1 Headache & Orofacial Pain Effort, Biologic & Materials Sciences Department, University of Michigan School of Dentistry, Ann Arbor, MI, USA.
2 Center for Human Growth and Development, University of Michigan, Ann Arbor, MI, USA.
J Dent Res. 2018 May;97(5):523-529. doi: 10.1177/0022034517750136. Epub 2018 Jan 11.
This study used an emerging brain imaging technique, functional near-infrared spectroscopy (fNIRS), to investigate functional brain activation and connectivity that modulates sometimes traumatic pain experience in a clinical setting. Hemodynamic responses were recorded at bilateral somatosensory (S1) and prefrontal cortices (PFCs) from 12 patients with dentin hypersensitivity in a dental chair before, during, and after clinical pain. Clinical dental pain was triggered with 20 consecutive descending cold stimulations (32° to 0°C) to the affected teeth. We used a partial least squares path modeling framework to link patients' clinical pain experience with recorded hemodynamic responses at sequential stages and baseline resting-state functional connectivity (RSFC). Hemodynamic responses at PFC/S1 were sequentially elicited by expectation, cold detection, and pain perception at a high-level coefficient (coefficients: 0.92, 0.98, and 0.99, P < 0.05). We found that the pain ratings were positively affected only at a moderate level of coefficients by such sequence of functional activation (coefficient: 0.52, P < 0.05) and the baseline PFC-S1 RSFC (coefficient: 0.59, P < 0.05). Furthermore, when the dental pain had finally subsided, the PFC increased its functional connection with the affected S1 orofacial region contralateral to the pain stimulus and, in contrast, decreased with the ipsilateral homuncular S1 regions ( P < 0.05). Our study indicated for the first time that patients' clinical pain experience in the dental chair can be predicted concomitantly by their baseline functional connectivity between S1 and PFC, as well as their sequence of ongoing hemodynamic responses. In addition, this linked cascade of events had immediate after-effects on the patients' brain connectivity, even when clinical pain had already ceased. Our findings offer a better understating of the ongoing impact of affective and sensory experience in the brain before, during, and after clinical dental pain.
本研究采用新兴的脑成像技术——功能近红外光谱（fNIRS），在临床环境中研究调节有时创伤性疼痛体验的大脑功能激活和连接。在牙科椅上，12 名牙本质过敏患者在临床疼痛之前、期间和之后，从双侧体感（S1）和前额叶皮质（PFC）记录血流动力学反应。临床牙科疼痛通过 20 次连续下降冷刺激（32°至 0°C）引发到受影响的牙齿。我们使用偏最小二乘路径建模框架将患者的临床疼痛体验与连续阶段和基线静息状态功能连接（RSFC）记录的血流动力学反应联系起来。在高水平系数（系数：0.92、0.98 和 0.99，P < 0.05）下，PFC/S1 的血流动力学反应依次由期望、冷探测和疼痛感知引发。我们发现，只有在功能激活的中等水平系数（系数：0.52，P < 0.05）和基线 PFC-S1 RSFC（系数：0.59，P < 0.05）的情况下，疼痛评分才会受到正影响。此外，当牙科疼痛最终消退时，PFC 增加了与疼痛刺激对侧的受影响 S1 或面区域的功能连接，而与同侧同源 S1 区域相反（P < 0.05）。我们的研究首次表明，患者在牙科椅上的临床疼痛体验可以通过他们在 S1 和 PFC 之间的基线功能连接以及他们正在进行的血流动力学反应序列来同时预测。此外，即使临床疼痛已经停止，这种连锁事件对患者的大脑连接也有即时的后续影响。我们的发现更好地理解了临床牙科疼痛之前、期间和之后大脑中情感和感觉体验的持续影响。
