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G. Holmes, MD
Dept of Neurology Univ of Virginia Med Center Charlottesville, VA 22901

Arch Neurol. 1977;34(5):321.

	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.—

The recent article by Trauner et al (Arch Neurol 34:116, 1977) on EEG correlation with serum short-chain fatty acids in Reye's syndrome raised a possibility that the severity of the encephalopathy and associated EEG abnormalities in Reye's syndrome may be partly the result of organic acid effects on the CNS. They concluded the article by encouraging other investigators to continuously monitor EEG in a series of patients with Reye's syndrome in order to fully study the effects of biochemical abnormalities on the EEG pattern. In view of the evidence for increased intracranial pressure secondary to cerebral edema being the major contributing factor to death in Reye's syndrome^1,2 and the improvement both clinically and on EEG with control of the pressure,³ the question is raised whether the improvement in EEG mentioned in the article by Trauner et al was a reflexion of the change in short-chain . . . [Full Text PDF of this Article]

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