• Journal of Biomedical Engineering Research
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• v.22 no.3
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• pp.249-257
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• 2001

The voluntary contracted EMG signal of spinal cord injured patients is very small because the information from central nervous system is not sufficiently transmitted to $\alpha$ motor neuron or muscle fiber. Therefore the acquisited EMG signal from needle or surface electrodes can not be identified obvious voluntary contraction pattern by muscle movement. In this paper we propose the extraction technique of voluntary muscle contraction and relaxation pattern from EMG signal of spinal cord injured patient whose EMG signal is composed of the linear sum of mo색 unit action potentials with two noise sources, additive noise assumed to be white Gaussian noise and high frequency discharge assumed to be not motor unit action potential but impulsive noise. In order to eliminate impulsive noise and additive noise from voluntary contracted EMG signal, we use the FatBear filter which is a nonarithmetic piecewise constant filter, and multiscale nonlinear wavelet denoising processing, respectively. The proposed technique is applied to the EMG signal acquisited from transverse myelitis patients to extract voluntary muscle contraction pattern.

• Physical Therapy Korea
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• v.8 no.4
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• pp.81-89
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• 2001

There are two independent mechanisms to control the segmental reflex gain in humans during gait. They are presynaptic inhibition and homosynaptic depression. Through the mechanism of the presynaptic inhibition, the muscle spindle afferent feedback can be properly gated during eccentric phase of gait. The modulation of the presynaptic inhibition is reflected in the level of H-reflex at a constant EMG level. During the eccentric muscle activation presynaptic inhibition should increase to account for the lower amplitude level of H-reflex at a constant level of EMG. Homosynaptic depression is another mechanism responsible for regulating the effectiveness of the muscle spindle afferent feedback. Both the presynaptic inhibition and the monosynaptic depression are responsible for modulating reflex gain during gait initiation. Reflex modulation is influenced not only as a passive consequence of the alpha motor neuron excitation level, but also through supraspinal mechanisms. Spastic paretic patients show the impaired soleus H-reflex modulation either during the initial stance phase, or during the swing phase. This abnormal modulatory mechanism can partially and artificially be restored by the application of peripheral stimulus to the sole of the foot, provided that the segmental circuitry remains functional.

• The Journal of Korean Physical Therapy
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• v.22 no.4
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• pp.15-20
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• 2010

Purpose: The purpose of this study was to measure changes in the H-reflex and V wave under loading conditions (e.g. prone and standing position) and to investigate whether postural change would affect the H-reflex and V wave in post stroke hemiplegic patients. Methods: Thirty persons with hemiplegia resulting from stroke (20 males, 10 females) participated in this study. Electromyography (EMG) was used to electrically stimulate and record the soleus H-reflexes and V waves under various loading conditions. The normality of the distribution of each variable (H latency, $H_{max}/M_{max}$ ratio, $V_{max}/M_{max}$ ratio) was tested using the Kolmogorov-Smirnov test. The means of normally distributed continuous data were assessed by independent t-test (${\alpha}$=0.05). Results: There were statistically significant differences in $H_{max}/M_{max}$ ratio (p<0.01), $V_{max}/M_{max}$ ratio (p<0.01), H latency (p<0.01) among the prone and standing position. Conclusion: We found that the H-reflex and V wave in standing position was more active to weight bearing load than prone position.

• Journal of Korean Medicine Rehabilitation
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• v.19 no.2
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• pp.73-88
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• 2009

Objectives : Neuronal changes that result from treadmill exercise for patients with Parkinson's disease(PD) have not been well documented, although some clinical and laboratory reports suggest that regular exercise may produce a neuroprotective effect and restore dopaminergic and motor functions. However, it is not clear if the improvements are due to neuronal alterations within the affected nigrostriatal region or result from a more general effect of exercise on affect areas and motivation. In this study, we demonstrate that motorized treadmill exercise improves the neuronal outcomes in rodent models of PD. Methods : We used a chronic mouse model of parkinsonism, which was induced by injecting male C57BL/6 mice with 10 doses(Every 12 hour) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (30 mg/kg) and probenecid (20 mg/kg) over 5 days. These mice were able to sustain an exercise training program on a motorized rodent treadmill at a speed of 18 m/min, $0^{\circ}$ of inclination, 40 min/day, 5 days/week for 4 weeks. At the end of exercise training, we extracted the brain and compared their neuronal and neurochemical changes with the control(saline and sedentary) mice groups. Synphilin protein is the substance that manifestly reacts with ${\alpha}$-synuclein. In this study, we used Synphilin as a manifest sign of recovery from neurodegeneration. We analyze the brain stems of the substantia nigra and striatum region using the western blotting technique. Results : There were no expression of synphilin in the saline-induced groups. The addition of MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) greatly accelerated synphilin expression which meant an aggregation of ${\alpha}$-synuclein. But, the MPTP-induced treadmill exercise group showed significantly lower expression than the MPTP-induced sedentary group. This means treadmill exercise has a definite effect on the decrease of ${\alpha}$-synuclein aggregation. Conclusions : In this study, our results suggest that treadmill exercise promoted the removal of the aggregation of ${\alpha}$-synuclein, resulting in protection against disease development and blocks the apoptotic process in the chronic parkinsonian mice brain with severe neurodegeneration.