Sunzini Flavia, Stefanov Kristian, Al-Wasity Salim, Kaplan Chelsea, Schrepf Andrew, Waller Noah, Harte Steven, Harris Richard, Clauw Daniel J, McLean John, Siebert Stefan, Goodyear Carl S, Waiter Gordon D, Basu Neil
School of Infection & Immunity, University of Glasgow, Glasgow, Scotland, UK.
Chronic Pain and Fatigue Research Centre, Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, MI, USA.
Arthritis Res Ther. 2025 Mar 31;27(1):70. doi: 10.1186/s13075-025-03526-7.
Pain remains a principal complaint for people with psoriatic arthritis (PsA), despite successful mitigation of inflammation. This situation alludes to the co-existence of distinct pain mechanisms. Nociceptive and nociplastic mechanisms are clinically challenging to distinguish. Advances in brain functional magnetic resonance imaging (fMRI) have successfully characterised distinct pain mechanisms across several disorders, in particular implicating the insula. This is the first study to characterise neurobiological markers of pain mechanisms in PsA employing fMRI.
PsA participants underwent a 6-minutes resting-state fMRI brain scan, and questionnaire assessments of nociplastic pain (2011 ACR fibromyalgia criteria) and body pain, assessed using the Numeric Rating Scale (NRS, 0-100). Functional connectivity between insula seeds (anterior, mid, posterior), and the whole brain was correlated with the above pain outcomes correcting for age and sex, and false discovery rate (FDR) for multiple comparisons.
A total of 46 participants were included (age 49 ± 11.2; 52% female; FM score 12.5 ± 5.7; overall pain 34.8 ± 23.5). PsA participants with higher fibromyalgia scores displayed increased connectivity between: (1) right anterior insula to DMN (P < 0.05), (2) right mid and left posterior insula to parahippocampal gyri (P < 0.01 FDR); and (3) right mid insula to left frontal pole (P = 0.001 FDR). Overall pain was correlated with connectivity of left posterior insula to classical nociceptive regions, including thalamus (P = 0.01 FDR) and brainstem (P = 0.002 FDR).
For the first time, we demonstrate objectively that nociceptive and nociplastic pain mechanisms co-exist in PsA. PsA pain cannot be assumed to be only nociceptive in origin and screening for nociplastic pain in the future will inform supplementary analgesic approaches.
尽管炎症得到了有效缓解,但疼痛仍是银屑病关节炎(PsA)患者的主要诉求。这种情况表明存在不同的疼痛机制。伤害性和神经病理性疼痛机制在临床上难以区分。脑功能磁共振成像(fMRI)的进展已成功地在多种疾病中描绘出不同的疼痛机制,特别是涉及脑岛。这是第一项采用fMRI来描绘PsA疼痛机制的神经生物学标志物的研究。
PsA参与者接受了6分钟的静息态fMRI脑部扫描,并使用数字评分量表(NRS,0 - 100)对神经病理性疼痛(2011年美国风湿病学会纤维肌痛标准)和身体疼痛进行问卷调查评估。脑岛种子区(前、中、后)与全脑之间的功能连接与上述疼痛结果进行相关性分析,并对年龄和性别进行校正,同时对多重比较采用错误发现率(FDR)进行校正。
共纳入46名参与者(年龄49±11.2;52%为女性;纤维肌痛评分12.5±5.7;总体疼痛34.8±23.5)。纤维肌痛评分较高的PsA参与者在以下区域之间显示出连接增加:(1)右侧前脑岛与默认模式网络(P < 0.05),(2)右侧脑岛中部和左侧脑岛后部与海马旁回(P < 0.01 FDR);以及(3)右侧脑岛中部与左侧额极(P = 0.001 FDR)。总体疼痛与左侧脑岛后部与经典伤害性感受区域(包括丘脑,P = 0.01 FDR;脑干,P = 0.002 FDR)的连接性相关。
我们首次客观地证明了伤害性和神经病理性疼痛机制在PsA中共存。不能认为PsA疼痛仅源于伤害性感受,未来对神经病理性疼痛的筛查将为辅助镇痛方法提供依据。