Casey K L, Beydoun A, Boivie J, Sjolund B, Holmgren H, Leijon G, Morrow T J, Rosen I
Department of Neurology, University of Michigan, Ann Arbor, MI, USA Department of Physiology, University of Michigan, Ann Arbor, MI, USA Neurology Research Laboratories, VA Medical Center, Ann Arbor, MI 48105 USA Department of Neurology, University of Linkoping, Linkoping, Sweden Department of Anesthesiology, University of Lund, Lund, Sweden Department of Clinical Neurophysiology, University of Lund, Lund, Sweden.
Pain. 1996 Mar;64(3):485-491. doi: 10.1016/0304-3959(95)00143-3.
Central pain syndromes (CPS) could be caused by disinhibition of spinothalamic excitability or by other central nervous system (CNS) changes caused by reduced spinothalamic function. To examine these possibilities, we studied 11 patients (ages 51-82 years) with unilateral central pain and with reproducible cerebral evoked vertex potentials in response to cutaneous stimulation of the normal side with pulses from an infra-red CO2 laser. All patients had normal tactile and kinesthetic sensation; one had slightly decreased vibratory sense bilaterally. All showed, from the unaffected (asymptomatic) side, laser evoked potentials (LEPs) with negative (N) components ranging from 208 to 280 msec peak latency (av: 240 +/- 6 SE msec) and peak amplitudes of 1-7 microV (av: 2.9 +/- 0.5 SE microV), followed, in all but 1 patient, by positive (P) potentials ranging from 288 to 370 msec peak latency (av: 319 +/- 7.7 SE msec) with peak amplitudes of 1-7 microV (2.8 +/- 0.5 SE microV). Laser stimulation of the affected (symptomatic) side in 5 patients evoked LEPs with N-P interpeak amplitudes that were within 20% of those evoked from the normal side. All but one of these patients had thresholds for warm, heat pain, and deep pain that were normal in comparison with the unaffected side. The excepted patient had the largest N-P interpeak amplitude asymmetry (18.5%) of this group. Ratings of laser pulse intensity were either symmetrical (n = 2) or increased on the affected side (n = 3) in these patients. In contrast, laser stimulation of the affected side failed to evoke either N or P potentials in 6 patients, all of whom had lateralized increased thresholds for warm, heat pain, or deep pain, or reduced ratings of laser pulse sensation. Although 1 patient had increased ratings of laser pulse sensation, the amplitude of the LEP was always reduced on the side of increased pain or heat threshold in these CPS patients (Fisher exact test: P = 0.015). These results reflect primarily a deficit in spinothalamic tract function and do not suggest excessive CNS responses to synchronous activation of cutaneous heat nociceptors in patients with CPS.
中枢性疼痛综合征（CPS）可能是由于脊髓丘脑束兴奋性的去抑制，或因脊髓丘脑束功能减退引起的其他中枢神经系统（CNS）变化所致。为研究这些可能性，我们对11例（年龄51 - 82岁）单侧中枢性疼痛患者进行了研究，这些患者对正常侧皮肤进行红外二氧化碳激光脉冲刺激时，可诱发出可重复的脑诱发顶点电位。所有患者的触觉和本体感觉均正常；1例患者双侧振动觉略有减退。所有患者从未受影响（无症状）侧均可诱发出激光诱发电位（LEP），负性（N）成分的峰潜伏期为208至280毫秒（平均：240±6标准误毫秒），峰幅度为1 - 7微伏（平均：2.9±0.5标准误微伏），除1例患者外，随后均出现正性（P）电位，峰潜伏期为288至370毫秒（平均：319±7.7标准误毫秒），峰幅度为1 - 7微伏（2.8±0.5标准误微伏）。对5例患者的患侧（有症状侧）进行激光刺激，诱发出的LEP的N - P峰间幅度在正常侧诱发出的幅度的20%以内。除1例患者外，所有这些患者的温热、热痛和深部痛阈值与未受影响侧相比均正常。该例外患者是该组中N - P峰间幅度不对称性最大的（18.5%）。在这些患者中，激光脉冲强度评分在两侧要么对称（n = 2），要么患侧增加（n = 3）。相比之下，对6例患者的患侧进行激光刺激未能诱发出N或P电位，所有这些患者的温热、热痛或深部痛阈值均有侧化性升高，或激光脉冲感觉评分降低。尽管1例患者的激光脉冲感觉评分增加，但在这些CPS患者中，疼痛或热阈值升高侧的LEP幅度总是降低（Fisher精确检验：P = 0.015）。这些结果主要反映了脊髓丘脑束功能的缺陷，并未提示CPS患者中枢神经系统对皮肤热伤害感受器同步激活存在过度反应。
