PT  - JOURNAL ARTICLE
AU  - Daniel W. Grupe
AU  - Ted Imhoff-Smith
AU  - Joseph Wielgosz
AU  - Jack B. Nitschke
AU  - Richard J. Davidson
TI  - A common neural substrate for elevated PTSD symptoms and reduced pulse rate variability in combat-exposed veterans
AID  - 10.1101/364455
DP  - 2018 Jan 01
TA  - bioRxiv
PG  - 364455
4099  - http://biorxiv.org/content/early/2018/07/10/364455.short
4100  - http://biorxiv.org/content/early/2018/07/10/364455.full
AB  - Background Previous studies have identified reduced heart rate variability (HRV) in posttraumatic stress disorder (PTSD), which may temporally precede the onset of the disorder. A separate line of functional neuroimaging research suggests that the ventromedial prefrontal cortex (vmPFC) — a key aspect of a descending neuromodulatory system that exerts inhibitory control over heart rate — shows functional and structural abnormalities in PTSD. No research to date, however, has simultaneously investigated whether altered vmPFC activation is associated with reduced HRV and elevated PTSD symptoms in the same individuals.Methods We collected fMRI data during alternating conditions of threat of shock and safety from shock in 51 male, combat-exposed veterans with either high or low levels of PTSD symptoms. Pulse rate variability (PRV) – an HRV surrogate calculated from pulse oximetry – was assessed during a subsequent resting scan. Correlational analyses tested for hypothesized relationships between vmPFC activation, PRV, and distinct dimensions of PTSD symptomatology.Results Re-experiencing PTSD symptoms were inversely associated with high-frequency (HF)-PRV, thought to primarily reflect parasympathetic control of heart rate, in veterans with elevated PTSD symptoms. Lower HF-PRV was associated with reduced vmPFC activation for the contrast of safety-threat in a region that also showed an inverse relationship with re-experiencing symptoms.Conclusions Reduced vmPFC responses to safety vs. threat were associated with both reduced HF-PRV and increased re-experiencing symptoms. These results tie together previous observations of reduced HRV/PRV and impaired vmPFC function in PTSD and call for further research on reciprocal brain-body relationships in understanding PTSD pathophysiology.