Department of Clinical Oral Physiology, School of Dentistry, Aarhus University, Aarhus, Denmark Center of Functionally Integrative Neuroscience, Aarhus University, Aarhus, Denmark Psychooncology Research Unit, Aarhus University Hospital, Aarhus, Denmark Department of Oral Maxillofacial Surgery, Aarhus University Hospital, Denmark.
Pain. 2010 Dec;151(3):825-833. doi: 10.1016/j.pain.2010.09.020. Epub 2010 Oct 8.
Hypnosis modulates pain perception but the associated brain mechanisms in chronic pain conditions are poorly understood. Brain activity evoked by painful repetitive pin-prick stimulation of the left mental nerve region was investigated with use of fMRI in 19 patients with painful temporomandibular disorders (TMD) during hypnotic hypoalgesia and hyperalgesia and a control condition. Pain intensity and unpleasantness of the painful stimulation was scored on a 0-10 Numerical Rating Scale (NRS). NRS pain and unpleasantness scores during hypnotic hypoalgesia were significantly lower than in the control condition and significantly higher in the hypnotic hyperalgesia condition. In the control condition, painful stimulation caused significant activation of right posterior insula, primary somatosensory cortex (SI), BA21, and BA6, and left BA40 and BA4. Painful stimulation during hypnotic hyperalgesia was associated with increased activity in right posterior insula and BA6 and left BA40 whereas hypnotic hypoalgesia only was associated with activity in right posterior insula. Unexpectedly, direct contrasts between control and hypnotic hyperalgesia conditions revealed significant decreases in S1 during hyperalgesia. Direct contrasts between control and hypnotic hypoalgesia conditions demonstrated significant decreases in right posterior insula and BA21, as well as left BA40 during hypoalgesia. These findings are the first to describe hypnotic modulation of brain activity associated with nociceptive processing in chronic TMD pain patients and demonstrate that hypnotic hypoalgesia is associated with a pronounced suppression of cortical activity and a disconnection between patient-based scores and cortical activity in S1 during hypnotic hyperalgesia.
催眠可以调节疼痛感知，但慢性疼痛情况下相关的大脑机制仍不清楚。本研究使用 fMRI 技术，观察 19 例患有颞下颌关节紊乱（TMD）的慢性疼痛患者在催眠镇痛和超敏状态下以及对照状态下，左侧精神神经区域的疼痛性重复刺痛刺激所引起的大脑活动。使用 0-10 数字评分量表（NRS）对疼痛强度和疼痛刺激的不愉快程度进行评分。催眠镇痛状态下的 NRS 疼痛和不愉快评分明显低于对照状态，而在催眠超敏状态下则明显升高。在对照状态下，疼痛刺激引起右侧后岛叶、初级体感皮层（SI）、BA21 和 BA6 以及左侧 BA40 和 BA4 的显著激活。在催眠超敏状态下，疼痛刺激与右侧后岛叶和 BA6 以及左侧 BA40 的活动增加相关，而催眠镇痛仅与右侧后岛叶的活动相关。出乎意料的是，对照和催眠超敏状态之间的直接对比显示，在超敏状态下 SI 的活动显著降低。对照和催眠镇痛状态之间的直接对比显示，在镇痛状态下，右侧后岛叶和 BA21 以及左侧 BA40 的活动显著降低。这些发现首次描述了催眠对慢性 TMD 疼痛患者疼痛处理相关大脑活动的调节作用，并表明催眠镇痛与皮质活动的明显抑制以及在催眠超敏状态下患者评分与 SI 皮质活动之间的脱钩有关。
