Author:

Keywords:

Spinal cord stimulator, Proton magnetic resonance spectroscopy, GABA, Thalamus, Science & Technology, Life Sciences & Biomedicine, Clinical Neurology, Neuroimaging, Radiology, Nuclear Medicine & Medical Imaging, Neurosciences & Neurology, BACK-SURGERY-SYNDROME, RANDOMIZED CONTROLLED-TRIAL, REGIONAL PAIN SYNDROME, NEUROPATHIC PAIN, DORSAL-HORN, BRAIN CHEMISTRY, FMRI, MODEL, FIBROMYALGIA, ACTIVATION, Aged, Chronic Pain, Cohort Studies, Female, Glucose, Humans, Magnetic Resonance Spectroscopy, Male, Middle Aged, Neuralgia, Protons, Spinal Cord Stimulation, Treatment Outcome, Young Adult, gamma-Aminobutyric Acid, 1103 Clinical Sciences, 1109 Neurosciences, Nuclear Medicine & Medical Imaging, 3202 Clinical sciences, 3209 Neurosciences

Abstract:

Introduction Although spinal cord stimulation (SCS) is a widely used treatment for chronic neuropathic pain secondary to spinal surgery, little is known about the underlying physiological mechanisms. Methods The primary aim of this study is to investigate the neural substrate underlying short-term SCS by means of 1H MR spectroscopy with short echo time, in 20 patients with failed back surgery syndrome. Results Marked increase of γ-aminobutyric acid (GABA) and decrease in glucose in the ipsilateral thalamus were found between baseline situation without SCS and after 9′ of SCS, indicating the key role of the ipsilateral thalamus as a mediator of chronic neuropathic pain. In addition, this study also showed a progressive decrease in glucose in the ipsilateral thalamus over time, which is in line with the findings of previous studies reporting deactivation in the ipsilateral thalamic region. Conclusions The observation of GABA increase and glucose decrease over time in the ipsilateral thalamus may be the causal mechanism of the pain relief due to SCS or an epiphenomenon.