Neuropathic Pain in Ankylosing Spondylitis: A Psychophysics and Brain Imaging Study

Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS. Methods Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age‐ and sex‐matched h...

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Published inArthritis & rheumatology (Hoboken, N.J.) Vol. 65; no. 6; pp. 1494 - 1503
Main Authors Wu, Qi, Inman, Robert D., Davis, Karen D.
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.06.2013
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Abstract Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS. Methods Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age‐ and sex‐matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging. Results Eleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid‐cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum. Conclusion The present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.
AbstractList Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS. Methods Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age‐ and sex‐matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging. Results Eleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid‐cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum. Conclusion The present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.
Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS. Methods Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age- and sex-matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging. Results Eleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid-cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum. Conclusion The present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component. [PUBLICATION ABSTRACT]
To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS.OBJECTIVETo determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS.Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age- and sex-matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging.METHODSSeventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age- and sex-matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging.Eleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid-cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum.RESULTSEleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid-cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum.The present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.CONCLUSIONThe present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.
To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with AS. Seventeen patients with back pain secondary to AS who were not receiving biologic agents and 17 age- and sex-matched healthy controls consented to participate in the study and were assessed using the painDETECT instrument (scores of ≤12 indicating low probability of neuropathic pain) and the McGill Pain Questionnaire. Mechanical and thermal thresholds were determined in all subjects, and brain gray matter was assessed by 3T magnetic resonance imaging. Eleven of the 17 AS patients had painDETECT scores of >12. The patients had decreased mechanical and cold sensitivity on the dorsum of their feet but did not have altered pain thresholds. Compared to controls, the AS patients exhibited cortical thinning in the primary somatosensory, insular, anterior cingulate, and anterior mid-cingulate cortices and the supplemental motor area, and increased gray matter volume in the thalamus and putamen. Scores on the painDETECT in AS patients were correlated with decreased gray matter in the primary somatosensory cortex and with increased gray matter in the motor cortex, anterior cingulate cortex, prefrontal cortex, thalamus, and striatum. The present findings indicate that neuropathic pain occurs in AS. Furthermore, abnormal brain gray matter and neural correlates of neuropathic pain are concordant with the clinical picture of AS, which includes sensorimotor and mood deficits as well as neuropathic pain symptoms. These results suggest that back pain in AS is a mixed pain condition that includes a neuropathic pain component.
Author Wu, Qi
Inman, Robert D.
Davis, Karen D.
Author_xml – sequence: 1
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  givenname: Karen D.
  surname: Davis
  fullname: Davis, Karen D.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23460087$$D View this record in MEDLINE/PubMed
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PublicationPlace United States
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PublicationTitle Arthritis & rheumatology (Hoboken, N.J.)
PublicationTitleAlternate Arthritis Rheum
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Publisher Wiley Subscription Services, Inc
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Snippet Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities...
To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities associated with...
Objective To determine whether there is a neuropathic component in ankylosing spondylitis (AS) back pain and to delineate gray matter brain abnormalities...
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StartPage 1494
SubjectTerms Adolescent
Adult
Back pain
Brain
Brain - physiopathology
Female
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Neuralgia - physiopathology
Neuroimaging - methods
Pain Measurement
Psychophysics
Spondylitis, Ankylosing - physiopathology
Young Adult
Title Neuropathic Pain in Ankylosing Spondylitis: A Psychophysics and Brain Imaging Study
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fart.37920
https://www.ncbi.nlm.nih.gov/pubmed/23460087
https://www.proquest.com/docview/1356997544
https://www.proquest.com/docview/1364707269
Volume 65
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