Before his death in 1824, Parkinson expressed the hope that in the future, researchers would investigate the pathology of the disease because he was unable to. Many tried to tackle this feat. In 1871, Theodor Meynert suggested that the disease was due to some dysfunction of the basal ganglia. Through 1902, Hermann Oppenheim considered the disease a neurosis. Edouard Brissaud suggested that the disease was due to a lesion in the substantia nigra in 1894. Kinnie Wilson, in 1912, termed the pathway that he thought to be involved with the development of rigidity as the "extrapyramidal pathway". By 1919, the idea that the substantia nigra was the affected region of the brain was accepted, and many studies were done investigating this area.
At this time, the symptoms used to describe PD were also used to describe encephalitis lethargica, which caused an epidemic in Europe in 1915. There was continued debate that the basis for the disease lied in the stubstantia nigra. It wasn't until 1925 that it was widely accepted that the rigidity and tremor characteristic of Parkinson's Disease were due to the loss of inhibition in the pathway that included the axon cells of the substantia nigra which end primarily in the lenticular nucleus of the corpus striatum. Years after this agreement, PD was associated with depleted dopamine production in the subcortical motor circuitry. (Finger, 1994)