Gait control in spinal palsy
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Published on: January 15, 2016
Bernard Dan1, Ethel Bouillot, Leena D Mewasingh
1Department of Neurology, Hôpital Universitaire des Enfants Reine Fabiola, Free University of Brussels (ULB), 15 Avenue JJ Crocq, 1020 Brussels, Belgium. bermard.dan@ulb.ac.be
Insights
This study presents a case of spinal cord compression causing spastic paraparesis in a child. Her unique gait pattern highlights differences between spinal and cerebral origins of developmental motor impairment.
Area of Science:
- Neurology
- Pediatrics
- Biomechanical Engineering
Background:
- Developmental motor impairment with spasticity often indicates cerebral palsy.
- Spastic diplegia is the most common type of cerebral palsy affecting lower limbs.
Observation:
- A 4-year-old girl presented with spastic paraparesis due to D4-D8 spinal cord compression.
- Her gait was analyzed using the ELITE optoelectronic system and compared to healthy children and those with spastic diplegia.
Findings:
- The patient maintained head orientation and arm swing like controls, unlike spastic diplegia patients.
- She exhibited truncal instability and limited lower limb movement selectivity, similar to spastic diplegia.
Implications:
- These findings suggest distinct locomotor control mechanisms in spinal versus cerebral spasticity.
- The concept of 'spinal palsy' is proposed for motor disorders from immature spinal cord lesions.
Abstract:
Developmental motor impairment with lower limb spasticity most commonly corresponds to cerebral palsy of the spastic diplegia type. Here we describe a 4-year-old girl whose locomotor phenotype reflects early cortico-spinal lesion at the spinal level. This child has developmental spastic paraparesis secondary to D4-D8 cord compression. We analysed her gait using the ELITE optoelectronic system and compared it to that of six normal age-matched controls and six age-matched children with leucomalacic spastic diplegia. Gait characteristics of the patient included preservation of head orientation and arm swing similar to findings in normal controls and contrasting with children with spastic diplegia. She also had truncal instability and displayed lack of selectivity in lower limb movement as in spastic diplegia and in contrast with normal controls. This may reflect differences in locomotor control between developmental spasticity of cerebral and spinal origin. The latter might correspond to spinal palsy defined as abnormal movement and posture secondary to non-progressive pathological processes affecting the immature spinal cord.
