<unk>  has long been thought to arise through pathological alterations in pre-synaptic and post-synaptic signal transduction in the nigrostriatal pathway (dorsal striatum). It is thought that the stage of illness, dosage of l-DOPA, frequency of l-DOPA treatment and the youth of the patient at the onset of symptoms; contributes to the severity of the involuntary movements associated with<unk> . In experiments employing real-time electrophysiological recordings in awake and active animals,<unk> s have been shown to be strongly associated with cortical gamma-oscillations with accompanying Δc-fos overexpression, proposedly due to a dysregulation of dopamine signaling in the cortico-basal ganglia circuitry. This was concluded partially from reduced tyrosine hydroxylase (TH) staining in the cortex - and the fact that a dopamine receptor 1 antagonist, delivered exclusively to the cortex, relieved the dyskinesia at its peak-time. ΔFosB overexpression in the dorsal striatum (nigrostriatal dopamine pathway) via viral vectors generates<unk>  in animal models of Parkinson's disease. Dorsal striatal ΔFosB is overexpressed in rodents and primates with dyskinesias; moreover, postmortem studies of individuals with Parkinson's disease that were treated with<unk>  have also observed similar dorsal striatal ΔFosB overexpression.
Levodopa-induced dyskinesia
Dopamine-responsive dystonia
Post-encephalitic parkinsonism
Paroxysmal exercise-induced dystonia
Parkinson-plus syndrome
Hyperkalemic periodic paralysis
Tardive dyskinesia
Cerebellar cognitive affective syndrome