Abstract
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
healthy controls during a simple Go/No-Go task (response inhibition) while they underwent
functional magnetic resonance imaging (fMRI). Performance was not different between
FM and healthy control, in either reaction time or accuracy. However, fMRI revealed
that FM patients had lower activation in the right premotor cortex, supplementary
motor area, midcingulate cortex, putamen and, after controlling for anxiety, in the
right insular cortex and right inferior frontal gyrus. A hyperactivation in FM patients
was seen in the right inferior temporal gyrus/fusiform gyrus. Despite the same reaction
times 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 a par with control groups.
Perspective
Neural activation (fMRI) during response inhibition was measured in fibromyalgia patients
and controls. FM patients show lower activation in the inhibition and attention networks
and increased activation in other areas. Inhibition and pain perception may use overlapping
networks: resources taken up by pain processing may be unavailable for other processes.
Key words
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Article Info
Publication History
Published online: September 26, 2011
Accepted:
June 23,
2011
Received in revised form:
June 21,
2011
Received:
February 18,
2011
Footnotes
Supported in part by grant numbers R01-AR050044 (NIAMS/NIH) , and DAMD 17-00-2-0018 (Department of Defense) to David Williams and Daniel Clauw and by a grant of the DFG (Deutsche Forschungsgemeinschaft, GZ: SchM 2665/1-1 ) to Tobias Schmidt-Wilcke.
The authors have no conflicts of interest to report.
Identification
Copyright
© 2011 American Pain Society. Published by Elsevier Inc. All rights reserved.
