Elsevier

NeuroImage: Clinical

Volume 12, February 2016, Pages 715-723
NeuroImage: Clinical

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

https://doi.org/10.1016/j.nicl.2016.10.007Get rights and content
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Highlights

  • Deficient recall of extinguished fear (extinction recall; ER) has been associated with PTSD.

  • Prolonged exposure (PE) is a first line treatment for PTSD which relies on extinction.

  • Changes in prefrontal activation and functional connectivity during ER appeared following PE.

  • Changes in ER following PE corresponded to changes in PTSD severity.

  • Taken together, these findings suggest normalization of ER deficits in PTSD following PE.

Abstract

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.

Cited by (0)

This study was supported by NIMH grant R01 MH072833 (Dr. Neria, principal investigator). Dr. Helpman is supported by National Institutes of Health (NIH) grant 5T32MH096724-03.

1

Equal contribution.