EEG for Aneurysms and AVMs

EEG for Aneurysms and Arteriovenous Malformations

GUIDELINES FOR INTRAOPERATIVE NEUROMONITORING USING RAW (ANALOG OR DIGITAL WAVEFORMS) ANDQUANTITATIVE ELECTROENCEPHALOGRAPHY

A POSITION STATEMENT BY THE AMERICAN SOCIETY OF NEUROPHYSIOLOGICAL MONITORING :http://www.asnm.org/EEG41.pdf

Aneurysms and Arteriovenous Malformations

Intraoperative neuromonitoring using rEEGand qEEG during the clipping of cerebral aneurysms has traditionally been used for two purposes. The first is the detection of cerebral ischemia during the dissection and clipping of an intracranial aneurysm, which is of paramount importance. Compromised cerebral perfusion can occur during either placement of retractors for surgical exposure and placement of the aneurysm clip, or both. Both the rEEG and qEEG are neuromonitoring modalities which can be used, although may not necessarily be the primary ones. In addition, other neuromodalities are also strongly recommended:

1) upper and lower extremity SSEPs for aneuryms of the anterior vessels of the Circle of Willis (e. g., internal carotid, middle and anterior cerebral arteries)

2)microvascular Doppler for any cerebral aneurysmfor evaluation of cerebral blood flow velocity of the arterial branches and its perforators, and to confirmthe absence of pulsatile flow in the “dome” of the clipped aneurysm.

The second use of rEEG and qEEG monitoring during intracranial aneurysm surgery is for cerebral protection. Pharmacological protection of the brain is a relatively common practice during surgical manipulation and clipping of a cerebral aneurysm, although the efficacy of a barbiturate coma to produce cerebral protection is still debated. In general, barbiturates and other IV drugs (e. g., etomidate) are often titrated to produce a burst-suppression pattern or even isoelectric waveforms prior to aneurysm clipping in order to reduce the cerebral metabolic rate by about 50%. Most feel barbiturates are the preferred drug. The "typical" dose of barbiturates necessary to induce burst suppression varies greatly among individuals, ranging from as little as 2 mg/kg to as much as 25 mg/kg [71]. "With such a wide range of dosage necessary for the desired effect, is clear that the only rational way to administer barbiturates ..... is using EEG" (p. 566) [71]. Lastly, titration of these agents to a specific degree of burst suppression can be quantified by the burst suppression ratio (BSR) which is available on virtually all commercially-available neuromonitoring systems. One method used to calculate the BSR is the sum of the intervals of suppression (voltages < 5μV) that last at least 0.5 s divided by the epoch length [72]. The alarm criteria for detection of a cerebral ischemic event are listed in Sections 5.1.7 and 6.2. Obviously, if the rEEG is pharmacologically depressed, detection of ischemia is compromised. Thus, other neuromonitoring modalities, such as SSEPs, motor evoked potentials or microvascular Doppler may be more efficacious during such anesthetic maneuvers.