The developing cerebellum is susceptible in unique ways to disruptions, both in utero and after birth. This is in part because of its relatively late and prolonged program of neuronal migration and differentiation, as compared to those of the hemispheres, brainstem, and spinal cord (see Chapters 20 and 23). As in other neuroanatomic sites, selective vulnerability is in play in the immature external granule cells which, while derived from the rhombic lip, are analogous in many ways to the immature cells of the germinal matrix originating from the ventricular zone. Thus, the external granule cells are thought to be the cerebellar elements at risk of injury from hypoxia-ischemia and/or hemorrhage, resulting in free radical toxicity, neuroinflammation, and excitotoxicity. The short-term effect is an irreversible injury to or delayed function of these precursor cells of the cerebellar cortex, and the long-term result is overall underdevelopment of the cerebellum (hypoplasia) [1].