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1.  Suppression of Stimulus Artifact Contaminating Electrically Evoked Electromyography 
NeuroRehabilitation  2014;34(2):381-389.
Background
Electrical stimulation of muscle or nerve is a very useful technique for understanding of muscle activity and its pathological changes for both diagnostic and therapeutic purposes. During electrical stimulation of a muscle, the recorded M wave is often contaminated by a stimulus artifact. The stimulus artifact must be removed for appropriate analysis and interpretation of M waves.
Objectives
The objective of this study was to develop a novel software based method to remove stimulus artifacts contaminating or superimposing with electrically evoked surface electromyography (EMG) or M wave signals.
Methods
The multiple stage method uses a series of signal processing techniques, including highlighting and detection of stimulus artifacts using the Savitzky-Golay filtering, estimation of the artifact contaminated region with the Otsu thresholding, and reconstruction of such region using signal interpolation and smoothing. The developed method was tested using M wave signals recorded from biceps brachii muscles by a linear surface electrode array. To evaluate the performance, a series of semi-synthetic signals were constructed from clean M wave and stimulus artifact recordings with different degrees of overlap between them.
Results
The effectiveness of the developed method was quantified by a significant increase in correlation coefficient and a significant decrease in root mean square error between the clean M wave and the reconstructed M wave, compared with those between the clean M wave and the originally contaminated signal. The validity of the developed method was also demonstrated when tested on each channel’s M wave recording using the linear electrode array.
Conclusions
The developed method can suppress stimulus artifacts contaminating M wave recordings.
doi:10.3233/NRE-131045
PMCID: PMC4000584  PMID: 24419021
M wave; Stimulus artifact suppression; Electromyography (EMG)
2.  Differential Age-related Changes in Bone Geometry between the Humerus and the Femur in Healthy Men 
Aging and Disease  2011;3(2):156-163.
Muscle pull and weight-bearing are key mechanical determinants of bone geometry which is an important feature of bone strength that declines with adult aging. However, the relative importance of these determinants in young and old adults has not been evaluated systematically. To differentiate the influence of each type of mechanical loading we compared humeral and femoral bone shaft geometry and cross-sectional area (CSA) of the arm and thigh muscles in young and old men. Contiguous transverse MRI (Siemens 1.5T) scans of the arm and thigh were made in 10 young men (21.9 ± 1.0 years) and 10 old men (78.1 ± 4.9 years). Image analysis yielded total (TA), cortical (CA) and medullary (MA) CSA of the humeral and femoral shafts, as well as muscle CSA of the corresponding regions of the arm and thigh. Humeral CA was significantly greater in the young, whereas humeral and femoral MA were significantly greater in the older group. Significant correlations were found between arm muscle CSA and humeral CA (r = 0.73); between thigh muscle CSA and femoral CA (r = 0.69); and between body mass and femoral CA (r = 0.63) and TA (r = 0.55). Moderate correlations between muscle CSA and CA suggest that muscle pull is an important determinant of bone geometry. The significant difference observed between young and old in humeral, but not femoral CA, and the correlation between body mass and femoral, but not humeral cortical area, suggests that weight-bearing attenuates bone loss associated with adult aging.
PMCID: PMC3377827  PMID: 22724076
Aging; Femur; Humerus; Osteopenia; Osteoporosis; Muscle
3.  Effects of baclofen on motor units paralysed by chronic cervical spinal cord injury 
Brain  2009;133(1):117-125.
Baclofen, a gamma-aminobutyric acid receptorB agonist, is used to reduce symptoms of spasticity (hyperreflexia, increases in muscle tone, involuntary muscle activity), but the long-term effects of sustained baclofen use on skeletal muscle properties are unclear. The aim of our study was to evaluate whether baclofen use and paralysis due to cervical spinal cord injury change the contractile properties of human thenar motor units more than paralysis alone. Evoked electromyographic activity and force were recorded in response to intraneural stimulation of single motor axons to thenar motor units. Data from three groups of motor units were compared: 23 paralysed units from spinal cord injured subjects who take baclofen and have done so for a median of 7 years, 25 paralysed units from spinal cord injured subjects who do not take baclofen (median: 10 years) and 45 units from uninjured control subjects. Paralysed motor unit properties were independent of injury duration and level. With paralysis and baclofen, the median motor unit tetanic forces were significantly weaker, twitch half-relaxation times longer and half maximal forces reached at lower frequencies than for units from uninjured subjects. The median values for these same parameters after paralysis alone were comparable to control data. Axon conduction velocities differed across groups and were slowest for paralysed units from subjects who were not taking baclofen and fastest for units from the uninjured. Greater motor unit weakness with long-term baclofen use and paralysis will make the whole muscle weaker and more fatigable. Significantly more paralysed motor units need to be excited during patterned electrical stimulation to produce any given force over time. The short-term benefits of baclofen on spasticity (e.g. management of muscle spasms that may otherwise hinder movement or social interactions) therefore have to be considered in relation to its possible long-term effects on muscle rehabilitation. Restoring the strength and speed of paralysed muscles to pre-injury levels may require more extensive therapy when baclofen is used chronically.
doi:10.1093/brain/awp285
PMCID: PMC2857957  PMID: 19903733
baclofen; spinal cord injury; muscle paralysis; muscle weakness; axon conduction velocity; intraneural motor axon stimulation

Results 1-3 (3)