The primary symptom of fibromyalgia (FM) is chronic, widespread pain; however, patients report additional symptoms including decreased concentration and memory. Performance based deficits are seen mainly in tests of working memory and executive function. Neural correlates of executive function were investigated in 18 FM patients and 14 age-matched HCs during a simple go/no-go task (response inhibition) while they underwent functional magnetic resonance imaging (fMRI). Performance was not different between FM and HC, in either reaction time or accuracy. However, fMRI revealed that FM patients had lower activation in the right pre-motor cortex, supplementary motor area (SMA), mid cingulate cortex (MCC), putamen and, after controlling for anxiety, in the right insular cortex (IC) and right inferior frontal gyrus (IFG). A hyper-activation in FM patients was seen in the right inferior temporal gyrus/fusiform gyrus. Despite the same RTs and accuracy, FM patients show less brain activation in cortical structures in the inhibition network (specifically in areas involved in response selection/motor preparation) and the attention network along with increased activation in brain areas not normally part of the inhibition network. We hypothesize that response -inhibition and pain perception may rely on partially overlapping networks, and that in chronic pain patients resources taken up by pain processing may not be available for executive functioning tasks such as response inhibition. Compensatory cortical plasticity may be required to achieve performance on par with control groups.

Our results suggest that the clinical distribution of pain is associated with the BOLD response elicited by a cognitive task. The cingulate cortex and the supplementary motor area are critically involved in both the pain system as well as the response inhibition network. We hypothesize that increases in the spatial distribution of pain might engage greater neural resources, thereby reducing their availability for other networks. Our data also point to the potential for, at least partial, reversibility of these changes.

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Growing research has reported the presence of a clear impairment of working memory functioning in fibromyalgia. Although different genetic factors involving dopamine availability (i.e, the COMT gene) have been associated with the more severe presentation of key symptoms in fibromyalgia, scientific evidence regarding the influence of COMT genotypes on cognitive impairment in these patients is still lacking. To this end, 167 participants took part in the present investigation. Working memory performance was assessed by the application of the SST (Spatial Span Test) and LNST (Letter and Number Sequence Test) belonging to the Weschler Memory Scale III. Significant working memory impairment was shown by the fibromyalgia patients. Remarkably, our results suggest that performance according to different working memory measures might be influenced by different genotypes of the COMT gene. Specifically, fibromyalgia patients carrying the Val/Val genotype exhibited significantly worse outcomes for the span of SST backward, SST backward score, SST total score and the Working Memory Index (WMI) than the Val/Val healthy carriers. Furthermore, the Val/Val patients performed worse on the SST backward and SST score than heterozygotes. Our findings are the first to show a link between the COMT gene and working memory dysfunction in fibromyalgia, supporting the idea that higher COMT enzyme activity would contribute to more severe working memory impairment in fibromyalgia.