Elevated blood pressure variability (BPV) in the days after acute stroke onset is associated with worse clinical outcomes. However, the mechanism of increased BPV remains unknown. We hypothesize that sympathetic nervous system dysfunction causes increased BPV after stroke.

Pupillary light reflexes (PLR), measured with a bedside pupillometer, are mediated by parasympathetic and sympathetic components. We propose that biomarkers of sympathetic dysfunction, including baseline pupil diameter (bPD), pupil diameter after light stimulus (sPD), and  dilation velocity (DV), will correlate with increased BPV.

This is a retrospective analysis of acute stroke patients admitted to the Neurocritical Care Unit who had concurrently collected blood pressure and pupillometry readings during the first 24 hours of their admission. The PLRs were averaged for the 24-hour period and to represent BPV we calculated standard deviation (SD) and coefficient of variation (CV) of systolic blood pressure. We correlated PLRs and BPV using linear regression. 

We included 14 patients: 7 with ischemic and 7 with hemorrhagic stroke. The mean number of blood pressure and PLR readings per patient was 31 and 7. We found that both increased SD and CV correlated with smaller bPD and sPD, while there was a trend for a correlation with decreased DV. The beta coefficient for SD and bPD was -5.22 (95% CI -10.1, -0.3, p=0.039), for SD and sPD was -8.13 (95% CI -15.0, -1.2, p=0.025), and for SD and DV was -6.48 (95% CI -14.9, 2.0, p=0.121). There was no correlation between PLR biomarkers of parasympathetic function and BPV, including maximum constriction velocity (p=0.417), mean constriction velocity (p=0.338), and latency to constriction (p=0.901).

Our data provides preliminary support for the hypothesis that sympathetic nervous system dysfunction correlates with increased BPV after stroke and may represent both a mechanism and therapeutic target for BPV reduction.