Prenatal ischemia deteriorates white matter, brain organization, and function: implications for prematurity and cerebral palsy

Abstract

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.

All Wrapped Up: Environmental Effects on Myelination

“…Significant loss of the progenitor pool and gross reductions in the number of myelinating OLs underlies the maturation blockade seen with injury. Apneic, ischemic, and inflammatory events cause a delay maturation of neuronal and glial cell populations, and diffuse abnormalities in WM that result in a reduced capacity to synthesize myelin [46,164]. Accordingly, the resultant diffuse WM injury is believed to be a major cause of disability in survivors [165].…”

Characterization of a cerebral palsy‐like model in rats: Analysis of gait pattern and of brain and spinal cord motor areas

“…Thus, both LPS injections and asphyxia procedure used in the present study may have caused reactive astrogliosis, which could explain the increase observed in the number of glial cells in the primary somatosensory cortex and striatum (Haupt et al, 2007;Pekny et al, 2014). On the other hand, one of the most common encephalic lesions found in patients with CP is the PVL (Back and Rosenberg, 2014;Coq et al, 2016). This lesion is characterized by an increase in the size of ventricles associated with a lesion of the surrounding white matter (Hadders-Algra, 2004;Garel and Alberti, 2006;Coq et al, 2008;Clowry et al, 2014).…”

“…On the other hand, one of the most common encephalic lesions found in patients with CP is the PVL (Back and Rosenberg, 2014; Coq et al, 2016). This lesion is characterized by an increase in the size of ventricles associated with a lesion of the surrounding white matter (Hadders‐Algra, 2004; Garel and Alberti, 2006; Coq et al, 2008; Clowry et al, 2014).…”

Immunoreactivity of MAPK Signaling in a Rat Model of Intrauterine Growth Retardation Induced by Uterine Artery Ligation

“…Uterine artery ligation clearly decreased uterine blood flow and caused fetal weight reduction (29), which resulted in neuronal cell death (30). Further, impaired neuronal cell bodies were observed in the hippocampus and cerebral cortex (31), and were reduced in the entorhinal cortex (32). Hypoxic injury, like uterine artery ligation, was also associated with oligodendrocyte maturation (33) and defects in myelination (34).…”