Anatomical and Temporal Blind Spots Explain the High False-Negative Rate of Motor Evoked Potential Monitoring in Glioma Surgery: A Single-Center Analysis of 106 Consecutive Patients.

BACKGROUND

Intraoperative motor evoked potential (MEP) monitoring is standard during glioma surgery, yet its diagnostic performance in cohorts enriched for deep-seated tumors remains poorly characterized.

METHODS

We retrospectively analyzed 106 consecutive patients undergoing MEP-monitored glioma resection. False-negative cases were systematically reviewed to classify monitoring failure as anatomical blind spots (basal ganglia injury, supplementary motor area (SMA)/parietal involvement, thalamic injury) or temporal blind spots (delayed hemorrhage). Preoperative MRI variables were compared between false-negative and true-positive cases.

RESULTS

Twenty-five patients (24%) developed new-onset motor deficits at the time of hospital discharge. MEP sensitivity was 28% (95% CI: 12%-49%), and specificity was 95% (95% CI: 88%-99%), with a false-negative rate of 72% (18/25). Systematic review attributed 89% of false-negative events to anatomical blind spots: basal ganglia injury (n = 9), SMA/parietal involvement (n = 4), and thalamic injury (n = 3); 2 cases (11%) resulted from delayed postoperative hemorrhage. No preoperative magnetic resonance imaging (MRI) variable significantly differentiated false-negative from true-positive cases (all P > 0.05).

CONCLUSIONS

These metrics apply to a selectively monitored cohort enriched for deep-seated lesions and should not be generalized to unselected glioma populations. The low sensitivity most plausibly reflects the high proportion of basal ganglia-involving tumors rather than undetected corticospinal tract injury, though this remains inferential without tractographic confirmation. Patients with deep-seated tumors should be counseled that stable MEP does not reliably predict the absence of motor deterioration at discharge from non-corticospinal structures. These findings quantify a specific monitoring gap and underscore the need for supplementary strategies targeting non-corticospinal motor circuits.