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New Data on the Genetics of Parkinson’s Disease

Published online by Cambridge University Press:  18 September 2015

André Barbeau  and
Emmanuelle Pourcher
André Barbeau*
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal and University of Montreal
Emmanuelle Pourcher
Affiliation:
Department of Neurobiology, Clinical Research Institute of Montreal and University of Montreal
*
Clinical Research Institute of Montreal, 110 West Pine Ave, Montreal, Quebec, Canada, H2W 1R7
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We investigated the clinical and metabolic characteristics of Parkinsonian patients whose illness started before the age of 40. A pilot study of 32 of our own such cases revealed the existence of 3 subgroups: 1. Post-Encephalitic, 2. Onset and course with predominant tremor, 3. Onset and course with akinesia and rigidity. In this early onset group of patients, there was a 46% incidence of familial cases (as opposed to 10-15% in the general Parkinson population). The cases with tremor onset had a high prevalence of essential tremor in their families, while those with an akinetorigid onset had a high familial incidence of other cases of Parkinson’s Disease. Familial grey hair, hypertension, diabetes and thyroidopathies appeared to be in higher than expected frequency.

These trends were confirmed in a larger series of 135 cases of early onset Parkinson obtained through a mail survey. When the same clinical material was analysed for the familial cases only, two new genetic subgroups emerged: 1) a familial metabolic akineto-rigid syndrome (with hypertension, familial diabetes, hypothyroidism and a more severe course) and, 2) a familial essential tremor-related Parkinsonian syndrome (with familial grey hair trait and hyperthyroidism). These new genetic syndromes along with the recently described “Familial juvenile Parkinsonism” require many further prospectives metabolic and clinical investigations for full characterization, but confirm our hypothesis that “idiopathic” Parkinson’s disease is not a single homogeneous entity.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 9 , Issue 1 , February 1982 , pp. 53 - 60
Copyright
Copyright © Canadian Neurological Sciences Federation 1982

References

REFERENCES

Ayd, F.J. (1961). A survey of drug-induced extrapyramidal reactions. J. Am Med. Ass. 197: 1054–1069CrossRefGoogle Scholar
Barbeau, A. and Joly, J.G. (1963). Parkinson et cancer. Union médicale du Canada 92: 169–174Google Scholar
Barbeau, A. and Raymond-Tremblay, W. (1965). Recent biochemical studies in Parkinson’s Disease and position of the problem. In: Parkinson’s Disease – Trends in Research and Treatment, (ed. Barbeau, A.Doshay, L. and Spiegel, E.A.) Grune & Stratton, pp. 79–94Google Scholar
Bartels, E.C. and Rohart, R.R. (1958). The Relationship of Hyperthyroidism and Parkinsonism. AMA Arch. Int. Med. 101: 562–568CrossRefGoogle ScholarPubMed
Baumann, R.J.; Jameson, H.D.; McKean, H.E.; Haack, D.G. and Weisberg, L.M. (1980). Cigarette smoking and Parkinson’s Disease: 1. A comparison of cases with matched neighbors. Neurology (NY) 30: 839–843CrossRefGoogle ScholarPubMed
Berger, J.R. and Kelley, R.E. (1981) Thyroid function in Parkinson Disease. Neurology (NY) 31: 93–95CrossRefGoogle ScholarPubMed
Berger, J.R. and Ross, D.B. (1981). Reversible Parkinson syndrome complicating postoperative hypoparathyroidism. Neurology (NY) 31: 881–882CrossRefGoogle ScholarPubMed
Birmayer, W., Reiderer, P. and Youdim, J.B.H. (1979). Distinction between benign and malignant type of Parkinson’s Disease. Clin. Neurol. Neurosurg. 81: 158–164CrossRefGoogle Scholar
Clarke, H.A. and Frame, B. (1962). Parkinson’s Disease associated with hypothyroidism. Henry Ford Hospital Med. Bull. 10: 51–53Google Scholar
Duvoisin, R.C., Gearing, F.R.; Schweitzer, M.D., and Yahr, M.D. (1969). A family study of Parkinsonism. In: Progress in neuro-genetics (Ed. Barbeau, A. and Brunette, J.R.) Excerpta Medica Foundation, Amsterdam pp. 492–496Google Scholar
Kessler, I.I. (1978). “Parkinson’s Disease in Epidemiologic Perspective”. Advances in Neurology 19: 355–384Google ScholarPubMed
Kondo, K., Jurland, L.T. and Schull, W.J. (1973). Parkinson’s Disease. Genetic Analysis and Evidence of a Multifactorial Etiology. Mayo Clinic Proc 48: 465–475Google ScholarPubMed
Martin, W.E., Resch, J.A. and Baker, A.B. (1971). Juvenile Parkinsonism. Arch. Neurol. 25: 494–500CrossRefGoogle ScholarPubMed
Martin, W.E., Young, W.I. and Anderson, V.E. (1973). Parkinson’s Disease – A genetic Study. Brain 96: 495–506CrossRefGoogle ScholarPubMed
MjöNes, H. (1949). Paralysis agitans: A clinical and genetic study. Acta Psychiat. Scand., Suppl. 54p. I.Munksgaard. Copenhagen.Google Scholar
Mortimer, J.A., Pirozzolo, F.J., Hansch, E.C. and Webster, D.A. (1981). Relation of motor symptoms to intellectual deficits in Parkinson’s Disease. Neurology (NY) 31: 61Google Scholar
Myrianthopoulos, N.C., Waldrop, F.N. and Vincent, B.L. (1969). A repeat study of hereditary predisposition in drug-induced Parkinsonism. In: Progress in Neuro-genetics (Ed. A. Barbeau and J.R. Brunette) Excerpta Medica Foundation, Amsterdam, pp. 486–491Google Scholar
Nowack, WJ. (1980). Hyperthyroidism, Parkinsonism and Tri-iodo thyronine receptors. Soc. Neurosciences Abst. 6: 803Google Scholar
Ward, CD., Duvoisin, R.C., Ince, S.E., Nutt, J.D., Eldridge, R. and Calne, D.B. (1981). Parkinson’s Disease in twins and in a set of quadruplets. Neurology (NY) 31: 110Google Scholar
Yokochi, M. and Narabayashi, H. (1981). Clinical characteristics in juvenile Parkinsonism. In: Research Progress in Parkinson’s Disease. (Rose, F. Clifford and Capildeo, R., Eds). Pitman Medical, Turnbridge Wells, pp 35–39.Google Scholar