Familial hemiplegic migraine (FHM) is a severe monogenic form of migraine with three main causal genes identified to date - CACNA1A, ATP1A2, and SCN1A - all related to ion channel function. However, the majority of hemiplegic migraine patients do not appear to have mutations in the known FHM genes, and a number of other genes have been linked with the disorder. PRRT2, in which mutations can cause paroxysmal movement disorders, has been proposed as a fourth hemiplegic migraine gene, and mutations in other genes - PNKD, SLC1A3, SLC2A1, SLC4A4, ATP1A4 and CSNK1D - have also been reported in hemiplegic or familial migraine cases. The aim of this study was to determine the contribution of these genes in an Australian cohort of hemiplegic migraine patients. Whole exome sequencing data from 180 probands referred for FHM genetic testing, but negative for exonic CACNA1A, ATP1A2 and SCN1A mutations, was analysed and assessed with in silico tools for potentially pathogenic variants in previously reported hemiplegic migraine genes. Sanger sequencing was used to determine the presence of the recurrent PRRT2 c.649dupC (p.Arg217ProfsX8) frameshift mutation. None of the patients had PRRT2 c.649dupC, however, rare or novel variants that may cause or contribute to hemiplegic migraine were identified in PRRT2, PNKD, SLC1A3, SLC2A1, SLC4A4, ATP1A4 and CSNK1D, in some patients. Multiple predicted deleterious rare variants were identified in ATP1A4, suggesting further investigation of this gene is warranted. This study suggests that all genes previously reported in respect to hemiplegic and familial migraine should be considered in genetic testing of patients. It also comprehensively shows that the majority of referred patients do not have exonic mutations in the known genes; further analysis of WES data is likely to implicate other genes and variants that contribute to hemiplegic migraine and reveal the genetic heterogeneity of the disorder.