SPG7 mutations can cause both pure and complex phenotypes, especially later in the course of the disease, including cerebellar ataxia and atrophy, optic atrophy, chronic progressive external ophthalmoparesis, supranuclear palsy, cognitive impairment, thin corpus callosum, and polyneuropathy [10,16,32,33]. This evidence concerns the gene SPG7 and hereditary optic atrophy.