Strigo I A, Spadoni A D, Lohr J, Simmons A N
1] Veterans Affairs San Diego Healthcare System, San Diego, CA, USA [2] University of California San Diego, La Jolla, CA, USA [3] BioCircuits Institute, University of California San Diego, La Jolla, CA, USA.
1] Veterans Affairs San Diego Healthcare System, San Diego, CA, USA [2] University of California San Diego, La Jolla, CA, USA.
Transl Psychiatry. 2014 Jan 7;4(1):e340. doi: 10.1038/tp.2013.116.
Mild traumatic brain injury (MTBI) is a vulnerability factor for the development of pain-related conditions above and beyond those related to comorbid traumatic and emotional symptoms. We acquired functional magnetic resonance imaging (fMRI) on a validated pain anticipation task and tested the hypotheses that individuals with a reported history of MTBI, compared with healthy comparison subjects, would show increased brain response to pain anticipation and ineffective pain modulation after controlling for psychiatric symptoms. Eighteen male subjects with a reported history of blast-related MTBI related to combat, and eighteen healthy male subjects with no reported history of MTBI (healthy controls) underwent fMRI during an event-related experimental pain paradigm with cued high or low intensity painful heat stimuli. No subjects in either group met diagnostic criteria for current mood or anxiety disorder. We found that relative to healthy comparison subjects, after controlling for traumatic and depressive symptoms, participants with a reported history of MTBI showed significantly stronger activations within midbrain periaqueductual grey (PAG), right dorsolateral prefrontal cortex and cuneus during pain anticipation. Furthermore, we found that brain injury was a significant moderator of the relationship between anticipatory PAG activation and reported subjective pain. Our results suggest that a potentially disrupted neurocognitive anticipatory network may result from damage to the endogenous pain modulatory system and underlie difficulties with regulatory pain processing following MTBI. In other words, our findings are consistent with a notion that brain injury makes it more difficult to control acute pain. Understanding these mechanisms of dysfunctional acute pain processing following MTBI may help shed light on the underlying causes of increased vulnerability for the development of pain-related conditions in this population.
轻度创伤性脑损伤（MTBI）是疼痛相关疾病发生的一个易患因素，其影响超出了与创伤性和情绪性共病症状相关的范围。我们在一项经过验证的疼痛预期任务中进行了功能磁共振成像（fMRI），并检验了以下假设：与健康对照受试者相比，有MTBI病史报告的个体在控制精神症状后，对疼痛预期的脑反应会增强，且疼痛调节无效。18名有与战斗相关的爆炸所致MTBI病史报告的男性受试者和18名无MTBI病史报告的健康男性受试者（健康对照组）在一个事件相关的实验性疼痛范式中接受了fMRI检查，该范式采用了提示高强度或低强度疼痛热刺激。两组中均无受试者符合当前情绪或焦虑障碍的诊断标准。我们发现，与健康对照受试者相比，在控制创伤性和抑郁性症状后，有MTBI病史报告的参与者在疼痛预期期间中脑导水管周围灰质（PAG）、右侧背外侧前额叶皮质和楔叶内的激活明显更强。此外，我们发现脑损伤是预期性PAG激活与报告的主观疼痛之间关系的一个显著调节因素。我们的结果表明，内源性疼痛调节系统受损可能导致潜在的神经认知预期网络中断，并成为MTBI后调节性疼痛处理困难的基础。换句话说，我们的研究结果与脑损伤使控制急性疼痛更加困难这一观点一致。了解MTBI后功能失调的急性疼痛处理机制可能有助于阐明该人群中疼痛相关疾病易患性增加的潜在原因。
