Background: Deafferentation pain secondary to brachial plexus avulsion, spinal cord injury, and other peripheral nerve injuries is often refractory to conventional treatments. Stimulation of the primary motor cortex (M1) has been proven to be an effective treatment for intractable deafferentation pain. The mechanisms underlying the attenuation of deafferentation pain by motor cortex stimulation remain hypothetical.
Objectives: The purpose of this case report is to: (1) summarize a case in which a patient suffering chronic intractable deafferentation pain for 25 years underwent rTMS treatment over M1, (2) describe the evidence from PET imaging, and (3) reveal a possible relief mechanism with cortical plasticity.
Study design: Case report.
Setting: University hospital.
Results: This patient had successful pain control with no transient or lasting side effects. The pain relief remained stable for at least one week. At the end of the 20-day procedure, pain relief was obtained according to the Visual Analog Scale (VAS) (-34.6%) and the McGill Pain Questionnaire (MPQ) (-31.6%). In the PET/CT scans, the glucose metabolism was significantly reduced contralaterally to the pain side in the anterior cingulate cortex (ACC), insula, and caudate nucleus. There was no statistically significant difference in any other cortical area.
Limitations: Single case of a patient with long-term intractable deafferentation pain having a PET study.
Conclusion: This study implies that a single session of 20 Hz rTMS over the motor cortex could reduce the pain level in patients suffering from long-term, intractable deafferentation pain. The stimulation of the M1 induces deactivation in the ACC, insula, and caudate nucleus. The changes in these pain-related regions may mirror an adaptive mechanism to pain relief after rTMS treatment.