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H. S. Pall, MD; A. C. Williams, MD; D. R. Blake, MD
Department of Neurology Queen Elizabeth Hospital Edgbaston Birmingham B15 2TH, England.

Arch Neurol. 1989;46(4):359-360.

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

To the Editor.

—Brewer and coworkers¹ suggest that the phenomenon of neurologic deterioration seen in some patients with Wilson's disease after starting penicillamine therapy may result from the redistribution of copper. Curzon² has previously suggested this mechanism, and Blake and coworkers³ and Pall and coworkers⁴ have shown that increases in copper in the cerebrospinal fluid occur during chelation therapy with desferrioxamine, relating this to the neurologic and the ophthalmic toxicity of the drug. The copper chelating agent, diethyl dithiocarbamate, has been shown to increase the copper content of neural tissue (spinal cord) in experimental animals.⁵ Other compounds that are capable of ligating with metal ions, such as the phenothiazines,⁶ can cause alterations of neural copper content,⁷ and can result in permanent neurologic deficit.⁸

The postulate of abnormalities of metal distribution being caused by metal chelating agents is not restricted to copper. British . . . [Full Text PDF of this Article]

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