Autosomal dominant and autosomal recessive forms of the disease have been reported. Mutations in several genes have been shown to cause<unk> . The precursor of the neurotransmitter<unk> , L-dopa, is synthesised from tyrosine by the enzyme tyrosine hydroxylase and utilises tetrahydrobiopterin (BH4) as a cofactor. A mutation in the gene GCH1, which encodes the enzyme GTP cyclohydrolase I, disrupts the production of BH4, decreasing<unk>  levels (hypodopaminergia). This results in autosomal-dominant<unk> . Mutations in the gene for tyrosine hydroxylase may lead to tyrosine hydroxylase deficiency, a rare form of<unk>  inherited in an autosomal recessive manner. The activity of<unk> rgic neurons in the nigrostriatal pathway normally peaks during the morning and also decreases with age until after age 20, which explains why the symptoms worsen during the course of the day and with increasing age until the third decade of life.
Dopamine-responsive dystonia
Paroxysmal exercise-induced dystonia
Levodopa-induced dyskinesia
Post-encephalitic parkinsonism
Myoclonic dystonia
Focal dystonia
Paroxysmal kinesigenic choreoathetosis
Cerebellar cognitive affective syndrome