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Research Paper|Volume 13, Issue 11|pp 15139—15150

Dexmedetomidine inhibits unstable motor network in patients with primary motor area gliomas

Tao Yu1,2, Songlin Yu1,2,5, Zhentao Zuo3,4,5, Nan Lin6, Jing Wang7, Yuanli Zhao1,2,7, Song Lin1,2,8
  • 1Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China
  • 2China National Clinical Research Center for Neurological Diseases, Beijing 100070, China
  • 3State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China
  • 4University of Chinese Academy of Sciences, Beijing 100049, China
  • 5CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai 200031, China
  • 6Department of Anesthesiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China
  • 7Department of Neurosurgery, Peking University International Hospital, Peking University Health Science Center, Beijing 102206, China
  • 8Department of Neurosurgery, Beijing Neurosurgical Institute, Capital Medical University, Beijing 100070, China
* Equal contribution
Received: January 7, 2021Accepted: March 13, 2021Published: May 25, 2021
https://doi.org/10.18632/aging.203077

Copyright: © 2021 Yu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Sedative agents such as dexmedetomidine have been found to transiently exacerbate or unmask limb motor dysfunction in patients with eloquent area brain gliomas. The present study aims to investigate whether dexmedetomidine can inhibit motor plasticity in patients with glioma via fMRI.

Methods: 21 patients with brain glioma were prospectively recruited between September 2017 and December 2018. Patients were classified into pre-M1 (primary motor cortex) group (n=9), post-M1 group (n=6), and non-eloquent group (control group) (n=6) according to the tumor position related to M1. The hand movement task-fMRI and resting state fMRI (rs-fMRI) were performed before and after sedation using dexmedetomidine. The lateralization index (LI) of activation voxels and magnitude and the functional connectivity (FC) of motor network were compared before and after sedation and among different groups.

Results: Permanent postoperative motor deficit of the upper limb was found in 5 of 6 patients in the pre-M1 group, and none in other groups (P < .01). Task-fMRI showed the LI of activation volume and activation magnitude at M1 significantly increased only in the pre-M1 group after sedation (P < .05). Rs-fMRI showed 60.0% (27 of 45) FCs of motor network decreased in pre-M1 group after sedation (p[FDR] < .05); whereas there was no FC reduction in post-M1 and control groups (p[FDR] > .05).

Conclusions: In patients with eloquent area gliomas, dexmedetomidine can inhibit the unstable compensative motor plasticity on both task- and rs-fMRI. fMRI may be a promising method for elucidating the effect of sedative agents on motor plasticity.