Abstract
The aim of this prospective study was to investigate changes in muscle activity during gait in children with Duchenne muscular Dystrophy (DMD). Dynamic surface electromyography recordings (EMGs) of 16 children with DMD and pathological gait were compared with those of 15 control children. The activity of the rectus femoris (RF), vastus lateralis (VL), medial hamstrings (HS), tibialis anterior (TA) and gastrocnemius soleus (GAS) muscles was recorded and analysed quantitatively and qualitatively. The overall muscle activity in the children with DMD was significantly different from that of the control group. Percentage activation amplitudes of RF, HS and TA were greater throughout the gait cycle in the children with DMD and the timing of GAS activity differed from the control children. Significantly greater muscle coactivation was found in the children with DMD. There were no significant differences between sides. Since the motor command is normal in DMD, the hyper-activity and co-contractions likely compensate for gait instability and muscle weakness, however may have negative consequences on the muscles and may increase the energy cost of gait. Simple rehabilitative strategies such as targeted physical therapies may improve stability and thus the pattern of muscle activity.
Highlights
Duchenne Muscular Dystrophy (DMD) is the most common neuromuscular disease in children, with an incidence of 1 in 3500 male births [1]
The KeR-EGI of the children with DMD was more than 2 standard deviations lower than that of the control children (76.88 ±16.9 vs 100.10 ±7.90, p
Mean Electromyography-profil score (EMG-PS) and EMG-PS by phase were significantly higher in the children with DMD for the rectus femoris (RF), HS, GAS and tibialis anterior (TA) muscles
Summary
Duchenne Muscular Dystrophy (DMD) is the most common neuromuscular disease in children, with an incidence of 1 in 3500 male births [1]. Case-control studies using optoelectronic systems to analyse gait have shown kinematic anomalies at the pelvis (lumbar hyperlordosis, excessive anterior pelvic tilt, double bump pattern), the knee (loss of knee flexion in stance and excessive extension at the end of stance) and the ankle (increased plantarflexion in swing, toe-walking) [3,5,6,7,8,9,10,11,12,13,14] These pathological patterns are the result of a slow, poorly-understood process caused by a combination of muscle weakness, muscle shortening and osteo-articular changes, along with postural adaptations
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