All PD associated subtypes have genetic contributions and are likely to run in a families genetic history due to dominant allele mutations. Mutations of identified genes have been leading areas of research in the study and treatment of paroxysmal dyskinesia. PKD, PNKD, and PED are classified as separate subtypes because they all have different presentations of symptoms, but also, because they are believed to have different pathologies.

Interestingly, studies on diseases that are similar in nature to PD have revealed insights into the causes of movement disorders. Hypnogenic paroxysmal dyskinesia is a form of epilepsy affecting the frontal lobe. Single genes have been identified on chromosomes 15, 20, and 21, which contribute to the pathology of these epilepsy disorders. Utilizing new knowledge about pathologies of related and similar disease can shed insight on the causal relationships in paroxysmal dyskinesia.

Numerous causes have been proposed for PKD, such as genetic mutations, multiple sclerosis, brain trauma, and endocrine dysfunction. This is not an exhaustive list; many other causes are being proposed and studied. Until causal genes can be identified, the pathology of PKD will not be fully understood. Researchers have identified specific loci in chromosomes 16 and 22, which have been reported to have a genotype-phenotype correlation.