Abstract

To the Editor: With great interest we read the article by Thomas et al1 recently published in Stroke. The authors proposed the intrathecal administration of the nitric oxide donor sodium nitroprusside (SNP) as a novel means to treat refractory cerebral vasospasm. However, although amelioration or even reversal of large cerebral vessel constriction was shown by cerebral angiography, the article failed to provide data on the acute and long-term effect of SNP on cerebral vasospasm–associated ischemia and hypoxia. Therefore, in addition to their report, we here show the effect of intrathecal SNP on episodes of severely reduced cerebral blood flow and brain tissue oxygenation in a patient suffering from refractory cerebral vasospasm. Seven days after subarachnoid hemorrhage (Hunt and Hess grade II) and uneventful operation of bilateral middle cerebral artery (MCA) aneurysms, a 31-year-old female patient presented with right-sided hemiparesis and progressive neurological deterioration. Transcranial Doppler recordings of the MCAs had elevated from values <100 cm/s to 205 cm/s and 180 cm/s on the left and right sides, respectively. Cerebral angiography revealed severe cerebral vasospasm, which was most pronounced in the left MCA (M1 and M2 segments). Consequently, the patient was sedated and intubated, and a right frontal ventriculostomy for intracranial pressure (ICP) monitoring was performed. In addition, a polarographic brain tissue oxygen (ptiO2) microprobe2 and a thermal diffusion regional cerebral blood flow (rCBF) microprobe3 were implanted subcortically into the white matter of the left frontal MCA territory. Thereby, using a PC-based multimodality neuromonitoring system, mean arterial blood pressure (MABP), ICP, cerebral perfusion pressure (CPP=MABP−ICP), ptiO2, and rCBF were monitored continuously at the bedside with a sampling rate of 1 Hz. Thresholds for severe ischemia and hypoxia were defined as rCBF <6 mL/100 g/min and ptiO2 <10 mm Hg, as previously reported.3 4 …

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