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JOHN F. KURTZKE, M.D.

Arch Neurol. 1962;7(5):371-376.

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

Deficiency of ceruloplasmin, a copper-binding ₂-globulin, is considered to be a primary feature of Wilson's disease, or hepatolenticular degeneration.^1,2 In almost all instances of this disease this protein is present in small amounts averaging 10 mg/100 ml, whereas the normal is about 30 mg. However, there have been a number of cases reported (Table) in which ceruloplasmin has been found to be within the normal range. For this reason the pathogenic role of ceruloplasmin deficiency in this disorder has been questioned by Rosenoer³ in presenting such a case, a 14-year-old girl with neurologic dysfunction but no symptoms referable to the liver. The patients of Enger⁴ and Sass Kortsak⁵ demonstrated cirrhosis, Kayser-Fleischer rings, and cupriuria, but no neurologic defects; these too had normal ceruloplasmin. In Walshe's⁶ cases only the liver defects of the disease were found in one (Case V, Table) while another (Case . . . [Full Text PDF of this Article]

Author Affiliations
COATESVILLE, PA.

Neurology Service, Veterans Administration Hospital, Coatesville, Pa., and Department of Neurology, Jefferson Medical College, Philadelphia.

Footnotes
Submitted for publication May 15, 1962.

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