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Wayne L. Chandler, MD; Kathleen J. Clayson, MS; James S. Fine, MD
Department of Laboratory Medicine

W. T. Longstreth, Jr, MD
Division of Neurology Department of Medicine University of Washington Seattle, WA 98195

Arch Neurol. 1987;44(5):471-472.

	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.

—Several investigators have described creatine kinase (CK) activity in the cerebrospinal fluid (CSF) of patients with stroke.^1-4 In a recent investigation, Vaagenes et al⁴ used an assay to measure CSF CK that did not include the addition of reactivating agents prior to analysis.^5,6 We have found that the majority of the CK in CSF from patients with acute neurologic injury was present in a reversibly inactivated form.^7,8 The presence of dithiothreitol or N-acetylcysteine in the CK reagents alone was not sufficient to fully reactivate the CK. To regain maximum CK activity in CSF, the sample should be reactivated by adding dithiothreitol directly to the CSF (10 mg/mL) and then incubated at room temperature for at least ten minutes.

In addition, Vaagenes and associates estimated activity of the CSF CK-B subunit by measuring total CSF CK after immunoinhibition with anti-CK-M antibodies. This assumes that . . . [Full Text PDF of this Article]

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