Central neuroimaging of pain has emerged as an effective way to assess central nervous system correlates and potentially also to characterize mechanisms of human pain perception, modulation, and plasticity. Central neuroimaging has allowed us to open windows into the brain to observe the roles of attention,
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Pain-related cerebral activation is altered by a distracting cognitive task.
Pain. 2000; 85: 19-30
- Koyama T.
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- Coghill R.C.
The subjective experience of pain: Where expectations become reality.
Proc Natl Acad Sci USA. 2005; 102: 12950-12955
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- Mackey S.C.
Neural correlates of individual differences in pain-related fear and anxiety.
Pain. 2006; 120: 69-77
- Benedetti F.
- Maybert H.S.
- Wager T.D.
- Stohler C.S.
- Zubieta J.K.
Neurobiological mechanisms of the placebo effect.
J Neurosci. 2005; 25: 10390-10402
6and other factors. We now better understand the changes in the brain associated with chronicity of pain,
- deCharms R.C.
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Proc Natl Acad Sci USA. 2005; 102: 18626-18631
- Apkarian A.V.
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- Parrish T.B.
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Chronic back pain is associated with decreased prefrontal and thalamic gray matter density.
J Neurosci. 2004; 24: 10410-10415
28the effects of opioids,
- Younger J.W.
- Shen Y.F.
- Goddard G.
- Mackey S.C.
Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems.
Pain. 2010; 149: 222-228
- Upadhyay J.
- Maleki N.
- Potter J.
- Elman I.
- Rudrauf D.
- Knudsen J.
- Wallin D.
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Alterations in brain structure and functional connectivity in prescription opioid-dependent patients.
Brain. 2010; 133: 2098-2114
27and effects of nonopioid therapies.
- Younger J.W.
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Prescription opioid analgesics rapidly change the human brain.
Pain. 2011; 152: 1803-1810
21The benefits we have gained from using central neuroimaging clearly advance our scientific knowledge of pain. However, the authors of 2 articles in this issue of the Journal of Pain suggest that perhaps our use of neuroimaging overreaches in our attempt to address 2 important questions: 1) Does brain neuroimaging replace self-reporting of pain or will it do so in the future? and 2) Do central neuroimaging findings alone define pain as a disease? The authors of these articles
- Seminowicz D.A.
- Wideman T.H.
- Naso L.
- Hatami-Khoroushahi Z.
- Fallatah S.
- Ware M.A.
- Jarzem P.
- Bushnell M.C.
- Shir Y.
- Ouellet J.A.
- Stone L.S.
Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function.
J Neurosci. 2011; 31: 7540-7550
- Robinson M.E.
- Staud R.
- Price D.D.
Pain Measurement and brain activity: Will neuroimages replace pain ratings?.
J Pain. 2013; 14: 323-327
23make compelling arguments that the answers to both these questions are an emphatic “No.” I would agree. However, it would be too easy to lose sight of neuroimaging’s potential role in augmenting self-report of pain, detecting or classifying pain and pain states, and helping define chronic pain as a disease. The story is much richer and deserves further consideration.
- Sullivan M.D.
- Cahan A.
- Derbyshire S.
- Loeser J.D.
What does it mean to call chronic pain a brain disease?.
J Pain. 2013; 14: 317-322
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- Chronic back pain is associated with decreased prefrontal and thalamic gray matter density.J Neurosci. 2004; 24: 10410-10415
- Neurobiological mechanisms of the placebo effect.J Neurosci. 2005; 25: 10390-10402
- Decoding sequential stages of task preparation in the human brain.Neuroimage. 2009; 45: 606-613
- Biomarkers for chronic pain and analgesia. Part 1: The need, reality, challenges, and solutions.Discov Med. 2011; 11: 197-207
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- Quantitative prediction of subjective pain intensity from whole-brain fMRI data using Gaussian processes.Neuroimage. 2010; 49: 2178-2189
- Visual image reconstruction from human brain activity using a combination of multiscale local image decoders.Neuron. 2008; 60: 915-929
- Multi-centre diagnostic classification of individual structural neuroimaging scans from patients with major depressive disorder.Brain. 2012; 135: 1508-1521
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- Prescription opioid analgesics rapidly change the human brain.Pain. 2011; 152: 1803-1810
- Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems.Pain. 2010; 149: 222-228
© 2013 American Pain Society. Published by Elsevier Inc. All rights reserved.
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- What Does It Mean to Call Chronic Pain a Brain Disease?The Journal of PainVol. 14Issue 4
- PreviewMultiple investigators have recently asked whether neuroimaging has shown that chronic pain is a brain disease. We review the clinical implications of seeing chronic pain as a brain disease. Abnormalities noted on imaging of peripheral structures have previously misled the clinical care of patients with chronic pain. We also cannot assume that the changes associated with chronic pain on neuroimaging are causal. When considering the significance of neuroimaging results, it is important to remember that “disease” is a concept that arises out of clinical medicine, not laboratory science.
- Pain Measurement and Brain Activity: Will Neuroimages Replace Pain Ratings?The Journal of PainVol. 14Issue 4
- PreviewArguments made for the advantages of replacing pain ratings with brain-imaging data include assumptions that pain ratings are less reliable and objective and that brain image data would greatly benefit the measurement of treatment efficacy. None of these assumptions are supported by available evidence. Self-report of pain is predictable and does not necessarily reflect unreliability or error. Because pain is defined as an experience, magnitudes of its dimensions can be estimated by well-established methods, including those used to validate brain imaging of pain.
- Reply to CommentariesThe Journal of PainVol. 14Issue 4
- Reply to CommentaryThe Journal of PainVol. 14Issue 4
- PreviewThe commentary by Sean Mackey3 makes several interesting points, many of which show strong agreement with the points raised by all of the other articles. Within the early part of his article he agrees that brain neuroimaging will not replace self-reporting of pain nor will it do so in the future and that central neuroimaging findings alone do not define pain as a disease. He then raises concerns that, based on our arguments forcefully presented to readers,6 they “may lose sight of the real value of central neuroimaging—a way to augment self-report of pain and a potential, objective [italics ours] biomarker of pain and pain treatment.”3 There are several points we wish to make about Mackey’s concerns that we think help clarify our agreements and disagreements.