Neural changes in extinction recall following prolonged exposure treatment for PTSD: A longitudinal fMRI study

被引:84
|
作者
Helpman, Liat [1 ,2 ]
Marin, Marie-France [3 ,4 ]
Papini, Santiago [5 ]
Zhu, Xi [1 ,2 ]
Sullivan, Gregory M. [1 ,2 ]
Schneier, Franklin [1 ,2 ]
Neria, Mariana [1 ,2 ]
Shvil, Erel [1 ,2 ]
Aragon, Maria Josefa Malaga [1 ,2 ]
Markowitz, John C. [1 ,2 ]
Lindquist, Martin A. [6 ]
Wager, Tor D. [7 ]
Milad, Mohammed R. [6 ]
Neria, Yuval [1 ,2 ]
机构
[1] Columbia Univ, Dept Psychiat, 1051 Riverside Dr, New York, NY 10032 USA
[2] New York State Psychiat Inst & Hosp, 1051 Riverside Dr, New York, NY 10032 USA
[3] Massachusetts Gen Hosp, Dept Psychiat, 149 13th St, Charlestown, MA 02129 USA
[4] Harvard Med Sch, 149 13th St, Charlestown, MA 02129 USA
[5] Univ Texas Austin, Mental Hlth Res Inst, 305 E 23rd St,Stop E9000, Austin, TX 78712 USA
[6] Johns Hopkins Univ, Dept Biostat, 615 N Wolfe St,E3634, Baltimore, MD 21205 USA
[7] Univ Colorado, Dept Psychol & Neurosci, 345 UCB, Boulder, CO 80309 USA
基金
美国国家卫生研究院;
关键词
POSTTRAUMATIC-STRESS-DISORDER; VENTROMEDIAL PREFRONTAL CORTEX; IMPAIRED FEAR INHIBITION; CONDITIONED FEAR; EMOTIONAL PERSEVERATION; HORMONAL CONTRACEPTIVES; SEX-DIFFERENCES; AMYGDALA; TRAUMA; ACTIVATION;
D O I
10.1016/j.nicl.2016.10.007
中图分类号
R445 [影像诊断学];
学科分类号
100207 ;
摘要
Background: Neurobiological models of posttraumatic stress disorder (PTSD) implicate fear processing impairments in the maintenance of the disorder. Specific deficits in extinction recall, the retention of learned extinction, have been demonstrated. While deficient extinction recall, and the associated activation pattern of prefrontal and hippocampal regions, distinguishes individuals with PTSD from controls, research has not yet examined changes following treatment. We examined the behavioral and neural correlates of extinction recall before and after cognitive behavioral treatment of PTSD. Methods: Fifty-eight participants (30 with PTSD, 28 trauma-exposed matched controls) underwent a 2-day behavioral fear conditioning, extinction, and recall paradigm during functional magnetic resonance imaging (fMRI). The same procedures were repeated 10 weeks later, after PTSD patients had completed prolonged exposure treatment. We analyzed fMRI data from 32 subjects (16 PTSD; 16 controls) and skin conductance response (SCR) data from 33 subjects (16 PTSD; 17 controls). Neural activity during extinction recall, SCR, and PTSD symptoms were compared across groups and over time. Results: PTSD patients exhibited pre-to post-treatment reduction in rostral anterior cingulate cortex (rACC) activation during extinction recall, and increase in functional coherence between the rACC and the ventromedial prefrontal cortex (vmPFC) and subgenual anterior cingulate cortex (sgACC). Reduced PTSD symptom severity from pre-to post-treatment was significantly associated with reduced subgenual ACC and parahippocampal activation during this task. SCR during the extinction recall phase did not significantly change with treatment in the PTSD group, but change in SCR was associated with reduction in PTSD symptom severity. Conclusions: Prolonged exposure treatment appears to alter neural activation in PTSD patients during recall of fear extinction, and change in extinction recall (measured by SCR) is associated with symptom reduction. We discuss results in the context of neural systems involved in response to affective stimuli. (C) 2016 The Authors. Published by Elsevier Inc.
引用
收藏
页码:715 / 723
页数:9
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