Simple Summary
Insular glioma surgery carries a risk of motor deficits due to the proximity of the corticospinal tract and deep perforating arteries. This study investigates the relationship between intraoperative motor monitoring, postoperative ischemia, and persistent motor deficits. The findings suggest that the described intraoperative monitoring and stimulation technique helps identify the anatomical location of the corticospinal tract and supports its functional preservation during resection. However, all patients with persistent postoperative motor deficits had ischemic lesions, highlighting the importance of preserving perforating arteries arising from the middle cerebral artery. Intraoperative motor monitoring remains essential for assessing motor pathway function, but stable signals do not completely exclude postoperative injury, as false-negative results occurred. These findings emphasize that functional monitoring and meticulous vascular preservation must be complementary components of surgical strategy. Further refinement of monitoring techniques is needed to improve sensitivity and reduce undetected injuries, potentially enhancing neurological outcomes after insular glioma surgery.
Abstract
Background and Objectives: The proximity of insular gliomas to eloquent brain structures and complex vascular anatomy makes preservation of neurological function during resection challenging. This study investigates postoperative motor deficits after insular glioma resection and their association with intraoperative neuromonitoring and ischemia. Methods: In total, 64 patients who underwent insular glioma resection between 2018 and 2025 were included. Extent of resection (EOR), intraoperative MEP changes, subcortical stimulation thresholds, postoperative ischemic lesions and motor outcomes at 3 months were evaluated. Results: Median EOR was 93.4% (IQR 87.4–100%), and median residual tumor volume was 4.5 cm3 (IQR 0–8.1). MEP monitoring was performed in 56 patients (87.5%); deterioration occurred in 3 (5.4%), all of whom developed persistent deficits. MEP deterioration showed 60% sensitivity (95% CI 14.7–94.7%), 100% specificity (95% CI 93.0–100%), 100% positive predictive value (95% CI 29.2–100%), and 96.2% negative predictive value (95% CI 87.0–99.5%). The positive predictive value should be interpreted cautiously given the small number of events. Subcortical responses were elicited in 48 patients (85.7%). Tumors involving Berger–Sanai zones II and/or III had lower subcortical stimulation thresholds than tumors sparing both regions (median 4 vs. 8.5 mA; p = 0.012), although thresholds were not associated with motor deficits or ischemia. Postoperative ischemic lesions occurred in 20 patients (31.3%). Persistent motor deficits occurred in 6 patients (9.4%), all with associated ischemic lesions. Conclusions: Postoperative motor deficits were associated with ischemic lesions. MEP deterioration showed high specificity and positive predictive value, but limited sensitivity. Subcortical stimulation provided functional information about corticospinal tract proximity. These findings highlight the importance of preserving vascular supply to motor pathways during insular glioma surgery.