The aim of this research topic is to collate articles describing prediction of outcomes of pre- and perinatal lesions leading to cerebral palsy, basic research in animal models and human subjects, and ideas for, and trials of, interventions in the first two years of life.
CP arises from insults to the sensorimotor cortex, subcortical axon tracts and subplate. The aetiology is complex and often multifactorial, but commonly involves hypoxia in premature babies, or perinatal strokes. Corticospinal axons have just invaded the spinal grey matter and thalamic afferents the upper layers of the neocortex, and these systems are undergoing activity dependent development. The outcome is not simply a loss of voluntary control due to disruption of descending pathways, but also involves abnormal development of reflex and corticospinal circuitry including heteronymous and hyperexcitable reflexes, and uprated ipsilateral corticospinal inputs that are not functionally useful. CP may be viewed as aberrant plasticity in response to a lesion, indeed, abnormalities in movement are subtle at first but develop subsequently. It is misleading to suppose that developmental mechanisms are self-reparative. The challenge is to understand activity-dependent fine tuning of neural circuitry during normal development and to find how to promote desirable plasticity whilst limiting undesirable effects following developmental lesions. However, before proposing interventions, we have to develop our ability to predict the severity of neonatal insults.
We hope to solicit a variety of articles, including long and short reviews, original research or opinion pieces, from both basic scientists and clinicians. Likewise we, as editors, have complementary knowledge and experience in this area. Anna Basu is an academic pediatric neurologist and Gavin Clowry is a developmental neuroscientist.
The aim of this research topic is to collate articles describing prediction of outcomes of pre- and perinatal lesions leading to cerebral palsy, basic research in animal models and human subjects, and ideas for, and trials of, interventions in the first two years of life.
CP arises from insults to the sensorimotor cortex, subcortical axon tracts and subplate. The aetiology is complex and often multifactorial, but commonly involves hypoxia in premature babies, or perinatal strokes. Corticospinal axons have just invaded the spinal grey matter and thalamic afferents the upper layers of the neocortex, and these systems are undergoing activity dependent development. The outcome is not simply a loss of voluntary control due to disruption of descending pathways, but also involves abnormal development of reflex and corticospinal circuitry including heteronymous and hyperexcitable reflexes, and uprated ipsilateral corticospinal inputs that are not functionally useful. CP may be viewed as aberrant plasticity in response to a lesion, indeed, abnormalities in movement are subtle at first but develop subsequently. It is misleading to suppose that developmental mechanisms are self-reparative. The challenge is to understand activity-dependent fine tuning of neural circuitry during normal development and to find how to promote desirable plasticity whilst limiting undesirable effects following developmental lesions. However, before proposing interventions, we have to develop our ability to predict the severity of neonatal insults.
We hope to solicit a variety of articles, including long and short reviews, original research or opinion pieces, from both basic scientists and clinicians. Likewise we, as editors, have complementary knowledge and experience in this area. Anna Basu is an academic pediatric neurologist and Gavin Clowry is a developmental neuroscientist.
