TheRelationshipBetweenCorticalExcitabilityandPainCatastrophizinginMyofascialPain

Chronic pain is a major health problem that reduces quality of life and has substantial social and economic consequences. Myofascial pain syndrome (MPS), characterized by painful myofascial trigger points, is particularly common and may be the source of nociceptive input for 30 to 85% of patients seeking pain therapy. Beyond the physical symptoms, psychological factors play a crucial role in how patients experience and manage chronic pain. Pain catastrophizing—defined as dwelling on the worst possible outcomes of a painful situation—is one such factor that has been shown to worsen pain outcomes and disability.

While catastrophizing has been extensively studied from psychological and social perspectives, its underlying neurophysiological mechanisms remain poorly understood. Specifically, it was unknown whether catastrophizing is associated with changes in brain plasticity or cortical excitability. Understanding these mechanisms could lead to more targeted treatments for chronic pain patients who struggle with catastrophic thinking.

This exploratory study investigated whether pain catastrophizing is linked to cortical excitability in women with chronic myofascial pain syndrome. The researchers recruited 24 women aged 19 to 65 years who had been diagnosed with MPS for at least 3 months. All participants completed the Brazilian Portuguese Pain Catastrophizing Scale (B-PCS), which measures three dimensions of catastrophizing: rumination, magnification, and helplessness. They also completed assessments of pain severity, functional interference, and emotional burden using the Profile of Chronic Pain: Screen (B-PCP:S), as well as the Beck Depression Inventory.

To measure cortical excitability, the researchers used transcranial magnetic stimulation (TMS), a non-invasive technique that applies magnetic pulses to the brain and records motor responses in peripheral muscles. They assessed several TMS parameters: resting motor threshold, motor-evoked potential amplitude, cortical silent period, short intracortical inhibition (SICI), and intracortical facilitation (ICF). These parameters reflect the activity of different neurotransmitter systems, with ICF particularly associated with glutamatergic transmission.

For pain assessment, participants underwent multiple quantitative sensory tests including pressure pain threshold, heat detection and pain thresholds, maximal tolerable heat, and conditioned pain modulation (a measure of endogenous pain inhibition). The researchers then used linear regression analyses to examine relationships between cortical excitability measures and catastrophizing scores, while controlling for potential confounders like age, functional pain scores, and medication use.

The study revealed a significant association between intracortical facilitation (ICF) and pain catastrophizing. ICF was significantly correlated with all three subscales of catastrophizing—rumination (P = .009), magnification (P = .03), and helplessness (P = .004)—as well as the total B-PCS score (P = .001). The beta coefficient for the relationship between ICF and total catastrophizing score was .63, with catastrophizing accounting for 39% of the variance in ICF. This relationship remained significant after controlling for age, functional pain scores, and pain medication use, suggesting it was not confounded by these factors.

No significant associations were found between catastrophizing and other cortical excitability measures (resting motor threshold, motor-evoked potential amplitude, cortical silent period, or short intracortical inhibition). ICF also showed a trend toward association with heat pain threshold (P = .07), though this did not reach statistical significance.

In additional analyses, the researchers found that short intracortical inhibition (SICI) was significantly associated with pressure pain threshold (P = .04), with PPT accounting for 19% of SICI variance. Motor-evoked potential amplitude was inversely correlated with conditioned pain modulation effect (P = .03), explaining 20% of the variance. These findings suggest that different aspects of cortical excitability relate to different pain measures, with catastrophizing specifically linked to facilitatory (glutamatergic) mechanisms.

These findings suggest that pain catastrophizing in myofascial pain patients may be mediated by increased glutamatergic activity in the brain, as reflected by elevated intracortical facilitation. Glutamate is the brain's primary excitatory neurotransmitter, and its overactivity has been implicated in various conditions involving heightened emotional states, including anxiety. The researchers propose that catastrophizing may represent a state of increased glutamatergic activity that becomes functionally and anatomically connected with chronic pain over time.

For clinicians, this study highlights the importance of assessing and addressing catastrophizing in chronic pain management. The neurophysiological basis of catastrophizing implies that psychological interventions alone may not be sufficient—treatments that modulate glutamatergic neurotransmission, such as certain medications or neuromodulation approaches, might be particularly beneficial for patients with high catastrophizing scores. The finding that baseline cortical excitability measures predict pain sensitivity also suggests that TMS could potentially serve as a biomarker to identify patients who might respond to specific treatments.

For patients, this research validates that catastrophic thinking about pain is not simply "all in your head"—it has measurable biological correlates in the brain's excitatory systems. Understanding this connection may help reduce stigma and encourage engagement in both psychological and medical treatments. The study also points to the need for further research to determine whether reducing catastrophizing can normalize cortical excitability, or vice versa, which could open new therapeutic avenues for chronic myofascial pain.