ArticleBrain imaging and behavior2026
Altered brain function and its spatial correlations with neurotransmitter maps in anterior shoulder pain patients.
Article in Brain imaging and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neuroimaging studies have reported that chronic pain may be associated with brain functional changes and related molecular mechanisms. However, there are few studies in anterior shoulder pain (ASP). Thus, we aimed to assess the possible brain functional changes and their associations with neurotransmitter receptor maps in ASP patients. Resting-state functional magnetic resonance imaging data were obtained from 27 ASP patients and 20 healthy controls (HCs). Regional homogeneity (ReHo) and fractional amplitude of low-frequency fluctuation (fALFF) methods were used to examine altered brain functions. JuSpace toolbox was employed for evaluating the spatial correlations between ReHo and fALFF changes and neurotransmitter receptor maps. Regression analysis was conducted to explore the associations between neuroimaging findings and clinical characteristics in ASP patients. Furthermore, we investigated reliable biomarkers to distinguish ASP patients from HCs using receiver operating characteristic (ROC) curve analysis. ASP patients had abnormal ReHo/fALFF in the middle temporal gyrus, putamen, caudate, pallidum, precentral gyrus, medial prefrontal cortex, precuneus, posterior cingulate cortex and inferior temporal gyrus. ReHo/fALFF alterations in ASP patients were associated with the serotonin, dopamine, GABA, choline, glutamate and norepinephrine neurotransmitter systems. Visual analog scale was positively correlated with ReHo in the right insula. Moreover, ROC analysis showed higher classification accuracy in the middle temporal gyrus, precentral gyrus and putamen. Our study investigated abnormal brain function and associated neurotransmitter receptor maps in ASP patients, which may contribute to improving our understanding of the pathophysiological mechanisms in ASP.
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