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EEG monitoring for induced hypotension for surgery of intracranial aneurysms

EEG was monitored at bilateral scalp sites outside the operative field during hypotensive aneurysm surgery in 21 patients. Mean arterial blood pressure at axillary level was 50-60 mm Hg (average 55 mm) for 1.9-5.3 hours (average 3.6). Four new deficits were noted immediately post-operatively, all re...

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Published in:Stroke (1970) 1979-05, Vol.10 (3), p.292-294
Main Authors: Jones, T H, Chiappa, K H, Young, R R, Ojemann, R G, Crowell, R M
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container_end_page 294
container_issue 3
container_start_page 292
container_title Stroke (1970)
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creator Jones, T H
Chiappa, K H
Young, R R
Ojemann, R G
Crowell, R M
description EEG was monitored at bilateral scalp sites outside the operative field during hypotensive aneurysm surgery in 21 patients. Mean arterial blood pressure at axillary level was 50-60 mm Hg (average 55 mm) for 1.9-5.3 hours (average 3.6). Four new deficits were noted immediately post-operatively, all related to the operated site: these were attributable to intra-operative rupture with forced vascular clipping, vasospasm, or edema. In no instance was hypotension solely responsible for a new deficit. EEG showed persistent slowing in relation to surgery in only 1 patient, where aneurysmal rupture led to severe hypotension, forced clipping of 1 posterior cerebral artery, and subsequent brain stem infarction. In the 3 other patients with fresh focal postoperative deficits, no persistent intraoperative EEG changes were observed. EEG monitoring did not detect ischemia in these 3 patients because 1) hypotension was moderate and did not per se cause new deficit, and 2) EEG electrodes did not survey the area at maximal risk, namely the operative field. EEG scalp electrodes near but outside the operative site do not seem useful for monitoring cerebral function in the region of aneurysm surgery. Epidural or cortical electrodes in the operative field may prove to be more useful.
doi_str_mv 10.1161/01.STR.10.3.292
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Mean arterial blood pressure at axillary level was 50-60 mm Hg (average 55 mm) for 1.9-5.3 hours (average 3.6). Four new deficits were noted immediately post-operatively, all related to the operated site: these were attributable to intra-operative rupture with forced vascular clipping, vasospasm, or edema. In no instance was hypotension solely responsible for a new deficit. EEG showed persistent slowing in relation to surgery in only 1 patient, where aneurysmal rupture led to severe hypotension, forced clipping of 1 posterior cerebral artery, and subsequent brain stem infarction. In the 3 other patients with fresh focal postoperative deficits, no persistent intraoperative EEG changes were observed. EEG monitoring did not detect ischemia in these 3 patients because 1) hypotension was moderate and did not per se cause new deficit, and 2) EEG electrodes did not survey the area at maximal risk, namely the operative field. EEG scalp electrodes near but outside the operative site do not seem useful for monitoring cerebral function in the region of aneurysm surgery. 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EEG scalp electrodes near but outside the operative site do not seem useful for monitoring cerebral function in the region of aneurysm surgery. 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subjects Adult
Blood Pressure
Brain Damage, Chronic - etiology
Brain Ischemia - etiology
Electroencephalography
Female
Humans
Hypotension, Controlled
Intracranial Aneurysm - surgery
Male
Middle Aged
Postoperative Complications - etiology
title EEG monitoring for induced hypotension for surgery of intracranial aneurysms
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