Dysfonctionnement de circuits neuronaux spinaux impliqués dans la motricité chez des patients présentant une paralysie cérébrale spastique

Cerebral palsy is defined as a non-progressive postural and movement impairment related to a perinatal lesion in an immature brain. The development of spasticity, i.e. the hyperexcitability of the stretch reflex certainly contribute to the appearance of contracture, structural deformations and functional impairments. Among presynaptic mechanisms regulating the stretch reflex, only homosynaptic depression of fibre Ia-motoneurone α, which is decreased in cerebral palsy patients, is correlated with the level of spasticity suggesting that it could play a role in spasticity. Central nervous system lesions present in cerebral palsy patients suggest two hypotheses explaining the decrease of homosynaptic depression: a phenomena similar to denervation hypersensitivity and changes in the motoneurones discharge induced by decending monoaminergic pathways. These two hypotheses may coexist but suggest two different new therapeutics options. These two pathophysiological mechanisms could be linked with the lesions of the central nervous system present in cerebral palsy patients and could coexist to varying degrees. However, these two physiopathological hypotheses suggest different therapeutic ways.