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PTSD Specific Deficits in Default Mode Network Strength: At Baseline and Following Experimental Stress

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Abstract Reductions in default mode (DMN) connectivity strength have been reported in posttraumatic stress disorder (PTSD). However, the specificity of DMN connectivity deficits in PTSD compared to major depressive disorder (MDD), and the sensitivity of these alterations to acute stressors are not yet known. 52 participants with primary diagnosis of PTSD (n = 28) or MDD (n = 24) completed resting state functional magnetic resonance imaging immediately before and after a mild affective stressor. A 2x2 design was conducted to determine the effects of group, stress, and group*stress on DMN connectivity strength. Exploratory analyses were completed to identify the brain region(s) underlying the DMN alterations. We found 13% reduction in DMN strength in PTSD compared to MDD (p = 0.04). There was significant group*stress interaction (p = 0.03), reflecting stress-induced reduction in DMN strength in PTSD (p = 0.02), but not MDD (p = 0.50). Nodal exploration of connectivity strength in the DMN identified regions of the ventromedial prefrontal cortex and the precuneus contributing to DMN connectivity deficits. The findings indicate distinct, disease-specific, patterns of connectivity strength reduction in the DMN in PTSD, especially following an experimental stressor. The identified stress-induced dynamic shift in functional connectivity underscores the potential utility of the DMN connectivity and raises the question whether these disruptions are inversely affected by antidepressants known to treat both MDD and PTSD psychopathology.
Title: PTSD Specific Deficits in Default Mode Network Strength: At Baseline and Following Experimental Stress
Description:
Abstract Reductions in default mode (DMN) connectivity strength have been reported in posttraumatic stress disorder (PTSD).
However, the specificity of DMN connectivity deficits in PTSD compared to major depressive disorder (MDD), and the sensitivity of these alterations to acute stressors are not yet known.
52 participants with primary diagnosis of PTSD (n = 28) or MDD (n = 24) completed resting state functional magnetic resonance imaging immediately before and after a mild affective stressor.
A 2x2 design was conducted to determine the effects of group, stress, and group*stress on DMN connectivity strength.
Exploratory analyses were completed to identify the brain region(s) underlying the DMN alterations.
We found 13% reduction in DMN strength in PTSD compared to MDD (p = 0.
04).
There was significant group*stress interaction (p = 0.
03), reflecting stress-induced reduction in DMN strength in PTSD (p = 0.
02), but not MDD (p = 0.
50).
Nodal exploration of connectivity strength in the DMN identified regions of the ventromedial prefrontal cortex and the precuneus contributing to DMN connectivity deficits.
The findings indicate distinct, disease-specific, patterns of connectivity strength reduction in the DMN in PTSD, especially following an experimental stressor.
The identified stress-induced dynamic shift in functional connectivity underscores the potential utility of the DMN connectivity and raises the question whether these disruptions are inversely affected by antidepressants known to treat both MDD and PTSD psychopathology.

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