Disruption of Sensorimotor Network Connectivity in Patients With Supratentorial Gliomas During Mild Sedation With...

Midazolam has been shown to induce transient motor deficits in patients with supratentorial gliomas. However, its effects on brain networks remain unclear, given the compensatory network reorganization in response to tumor-induced damage. This study examined sensorimotor network (SMN) intra- and internetwork functional connectivity before and after midazolam mild sedation in patients with motor cortex gliomas, compared with healthy controls.

Glioma patients and healthy volunteers underwent resting-state functional MRI in the awake state and mild midazolam sedation. Regions of interest were defined in the primary motor cortex (M1) using a 6 mm radius. Statistical significance was set at an uncorrected voxel-wise threshold of P<0.001 and a false discovery rate-corrected cluster-wise threshold of P<0.05. This trial was registered at clinicaltrials.gov (NCT03984240) on June 11, 2019.

Thirty-four participants (18 glioma patients and 16 healthy volunteers) were analyzed. Glioma patients showed reduced negative functional connectivity between the SMN and the default mode network (DMN) in the awake state (P<0.05) and decreased SMN intranetwork connectivity. Following mild midazolam sedation, glioma patients demonstrated enhanced SMN intranetwork connectivity, with increased connectivity between M1 and the bilateral precentral gyrus, postcentral gyrus, and supramarginal regions (all P<0.001). Internetwork connectivity was decreased between M1 and the temporal fusiform cortex (T=8.05 and P=0.01), and between M1 and the occipital fusiform gyrus/inferior lateral occipital cortex (T=5.88 and P=0.002).

Midazolam mild sedation alters SMN connectivity in glioma patients, characterized by enhanced intranetwork compensation and impaired cross-network integration. These findings suggest potential vulnerabilities of functional brain networks during the perioperative period.