Ethel Bouillot

Early emergence of temporal co-ordination of lower limb segments elevation angles in human locomotion

We analysed the co-ordination of the elevation angles of the thigh (alpha(t)), shank (alpha(s)) and foot (alpha(f)) during walking in 19 adults and 21 children (aged 11--144 months), including the very first unsupported steps in four. Cross-correlation functions (CCF) maturation of pairs of elevation angles was quantified by a global error parameter (Et((CCF))) reflecting the difference between particular CCF value of toddlers and mean adult value (Ea((CCF))). During the very first step, Et((CCF)) could be five times higher than Ea((CCF)). With walking experience, Et((CCF)) for both alpha(t)-alpha(s) and alpha(s)-alpha(f) pairs evolved following a biexponential profile, with a fast time constant below 6 months. Adult-like CCF parameters were reached earlier for alpha(s)-alpha(f) than alpha(t)-alpha(s), indicating disto-proximal maturation of the temporal co-ordination of the lower limb segments in human locomotion.

Distinct multi-joint control strategies in spastic diplegia associated with prematurity or Angelman syndrome

Spastic diplegia is commonly due to periventricular leucomalacia associated with premature birth. It is also a feature of Angelman syndrome (AS), a neurogenetic disorder with developmental delay, absent speech and mirthful behaviour. We studied the kinematics and kinetics of the squatting movement and associated electromyographic (EMG) activities in 20 children with spastic diplegia associated with periventricular leucomalacia (SDPL) or AS and 18 unimpaired children. While movement of normal subjects consisted of vertical translation of most body segments, the movement of SDPL children was operated around the fixed knee with backward shift of the hip, and AS children performed a forward flexion of the trunk over the thigh. Trunk stability was correlated with movement velocity in both pathological groups. In normal subjects, anticipatory EMG pattern consisted of silencing of hamstring muscle tonic activity prior to movement onset. This deactivation was not present in spastic diplegia. In SDPL, anticipatory overactivation of ankle joint actuators was recorded and tonic co-contraction persisted throughout the movement. In AS, rhythmic EMG bursting was seen during the movement. Shoulder, hip and knee trajectories in the sagittal plane showed marked within-group stereotypies in orientation, shape and length. The patterns in both pathological groups were therefore distinctive. We speculate that they reflect corticospinal impairment in SDPL and combined corticospinal and cerebellar dysfunction in AS.

Head stability during whole body movements in spastic diplegia.

Head angular stability is essential for postural control in whole body movement. Using the opto-electronic ELITE system, we have studied head orientation during the movements of squatting from the standing position and straightening-up from the squatting position in 12 children with spastic diplegia and 12 age-matched controls. Although no instruction was given regarding the head, diplegic children consistently performed excessive neck flexion in the squatting movement and excessive hyperextension in the straightening-up movement, whereas normal children maintained the initial orientation throughout both movements. We discuss pathophysiological implications.

Adaptive motor strategy for squatting in spastic diplegia.

Motor strategies, defined by kinetic, kinematic and/or muscle activation patterns, reflect neural planning of movement, which takes into account central as well as peripheral constraints. Major alteration is expected in cerebral palsy, a condition characterized by abnormal posture and movement secondary to early lesion of the brain. The objective of this study was to characterize the motor strategies involved in disruption of posture in cerebral palsy of the spastic diplegia type and compare them with normal controls. The optoelectronic ELITE system was used to record and analyse the movement of squatting from the standing position with the arms extended forward in 11 children with spastic diplegia aged between 3 and 12 years and 11 age-matched normal controls. Normal children maintained gaze and arm horizontality and trunk verticality throughout the movement. The knee followed an oblique trajectory. Its angular velocity profile showed a short, single-peaked, ascending phase. The onset of movement was preceded by deactivation of the semimembranous muscle. In diplegic children, gaze and arm horizontality and trunk verticality were lost. The ankle was rigidified, resulting in spatial fixation of the knee. The ascending phase of the knee velocity profile was prolonged and multi-peaked. There was widespread muscle co-contraction from the outset of movement. No anticipatory deactivation was evidenced, but anticipatory bursts appeared in the soleus. Patients with cerebral palsy have to organize a limited motor repertoire from a restricted neural potential. Consequent motor strategies presently demonstrated in spastic diplegia are distinct and appear as an original alternative to those of normal subjects.

Gait control in spinal palsy

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.