Abstract
The clinical picture of cerebral palsy (CP) develops subsequently to hypoxic/ischaemic or inflammatory/toxic injury of the developing central nervous system in the pre-, peri- or postnatal period. The distribution of lesions reflects peculiarities of foetal vascular development, increased vulnerabilities of developing cells or supply territories of the basal cerebral arteries. The present chapter focuses on pathophysiological aspects and the neuropathological alterations observed in CP. The pathologies described comprise (a) periventricular leukoencephalopathy which is predominantly seen in preterm births and may impress as small infarcts or gliotic foci, (b) germinal/ventricular haemorrhage mainly affecting preterm neonates presumably resulting from hypoxic damage to the endothelium of immature vessels in the germinal layer, (c) por-/hydranencephaly developing in the 5th gestational month following systemic hypotension, (d) pontosubicular neuronal apoptotic necrosis observed between the 30th gestational week and the 2nd postnatal month after severe systemic hypoxia, (e) cortical border zone infarction/ulegyria, (f) territorial infarction due to occlusion of a basal cerebral artery in mature neonates up to infant age, (g) marbled state referring to bilaterally abnormally myelinated scars in the basal ganglia and thalami due to lesioning in the perinatal period until an age of 6–9 months, and (h) multicystic encephalopathy, a global hemispheric necrosis developing postnatally up to an age of 18 months. The neuropathological findings particularly underline the importance of localization, extent and timing of brain injury for the clinical picture, whereas data on brain development may indicate possible time windows for therapeutic intervention.
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Hagel, C. (2018). Neuropathology of Cerebral Palsy. In: Panteliadis, C. (eds) Cerebral Palsy. Springer, Cham. https://doi.org/10.1007/978-3-319-67858-0_5
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