Parkinson Disease

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James Parkinson first described Parkinson disease (PD), a neurodegenerative disorder with an incidence range from 4.9 to 26 per 100,000 and prevalence of approximately 200 per 100,000, in 1817 in his monograph Essay on the Shaking Palsy. Parkinson termed the disease "paralysis agitans" and reported resting tremor, festinant gait, flexed posture, dysarthria, dysphagia, insomnia, and constipation as the hallmarks of the condition. Charcot subsequently used the term "Parkinson's disease," and differentiated the resting tremor of PD from the cerebellar outflow action tremor seen in multiple sclerosis. He also noted that tremor was not always present in all PD cases, and that cognitive decline may also be a part of the disease. In 1893 researchers discovered that the substantia nigra was abnormal in those afflicted with PD. Subsequent examinations of the brains of patients dying with idiopathic PD demonstrated depigmentation of the substantia nigra in the midbrain, associated with a loss of dopamine-producing cells (Duvoisin 1992).

In 1957, after demonstrating a reversal of the reserpine effects (depletion of central monoamines) in rabbits and mice, Carlsson reported that approximately 80% of all brain-derived dopamine was localized within the basal ganglia. Hornykiewicz and Birkmeyer and Barbeau independently reported therapeutic benefit from levodopa, and PD became the first disease treated by neurotransmitter replacement (Duvoisin 1992). In 1983 an effort led by Langston determined that a group of intravenous narcotic users developed a profound Parkinsonian syndrome after self-injecting 1-methyl-4-phenyl-1,2,26-tetrahydropyridine (MPTP), a meperidine analog (Ballard et al. 1985). The discovery of this compound led to the creation of animal models, and served as the observation leading to the Deprenyl and Tocopherol Antioxidant Therapy for Parkinson Disease (DATATOP) clinical trial, the initial study of the Parkinson Study Group.

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