Frontotemporal dementia (Picks disease)
Gerstmann–Sträussler–Scheinker syndrome
Huntingtons disease
Lytico-bodig disease (ALS complex of Guam)
Multiple system atrophy (Shy–Drager syndrome)
Neuroacanthocytosis
Neuronal ceroid lipofuscinosis
Olivopontocerebellar atrophy
Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation
Parkin mutation (hereditary juvenile dystonia)
Parkinsons disease
Parkinsons disease dementia
Progressive supranuclear palsy
Wilsons disease
X-linked dystonia parkinsonism (Lubag syndrome)

Drug-induced ("pseudoparkinsonism")
About 7% of people with parkinsonism developed symptoms as a result of side effects of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), and rarely, antidepressants. Yet another drug that can induce parkinsonism is the antihistaminic medication cinnarizine, usually prescribed for motion sickness; this is because besides antagonizing histamine receptors this drug antagonizes the dopamine D2 receptors. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level and does not worsen like Parkinsons disease.Implicated medications include:

Antipsychotics
Lithium
Metoclopramide
MDMA addiction and frequent use
Tetrabenazine
Cinnarizine

Infectious
Creutzfeldt–Jakob disease
Encephalitis lethargica
HIV infection and AIDS

Toxins
Evidence exists of a link between exposure to pesticides and herbicides and PD; a two-fold increase in risk was seen with paraquat or maneb/mancozeb exposure.Chronic manganese (Mn) exposure has been shown to produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this parkinsonism-like disease.
That is, it cannot be transferred directly from person to person.Researchers are challenged in understanding the prevalence of RBF. One factor that limits the known number of cases of RBF in the United States is that it is not a reportable disease there. RBF is classified as a notifiable disease, which means it is required by the state to be reported, however, the state is not mandated to provide that information to the United States Centers for Disease Control. Identification of RBF is also hindered due to the presence of two different etiological bacterial agents, Streptobacillus moniliformis and Spirillum minus. RBF caused by Sp. minus is more commonly found in Asia and is termed Sodoku, whereas St. moniliformis is found more often in the United States and in the Western Hemisphere. Although cases of RBF have been reported all over the world, the majority of cases that have been documented are caused by St. moniliformis primarily in the United States, where approximately 200 cases have been identified and reported. Due to increasing population density, this illness is being seen more frequently, as humans have increased their contact with animals and the zoonotic diseases they carry. Most cases of the disease have been reported from densely populated regions, such as big cities. The populations at risk have broadened due to the fact that domestic rats have become a common household pet.