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The Epidemiology of Parkinson's DiseaseA Case-Control Study of Young-Onset and Old-Onset Patients
Matthew Stern, MD;
Eugene Dulaney;
Stephen B. Gruber, PhD;
Larry Golbe, MD;
Mary Bergen, RN;
Howard Hurtig, MD;
Steve Gollomp, MD;
Paul Stolley, MD, MPH
Arch Neurol. 1991;48(9):903-907.
Abstract
• While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio=2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio=0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors. While we were unable to link specific environmental agents with PD, our study suggests that head trauma should be reassessed as a potential risk factor for PD.
Author Affiliations
From the Department of Neurology, Graduate Hospital (Drs Stern, Hurtig, and Gollomp and Mr Dulaney), Clinical Epidemiology Unit, Department of Medicine (Drs Gruber and Stolley), University of Pennsylvania, Philadelphia; and Department of Neurology, University of Medicine and Dentistry of New Jersey, New Brunswick (Dr Golbe and Ms Bergen).
Footnotes
Accepted for publication March 12, 1991.
Reprint requests to Department of Neurology, Graduate Hospital, Pepper Pavilion, Suite 900, 18th and Lombard streets, Philadelphia, PA 19146 (Dr Stern).
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