Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder (PTSD)
Ida T. Fonkoue, Paul J. Marvar, Seth Norrholm, Yunxiao Li, Melanie L. Kankam, Toure N. Jones, Monica Vemulapalli, Barbara Rothbaum, J.Douglas Bremner, Ngoc-Anh Le, Jeanie Park
Brain Behav Immun. 2020 Jan;83:260-269
1) Summarize your work in one sentence.
My scientific interest is geared toward understanding how the autonomic nervous system, the vasculature and the kidney interact to contribute to the high cardiovascular disease risk of patients living with chronic stress exposure.
2) Summarize your findings in one sentence.
Our latest manuscript “Symptom severity impacts sympathetic dysregulation and inflammation in post-traumatic stress disorder” highlights the fact that individuals with severe post-traumatic stress disorder (PTSD) symptoms have a higher level of low-grade inflammation and greater impairment of the autonomic control of blood pressure at rest and in response to acute stress that may contribute to higher cardiovascular risk.
3) Which were the more important methods you used in this work? If it is not a traditional method you can briefly explain the concept of that methodology.
To address our research question, we used: 1) The Clinician Administered PTSD Scale (CAPS) fourth edition and the PTSD Checklist Military version (PCL-M) as diagnostic tools. CAPS and PCL-M are both validated and reliable measure of PTSD diagnostic and severity. 2) Immunohistochemical analyses of blood samples to quantify inflammatory biomarkers. 3) The modified Oxford technique for arterial baroreflex sensitivity and microneurography to measure muscle sympathetic nerve activity. Briefly, the modified Oxford technique is the gold-standard method for evaluation of arterial baroreflex sensitivity and is done by pharmacologically modifying blood pressure to force the activation of the baroreceptors. Microneurography is the most direct method to record multiunit postganglionic sympathetic nerve activity directed to muscle in humans. These techniques are described in details in the manuscript.
4) What did you learn from this paper, what was your take-home message?
A growing number of studies in recent years have highlighted the role of inflammation as an early mechanism contributing to the development of cardiovascular diseases. An important take-home message from our study is that higher severity of PTSD symptoms not only contributes to increased psychological distress, but is also associated with higher risk of hypertension and cardiovascular disease that may be mediated by greater inflammation and autonomic dysfunction. Moreover,these results might have treatment implications. Early pharmacologic and nonpharmacologic interventions aimed at reducing inflammation and sympathetic activity, as well as the treatment of PTSD symptoms themselves, particularly in severe PTSD, may have long-term beneficial effects on cardiovascular disease risk and should be investigated in future studies.