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Jack E. Riggs, MD

Arch Neurol. 1993;50(6):653-656.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Parkinson's disease is one of the more prevalent neuro-degenerative disorders. Over the past two decades, mortality attributed to Parkinson's disease in industrialized nations has risen significantly (Fig 1).^1,2 This recent increase in mortality has occurred on a background of overall Parkinson's disease mortality rates that had been stable for decades^3-5 and following the introduction of levodopa therapy, a treatment that has significantly enhanced survival.⁶ This evolving mortality pattern in Parkinson's disease has been attributed to better case ascertainment and environmental toxins that may have assumed an increased role in the etiopathogenesis of Parkinson's disease.^1,2 The purpose of this communication is to demonstrate a theoretical model of human aging and mortality that is remarkably consistent with available Parkinson's disease mortality data. This model suggests that neither environmental influences nor changing diagnostic practices are responsible for the rise in overall Parkinson's disease mortality.

BACKGROUND

In 1825, Gompertz⁷ . . . [Full Text PDF of this Article]

Author Affiliations
From the Departments of Neurology, Medicine, and Community Medicine, West Virginia University School of Medicine, Morgantown.

Footnotes
Accepted for publication December 10, 1992.

Reprint requests to Department of Neurology, West Virginia University Health Sciences Center, Morgantown, WV 26506 (Dr Riggs).

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