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Review
. 2012 Dec 12;16(2):216.
doi: 10.1186/cc11230.

Quantitative EEG for the detection of brain ischemia

Affiliations
Review

Quantitative EEG for the detection of brain ischemia

Brandon Foreman et al. Crit Care. .
No abstract available

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Figures

Figure 1
Figure 1
The relationship of cerebral blood flow to electroencephalogram (EEG) and pathophysiology. ATP, adenosine triphosphate (CBF). Data from [2,4].
Figure 2
Figure 2
(a) Alpha/delta ratio (ADR) calculated every 15 min and Glasgow Coma Score (GCS), shown for days 6-8 of continuous EEG (cEEG) monitoring. (b) A 57-year old woman admitted for acute subarachnoid hemorrhage (admission Hunt-Hess grade 4) from a right posterior communicating aneurysm. Admission angiography did not show vasospasm. The aneurysm was clipped on SAH day 2. No infarcts were seen on postoperative computed tomography (CT) scan. Postoperatively she had a GCS of 14. cEEG monitoring was performed from SAH days 3 to 8. The ADR progressively decreased after day 6, particularly in the right anterior region (blue arrow), to settle into a steady trough level later that night, reflecting loss of fast frequencies and increased slowing over the right hemisphere in the raw cEEG (c; EEG2 compared with EEG1). On SAH day 6, flow velocities in the right MCA were marginally elevated (144cm/s), but the patient remained clinically stable with hypertensive, hypervolemic therapy (systolic blood pressure >180 mmHg). On day 7, the GCS dropped from 14 to 12 and a CT scan showed a right internal capsule and hypothalamic infarction (b, Day 7). Angiography demonstrated severe distal right MCA and left vertebral artery spasm; however, due to the marked tortuosity of the parent vessels and the location of vasospasm, a decision was made not to perform angioplasty, but to infuse verapamil and papaverine. This resulted in a marked, but transient increase of the right anterior and posterior alpha/delta ratios (blue shaded area). Later that day the patient further deteriorated clinically to a GCS of 7, with a new onset left hemiparesis, and died on SAH day 9 from widespread infarction due to vasospasm. From [9] with permission.

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