期刊
ANNALS OF PHYSICAL AND REHABILITATION MEDICINE
卷 63, 期 5, 页码 422-430出版社
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.rehab.2019.10.002
关键词
Cerebral palsy; Prematurity; Developmental Coordination Disorder; Intrauterine growth retardation; Hypoperfusion; Sensorimotor restriction; White matter injury
资金
- Fondation Paralysie Cerebrale
- Cerebral Palsy Alliance
- Fondation NRJ - Institut de France
- Region Provence-Alpes-Cote-d'Azur
- Centre National de la Recherche Scientifique (CNRS)
- Aix-Marseille Universite
- Ministere des Affaires Etrangeres et du Developpement International
- National Institute of Mental Health of the National Institute of Health [P30 MH092177]
- Temple University
- National Cerebral and Vascular Center in Osaka
Cerebral palsy (CP) is a complex syndrome of various sensory, motor and cognitive deficits. Its prevalence has recently decreased in some developed countries and its symptoms have also shifted since the 1960s. From the 1990s, CP has been associated with prematurity, but recent epidemiologic studies show reduced or absent brain damage, which recapitulates developmental coordination disorder (DCD). In previous studies, we developed a rat model based on mild intrauterine hypoperfusion (MIUH) that recapitulated the diversity of symptoms observed in preterm survivors. Briefly, MIUH led to early inflammatory processes, diffuse brain damage, minor locomotor deficits, musculoskeletal pathologies, neuroanatomical and functional disorganization of the primary somatosensory (S1) cortex but not in the motor cortex (M1), delayed sensorimotor reflexes, spontaneous hyperactivity, deficits in sensory information processing, and memory and learning impairments in adult rats. Adult MIUH rats also exhibited changes in muscle contractile properties and phenotype, enduring hyperreflexia and spasticity, as well as hyperexcitability in the sensorimotor cortex. We recently developed a rat model of DCD based on postnatal sensorimotor restriction (SMR) without brain damage. Briefly, SMR led to digitigrade locomotion (i.e., toe walking) related to ankle-knee overextension, degraded musculo-skeletal tissues (e.g., gastrocnemius atrophy), and lumbar hyperreflexia. The postnatal SMR then led to secondary degradation of the hind-limb maps in S1 and M1 cortices, altered cortical response properties and cortical hyperexcitability, but no brain damage. Thus, our 2 rat models appear to recapitulate the diversity of symptoms ranging from CP to DCD and contribute to understanding the emergence and mechanisms underlying the corresponding neurodevelopmental disorders. These preclinical models seem promising for testing strategies of rehabilitation based on both physical and cognitive training to promote adaptive brain plasticity and to improve physical body conditions. (C) 2019 Elsevier Masson SAS. All rights reserved.
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