Hsieh Jen-Chuen, Belfrage Måns, Stone-Elander Sharon, Hansson Per, Ingvar Martin
Clinical Neurophysiology, Department of Clinical Neuroscience, Karolinska Hospital/Karolinska Institute, 171 76 Stockholm, Sweden Pain Section, Department of Anesthesiology, Karolinska Hospital/Karolinska Institute, 171 76 Stockholm, Sweden Intensive Care, Karolinska Pharmacy, Karolinska Hospital/Karolinska Institute, 171 76 Stockholm, Sweden Neurogenic Pain Unit, Department of Rehabilitation Medicine, Karolinska Hospital/Karolinska Institute, 171 76 Stockholm, Sweden Neuroanesthesia and Pain Unit, Department of Anesthesiology, Veterans General Hospital-Taipei, and School of Medicine, National Yang-Ming University, Taipei 11217, Taiwan.
Pain. 1995 Nov;63(2):225-236. doi: 10.1016/0304-3959(95)00048-W.
This study was undertaken to explore whether the neural substrates demonstrated in brain imaging studies on experimentally induced pain are involved in the perception of chronic neuropathic pain. We investigated the cerebral representation of chronic lateralised ongoing pain in patients with painful mononeuropathy (PMN, i.e., pain in the distribution of a nerve, neuralgia) with positron emission tomography (PET), using regional cerebral blood flow (rCBF) as an index for neuronal activity. Eight patients (29-53 years) with PMN in the lower extremity (4 in the right, 4 in the left) were recruited. Paired comparisons of rCBF were made between the patient's habitual pain (HP) state and the pain alleviated (PA) state following a successful regional nerve block (RNB) with lidocaine. The ongoing neuropathic pain resulted in activation of bilateral anterior insula, posterior parietal, lateral inferior prefrontal, and posterior cingulate cortices as well as the posterior sector of the right anterior cingulate cortex (ACC), Brodmann area (BA) 24, regardless of the side of PMN. In addition, a reduction in rCBF was noted in the contralateral posterior thalamus. No significant change of rCBF was detected in the somatosensory areas, i.e., SI and SII. The cerebral activation pattern, while addressing the differences between the HP and PA states, emphasises the affective-motivational dimension in chronic ongoing neuropathic pain. The striking preferential activation of the right ACC (BA 24), regardless of the side of the PMN, not only confirms that the ACC participates in the sensorial/affectional aspect of the pain experience but also suggests a possible right hemispheric lateralisation of the ACC for affective processing in chronic ongoing neuropathic pain. Our data suggests that the brain employs different central mechanisms for chronic neuropathic pain and experimentally induced acute pain, respectively.
本研究旨在探讨脑成像研究中显示的实验性诱导疼痛的神经基质是否参与慢性神经性疼痛的感知。我们使用正电子发射断层扫描(PET),以局部脑血流量(rCBF)作为神经元活动指标,研究了患有疼痛性单神经病(PMN,即神经分布区域的疼痛、神经痛)患者慢性偏侧持续性疼痛的脑表征。招募了8名患有下肢PMN的患者(年龄29 - 53岁,右侧4例,左侧4例)。在患者的习惯性疼痛(HP)状态与利多卡因成功进行局部神经阻滞(RNB)后疼痛缓解(PA)状态之间进行rCBF的配对比较。无论PMN位于哪一侧,持续性神经性疼痛都会导致双侧前脑岛、顶叶后部、外侧前额叶下部、后扣带回皮质以及右侧前扣带回皮质(ACC)的后部区域(Brodmann区(BA)24)激活。此外,对侧后丘脑的rCBF降低。在躯体感觉区,即初级躯体感觉皮层(SI)和次级躯体感觉皮层(SII)未检测到rCBF的显著变化。脑激活模式在解决HP和PA状态之间差异的同时,强调了慢性持续性神经性疼痛中的情感 - 动机维度。无论PMN位于哪一侧,右侧ACC(BA 24)的显著优先激活不仅证实了ACC参与疼痛体验的感觉/情感方面,还表明在慢性持续性神经性疼痛的情感处理中ACC可能存在右半球偏侧化。我们的数据表明,大脑分别采用不同的中枢机制来处理慢性神经性疼痛和实验性诱导的急性疼痛。