Purpose: Prior neuroimaging studies in fibromyalgia (FM) have identified augmented neuronal activity in response to evoked pain when compared to healthy controls (HC). Affected regions are largely contained within the pain matrix [regions in the brain that can be activated by pain alone], e.g., insula, thalamus, primary and secondary somatosensory cortex, anterior cingulate and the inferior parietal lobe).
To date, the majority of the functional magnetic resonance imaging (fMRI) studies in FM have been on a relatively small scale. Heterogeneity within FM as a disease state however suggests the need to replicate earlier findings in a larger sample.
Methods: 57 individuals (mean age 45) satisfying American College of Rheumatology criteria for FM and 20 healthy controls (mean age 42) were studied.
During a 10 min fMRI scan, 2 Kg. of pressure (mild pressure) was applied three times to the left thumbnail in random sequence for 25s. A 3-Tesla GE Sigma Scanner with neuro-optimized gradients (FOV = 22cm, T2* weighted, single shot, reverse spinal acquisition, GRE, TR = 2500, TE = 30, FA = 90, 64 x 64) was used to acquire fMRI data. Pre-processing and analysis of BOLD signal was performed using SPM2. Group level T statistical images were generated and uncorrected voxel level threshold of p<0.002 was used to identify significant activations.
In FM, 2 Kg. of pressure resulted in significant neural activity in:
• Insula (Z = 3.21).
• Bilateral inferior parietal lobes (BA 40, Z = 4.48-4.81),
• Primary somatosensory cortex (Z = 4.03)
• And secondary somatosensory cortex (Z = 4.69),
• Putamen (Z = 3.27)
• And caudate (Z = 3.24).
Additional activations were observed in:
• The cerebellum (Z = 4.95)
• And the middle frontal gyrus (Z = 4.37).
Healthy controls only had significant activation in the contralateral inferior parietal lobe (BA 40, Z = 3.18) using the same stimulus intensity.
In contrast to healthy controls, mild pressure stimuli resulted in more extensive activation of pain matrix regions in individuals with FM.
This study reconfirms an augmented involvement of the “pain matrix” in the processing of evoked pain in FM and supports the role of central mechanisms being responsible for the pain of FM.
Source: ACR/ARHP Scientific Meeting 2009, Presentation # 89, Oct 18, 2009. (Fibromyalgia and Soft Tissue Disorders). Ichesco E, Bhavsar R, Harris R, Clauw D, Gracely R, Williams DA. University of Michigan, Ann Arbor, University of North Carolina, Chapel Hill.