To understand the mechanism of action of stem cells in the treatment of cerebral palsy, it is
important to understand the empirical neuropathophysiology. In spite of the vast and varied
etiology; underlying cellular mechanisms, that cause the morbidity or mortality associated
with cerebral palsy, are tissue damage caused by hypoxia and ischemia. The clinical manifestations
of this cellular damage, depends on a range of factors including the time of insult, the
severity of insult and cause of the insult. Brain tissue is heterogeneous and responds differently
to hypoxia and ischemia. Therefore, a certain type of brain tissue is implicated to cause cerebral
palsy. Recent preclinical, immunohistochemical and imaging evidence suggests periventricular
white matter injury (PWMI), particularly damage to oligodendrocytes (OLs) as a primary
cause of cerebral palsy [40,41,42]. PWMI is a spectrum ranging from cystic focal necrotic
lesions, periventricular leuckomalacia (PVL) to specific cortical scarring in the deep regions of
sulci, Ulegyria to diffuse myelination disturbances. Oligodendrocyte progenitors are abundantly
present in the subventricular and periventricualr zones, therefore damage to these cells
is seen as PVL in neuroimaging investigations. The extent of the damage to the white matter
and its consequences are dependent on the developmental stage at which the damage occurred,
brain vascularization and the type of tissue