Université de Versailles St-Quentin, AP-HP, Hôpital Raymond Poincaré, Service d'Anesthésie Réanimation Chirurgicale, 104 boulevard Raymond Poincaré, 92380 Garches, France Université de Versailles St-Quentin, AP-HP, Hôpital Raymond Poincaré, Réanimation médico-chirurgicale, 104 boulevard Raymond Poincaré, 92380 Garches, France INSERM, U-987, Hôpital Ambroise Paré, AP-HP, Centre d'Evaluation et de Traitement de la Douleur, 9 avenue Charles de Gaulle, Boulogne-Billancourt F-92100, France Université Versailles Saint-Quentin, Versailles F-78035, France.
Pain. 2010 Oct;151(1):53-60. doi: 10.1016/j.pain.2010.05.017. Epub 2010 Jun 17.
The mechanisms of neuropathic pain (NP) in Guillain Barré syndrome (GBS) are currently unknown. It has recently been shown that acute neuropathy of GBS not only affects large myelinated fibres but also small nociceptive fibres. In this prospective longitudinal 18 months study, we investigated the role of small fibre impairment in NP in GBS (n=30). Small fibres were assessed by quantifying cold and warm detection and pain thresholds and responses to suprathreshold painful thermal and mechanical stimuli. Nerve conduction velocities and mechanical detection thresholds assessed large myelinated fibres. Detection thresholds particularly at the lower limbs were significantly impaired in patients with GBS compared to 15 healthy controls. GBS patients with NP (n=13) had more severe impairment of cold detection thresholds (p=0.04), heat pain thresholds (p=0.03) and responses to suprathreshold heat stimuli (p=0.017) in the foot compared with those without pain or with non-neuropathic pain (n=17). Large fibre dysfunction and motor disability were similar between groups. Small fibre sensory impairment at the acute stage was correlated with the intensity of burning pain (Rho: -0.72; p=0.01 for cold detection; Rho: 0.72; p=0.02 for heat pain) and predicted residual NP (odds 4.1 p=0.04 for heat pain). These findings emphasize the importance of nociceptive fibre impairment in NP in GBS at both acute and chronic stages and suggest similarities between the mechanisms of NP in GBS and those of small fibre painful sensory polyneuropathies.
格林-巴利综合征（GBS）中神经病理性疼痛（NP）的机制目前尚不清楚。最近的研究表明，GBS 的急性神经病变不仅影响大髓鞘纤维，而且还影响小伤害感受纤维。在这项前瞻性纵向 18 个月的研究中，我们研究了小纤维损伤在 GBS 中的 NP 中的作用（n=30）。通过定量冷觉和温觉检测以及对超阈值疼痛热刺激和机械刺激的疼痛反应来评估小纤维。神经传导速度和机械检测阈值评估大髓鞘纤维。与 15 名健康对照相比，GBS 患者的下肢感觉检测阈值明显受损。与无疼痛或非神经病理性疼痛（n=17）的患者相比，GBS 伴有 NP（n=13）的患者足部的冷觉检测阈值（p=0.04）、热痛阈值（p=0.03）和超阈值热刺激反应（p=0.017）受损更为严重。各组间大纤维功能障碍和运动障碍相似。急性时的小纤维感觉损伤与灼痛的强度相关（冷觉：Rho：-0.72；p=0.01；热痛：Rho：0.72；p=0.02），并预测残留 NP（热痛：优势比 4.1；p=0.04）。这些发现强调了在急性和慢性阶段，GBS 中 NP 中小伤害感受纤维损伤的重要性，并表明 GBS 中 NP 的机制与小纤维痛性感觉多发性神经病的机制相似。
