Abstract

Tumors of the paralimbic system were considered inoperable for a long time due to high risk of postoperative complications. However, there have been significant changes in surgical tactics for these neoplasms over the past decades. Despite the improvement of surgical principles for these tumors and development of new approaches, risks of surgical treatment are still high (up to 33.6%). To assess the results of surgical treatment of paralimbic glial tumors and identify predictors of adverse outcomes. We retrospectively analyzed postoperative outcomes in 52 patients with paralimbic glial tumors at the neurosurgical department of the Pirogov National Medical Surgical Center between 2016 and 2020. Tumor dimensions and topography with surrounding structures were evaluated using preoperative MRI. Resection quality was evaluated within the first postoperative day considering MRI data. We applied transcranial or transcortical electrostimulation, direct cortical and subcortical bi- and monopolar stimulation for intraoperative functional assessment of corticospinal tract. Neurological examination was performed prior to surgery, after 24 hours, 7 days, and 6 months. Total resection was performed in 39 patients, almost total - 5 patients, subtotal - 6 patients, partial resection - 2 patients. Mean volume of tumors before surgery was 95.1±55.1 cm3. After surgery, volume ranged from 0 to 24.7 cm3 (mean 2.2±5.01 cm3). After 24 hours, neurological symptoms de novo or aggravation of preoperative motor deficit was revealed in 17 (33%) patients. However, this impairment regressed in most patients, and only 4 (7%) patients retained these disorders after 6 months. Transcortical or combined surgical approach in conjunction with multimodal neurophysiological monitoring allows total or close to total resection of paralimbic glioma in 85% of cases. Risk of postoperative complications is 7%. Unfavorable prognostic factors of neurological impairment are decrease in muscle response amplitude ≥50% according to transcranial neurophysiological stimulation and tumor spread medial to perforator arteries.

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