4.6 Article

Motor Cortex Stimulation Suppresses Cortical Responses to Noxious Hindpaw Stimulation After Spinal Cord Lesion in Rats

Journal

BRAIN STIMULATION
Volume 7, Issue 2, Pages 182-189

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.brs.2013.12.013

Keywords

Functional magnetic resonance imaging (fMRI); Neuropathic pain; Central pain; Motor cortex stimulation; Noxious electrical stimulation

Funding

  1. National Institute of Neurological Disorders and Stroke Research [R01-NS069568]
  2. Department of Defense Research [SC090126]

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Background: Motor cortex stimulation (MCS) is a potentially effective treatment for chronic neuropathic pain. The neural mechanisms underlying the reduction of hyperalgesia and allodynia after MCS are not completely understood. Objective: To investigate the neural mechanisms responsible for analgesic effects after MCS. We test the hypothesis that MCS attenuates evoked blood oxygen-level dependent signals in cortical areas involved in nociceptive processing in an animal model of chronic neuropathic pain. Methods: We used adult female Sprague-Dawley rats (n = 10) that received unilateral electrolytic lesions of the right spinal cord at the level of C6 (SCL animals). In these animals, we performed magnetic resonance imaging (fMRI) experiments to study the analgesic effects of MCS. On the day of fMRI experiment, 14 days after spinal cord lesion, the animals were anesthetized and epidural bipolar platinum electrodes were placed above the left primary motor cortex. Two 10-min sessions of fMRI were performed before and after a session of MCS (50 mu A, 50 Hz, 300 mu s, for 30 min). During each fMRI session, the right hindpaw was electrically stimulated (noxious stimulation: 5 mA, 5 Hz, 3 ms) using a block design of 20 s stimulation off and 20 s stimulation on. A general linear model-based statistical parametric analysis was used to analyze whole brain activation maps. Region of interest (ROI) analysis and paired t-test were used to compare changes in activation before and after MCS in these ROI. Results: MCS suppressed evoked blood oxygen dependent signals significantly (Family-wise error corrected P < 0.05) and bilaterally in 2 areas heavily implicated in nociceptive processing. These areas consisted of the primary somatosensory cortex and the prefrontal cortex. Conclusions: These findings suggest that, in animals with SCL, MCS attenuates hypersensitivity by suppressing activity in the primary somatosensory cortex and prefrontal cortex. (C) 2014 Published by Elsevier Inc.

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