Ding Fangfang, Fan Fengqi, Ji Feng, Xu Hua
Department of Anesthesiology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Front Med (Lausanne). 2025 Aug 22;12:1650218. doi: 10.3389/fmed.2025.1650218. eCollection 2025.
In the complex pathological context of mixed pain, where nociceptive, neuropathic, and nociplastic mechanisms coexist and interact, we present an innovative diagnostic and therapeutic model for refractory chronic scrotal pain (CSP) in a 49-year-old man. The pain originated from pudendal nerve entrapment secondary to piriformis scarring. Comprehensive evaluation revealed mixed pain mechanisms: neuropathic (lancinating pain, S2-S4 dermatomal hypoesthesia, and MRI-confirmed nerve compression), nociceptive (MRI-documented proven inflammation and mechanical stress exacerbation), and nociplastic (central sensitization with prolonged pain duration and psychological comorbidities). To address the stratified intervention needs of mixed pain, we implemented a mechanism-targeted strategy that included ultrasound-guided pulsed radiofrequency (PRF, 42 °C/240 s) at the inferior margin of the piriformis muscle to neuromodulate compressed nerves, perineural ozone/steroid injections to modulate the immunoinflammatory microenvironment, and citalopram to manage central sensitization, with complete pain resolution (VAS 8 → 0) sustained at 3-month follow-up. This case uniquely demonstrates how post-surgical piriformis scarring causes tripartite pain pathogenesis through neuro-immune-myofascial interactions, such as mechanical nerve compression, local inflammation, and subsequent central sensitization. The therapeutic strategy synergistically addressed all three cascades of mechanisms via C-fiber modulation, reduction of pro-inflammatory cytokines, and reversal of neuroplasticity. This study advances the understanding of CSP etiology beyond idiopathic causes by providing a reproducible mechanism-based precision model for mixed pain syndromes and advocating for multidisciplinary management that integrates interventional techniques, pharmacotherapy, and psychorehabilitation.
在混合性疼痛的复杂病理背景下,伤害性、神经性和神经可塑性机制共存并相互作用,我们为一名49岁男性难治性慢性阴囊疼痛(CSP)提出了一种创新的诊断和治疗模型。疼痛源于梨状肌瘢痕化继发的阴部神经卡压。综合评估显示存在混合性疼痛机制:神经性(刺痛、S2 - S4皮节感觉减退以及MRI证实的神经受压)、伤害性(MRI记录的炎症和机械应力加重)和神经可塑性(疼痛持续时间延长和心理合并症导致的中枢敏化)。为满足混合性疼痛的分层干预需求,我们实施了一种针对机制的策略,包括在梨状肌下缘进行超声引导下的脉冲射频(PRF,42°C/240秒)以对受压神经进行神经调节,神经周围臭氧/类固醇注射以调节免疫炎症微环境,以及使用西酞普兰来管理中枢敏化,在3个月的随访中疼痛完全缓解(VAS从8降至0)。该病例独特地展示了手术后梨状肌瘢痕化如何通过神经 - 免疫 - 肌筋膜相互作用导致三方疼痛发病机制,如机械性神经受压、局部炎症以及随后的中枢敏化。治疗策略通过C纤维调节、促炎细胞因子的减少以及神经可塑性的逆转,协同解决了所有三个机制级联。本研究通过为混合性疼痛综合征提供一个可重复的基于机制的精准模型,并倡导整合介入技术、药物治疗和心理康复的多学科管理,推进了对CSP病因的理解,超越了特发性病因。