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JOHN A. CHURCHILL, MD; ROBERT H. COLFELT, MD

Arch Neurol. 1963;9(4):400-406.

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

Prevailing opinion still holds that athetotic cerebral palsy has multiple causes in common with other types of cerebral palsy.¹ To some extent this viewpoint has been changed by the recognition that the history of neonatal jaundice is a factor commonly occurring with athetotic cerebral palsy,² whereas the history of prematurity commonly occurs with spastic diplegic cerebral palsy.^3-5 Conversely, histories of prematurity are not common in athetotic cerebral palsy, and histories of jaundice are not common in spastic diplegia. However, neonatal jaundice clearly is not the only factor important in the pathogenesis of athetotic cerebral palsy, since the history of neonatal jaundice is absent in a large proportion of cases with this kind of cerebral palsy.

Ideas relevant to the cause of athetosis, in cases lacking neonatal jaundice, have for the most part been based upon neuropathologic studies. Much attention has been paid to status marmoratus (état marbré) . . . [Full Text PDF of this Article]

Author Affiliations
DETROIT; SEATTLE

Footnotes
Submitted for publication May 17, 1963; accepted July 23, 1963.

Chief, Department of Research in Child Neurology, Lafayette Clinic, and Associate Professor, Department of Neurology, Wayne State University College of Medicine, Detroit (Dr. Churchill); Division of Neurology, University of Washington, Seattle (Dr. Colfelt).

This project was supported in part from the USPHS grant B-1309.

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