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Late Progression of Post-Encephalitic Parkinson's Syndrome

Published online by Cambridge University Press:  18 September 2015

Donald B. Calne  and
Andrew J. Lees
Donald B. Calne*
Affiliation:
Belzberg Laboratory of Clinical Neuroscience, University of British Columbia, Vancouver, British Columbia
Andrew J. Lees
Affiliation:
The National Hospital for Nervous Diseases, Queen Square, London, England
*
Division of Neurology, U.B.C., Health Sciences Centre Hospital, 2211 Westbrook Mall, Vancouver, British Columbia, Canada V6T IW5
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Abstract:

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We have studied 11 patients with neurological deficits due to the pandemic of encephalitis lethargica, all of whom had remained in hospital for more than forty years. Retrospective information obtained from physicians and nurses dating back as far as 1931, our own Webster and Northwestern University Disability Rating Scales available from 1976, photographic records, published narrative and hospital charts all indicate that neurological disabilities attributable to basal ganglia damage frequently increase in late life. Deterioration was most marked in motor function and largely spared the intellect, special senses and somatosensory system. The findings are discussed in relation to current hypotheses concerning the aetiology of Parkinson's disease.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 15 , Issue 2 , May 1988 , pp. 135 - 138
Copyright
Copyright © Canadian Neurological Sciences Federation 1988

References

REFERENCES

1.Howard, RS, Lees, AJ. Encephalitis lethargica. A report of four recent cases. Brain 1987; 110: 19–33.CrossRefGoogle ScholarPubMed
2.Williams, A, Houff, S, Lees, A, Calne, DB. Oligoclonal banding in the cerebrospinal fluid of patients with postencephalitic parkinsonism. Journal of Neurology, Neurosurgery and Psychiatry 1979; 42: 790–792.CrossRefGoogle ScholarPubMed
3.Calne, DB, Langston, JW. Aetiology of Parkinson’s disease. Lancet 1983; 31: 1457–1459.CrossRefGoogle Scholar
4.Calne, DB, Eisen, A, McGeer, E, Spencer, P. Alzheimer’s disease, Parkinson’s disease, and Motorneuron disease: Abiotrophic interaction between aging and environment? The Lancet 1986; 2: 1067–1070.CrossRefGoogle Scholar
5.Martin, JP. The Basal Ganglia and Posture. London: Pitman Medical Publishing Co. Ltd., 1967.Google Scholar
6.Webster, DD. Clinical analysis of the disability in Parkinson’s disease. Mod Treat 1968; 5: 257–282.Google Scholar
7.Canter, CJ, de la Torr, R, Mier, M. A method of evaluating disability in patients with Alzheimer’s disease. J Nerv Mental Dis 1961; 133: 143–147.CrossRefGoogle Scholar
8.Wilson, SAK. Neurology. Edited by Bruce, ANLondon: Arnold 1940: 99–144.Google Scholar
9.Duvoisin, RC, Yahr, MD. Encephalitis and parkinsonism. Arch Neurol 1965; 12: 227–239.CrossRefGoogle ScholarPubMed
10.Duncan, AG. The sequelae of encephalitis lethargica. Brain 1924; 47: 76–108.CrossRefGoogle Scholar
11.Teravainen, H, Calne, DB. Motor system in normal aging and Parkinson’s disease. In: Katzman, R, Terry, RD (eds.). Neurology of Aging: Contemporary Neurology Series. F.A. Davis Company, Philadelphia 1981; 85–109.Google Scholar
12.Gibb, WRG, Lees, AJ. The progression of idiopathic Parkinson’s disease is not explained by age-related changes. Clinical and pathological comparisons with post-encephalitis parkinsonian syndrome. Acta Neuropathol 1987 (in press).Google Scholar
13.Shoulson, I. Experimental therapeutics directed at the pathogenesis of Parkinson’s disease. In: Calne, DB (ed.) Handbook of Experimental Pharmacology: Drugs for the treatment of Parkinson’s disease. Springer-Verlag, Heidelberg 1988 (in press).Google Scholar