University of Otago, School of Physiotherapy, New Zealand.
University of Otago, School of Medicine, New Zealand.
Med Hypotheses. 2019 Aug;129:109243. doi: 10.1016/j.mehy.2019.109243. Epub 2019 May 22.
Pain is reported to affect over 70% of individuals with inflammatory bowel diseases (IBD), with abdominal and musculoskeletal (MSK) pain representing the most common complaints. MSK pain is typically considered within the narrow framework of inflammatory extraintestinal manifestations of IBD, resulting in a limited scope for the nature and underlying mechanisms participating in MSK pain experiences in this population. Symptoms related to central sensitization have recently demonstrated association with active IBD and worse MSK pain experiences, suggesting a potential roll for central mechanisms in MSK-related pain. Current literature exploring persistent pain in chronic inflammatory and MSK populations propose complex pain models comprised of dynamic nervous system relationships influenced by primary disease features and concomitant pain states, as well as affective and cognitive components. Nervous system contributions in the development and maintenance of persistent pain are postulated to include mechanisms of peripheral and central sensitization, changes in descending central modulation, as well as structural brain changes. These models go beyond current MSK pain models described in IBD literature, highlighting the need for new frameworks for considering MSK-related pain in IBD. Consequently, this paper proposes a broader theoretical model whereby central mechanisms, such as central sensitization and grey matter changes, as well as psychological and disease factors are suggested to modulate pain experiences in this population. Exploration of relationships within the proposed framework may provide not only a deeper understanding of the generation and maintenance of persistent MSK pain in IBD, but also highlight the need for new targeted management pathways in this population. This paper hypothesizes that exploration of central sensitization in IBD patients will demonstrate altered somatosensory functioning in patients with MSK pain, and that IBD activity and psychological factors will be associated with altered somatosensory functioning and worse pain experiences.
疼痛据报道影响超过 70%的炎症性肠病（IBD）患者，其中腹部和肌肉骨骼（MSK）疼痛是最常见的主诉。MSK 疼痛通常被认为是 IBD 的炎症性肠外表现的狭隘框架内，导致对参与该人群 MSK 疼痛体验的性质和潜在机制的研究范围有限。最近的研究表明，与中枢敏化相关的症状与活动期 IBD 和更严重的 MSK 疼痛体验有关，这表明中枢机制在 MSK 相关疼痛中可能发挥作用。目前探索慢性炎症和 MSK 人群持续性疼痛的文献提出了复杂的疼痛模型，该模型由受主要疾病特征和伴随疼痛状态以及情感和认知成分影响的动态神经系统关系组成。假设神经系统在持续性疼痛的发展和维持中的作用包括外周和中枢敏化的机制、下行中枢调节的变化，以及结构脑变化。这些模型超越了 IBD 文献中描述的当前 MSK 疼痛模型，强调了需要为 IBD 中的 MSK 相关疼痛考虑新的框架。因此，本文提出了一个更广泛的理论模型，即中枢机制（如中枢敏化和灰质变化）以及心理和疾病因素被认为可以调节该人群的疼痛体验。在提出的框架内探索关系不仅可以更深入地了解 IBD 中持续性 MSK 疼痛的产生和维持，还可以强调该人群需要新的靶向管理途径。本文假设，在 IBD 患者中探索中枢敏化将显示出 MSK 疼痛患者的感觉功能改变，并且 IBD 活动和心理因素与感觉功能改变和更严重的疼痛体验相关。
