Brain activity for tactile allodynia: a longitudinal awake rat functional magnetic resonance imaging study tracking emergence of neuropathic pain.
Brain activity for tactile allodynia: a longitudinal awake rat functional magnetic resonance imaging study tracking emergence of neuropathic pain.
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DOI：
10.1097/j.pain.0000000000000788
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发表时间：
2017-03
期刊：
影响因子：
7.4
通讯作者：
Apkarian AV
中科院分区：
文献类型：
--
作者：
Chang PC;Centeno MV;Procissi D;Baria A;Apkarian AV
触觉异常性疼痛是一种将无害的机械刺激感知为疼痛的状况，是慢性疼痛的常见特征。然而，大脑如何重组与触觉异常性疼痛的出现在很大程度上仍然是未知的。这可能源于这样一个事实，即人类实验本质上是横断面的，而动物脑成像研究通常需要麻醉，使大脑无法有意识地感知或对疼痛做出反应。在这项对清醒大鼠的纵向fMRI研究中，我们跟踪了触觉异常性疼痛发展过程中的大脑活动。损伤前，无害的空气刺激诱发了一个分布式的感觉网络的激活，包括对侧的躯体感觉皮层，丘脑，丘脑和扣带皮层。此外，初级躯体感觉皮层显示出分级响应跟踪喷气刺激强度。在神经性损伤后，对于强度超过缩爪阈值的刺激（诱发触觉异常性疼痛），初级体感皮层中的BOLD反应相当于损伤前由相同刺激诱发的反应。与此相反，正常无害的刺激时，这些刺激诱导的触觉异常性疼痛，在外周神经损伤后28天，这并没有在伤后5天的情况下，脑桥核和前额叶脑区显示异常活动。我们的数据表明，触觉异常性疼痛相关的伤害性输入在初级体感皮层BOLD反应中是不可观察的。相反，我们的数据表明，随着时间的推移，触觉异常性疼痛差异参与调节疼痛的情感和动机成分的神经回路。
Tactile allodynia, a condition in which innocuous mechanical stimuli are perceived as painful, is a common feature of chronic pain. However, how the brain reorganizes in relation to the emergence of tactile allodynia is still largely unknown. This may stem from the fact that experiments in humans are cross-sectional in nature, while animal brain imaging studies typically require anaesthesia rendering the brain incapable of consciously sensing or responding to pain. In this longitudinal fMRI study in awake rats, we tracked brain activity with the development of tactile allodynia. Prior to injury, innocuous air puff stimuli evoked a distributed sensory network of activations, including contralateral somatosensory cortices, thalamus, insula, and cingulate cortex. Moreover, the primary somatosensory cortex displayed a graded response tracking airpuff stimulus intensities. After neuropathic injury, and for stimuli where the intensity exceeded the paw withdrawal threshold (evoking tactile allodynia), the BOLD response in the primary somatosensory cortex was equivalent to that evoked by the identical stimulus prior to injury. In contrast, nucleus accumbens and prefrontal brain areas displayed abnormal activity to normally innocuous stimuli when such stimuli induced tactile allodynia at 28 days after peripheral nerve injury, which had not been the case at 5 days post-injury. Our data indicate that tactile allodynia-related nociceptive inputs are not observable in the primary somatosensory cortex BOLD response. Instead, our data suggests that, in time, tactile allodynia differentially engages neural circuits that regulate the affective and motivational components of pain.