Abstract
Over the years, studies have demonstrated morphological changes in the brain of fibromyalgia (FMS). We aimed to conduct a coordinate-based meta-analytic research through systemic review on voxel-based morphometry (VBM) imaging results to identify consistent gray matter (GM) difference between FMS patients and healthy subjects. We performed a comprehensive literature search in PubMed (January 2000–December 2015) and included six VBM publication on FMS. Stereotactic data were extracted from 180 patients of FMS and 123 healthy controls. By means of activation likelihood estimation (ALE) technique, regional GM reduction in left medial prefrontal cortex and right dorsal posterior cingulate cortex was identified. Both regions are within the default mode network. In conclusion, the gray matter deficit is related to the both affective and nonaffective components of pain processing. This result also provided the neuroanatomical correlates for emotional and cognitive symptoms in FMS.
Highlights
Fibromyalgia (FM) is characterized by chronic widespread pain with accompanying symptoms, such as fatigue, morning stiffness, insomnia, cognitive dullness, depression, and anxiety [1, 2]
A total of 47 peak coordinates were reported for brain structural changes, of which 31 were included for decreased gray matter and 16 were included for increased gray matter, in patients of FMS compared with NC
The activation likelihood estimation (ALE) metaanalysis revealed gray matter decreased in patients of FMS in 2 clusters, including left medial prefrontal cortex, extending partly to anterior cingulate area and right dorsal posterior cingulate cortex, extending to posterior-midcingulate cortex
Summary
Fibromyalgia (FM) is characterized by chronic widespread pain with accompanying symptoms, such as fatigue, morning stiffness, insomnia, cognitive dullness, depression, and anxiety [1, 2]. Does FM impair life quality [3], but it increases disability and absence from work [4]. Environmental, and biochemical factors proposed as the underlying pathophysiology [8, 9], the exact mechanism pertaining to FM is still under debate. Central sensitization has been proposed to explain the features of FM, including allodynia (increased sensitivity to stimulus that does not normally provoke pain) and hyperalgesia (heightened response to painful stimulus) [11, 12]
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