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(Stroke. 2005;36:2532.)
© 2005 American Heart Association, Inc.
Letters to the Editor |
Division of Neurosurgery, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong, China
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
To the Editor:
We read with great interest the article by Naidech et al.1 The authors started from the abstract statement that "Phenytoin is routinely used for seizure prophylaxis after subarachnoid hemorrhage ... ... " and went on to investigate the possible harmful effects on cognitive and neurological outcome. After a study of 527 subarachnoid hemorrhage patients, the authors concluded that higher quartiles of phenytoin burden were associated with worse telephone interviews for cognitive status scores at hospital discharge (P<0.001) and at 3 months (P=0.003) as well as poor functional outcome at 14 days (P<0.001) but not at 3 months (P=0.09). The authors then suggested that exposure to phenytoin after subarachnoid hemorrhage should be minimized and argued for a prospective study of phenytoin in patients at high risk for seizures after subarachnoid hemorrhage.
We avoid using phenytoin as anticonvulsant prophylaxis in patients with aneurysmal subarachnoid hemorrhage in our center for another reason. Oral nimodipine is currently indicated in patients with aneurysmal subarachnoid hemorrhage to reduce the risk of poor outcome and secondary ischemia after aneurysmal subarachnoid hemorrhage.2 Nimodipine is metabolized via the cytochrome P450 3A4 system located in both the intestinal mucosa and in the liver. Drugs that are known to either inhibit or to induce this enzyme system may therefore alter the first pass metabolism or clearance of nimodipine. As recommended by the company information sheet (UK),3 Nimotop tablets should not be administered concomitantly with drugs which induce the CYP 3A4
Northern University, Neurology, Chicago, IL
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