Brain activity for chronic knee osteoarthritis: Dissociating evoked pain from spontaneous pain

Abstract

Chronic pain is a hallmark of osteoarthritis (OA), yet little is known about its properties and representation in the brain. Here we use fMRI combined with psychophysics to study knee pain in 14 OA patients and 9 healthy controls. Mechanical painful pressure stimuli were applied to the knee in both groups and ratings of evoked pain and related brain activity examined. We observe that psychophysical properties and brain activation patterns of evoked pain are essentially the same between OA patients and healthy subjects, and between worse and better OA knees. In OA patients, stimulus-related brain activity could be distinguished from brain activity associated with spontaneous pain. The former activated brain regions commonly observed for acute painful stimuli in healthy subjects, while the spontaneous pain of OA engaged prefrontal-limbic regions closely corresponding to areas observed for spontaneous pain in other chronic pain conditions, such as chronic back pain and post-herpetic neuralgia. Arthritis-related clinical characteristics of knee OA also mapped to prefrontal-limbic regions. In a subgroup of patients (n = 6) we examined brain activity changes for a 2-week, repeat measure, cyclooxygenase-2 inhibitor (valdecoxib) therapy. Treatment decreased spontaneous pain for the worse knee and clinical characteristics of OA, and increased blood and csf levels of the drug which correlated positively with prefrontal-limbic brain activity. These findings indicate dissociation between mechanically induced and spontaneous OA knee pain, the latter engaging brain regions involved in emotional assessment of the self, and challenge the standard clinical view regarding the nature of OA pain.

Mechanisms and Mediators That Drive Arthritis Pain

“…Furthermore, there was no correlation between disease severity and evoked nerve firing, corroborating the clinical observation that joint destruction is a poor predictor of pain [63]. Brain imaging of OA patients revealed increased brain activity in regions commonly associated with the emotional aspect of pain, compared to normal subjects receiving a noxious thermal stimulus [64]. This finding points to neuroplastic changes in the brain of OA patients, although this outcome may not be purely driven by peripheral neuropathy.…”

[18F]-fluorodeoxyglucose positron emission tomography of the cat brain: A feasibility study to investigate osteoarthritis-associated pain

“…These changes also indicate brain plasticity, which induces a facilitation of nociceptive inputs (Gwilym et al, 2009) and an increased modulation of pain by the medial pain pathway (associated with affective dimension of pain) (Kulkarni et al, 2007;Parks et al, 2011). In a functional MRI study during quantitative sensory testing, human OA patients presented enhanced activity in the PAG compared with healthy controls (Gwilym et al, 2009).…”

Divergent Sensory Phenotypes in Nonspecific Arm Pain: Comparisons With Cervical Radiculopathy

“…A final consideration is that QST, which quantifies responses to experimentally induced pain, may evoke different central nervous system responses than does spontaneous pain, normally experienced by patients, as demonstrated by brain imaging studies. 44 Therefore, the development of better clinical tools for the assessment of sensory hypersensitivity is needed. The recommendation that the assessment of descending pain modulation and pain magnitude rating for a suprathreshold stimulus might facilitate a better 1 (2.5) 1 (2.5) 1 (2.5) 1 (2.5) 1 (6) 2 (12) 1 (6) 2 (12) Kinesiophobia (TSK!37/68) 3 (7.5) 2 (5) 2 (5) 4 (10) 2 (12) 4 (23.5) 0 (0) 4 (23.5) NPRS!5/10 5 (12.5) 4 (10) 7 (17.5) 9 (22.5) 4 (23.5) 4 (23.5) 1 (6) 4 (23.5) Hyperalgesia (yes) 3 (7.5) 2 (5) 1 (2.5) 0 (0) 2 (12) 0 (0) 1 (6) 1 (6) Allodynia (yes) 2 (5) 1 (2.5) 0 (0) 0 (0) 1 (6) 0 (0) 1 (6) 1 (6) NOTE.…”