Abstract
Substance P is released in painful and inflammatory conditions, affecting both peripheral processes and the central nervous system neurokinin 1 (NK1) receptor. There is a paucity of data on human brain alterations in NK1 expression, how this system may be affected by treatment, and interactions between central and peripheral tissue alterations. Ten subjects with chronic tennis elbow (lateral epicondylosis) were selected out of a larger (n = 120) randomized controlled trial evaluating graded exercise as a treatment for chronic tennis elbow (lateral epicondylosis). These ten subjects were examined by positron emission tomography (PET) with the NK1-specific radioligand 11C-GR205171 before, and eight patients were followed up after treatment with graded exercise. Brain binding in the ten patients before treatment, reflecting NK1-receptor availability (NK1-RA), was compared to that of 18 healthy subjects and, longitudinally, to the eight of the original ten patients that agreed to a second PET examination after treatment. Before treatment, patients had significantly lower NK1-RA in the insula, vmPFC, postcentral gyrus, anterior cingulate, caudate, putamen, amygdala and the midbrain but not the thalamus and cerebellum, with the largest difference in the insula contralateral to the injured elbow. No significant correlations between brain NK1-RA and pain, functional severity, or peripheral NK1-RA in the affected limb were observed. In the eight patients examined after treatment, pain ratings decreased in everyone, but there were no significant changes in NK1-RA. These findings indicate a role for the substance P (SP) / NK1 receptor system in musculoskeletal pain and tissue healing. As neither clinical parameters nor successful treatment response was reflected in brain NK1-RA after treatment, this may reflect the diverse function of the SP/NK1 system in CNS and peripheral tissue, or a change too small or slow to capture over the three-month treatment.
Highlights
Pain from the tendons that join the forearm muscles on the outside of the elbow, i.e. tennis elbow (TE) or lateral epicondylitis, has a prevalence of 1–3% in the population [1,2,3]
substance P (SP) and increased expression of neurokinin 1 (NK1) receptors has been demonstrated in human Achilles tendinosis [14], and we recently found that the radiolabeled NK1 receptor antagonist 11C-GR205171 has elevated retention in the affected regions in TE [27]
The diagnosis was verified by pain on palpation, stretching (Mills test), loading and Maudsleys middle finger test by a general practitioner and pain specialist (MP). 120 subjects were included in the larger randomized controlled trial (RCT), and each subject recruited in the RCT was invited to participate in the positron emission tomography (PET) study, until ten accepted
Summary
Pain from the tendons that join the forearm muscles on the outside of the elbow, i.e. tennis elbow (TE) or lateral epicondylitis, has a prevalence of 1–3% in the population [1,2,3]. SP contributes to local neurogenic inflammation [17,18,19], promotes tissue healing [20], [21]) by enhancing inflammatory response [22]), and serves as a neuropeptide in the nociceptive pathway via its primary receptor, the neurokinin 1 (NK1) receptor [23]. We investigated central NK1 receptor availability (NK1-RA) in patients with unilateral chronic tennis elbow before and after therapeutic exercise [28]. We further sought to characterize interactions between central NK1-RA alterations, pain ratings, functional severity, symptom duration and peripheral 11C-GR205171 uptake in the affected limb [27]
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