BACKGROUND AND PURPOSE: The determinants of ischemic complications in subarachnoid hemorrhage (SAH) are not well defined. The objective of this study is to evaluate the role of microemboli in SAH-related cerebral ischemia. METHODS: Forty patients with aneurysmal SAH were monitored with transcranial Doppler (TCD) for the presence of embolic signals (ES) and vasospasm, and followed clinically for the development of cerebral ischemic symptoms, from the time the aneurysm was secured until day 14 posthemorrhage or discharge. RESULTS: Microembolic signals were detected in 15/40 patients, appeared at a mean of 6.7 days after hemorrhage, and were often noted bilaterally. There was a close association between ES and cerebral ischemic symptoms (P= .003), and ES were commonly present in the distribution of the vessel with ischemic symptoms. Ultrasonographic vasospasm did not correlate with ischemia and there was no relationship between microembolic signals and vasospasm. CONCLUSIONS: In this study, ES detected in over a third of SAH victims, were associated with the development of cerebral ischemic symptoms, and were not related to vasospasm, but rather appeared to be an independent risk factor for the development of ischemic symptoms in SAH.
BACKGROUND AND PURPOSE: The determinants of ischemic complications in subarachnoid hemorrhage (SAH) are not well defined. The objective of this study is to evaluate the role of microemboli in SAH-related cerebral ischemia. METHODS: Forty patients with aneurysmalSAH were monitored with transcranial Doppler (TCD) for the presence of embolic signals (ES) and vasospasm, and followed clinically for the development of cerebral ischemic symptoms, from the time the aneurysm was secured until day 14 posthemorrhage or discharge. RESULTS: Microembolic signals were detected in 15/40 patients, appeared at a mean of 6.7 days after hemorrhage, and were often noted bilaterally. There was a close association between ES and cerebral ischemic symptoms (P= .003), and ES were commonly present in the distribution of the vessel with ischemic symptoms. Ultrasonographic vasospasm did not correlate with ischemia and there was no relationship between microembolic signals and vasospasm. CONCLUSIONS: In this study, ES detected in over a third of SAH victims, were associated with the development of cerebral ischemic symptoms, and were not related to vasospasm, but rather appeared to be an independent risk factor for the development of ischemic symptoms in SAH.
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