Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA Neurology Research Laboratory, VA Medical Center, Ann Arbor, MI 48105, USA Department of Pediatrics, University of Medicine and Pharmacy of Ho Chi Minh City, Ho Chi Minh City, Vietnam Medical School, University of Michigan, Ann Arbor, MI 48105, USA Department of Biomedical Engineering and Functional MRI Laboratory, University of Michigan, Ann Arbor, MI 48109, USA.
Pain. 2010 Jul;150(1):93-102. doi: 10.1016/j.pain.2010.04.001. Epub 2010 May 21.
Noxious cutaneous contact heat stimuli (48 degrees C) are perceived as increasingly painful when the stimulus duration is extended from 5 to 10s, reflecting the temporal summation of central neuronal activity mediating heat pain. However, the sensation of increasing heat pain disappears, reaching a plateau as stimulus duration increases from 10 to 20s. We used functional magnetic resonance imaging (fMRI) in 10 healthy subjects to determine if active central mechanisms could contribute to this psychophysical plateau. During heat pain durations ranging from 5 to 20s, activation intensities in the bilateral orbitofrontal cortices and the activation volume in the left primary (S1) somatosensory cortex correlated only with perceived stimulus intensity and not with stimulus duration. Activation volumes increased with both stimulus duration and perceived intensity in the left lateral thalamus, posterior insula, inferior parietal cortex, and hippocampus. In contrast, during the psychophysical plateau, both the intensity and volume of thalamic and cortical activations in the right medial thalamus, right posterior insula, and left secondary (S2) somatosensory cortex continued to increase with stimulus duration but not with perceived stimulus intensity. Activation volumes in the left medial and right lateral thalamus, and the bilateral mid-anterior cingulate, left orbitofrontal, and right S2 cortices also increased only with stimulus duration. The increased activity of specific thalamic and cortical structures as stimulus duration, but not perceived intensity, increases is consistent with the recruitment of a thalamocortical mechanism that participates in the modulation of pain-related cortical responses and the temporal summation of heat pain.
有害的皮肤接触热刺激（48°C）在刺激持续时间从 5 秒延长至 10 秒时，会被感知为越来越痛，这反映了介导热痛的中枢神经元活动的时间总和。然而，随着刺激持续时间从 10 秒增加到 20 秒，增加的热痛感觉消失，达到一个平台。我们使用 10 名健康受试者的功能磁共振成像（fMRI）来确定主动的中枢机制是否可以对此心理物理平台做出贡献。在热痛持续时间为 5 至 20 秒的过程中，双侧眶额皮质的激活强度和左侧初级（S1）体感皮质的激活体积仅与感知的刺激强度相关，而与刺激持续时间无关。在左侧外侧丘脑、后岛叶、下顶叶皮质和海马体中，激活体积随刺激持续时间和感知强度的增加而增加。相比之下，在心理物理平台期间，右侧内侧丘脑、右侧后岛叶和左侧次级（S2）体感皮质的丘脑和皮质激活的强度和体积继续随刺激持续时间增加而增加，但不随感知刺激强度增加。左侧内侧和右侧外侧丘脑以及双侧中前扣带回、左侧眶额皮质和右侧 S2 皮质的激活体积也仅随刺激持续时间增加而增加。随着刺激持续时间的增加而不是感知强度的增加，特定丘脑和皮质结构的活动增加与参与调制与疼痛相关的皮质反应和热痛的时间总和的丘脑皮质机制的募集一致。
