CTLT-03 STEROID RESPONSIVENESS PREDICTS FUNCTIONAL OUTCOME FOLLOWING LITT IN MOTOR CORTEX METASTASES

Abstract INTRODUCTION Metastases associated with the primary motor cortex (PMC) are associated with significant debility. Laser interstitial thermal therapy (LITT) could proffer less invasive treatment if the risk of thermal damage to corticospinal tracts is mitigated. We accordingly assessed functional outcomes of LITT relative to with open resection with motor mapping (OR) over time. METHODS A single-center retrospective review of patients receiving OR or LITT to PMC metastases from 2014 – 2024 was performed in collaboration with a board-certified neuroradiologist. Automated segmentation was performed to extract contrast-enhancing lesion volumes (CeLV). Functional outcomes out to 1 year were adjudicated. RESULTS Thirty-nine OR and 28 LITT cases were identified. More LITT patients had received prior SRS (100 vs 51.3%, P<0.0001), and had stable extracranial disease (53.6 vs 25.64%, P=0.018) on presentation. Median CeLV was 2.8 (LITT) vs 7.3 cm3 (OR), P <0.0001. Patients undergoing OR more frequently went to the neuro-ICU post-op (74.36 vs 17.86%, P <0.0001) and had a longer length of stay, median 2 vs 1 day (P=0.0007). Assessments at discharge, 30-, 90-, 180-, 270-, and 365 days showed no difference in KPS, mRS, or stable/improved symptoms between groups. A multivariate model of 30-day functional outcome revealed that of surgery type, CeLV, biopsy result, and extracranial disease status, only pre-operative responsiveness to steroids was predictive of symptomatic improvement or stability, OR 3.75 95%CI 1.06 – 13.26, P = 0.04. CONCLUSIONS For patients with recurrent motor cortex metastases following radiation and/or OR, LITT is a safe and feasible alternative. Functional outcomes do not differ between OR and LITT patients following treatment. During the early peak swelling window for LITT, good functional status is predicted by pre-operative steroid responsiveness rather than surgery type and intracranial or systemic disease biology.