Haroutounian Simon, Nikolajsen Lone, Bendtsen Thomas F, Finnerup Nanna B, Kristensen Anders D, Hasselstrøm Jørgen B, Jensen Troels S
Danish Pain Research Center, Aarhus University Hospital, Aarhus, Denmark Department of Anesthesiology, Aarhus University Hospital, Aarhus, Denmark Section for Toxicology and Drug Analysis, Department of Forensic Medicine, Aarhus University, Aarhus, Denmark Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
Pain. 2014 Jul;155(7):1272-1279. doi: 10.1016/j.pain.2014.03.022. Epub 2014 Apr 2.
Central sensitization after peripheral nerve injury may result in ectopic neuronal activity in the spinal cord dorsal horn, implying a potential autonomous pain-generating mechanism. This study used peripheral nerve blockade and systemic lidocaine administration, with detailed somatosensory assessment, to determine the contribution of primary afferent input in maintaining peripheral neuropathic pain. Fourteen patients with neuropathic pain (7 with unilateral foot pain due to peripheral nerve injury and 7 with bilateral pain in the feet due to distal polyneuropathy) underwent comprehensive characterization of somatosensory function by quantitative sensory testing. Patients were then administered an ultrasound-guided peripheral nerve block with lidocaine and intravenous lidocaine infusion in randomized order. The effect of these interventions on spontaneous pain intensity and on evoked cold, warm, pinprick, and brush responses was assessed at each session. All patients had sensory disturbances at baseline. The peripheral nerve block resulted in a complete abolition of ipsilateral pain within 10 min (median) in all patients, with lidocaine plasma concentrations being too low to account for a systemic effect of the drug. Intravenous lidocaine infusion reduced the spontaneous pain by 45.5% (±31.7%), and it reduced mechanical and thermal hypersensitivity in most patients who displayed such signs. However, the improvement in evoked hypersensitivity was not related to the effect of the drug on spontaneous pain intensity. This study demonstrated that regardless of the individual somatosensory phenotype and signs of central sensitization, primary afferent input is critical for maintaining neuropathic pain in peripheral nerve injury and distal polyneuropathy.
周围神经损伤后的中枢敏化可能导致脊髓背角出现异位神经元活动，这意味着存在一种潜在的自主疼痛产生机制。本研究采用周围神经阻滞和全身给予利多卡因，并进行详细的躯体感觉评估，以确定初级传入输入在维持周围神经病理性疼痛中的作用。14例神经病理性疼痛患者（7例因周围神经损伤导致单侧足部疼痛，7例因远端多发性神经病导致双侧足部疼痛）通过定量感觉测试对躯体感觉功能进行了全面表征。然后，患者以随机顺序接受超声引导下的利多卡因周围神经阻滞和静脉输注利多卡因。在每次治疗时评估这些干预措施对自发疼痛强度以及诱发的冷、热、针刺和轻刷反应的影响。所有患者在基线时均有感觉障碍。周围神经阻滞在所有患者中均在10分钟（中位数）内使同侧疼痛完全消失，此时利多卡因血浆浓度过低，无法解释药物的全身作用。静脉输注利多卡因使自发疼痛减轻了45.5%（±31.7%），并且在大多数有此类症状的患者中减轻了机械性和热性超敏反应。然而，诱发超敏反应的改善与药物对自发疼痛强度的影响无关。本研究表明，无论个体的躯体感觉表型和中枢敏化迹象如何，初级传入输入对于维持周围神经损伤和远端多发性神经病中的神经病理性疼痛至关重要。
