Distinct EEG microstate signatures across different pain types

Pain is known to trigger a reorganization of the brain's activity, which can be captured through the use of electroencephalographic measurements known as microstates. However, previous research on this topic has yielded inconsistent results, likely due to the repetitive nature of studies and the use of diverse analytical methods. In order to overcome these inconsistencies, a team of researchers conducted a comprehensive analysis of three distinct types of pain conditions using a standardized approach.

The three pain conditions examined were capsaicin-induced pain, non-chronic back pain, and chronic back pain. Capsaicin-induced pain was induced within the participants, while the other two conditions were compared against matched controls. The researchers focused on analyzing five distinct microstates - A through E - which correspond to various brain networks including auditory, visual, salience, and attentional networks.

Capsaicin pain was found to increase the expression of microstate C, while simultaneously reducing the expression of microstates A, D, and E. This suggests that pain activates certain brain networks more than others. Additionally, the transitions between microstates were also altered during capsaicin pain, indicating a shift towards salience-related processing at the expense of sensory and attentional dynamics.

When comparing the clinical back pain groups, the effects were smaller and differed based on the type of back pain. Non-chronic back pain showed a decrease in microstate C occurrence, the opposite of the effect seen in capsaicin pain. On the other hand, chronic back pain showed a decrease in the global explained variance of microstate D, which suggests differences in salience and attentional processing in clinical pain.

Direct comparisons between the different pain conditions revealed that the increases in microstate C expression during clinical back pain were weaker than in the capsaicin pain condition. Furthermore, there were additional differences involving microstates A, D, and E. These findings challenge the notion of a universal EEG microstate signature for pain, and instead highlight the importance of understanding pain-type-specific patterns of large-scale brain dynamics.

Microstate C, in particular, emerges as a critical distinguishing factor between experimental and clinical pain.