MicrostructuralAbnormalitiesWereFoundinBrainGrayMatterfromPatientswithChronicMyofascialPain

Myofascial pain syndrome is a widespread chronic pain condition affecting skeletal muscle, characterized by myofascial trigger points (MTrPs) — localized, sensitive areas in muscle that produce characteristic pain and referred pain when stimulated. With a prevalence of 21–30% in the general population and over 44 million affected individuals in the United States alone, this condition imposes substantial medical costs. Despite its prevalence, the underlying mechanisms remain poorly understood, and treatments targeting peripheral MTrPs often result in pain relapse. While previous research has established that various chronic pain conditions can induce structural changes in brain gray matter, it was unknown whether MTrPs-related chronic pain specifically causes such alterations.

This knowledge gap is important because understanding central nervous system changes could shift treatment approaches from purely peripheral interventions to strategies that also address central sensitization.

The researchers recruited 37 patients with chronic MTrPs-related neck pain and 36 healthy controls matched for age and gender. All patients had active trigger points in the left upper trapezius, pain duration exceeding 3 months, and pain scores of 5 or higher on a 0–10 visual analog scale (VAS). Participants underwent advanced brain imaging using Diffusion Kurtosis Imaging (DKI), a magnetic resonance technique particularly sensitive to microstructural changes in brain tissue. DKI measures three parameters: mean kurtosis (MK), axial kurtosis (AK), and radial kurtosis (RK), which reflect different aspects of water molecule diffusion in brain tissue and can detect subtle structural abnormalities not visible with conventional MRI.

The researchers compared DKI parameters between patients and controls, then analyzed correlations between brain changes and clinical features including pain duration, pain intensity, and age.

Patients with chronic myofascial pain showed significant microstructural abnormalities in multiple brain regions compared to healthy controls. Specifically, decreased mean kurtosis (MK) values were found in the right anterior cingulate cortex, right middle temporal gyrus, left parahippocampal gyrus, right superior frontal gyrus, right posterior cingulate cortex, and right thalamus. Decreased axial kurtosis (AK) appeared in the right parahippocampal gyrus, right medial prefrontal cortex, bilateral insula, right inferior frontal gyrus, and right caudate nucleus. Decreased radial kurtosis (RK) was observed in the left lingual gyrus, right precentral gyrus, left middle temporal gyrus, bilateral anterior cingulate cortex, and right precuneus.

Notably, no brain areas showed elevated DKI parameters in patients. The abnormalities were concentrated in two functional networks: the limbic system (involved in emotional processing) and the pain matrix (brain regions activated during pain perception). Critically, the MK values in the right anterior cingulate cortex showed significant negative correlations with both pain duration and VAS scores, while AK values in the right medial prefrontal cortex negatively correlated with VAS scores. No correlations were found with age.

This study provides the first direct evidence that chronic MTrPs-related pain causes measurable microstructural damage in brain gray matter, particularly in regions governing emotional responses to pain and pain perception itself. The negative correlations between pain duration/intensity and DKI parameters in the anterior cingulate and medial prefrontal cortex suggest that prolonged, severe pain progressively damages these structures — or alternatively, that individuals with more vulnerable brain microstructures develop worse pain. Either interpretation supports the clinical importance of early, effective intervention. The findings strengthen the argument that myofascial pain involves central nervous system changes, not merely peripheral muscle dysfunction.

For clinicians, this implies that treatment strategies should address central sensitization mechanisms alongside peripheral trigger point interventions. For patients, the research validates that chronic myofascial pain is a real condition with objective brain changes, and that prompt treatment may help prevent or limit progressive central nervous system alterations. Future research should investigate whether successful treatment can reverse these brain changes, which would have major implications for therapeutic approaches.