Wednesday, December 5, 2018

The brain’s hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers

My reading of this is that stress negatively affects blood flow, obviously with no medical knowledge on my own.  So with the massive amount of stress your doctor is causing you by not giving you any clear way to get 100% recovered you are in more danger  because lower blood flow negatively impacts your recovery.  Your doctor is worsening your recovery.

The brain’s hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers

Immanuel G. Elbau, Benedikt Brücklmeier, Manfred Uhr, Janine Arloth, Darina Czamara, Victor I. Spoormaker, Michael Czisch, Klaas Enno Stephan, Elisabeth B. Binder, and Philipp G. Sämann
  1. Edited by Bruce McEwen, The Rockefeller University, New York, NY, and approved August 14, 2018 (received for review April 6, 2018)
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Significance

Understanding how stress predisposes for psychopathology requires the identification of physiological stress-regulatory mechanisms with pathogenic potential. Here, we applied fMRI to investigate the interaction between acute psychosocial stress and the brain’s hemodynamic response function (HRF). The HRF models how local neural activity elicits cerebral blood flow changes, spanning several biophysical processes including neurovascular coupling (NVC). Stress replicably shifted the HRF peak in temporal, insular, and prefrontal brain regions, moderated by functional variants of KCNJ2, a protein involved in NVC. Hippocampal HRF markers correlated with the cortisol response and genetic variants that reflect transcriptional responses to glucocorticoids and the risk for depression. We suggest that acute psychosocial stress modulates hemodynamic response properties which could lead to previously undescribed endophenotypes of stress-related disorders.

Abstract

Ample evidence links dysregulation of the stress response to the risk for psychiatric disorders. However, we lack an integrated understanding of mechanisms that are adaptive during the acute stress response but potentially pathogenic when dysregulated. One mechanistic link emerging from rodent studies is the interaction between stress effectors and neurovascular coupling, a process that adjusts cerebral blood flow according to local metabolic demands. Here, using task-related fMRI, we show that acute psychosocial stress rapidly impacts the peak latency of the hemodynamic response function (HRF-PL) in temporal, insular, and prefrontal regions in two independent cohorts of healthy humans. These latency effects occurred in the absence of amplitude effects and were moderated by regulatory genetic variants of KCNJ2, a known mediator of the effect of stress on vascular responsivity. Further, hippocampal HRF-PL correlated with both cortisol response and genetic variants that influence the transcriptional response to stress hormones and are associated with risk for major depression. We conclude that acute stress modulates hemodynamic response properties as part of the physiological stress response and suggest that HRF indices could serve as endophenotype of stress-related disorders.

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