The clinical suspicion of an alternative aetiology was as follows: One patient progressed rapidly and developed autonomic dysfunction fulfilling the criteria for probable MSA-C, a second patient in his 20s had severe global cerebellar atrophy (unusual for anti-GAD ataxia) which lead to genetic testing confirming a pathogenic mutation for ANO10 and a third patient had mild spastic paraparesis and waddling gait which lead to a genetic diagnosis of SPG7. This evidence concerns the gene GAD1 and Ataxia.