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<unk> . 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. Studies on diseases that are similar in nature to PD have revealed insights into the causes of movement disorders. Hypnogenic<unk>  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<unk> . PKD 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. PNKD Research on the pathology for PNKD suggests that mutations to specific nucleotide sequences in chromosome 2, MR-1 (myofibrililogenesis regulator - 1) may be linked to PNKD. Studies on MR-1 reveal that it serves as a detoxifying agent. PNKD is sometimes induced by the consumption of alcohol or coffee. Individuals with a mutation in the MR-1 gene sequence may have problems detoxifying the body when alcohol or caffeine is ingested, perhaps resulting in the onset of PNKD. Other studies have revealed a possible mutation on the calcium sensitive potassium (BK) channel. A mutation affecting the influx and efflux of potassium and calcium can cause large scale changes in a neuron. This specific mutation leads to increased excitability of the neuron, often inducing rapid depolarization eliciting numerous action potentials. The pathogenesis of PKND is partially defined by the identification of mutations in the myofibrillogenesis regulator 1 (MR-1), whose gene product is an enzyme involved in the detoxification of methylglyoxal (a compound present in coffee, cola, and alcoholic beverages). PED Long periods of continuous physical exercise is often considered the causal factor involved in a PED diagnosis. It is important to note that PED a is sometimes co-diagnosed with epilepsy and young-onset Parkinson's disease. Correlations between the causes of young-onset Parkinson's disease and PED may be due to a similar problem, specifically a mutation of a potassium channel gene on chromosome 1. The pathogenesis of PED has also been linked to mutations in the GLUT1 glucose transporter which can result in transient energy deficits in the basal ganglia.
Paroxysmal dyskinesia
Paroxysmal nonkinesigenic dyskinesia
Pseudoathetosis
Tardive dyskinesia
Paroxysmal kinesigenic choreoathetosis
Choreoathetosis
Opsoclonus
Focal dystonia