Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury

被引:28
作者
Strigo, I. A. [1 ,2 ,3 ]
Spadoni, A. D. [1 ,2 ]
Lohr, J. [1 ,2 ]
Simmons, A. N. [1 ,2 ]
机构
[1] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA
[2] Univ Calif San Diego, La Jolla, CA 92161 USA
[3] Univ Calif San Diego, BioCircuits Inst, La Jolla, CA 92161 USA
来源
TRANSLATIONAL PSYCHIATRY | 2014年 / 4卷
关键词
concussion; dorsolateral prefrontal; emotion; imaging; PAG; post-traumatic stress; POSTTRAUMATIC-STRESS-DISORDER; PERSISTENT POSTCONCUSSIVE SYMPTOMS; MAJOR DEPRESSIVE DISORDER; INSULA ACTIVATION; BLAST EXPOSURE; WAR VETERAN; IRAQ; AFGHANISTAN; EMOTION; PTSD;
D O I
10.1038/tp.2013.116
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
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.
引用
收藏
页码:e340 / e340
页数:8
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