No phenotype associated with established lipopolysaccharide model for cerebral palsy

Abstract

Cerebral palsy (CP) is associated with childhood spasticity, seizures and paralysis. Oligodendrocyte damage resulting in periventricular leukomalacia (PVL) in the developing brain has been implicated. Animal models of CP have used prenatal hypoxia and infection with histopathology of PVL as the endpoint. To evaluate whether this histological endpoint is associated with a CP phenotype, we reproduced a lipoploysaccharide (LPS) model for PVL (Bell, 2002) and evaluated developmental, behavioral and motor outcomes.