Laboratoire de Neurosciences Intégratives et Adaptatives

Motor control and body representation in the central nervous system (CNS) as well as musculoskeletal architecture and physiology are shaped during development by sensorimotor experience and feedback, but the emergence of locomotor disorders during maturation and their persistence over time remain a matter of debate in the absence of brain damage. By using transient immobilization of the hind limbs, we investigated the enduring impact of postnatal sensorimotor restriction (SMR) on gait and posture on treadmill, age-related changes in locomotion, musculoskeletal histopathology and Hoffmann reflex in adult rats without brain damage. SMR degrades most gait parameters and induces overextended knees and ankles, leading to digitigrade locomotion that resembles equinus. Based on variations in gait parameters, SMR appears to alter age-dependent plasticity of treadmill locomotion. SMR also leads to small but significantly decreased tibial bone length, chondromalacia, degenerative changes in the knee joint, gastrocnemius myofiber atrophy and muscle hyperreflexia, suggestive of spasticity. We showed that reduced and atypical patterns of motor outputs, and somatosensory inputs and feedback to the immature CNS, even in the absence of perinatal brain damage, play a pivotal role in the emergence of movement disorders and musculoskeletal pathologies, and in their persistence over time. Understanding how atypical sensorimotor development likely contributes to these degradations may guide effective rehabilitation treatments in children with either acquired (ie, with brain damage) or developmental (ie, without brain injury) motor disabilities.

Cerebral palsy (CP) describes a group of neurodevelopmental disorders of posture and movement that are frequently associated with sensory, behavioral, and cognitive impairments. The clinical picture of CP has changed with improved neonatal care over the past few decades, resulting in higher survival rates of infants born very preterm. Children born preterm seem particularly vulnerable to perinatal hypoxia-ischemia insults at birth. Animal models of CP are crucial for elucidating underlying mechanisms and for development of strategies of neuroprotection and remediation. Most animal models of CP are based on hypoxia-ischemia around the time of birth. In this review, we focus on alterations of brain organization and functions, especially sensorimotor changes, induced by prenatal ischemia in rodents and rabbits, and relate these alterations to neurodevelopmental disorders found in preterm children. We also discuss recent literature that addresses the relationship between neural and myelin plasticity, as well as possible contributions of white matter injury to the emergence of brain dysfunctions induced by prenatal ischemia.

The effects of increasing postural task difficulty on balance control was investigated in 9 compensated vestibular loss patients whose results were compared to 11 healthy adults. Subjects were tested in static (stable support) and dynamic (sinusoidal translation of the support) conditions, both at floor level and at height (62 cm above the floor), and with and without vision, to create an additional postural threat. Wavelet analysis of the center of foot pressure displacement and motion analysis of the body segments were used to evaluate the postural performance. Evaluation questionnaires were used to examine the compensation level of the patients (DHI test), their general anxiety level (SAST), fear of height (subjective scale), and workload (NASA TLX test). (Vestibular loss patients rely more on vision and spend more energy maintaining balance than controls, but they use the same postural strategy as normals in both static and dynamic conditions.) Questionnaire data all showed differences in behavior and perceptions between the controls and the patients. However, at height and without vision, a whole body strategy leading to rigid posture replaces the head stabilization strategy found for standing at floor level. The effects of height on postural control can be attributable to an increase in postural threat and attention changes resulting from modifications in perception.