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Victor Ionasescu, MD; Hans Zellweger, MD; Lloyd J. Filer, Jr., MD, PhD; Thomas W. Conway, PhD

Arch Neurol. 1970;23(2):128-136.

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

THE etiology and pathogenesis of arthrogryposis multiplex congenita (AMC) are not well understood. Most investigators accept the concept that the disease is a syndrome with different causes. These may be genetic¹ or environmental² and can be associated with neurological lesions of supranuclear structures³ or of anterior horn cells,^4,5 primary muscle disorders,^6,7 or failure of muscle development (amyoplasia).⁸ In an attempt to evolve a unified hypothesis, McKusick⁹ proposed that several clinical features of AMC, such as changes in the joints or the skin and the occurrence of hernia, suggest a heritable disorder of connective tissue. Consistent with this view is the histopathological study of Hariga et al,¹⁰ suggesting that an increase of fibrous tissue precedes muscle fiber degeneration. Nevertheless, there is a clear need for biochemical data to support this idea.

As part of a broader study of protein synthesis in human . . . [Full Text PDF of this Article]

Author Affiliations
Iowa City

From the departments of pediatrics (Drs. Ionasescu, Zellweger, and Filer) and biochemistry (Dr. Conway), University of Iowa, Iowa City.

Footnotes
Submitted for publication Feb 12, 1970; accepted March 9.

Reprint requests to Department of Pediatrics, University Hospitals, Iowa City 52240 (Dr. Zellweger).

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