Central Neuropathic Pain

Neuropathic pain is a chronic debilitating condition caused by a lesion or a disease of the somatosensory system. It affects 7-10% of the general population and up to 50% of those with spinal cord injury.

People with spinal cord injury often report pain at or below the level of injury despite having limited or even no real sensation. Despite the availability of various pharmacological and non-pharmacological treatments, Neuropathic Pain remains refractory for many patients, seriously affecting their quality of life and necessitating the exploration of novel diagnostic and therapeutic approaches.

Abstract

Cross-sectional studies have shown that pain affects brain activity in Central Neuropathic Pain. However, more studies are needed to establish if mismatch negativity (MMN) is a biomarker for pain intensity. This work aims to determine whether the changes in MMN, i.e., amplitude and latency, is predictive of change in central neuropathic pain intensity due to medication.

In this longitudinal study, ten people with spinal cord injury-related central neuropathic pain recorded their response to MMN experiment using home-based self-guided EEG set-up for ten days both before and after taking medications over a period of several weeks. We found that the change in MMN was not predictive of change in central neuropathic pain intensity due to medications.

Conclusions: Duration-deviant or Frequency-deviant Mismatch Negativity was not able to detect self reported central neuropathic pain intensity. So we conclude that MMN may not be a surrogate or pharmacodynamic marker of Central Neuropathic Pain in people with Spinal Cord Injury.

Abstract

Chronic pain impacts millions worldwide, and places a significant strain upon healthcare systems, yet current treatments are largely suboptimal. Multiple studies have noted differences in various event-related potentials (ERP) in patients with chronic pain, and one of the primary ERP components of interest is mismatch negativity (MMN). It is currently not established whether alterations in MMN is a biomarker of chronic pain. The aim of this review is to assess how MMN is altered in patients with chronic pain. We carried out a systematic search of Embase, Medline and PubMed databases with the terms ‘chronic pain’ and ‘mismatch negativity’ and found seventeen studies. Seven screened studies were included in the final review. Of these, one cohort underwent experimentally induced chronic pain, whereas the other cohorts had a range of chronic pain conditions. Five studies measured magnitude of MMN responses, whilst two focused on latency. Three studies found smaller amplitudes in chronic pain, and both studies found longer latency. Both the studies with larger MMN reported that it was due to increased attention to the pain. In conclusion, this (first) literature review on MMN in chronic pain found that these studies offered wide-ranging applications of MMN, from understanding the neural pathophysiology of chronic pain to therapeutic advances. Given the limited number of studies and unexplored effect of pain medication on MMN, more studies are required to establish if MMN is a reliable pharmacodynamic marker of chronic pain.