I was intrigued by this article, because it shows what I suppose must be going on in my brain as I notice my blood pressure increasing when my stress system ramps up. (Being an introspective retired professor with sufficient time, I am increasingly noticing small changes in my breathing, heart rate, blood pressure, and relative sympathetic versus parasympathetic activation that accompany changes in context.)
In the article Gianaros et al. use the well-know Stroop color-word interference task to generate stress responses in a group of defined college students. They connect stressor processing with the brainstem cardiovascular control mechanisms regulating blood pressure. People with higher stressor-evoked blood pressure reactivity displayed more activation of the amygdala, especially in the dorsal part that contains the central nucleus. Individuals showing greater blood pressure reactivity also had a lower amygdala gray matter volume, which itself predicted greater amygdala activation. In addition, greater stressor- evoked blood pressure reactivity was correlated with stronger functional connectivity between the amygdala and the pons areas in the brainstem, which is critical for blood pressure control, as well the perigenual anterior cingulate cortex.
The data suggest that the amygdala and some of its projection areas play a role in mediating individual differences in autonomic stress responses and hence vulnerability to psychological stressors.
Figure - A. Greater mean arterial blood pressure (MAP) reactivity varied with greater amygdala activation to the incongruent condition. A, Clusters of the left and right amygdala where MAP reactivity varied with activation after covariate control for sex. Parametric maps are projected onto coronal (top) and axial (bottom) sections of a template derived from study participants. B, MAP reactivity (change from a resting baseline) is shown as a function of mean-centered and standardized amygdala BOLD activation values extracted from the peak voxels of the left (L; open circles, dashed line) and right (R; closed circles, solid line) amygdala clusters profiled in A.
Figure - Greater MAP reactivity varied with stronger positive amygdala-pons functional connectivity. A, Statistical parametric maps derived from an ROI regression analysis identifying pons areas where MAP reactivity varied as a function of connectivity with left (top) and right (bottom) amygdala seed regions. B, MAP reactivity is plotted as a function of amygdala-pons connectivity coefficients for the left (L; open circles, dashed line) and right (R; closed circles, solid line) amygdala.
Standard acquisitions at 3T with gradient echo EPI do not see the amygdala. We have the same scanner, and with 3mm thick axial or axial-oblique slices, the amygdala is _invisible_ due to signal loss from through-slice dephasing. What they could have observed is some kind of cardiac-related artifact that correlates with the blood pressure. But they definitely are not seeing enough amygdala signal (we see around 5% of the signal you get in typical cortex, which is why you have better luck seeing amygdala with a 1.5T scanner).ReplyDelete