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Per Vaagenes, MD
Department of Anesthesiology Akershus Central Hospital N-1474 Nordbyhagen, Norway

Petter Urdal, MD
Department of Clinical Chemistry Ullevål Hospital Oslo 1, Norway

Arch Neurol. 1987;44(5):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.

In Reply.

—Increased activity in cerebrospinal fluid (CSF) of creatine kinase (CK) or of its more brain-specific BB isoenzyme (CK-BB) now appears to reliably indicate brain damage after brain ischemia^1,2 and head trauma^3,4 and possibly also after stroke.⁵ Unfortunately, the clinical use of CK and CK-BB measurements has been, and to some extent still is, hampered by technical difficulties. Some of these problems have been discussed previously.^6,7 Chandler and coworkers focus on two of the more important ones: the use of a reactivator and the possible presence in CSF of mitochondrial CK (CK-mt) in addition to the cytoplasmic forms.

Creatine kinase is rapidly inactivated in serum and CSF but is reactivated prior to assay with the use of an SH-compound, which is a reactivator that is now included in all commercial CK reagents. We use reagents containing N-acetylcysteine (NAC) as a reactivator. Dithiothreitol (DTT) is a . . . [Full Text PDF of this Article]

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