Tonic pain: A SPET study in normal subjects and cluster headache patients
Tonic pain: A SPET study in normal subjects and cluster headache patients
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DOI：
10.1016/s0304-3959(96)03318-0
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发表时间：
1997-04-01
期刊：
影响因子：
7.4
通讯作者：
Pantano, P
中科院分区：
文献类型：
--
作者：
DiPiero, V;Fiacco, F;Pantano, P
丛集性头痛（CH）的发病机制是外周性的还是中枢性的仍然存在争议。据推测，与疼痛感知和调节相关的中枢结构受累，这也会导致 CH 疼痛感知生理模式的改变。我们通过使用强直性疼痛刺激实验模型冷水压试验 (CWPT) 评估脑血流量 (CBF) 变化，研究了正常受试者和 CH 患者的大脑对疼痛的反应模式。如前所述（Di Piero 等，1994），在休息时和 CWPT 期间，通过 Xe-133 吸入法和单光子发射断层扫描 (SPET) 对 CBF 进行定量评估。对 12 名志愿者和 7 名 CH 患者进行了 CWPT。所有 CH 患者均出现左侧头痛，并在集群期外的无头痛阶段进行研究。在CWPT期间，志愿者表现出对侧初级感觉运动（P < 0.001）、额叶（P < 0.01）和颞叶（P < 0.002）区域以及丘脑（P < 0.01）以及同侧颞叶（P < 0.005）和前扣带回（P < 0.01）区域的CBF显着增加。 CH 患者接受 CWPT 左手刺激（头痛侧同侧）时，CBF 变化显着低于志愿者对侧初级感觉运动区（P < 0.0005）和丘脑区（P < 0.01）。然后，在刺激头痛侧的对侧手时，观察到的大脑反应没有显着差异。总之，在丛集期的无头痛阶段，头痛侧手部强直性疼痛刺激期间，CH 患者的大脑激活模式在可能涉及刺激强度检测的区域发生了重大改变。这种改变可能反映了疼痛传递系统的生物改变的标志。事实上，它也存在于疾病的活跃期，这表明中枢性强直性疼痛机制可能参与 CH 的发病机制。 (C) 1997 年国际疼痛研究协会。
Whether the pathogenesis of cluster headache (CH) is peripheral or central is still matter of debate. An involvement of central structures related to pain perception and modulation, which also causes an alteration of the physiological pattern of pain perception in CH, has been hypothesized. We investigated the pattern of brain response to pain in normal subjects and CH patients by evaluating the cerebral blood flow (CBF) changes using an experimental model of tonic aching pain stimulation, the cold water presser test (CWPT). CBF was assessed quantitatively by the Xe-133 inhalation method and single photon emission tomography (SPET), at rest and during CWPT, as previously described (Di Piero et al., 1994). CWPT was performed in 12 volunteers and in seven patients with CH. All the CH patients had a left-sided headache and were studied in a headache-free phase out of the cluster period. During CWPT, volunteers showed a significant CBF increase in the contralateral primary sensorimotor (P < 0.001), frontal (P < 0.01) and temporal (P < 0.002) regions and thalamus (P < 0.01) and in the ipsilateral temporal (P < 0.005) and anterior cingulate (P < 0.01) regions. During left-hand stimulation (ipsilateral to the headache side) by CWPT in CH patients, CBF changes were significantly lower than those observed in volunteers in the contralateral primary sensorimotor region (P < 0.0005) and thalamus region (P < 0.01). Then were no significant differences in the brain response observed during the stimulation of the hand contralateral to the headache side. In conclusion, in a headache-free phase out of the cluster period, the pattern of cerebral activation during tonic pain stimulation of the hand ipsilateral to the headache side is critically modified in CH patients in areas which are probably involved in the detection of the stimulus intensity. This modification may reflect a marker of a biological modification of the pain conveyance system. The fact that it is also present out of the active period of the disease, suggests a possible involvement of central tonic pain mechanisms in the pathogenesis of CH. (C) 1997 International Association for the Study of Pain.