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Abstract Number: 587

Brain MRI and Psychophysics Analysis Demonstrate Neuropathic Pain to Be a Component of Back Pain in Ankylosing Spondylitis

Q. Wu1, Robert D. Inman2 and Karen Davis3, 1Research, Toronto Western Research Institute, Toronto, ON, Canada, 2Dept of Medicine/Rheumatology, Toronto Western Research Institute, University Health Network and University of Toronto, Toronto, ON, Canada, 3Department of Surgery, Toronto Western Research Institute, Toronto, ON, Canada

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Ankylosing spondylitis (AS), imaging techniques and pain

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Session Information

Title: Spondylarthritis and Psoriatic Arthritis - Pathogenesis, Etiology

Session Type: Abstract Submissions (ACR)

Background/Purpose: The mechanisms underlying pain in ankylosing spondylitis (AS) are unclear. The aim of this study was to investigate whether there is a neuropathic component in AS pain and to delineate gray matter brain abnormalities associated with AS

Methods: Seventeen patients with back pain secondary to AS (12M/5F; 34.4 +/-12.4yo) and age/sex-matched controls consented to the approved study. Mean BASDAI scores in the AS patients were 6.6 +/- 2.1, and none were on biologic agents at the time of the study. Patients were assessed with the PainDETECT (scores <12 indicate low probability of neuropathic pain) and McGill Pain Questionnaires. Mechanical and thermal pain thresholds were determined, 3T MRI scans obtained for all subjects. Brain gray matter was measured with cortical thickness analysis (Freesurfer) and voxel based morphology (FSL-VBM) for subcortical structures with age included as a covariate.

Results: The mean painDETECT score in AS patients was 15.1 ± 7.08 (eleven scored >12).  Compared to controls, AS patients had significantly decreased mechanical and cold sensitivity on their dorsal feet but pain thresholds were not abnormal. The gray matter analysis identified that AS patients had significant cortical thinning in left primary sensory (S1), insular, and anterior mid-cingulate cortices (MCC), and right supplemental motor area and ACC. Furthermore, painDETECT scores correlated with cortical thinning in the left S1 and thickening in the left motor cortex, right anterior cingulate and prefrontal cortex.  All cortical findings were significant at p< 0.05 image-wise, corrected for multiple comparisons.

Conclusion: Our psychophysical testing and self-reports identified signs of neuropathy. The imaging results of abnormal brain gray matter linked to neuropathic pain are concordant with the clinical picture of AS having sensorimotor and mood deficits as well as neuropathic pain. These data suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.


Disclosure:

Q. Wu,
None;

R. D. Inman,
None;

K. Davis,
None.

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