OBJECTIVE: Central nervous system pathways involving pain modulation shape the pain experience in patients with chronic pain. Our objectives were to understand the mechanisms underlying pain in rheumatoid arthritis (RA) and identify brain signals that may serve as imaging markers for developing targeted treatments for RA pain.
METHODS: Subjects with RA and matched controls underwent functional magnetic resonance imaging, using pulsed arterial spin labeling (pASL). The imaging conditions included: 1) resting state, 2) low intensity stimulus and 3) high intensity stimulus. Stimuli consisted of mechanical pressure applied to metacarpophalangeal (MCP) joints with an automated cuff inflator. The low intensity stimulus was 30 mmHg. The high intensity stimulus was the amount of pressure required to achieve 40/100 pain intensity for each RA patient, with the same amount of pressure given to the matched control.
RESULTS: Among RA patients, regional cerebral blood flow (rCBF) in medial frontal cortex (MFC) and dorsolateral prefrontal cortex increased during both low and high pressure stimuli. No rCBF changes were noted for pain-free controls. In region of interest analyses among RA patients, baseline rCBF in MFC was negatively correlated with pressure required for the high intensity stimulus (p<0.01) and positively correlated with pain induced by the low intensity stimulus (p<0.05). Baseline rCBF also marginally correlated with disease activity (p=0.05). rCBF during high pain was positively correlated with pain severity and interference (p's<0.05).
CONCLUSION: In response to clinically-relevant joint pain evoked by MCP pressure, neural processing in MFC increases and is directly associated with clinical pain in RA. This article is protected by copyright. All rights reserved.