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“Familial Parkinson's Disease” – A Case-Control Study of Families

Published online by Cambridge University Press:  18 September 2015

Ryan J. Uitti ,
Hitoshi Shinotoh ,
Margo Hayward ,
Michael Schulzer ,
Edwin Mak  and
Donald B. Calne
Ryan J. Uitti*
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
Hitoshi Shinotoh
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
Margo Hayward
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
Michael Schulzer
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
Edwin Mak
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
Donald B. Calne
Affiliation:
Neurodegenerative Disorders Centre, University of British Columbia, Vancouver.
*
Department of Neurology, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL USA 32224
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Abstract:

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Background:

Parkinson's disease (PD) patients frequently report a family history of PD and this may provide etiological clues to PD. It has also been suggested that a report of a negative family history is reliable. We studied the prevalence of PD in relatives of PD patients to assess the reliability of family history and to evaluate possible explanations of “familial PD”(fPD).

Methods:

81 of 650 (12.5%) PD probands (all PD patients seen at clinic in 4 years) reported a positive family history of PD. Each fPD proband was matched with non-familial PD (nfPD) proband by gender and year of birth. Screening and follow-up questionnaires were mailed to relatives to obtain information concerning pedigree and presence of neurodegenerative disease. Available family members (regardless of disease status) were examined.

Results:

On examination, 8 persons, said to be “normal” by probands, relatives and themselves, had definite or possible PD (5 fPD, 3 nfPD). The prevalence rate of PD among first and second degree living relatives of probands varied significantly between fPD and nfPD groups (6269/100 000 versus 1190/100 000; p < 0.001). The weighted prevalence (taking into account the proportions of fPD and nfPD within the clinic) was 1822/100 000, a value more than 5 times higher than reported prevalence rates of PD in the general population (p < 0.001). The prevalence rate was greater in first degree relatives than second degree.

Conclusions:

“Familial parkinsonism” cannot be explained merely by size of or advanced age within families. Significant numbers of previously unrecognized PD patients may be identified despite a “negative” family history. That is, the patient's report of an absence of familial parkinsonism is frequently inaccurate. The prevalence rate in relatives of PD patients appears to be higher than the general population – regardless of the family history reported by a PD patient. We believe our study suggests that genetic influences or early life environmental exposures are likely to be of etiological importance in PD.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 24 , Issue 2 , May 1997 , pp. 127 - 132
Copyright
Copyright © Canadian Neurological Sciences Federation 1997

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