area are involved in improvement of gait and balance function as well as motor learning in patients with cerebellar damage (Mihara M et al. NeuroImage 2007;37:1338–45, Mihara M et al. NeuroImage 2008:43:329–33, Mihara M et al. NeuroReport 2012;23:314–19, Hatakenaka H et al. Neurorehabil Neural Repair 2012;26:293–300). doi:10.1016/j.clinph.2013.02.050
S12-1. MMN in psychological research – A study of change in MMN peak latencies—Seiji Tamakoshi (Kwansei Gakuin University, Nishinomiya, Japan) In order to investigate how sound representations are compressed in sensory memory, we examined mismatch negativity (MMN), ERP component reflecting neural representations in sensory memory. Yabe et al. (2005) showed that the MMNm peak latencies by reversing standards to deviants from oddball sequences did not reflect physical time flow, and they suggested that the temporal information could be compressed in sensory memory. However, it is not clear that factors of the asymmetrical change in MMN peak latencies. The experiment 1 compared the conditions of the stimuli that included a silence gap and it replaced by a tone segment which was decreased intensity. As a result, duplicates as the finding of Yabe et al., and it indicates that the whole stimulus duration rather than only gap duration is compressed in sensory memory. The experiment 2 showed that the stimuli’s saliency affects the peak latency of MMN, examined by changing in sound intensity. The experiment 3 that examined to effect of stimuli’s duration, suggested that stimuli’s temporal element and saliency affect the asymmetrical change in MMN peak latencies. These findings suggest the temporal element