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Despite significant advancement in recent research and clinical treatments, the cellular pathologies that underlie SMA disease manifestations are not well characterized beyond those of spinal motor neurons (MNs). We previously reported cerebellar abnormalities in an SMA mouse model at the late stage of the disease, including volumetric deficits and lobule\u2010selective structural changes with Purkinje cell degeneration, with colocalized astrocytic reactivity. However, when these cerebellar defects arise and whether they are a consequence of MN degeneration remain unknown. We used magnetic resonance imaging, immunohistochemistry, and electrophysiology to characterize cerebellar pathology in early\u2010stage symptomatic SMN\u03947 mice and late\u2010stage SMA mice with transgenic rescue of SMN in MNs. We found disproportionate structural and lobule\u2010specific surface area deficits, as well as abnormal functional properties in the cerebella of early symptomatic SMA mice, suggesting that cerebellar pathologies may be a primary contributor to murine SMA phenotypes. Moreover, cerebellar pathologies were not ameliorated in SMA mice with MN rescue, suggesting that cerebellar neurons are independently vulnerable to reduced SMN expression. 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