Intraoperative monitoring of flash visual evoked potential under general anesthesia

Abstract

In neurosurgical procedures that may cause visual impairment in the intraoperative period, the monitoring of flash visual evoked potential (VEP) is clinically used to evaluate visual function. Patients are unconscious during surgery under general anesthesia, making flash VEP monitoring useful as it can objectively evaluate visual function. The flash stimulus input to the retina is transmitted to the optic nerve, optic chiasm, optic tract, lateral geniculate body, optic radiation (geniculocalcarine tract), and visual cortical area, and the VEP waveform is recorded from the occipital region. Intraoperative flash VEP monitoring allows detection of dysfunction arising anywhere in the optic pathway, from the retina to the visual cortex. Particularly important steps to obtain reproducible intraoperative flash VEP waveforms under general anesthesia are total intravenous anesthesia with propofol, use of retinal flash stimulation devices using high-intensity light-emitting diodes, and a combination of electroretinography to confirm that the flash stimulus has reached the retina. Relatively major postoperative visual impairment can be detected by intraoperative decreases in the flash VEP amplitude.

Keywords: Flash stimulation; General anesthesia; Intraoperative monitoring; Visual evoked potential.

Fig. 1. Retinal stimulation methods for VEP monitoring. The retina is stimulated by (A) pattern reversal stimulation or (B) flash stimulation. Flash stimulation-induced VEP monitoring is the only method capable of evaluating visual function under general anesthesia.

Fig. 2. Various types of visual impairment due to damage to areas of the optic pathway. The visual field defect portion is shown in black.

Fig. 3. Recording electrode locations for VEP monitoring. VEP is recorded from occipital scalp electrodes (O₁, O₂, O_z; International 10–20 System). The mid-occipital electrode (O_z) is placed above the external occipital protuberance (inion) calculated as 10% of the distance between the inion and nasion, which is 4 cm in most adults. The lateral occipital electrodes (O₁ and O₂) are placed 4 cm to the left and right of O_z.

Fig. 4. Flash VEP waveform. Flash VEP is evaluated by examining the peak-to-peak amplitude between negative wave near 75 ms (N75) and positive wave near 100 ms (P100). A significant decrease in flash VEP is defined as a decrease in peak-to-peak distance between N75 and P100 by at least 50% from the reference amplitude.

Fig. 5. Schematic diagram of VEP waveform induced by flash stimulation. Upward is negative (Partial modification from Electroenceph Clin Neurophysiol 1961; 13: 165-72).

Fig. 6. Comparison of the average latency of major positive vertices of VEP induced by flash stimulation and pattern reversal stimulation (Partial modification from Evoked Potentials in Clinical Testing, Churchill Livingston, 1982, p188).

Fig. 7. Effects of sevoflurane and propofol on flash VEP waveform. (A) Sevoflurane markedly suppresses flash VEP waveform by extending VEP latency and reducing VEP amplitude in a concentration-dependent manner, even at low concentrations. (B) Propofol has less suppressive effects on the flash VEP waveform. However, even propofol suppresses the flash VEP when administered in high doses (Partial modification from Masui 2006; 55: 692-8).