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Kinetics of compensatory gait in persons with myelomeningocele
Elena M Gutierrez1, Asa Bartonek, Yvonne Haglund-Akerlind
1Department of Surgical Sciences, Orthopedics Sect., Karolinska Institute, MotorikLab Q2:07 ALB, Karolinska Hospital, 17176 Stockholm, Sweden. lanie.gutierrez@kirurgi.ki.se
Insights
Children with lumbo-sacral myelomeningocele use compensatory mechanisms during gait. Hip abductor weakness significantly alters gait kinetics, with other joints compensating for ankle impairments.
Area of Science:
- Biomechanical analysis
- Pediatric orthopedics
- Neurorehabilitation
Background:
- Lumbo-sacral myelomeningocele often leads to muscle weakness affecting gait.
- Understanding compensatory strategies is crucial for improving mobility in affected children.
Purpose of the Study:
- To investigate the kinetic strategies and compensatory mechanisms in children with lumbo-sacral myelomeningocele during self-ambulatory gait.
- To analyze joint moments, power, and work to understand how muscle paresis impacts gait.
Main Methods:
- Three-dimensional gait analysis was performed on 31 children with myelomeningocele and 21 controls.
- Analysis included joint moments (hip, knee, ankle) and joint power/work.
Main Results:
- Orthotic support compensated for ankle weakness, but other joints were overloaded.
- Hip abductor weakness was a key factor, leading to altered hip moments and the hip acting as a power absorber.
- Children utilized stronger muscle groups to compensate for deficits.
Conclusions:
- Gait in children with myelomeningocele involves complex kinetic compensations.
- Hip abductor strength is critical for maintaining normal gait patterns.
- Combined kinetic and kinematic analysis provides a comprehensive understanding of gait adaptations.
Abstract:
This study investigated the kinetic strategy and compensatory mechanisms during self-ambulatory gait in children with lumbo-sacral myelomeningocele. Thirty-one children with mid-lumbar to low-sacral myelomeningocele who walked without aids and 21 control children were evaluated by three-dimensional gait analysis. Joint moments in all planes at the hip and knee and sagittal moments at the ankle, as well as joint power and work done at all three joints, were analyzed. Joint moment capacity lost due to plantarflexor and dorsiflexor weakness was provided instead by orthotic support, but other joints were loaded more to compensate for the weakness at the ankles and restricted ankle motion. Subjects with total plantarflexor and dorsiflexor paresis and strength in the hip abductors had more knee extensor loading due to plantarflexor weakness and dorsiflexion angle of the orthotic ankle joint. The subjects with orthoses also generated more power at the hip to supplement the power generation lost to plantarflexor weakness and fixed ankles. The most determinant muscle whose paresis changes gait kinetics was the hip abductor. Hip abductor weakness resulted in a characteristic pattern where the hips displayed an eccentric adduction moment, mediating energy transfer into the lower limbs, and the hips replaced the knees as power absorbers in early stance. Joint moment, power and work analyses complement a kinematic analysis to provide a complete picture of how children who have muscle paresis recruit stronger muscle groups to compensate for weaker ones.
