Dopamine Transporter Imaging for Distinguishing Between Idiopathic Parkinson’s Disease and Secondary Parkinsonism

Idiopathic Parkinson’s disease (IPD), first described by James Parkinson in 1817, is a sporadic neurodegenerative disorder. The main clinical features include masked face, resting tremor, bradykinesia, rigidity, festinating gait, and loss of postural reflexes. The clinical features are most insidious and usually asymmetric at onset. The asymmetry may persist even in a late stage and progress slowly. The pathological findings are characterized by loss of pigmented dopamine neurons in the substantia nigra, particularly the pars compacta and locus ceruleus, and the presence of Lewy bodies. The cause of IPD remains unknown. Parkinsonism (PM) is not a single disease but a common clinical presentation. The clinical syndrome is characterized by tremors, bradykinesia, rigidity, and postural instability. Exposure to toxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which was sold as “synthetic heroin,” manganese (Mn), carbon disulfide (CS2), carbon monoxide (CO), methanol, cyanide, and other organic solvents may cause brain damage, leading to features similar to PM. Many neurodegenerative disorders may present with PM, including progressive supranuclear palsy (PSP), multiple system atrophy (MSA), spinocerebellar atrophy (SCA), and corticobasal sundrome (CBS). Several genetic diseases, including doparesponsive dystonia (DRD), Wilson’s disease (WD), and Huntington’s disease (HD), may cause degeneration in the basal ganglia or affect the dopaminergic pathway. Furthermore, some dementia syndromes may be associated with PM, including vascular parkinsonism (multiple infarct parkinsonism), dementia with Lewy bodies (DLB), and frontotemporal dementia, and parkinsonism linked to chromosome 17 (FTD-17). The main treatment of IPD includes the use of dopamine, dopamine agonists, monoamine oxidase inhibitors, and catechol-o-methyltransferase inhibitors. The above medications are