Somatosensory Hypersensitivity in the Referred Pain Area in Patients With Chronic Biliary Pain and a Sphincter of Oddi Dysfunction: New Aspects of an Almost Forgotten Pathogenetic Mechanism

Somatosensory Hypersensitivity in the Referred Pain Area in Patients With Chronic Biliary Pain and a Sphincter of Oddi Dysfunction: New Aspects of an Almost Forgotten Pathogenetic Mechanism
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DOI:
10.1111/j.1572-0241.2008.02068.x
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发表时间:
2008-11-01
影响因子:
9.8
通讯作者:
Madacsy, Laszlo
Madacsy, Laszlo
中科院分区:
医学1区
文献类型:
--
作者:
Kurucsai, Gabor;Joo, Ildiko;Madacsy, Laszlo

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背景和目的:急、慢性腹痛综合征患者在牵涉痛区(RPA)的躯体感觉过敏可能是由于内脏和躯体组织的神经纤维在脊髓和脊柱上汇聚所致。胆囊术后综合征患者的慢性胆道疼痛(即胆道超敏反应)可通过中枢神经系统(CNS)神经元的持续性高兴奋性来解释。本研究的目的是评价慢性胆源性疼痛和Oddi括约肌(SO)功能障碍患者RPA中的皮肤神经感觉知觉。方法:对42例持续性胆源性疼痛患者和27例年龄匹配的健康志愿者和18例年龄匹配的无症状胆囊切除术患者进行前瞻性感觉测试。通过预先验证和标准化的问卷,在视觉模拟疼痛严重程度评分系统上对胆道症状和疼痛严重程度进行分类。患者帮助医生将RPA定位在右上腹。感觉检测阈值采用无创性(Neuroeter CPT),经皮电刺激频率分别为5、250和2000赫兹,不同电流强度(0.01~9.99 mA),采用单盲法。这三种频率选择性地兴奋小的无髓纤维(C纤维)、小的有髓纤维(A-Delta)和大的有髓纤维(A-beta),它们分别传递钝痛、尖锐痛和触摸。对侧腹部左上腹区作为对照区域。结果:在2,000 Hz频率下,胆道疼痛患者、健康志愿者、无症状胆囊切除患者、有症状但无超氧化物歧化酶的胆囊切除患者的感觉电流感觉阈值比分别为2.32+/-1.4、1.06+/-0.24、0.97+/-0.16、0.83+/-0.35;250赫兹时,2.19+/-1.0比1.01+/-0.26比1.02+/-0.25比0.88+/-0.35;5赫兹时2.19+/-1.1比1.12+/-0.26比0.99+/-0.37比0.84+/-0.32。胆源性疼痛患者的RPA在不同的刺激频率下均有明显的超敏反应,分别为5 Hz:P=0.00001,250 Hz:P=0.00001,2,000 Hz:P=0.0001。结论:胆源性疼痛或中枢神经系统功能障碍引起的持续性内脏痛可导致外周伤害性神经纤维的明显超敏反应。胆囊术后疼痛可能由中枢神经系统伤害性神经元持续的高兴奋性所致,并伴有或不伴有SO的客观运动障碍。
BACKGROUND AND AIMS: Somatosensory hyperalgesia in the referred pain area (RPA) in patients with acute or chronic abdominal pain syndromes may result from the convergence of nerve fibers from visceral and somatic tissues at the spinal and supraspinal levels. Chronic biliary pain in patients with the postcholecystectomy syndrome (i.e., biliary hypersensitivity) may be explained by persistent hyperexcitability of neurons in the central nervous system (CNS). The aim of this study was to evaluate the cutaneous neural sensory perception in the RPA in patients with chronic postcholecystectomy biliary pain and a sphincter of Oddi (SO) dysfunction (SOD).METHODS: Forty-two patients with persistent biliary pain and suspected SOD, 27 age-matched healthy volunteers, and 18 age-matched asymptomatic cholecystectomized controls were prospectively investigated by quantitative sensory testing (Neurometer CPT). The biliary symptoms and the severity of pain were classified on a visual analog pain severity scale system via a previously validated and standardized questionnaire. The patients helped the doctors locate the RPA in the right upper quadrant. The sensory detection threshold was determined noninvasively (Neurometer CPT) with transcutaneous electrical stimulation at 5, 250, and 2,000 Hz, and different current intensities (range from 0.01 to 9.99 mA) applied in a single (patient) blinded method. These three frequencies selectively excite small unmyelinated (C fibers), small myelinated (A-delta), and large myelinated (A-beta) fibers, which transmit dull pain, sharp pain, and touch, respectively. The contralateral region of the abdomen left upper quadrant served as the control area. The sensory current perception threshold ratio (SCPTR) of the data measured in the contralateral area and the RPA was calculated.RESULTS: The SCPTRs in the definite SOD patients with biliary pain, healthy volunteers, the asymptomatic cholecystectomized controls, and the symptomatic cholecystectomized patients but without SOD were 2.32 +/- 1.4 versus 1.06 +/- 0.24 versus 0.97 +/- 0.16 versus 0.83 +/- 0.35 at 2,000 Hz; 2.19 +/- 1.0 versus 1.01 +/- 0.26 versus 1.02 +/- 0.25 versus 0.88 +/- 0.35 at 250 Hz; and 2.19 +/- 1.1 versus 1.12 +/- 0.26 versus 0.99 +/- 0.37 versus 0.84 +/- 0.32 at 5 Hz, respectively. Significant hypersensitivity was detected in the RPA at different stimulation frequencies in the SOD patients with biliary pain versus the cholecystectomized controls: at 5 Hz: P = 0.00001; at 250 Hz: P = 0.00001; and at 2,000 Hz: P = 0.0001, respectively.CONCLUSION: Continuous visceral pain (biliary pain) caused by local inflammatory/sensitizing processes or a CNS malfunction could lead to significant hypersensitivity of the peripheral nociceptive nerve fibers in SOD patients. Postcholecystectomy pain may be explained by persistent hyperexcitability of the nociceptive neurons in the CNS with or without objective motility disorders of the SO.