Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury.
Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury.
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DOI：
10.1038/tp.2013.116
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发表时间：
2014-01-07
影响因子：
6.8
通讯作者：
Simmons AN
中科院分区：
文献类型：
--
作者：
Strigo IA;Spadoni AD;Lohr J;Simmons AN
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.
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影响因子：
3.7
作者：
Mac Donald C;Johnson A;Cooper D;Malone T;Sorrell J;Shimony J;Parsons M;Snyder A;Raichle M;Fang R;Flaherty S;Russell M;Brody DL
通讯作者：
Brody DL
影响因子：
--
作者：
Jack, Kirsten;McLean, Sionnadh Mairi;Moffett, Jennifer Klaber;Gardiner, Eric
通讯作者：
Gardiner, Eric
影响因子：
17.1
作者：
Goldstein LE;Fisher AM;Tagge CA;Zhang XL;Velisek L;Sullivan JA;Upreti C;Kracht JM;Ericsson M;Wojnarowicz MW;Goletiani CJ;Maglakelidze GM;Casey N;Moncaster JA;Minaeva O;Moir RD;Nowinski CJ;Stern RA;Cantu RC;Geiling J;Blusztajn JK;Wolozin BL;Ikezu T;Stein TD;Budson AE;Kowall NW;Chargin D;Sharon A;Saman S;Hall GF;Moss WC;Cleveland RO;Tanzi RE;Stanton PK;McKee AC
通讯作者：
McKee AC
影响因子：
--
作者：
Geuze, Elbert;Westenberg, Herman G. M.;Schmahl, Christian
通讯作者：
Schmahl, Christian
DOI：
10.1016/s0003-9993(96)90275-0
发表时间：
1996-09-01
影响因子：
4.3
作者：
Lahz, S;Bryant, RA
通讯作者：
Bryant, RA