
Intraoperative recordings from 31 patients revealed distinct pallidal firing patterns across dystonia genes. AOPEP, PANK2, and THAP1 showed high firing regularity, while GNAL, PLA2G6, and others displayed prominent bursting (>26.6%). TOR1A and VPS16 showed irregular spiking, bridging groups. Despite molecular differences, neural activity clustered by dynamics, suggesting burst-driven desynchronization may underlie DBS outcome variability and guide future adaptive therapies.
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