Spatial robustness of P100 latency compared with amplitude: a data-driven rationale for visual pathway monitoring...

Intraoperative visual evoked potential (VEP) monitoring has a reputation for being unreliable, and much of that belongs to P100 amplitude. Amplitude shifts with electrode position, anesthetic depth, and dipole geometry. Practice has nonetheless tended to lean on amplitude, and to treat latency as the weaker of the two. Neuroendovascular procedures give reason to shift that emphasis. During open surgery there can be a mixture of direct and ischemic neural injury, whereas in an endovascular procedure the brain is not dissected and the monitored pathway is threatened almost exclusively through perfusion. Oligodendrocytes are more vulnerable to ischemia than neurons, so myelinated conduction may slow before neurons are lost, and latency may prolong before amplitude falls. We first asked whether latency can be measured reliably enough. In a retrospective series of 49 eyes from 28 patients, the median spatial variability index across O1, Oz, and O2 was 2.10% for P100 latency and 40.9% for amplitude. Amplitude varied more than latency in 47 of 49 eyes and in all 28 patients. Latency behaves as a stable temporal measure of signal arrival, amplitude as a spatially sampled field measure. Some evidence for this exists in intraprocedural somatosensory monitoring. In an exploratory analysis of successfully reperfused thrombectomy patients, tree-based models separated 90-day functional outcome more consistently and efficiently by latency than by amplitude. If VEP latency behaves the same way, monitoring need not depend on the parameter that is hardest to trust, and VEP could be used actively in these procedures. We therefore propose that reproducible P100 latency prolongation may mark evolving visual pathway ischemia, and specify three studies that would test it. The first measures the temporal variability of intraoperative P100 latency and reports the smallest change it can resolve. That number sets the floor for any alarm threshold, including one below the conventional 10%. The second follows retrochiasmal perfusion-risk procedures with concurrent electroretinography, asking whether latency prolongation tracks angiographic events and precedes major amplitude loss. The third separates retinal from central contributions in ophthalmic-territory procedures. The present data establish spatial robustness only. Temporal stability and ischemia detection are the endpoints of those studies.