Offset analgesia is mediated by activation in the region of the periaqueductal grey and rostral ventromedial medulla
Offset analgesia is mediated by activation in the region of the periaqueductal grey and rostral ventromedial medulla
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DOI：
10.1016/j.neuroimage.2009.04.032
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发表时间：
2009-09-01
期刊：
影响因子：
5.7
通讯作者：
Osborn, J.
中科院分区：
文献类型：
--
作者：
Derbyshire, S. W. G.;Osborn, J.
当最初的有害热量返回时，用更大的有害热量中断持续的有害热量会导致快速和不成比例的疼痛减轻。这种疼痛体验的减少，被称为抵消镇痛，被认为是主动下行抑制控制起源于中脑导水管周围灰质(PAG)和延髓头端腹内侧部(RVM)的疼痛的结果。为了测试这种可能性，在补偿过程中，使用功能磁共振成像测量了12名健康对照的大脑激活。每个受试者都经历了六个第二周期的毒热，然后经历了相等的较高热期，然后再回到原始温度6 S。在对照试验中，受试者也接受了扫描，包括18个S的持续、不变的毒热，或者6个S毒热的相同周期，然后返回无毒基线，再经历6个S。每次试验的最后6个S的大脑激活与前6个S的大脑激活进行比较，并在不同的试验中对比这一差异。在OFFSET试验的最后6个S试验中观察到PAG/RVm的激活，而在两个对照试验中均未观察到PAG/RVm的激活，并且这一差异在各试验中是显着的。在偏置试验的最后6个S阶段，整个疼痛神经基质的激活被抑制，与热回到无毒基线时观察到的激活情况相当。这些发现提供了强有力的证据表明，抵消镇痛参与了起源于PAG/RVM区域的内源性抑制机制，该机制抑制了疼痛体验和疼痛神经基质的激活。(C)2009 Elsevier Inc.保留所有权利。
Interrupting a continuous noxious heat by a greater noxious heat causes rapid and disproportionate pain reduction when the original noxious heat returns. This reduction in pain experience, known as offset analgesia, is believed to be the consequence of active descending inhibitory control of pain originating in the periaqueductal grey (PAG) and rostral ventromedial medulla (RVM). To test this possibility, brain activation was measured using fMRI in twelve healthy controls during an offset procedure. Each Subject experienced six second periods of noxious heat followed by an equal period of more intense heat before returning to the original temperature for a further 6 s. Subjects were also scanned during control trials involving continuous, unchanging, noxious heat for 18 s or involving 6 s of noxious heat followed by an equal period Of More intense heat before returning to the non-noxious baseline for a further 6 s. Brain activation during the final 6 s of each trial was compared with activation during the first 6 s and this difference was contrasted across trials. PAG/RVM activation was observed during the final 6 s of offset trials but not during either of the control trials and this difference across trials was significant. Activation throughout the pain neuromatrix was inhibited during the final 6 s of the offset trials and was comparable to the activation observed when the heat returned to a non-noxious baseline. These findings provide strong evidence that offset analgesia engages an endogenous inhibitory mechanism originating in the PAG/RVM region, which inhibits pain experience and activation of the pain neuromatrix. (C) 2009 Elsevier Inc. All rights reserved.