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Shared Cause or Coincidence?

Ajit Kumar, DM; Susan M. Calne, RN; Michael Schulzer, MD, PhD; Edwin Mak, BSc; Zbigniew Wszolek, MD; Chris Van Netten, MD; Joseph K. C. Tsui, MD, FRCPC; A. Jon Stoessl, MD, FRCPC; Donald B. Calne, DM, FRSC

Arch Neurol. 2004;61:1057-1060.

Background  The spatial and temporal pattern of excessive disease occurrence, termed clustering, may provide clues about the underlying etiology.

Objective  To report the occurrence of 3 clusters of Parkinson disease (PD) in Canada.

Design and Patients  We determined the population groups containing the clusters, geographical limits, and duration of exposure to the specific environments. We tested whether there was an excessive presence of Parkinson disease by calculating the probability of the observed cases occurring under the null hypothesis that the disease developed independently and at random in cluster subjects. Results of genetic testing for mutations in the -synuclein, parkin, tau genes, and spinocerebellar ataxia genes (SCA2 and SCA3) were negative.

Results  The probabilities of random occurrence (P values) in the 3 clusters were P = 7.9 x 10 ^–7for cluster 1, P = 2.6 x 10 ^–7for cluster 2, and P = 1.5 x 10 ^–7for cluster 3.

Conclusions  Our findings indicate an important role for environmental causation in Parkinson disease. A possible role exists for environmental factors such as viral infection and toxins in the light of current evidence.

From the Pacific Parkinson's Research Centre, Vancouver Hospital and Health Sciences Centre (Drs Kumar, Schulzer, Tsui, Stoessl, and Calne, Ms Calne, and Mr Mak), and the Department of Health Care and Epidemiology (Dr Van Netten), University of British Columbia, Vancouver; and the Department of Neurology, Mayo Clinic, Jacksonville, Fla (Dr Wszolek).

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