Abstract Details

Title Impaired Cerebral Autoregulation Related Blood Pressure Reductions After Nimodipine Are Associated with Ischemic Changes on EEG After Subarachnoid Hemorrhage

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P13 - Poster Session 13 (8:00 AM-9:00 AM)

Poster/Presentation
Number 13-002

Background

aSAH is a severe, life-threatening hemorrhage that can result in impaired cerebral autoregulation. When BP falls outside the lower limits of autoregulation (LLA), patients are at higher risk for developing delayed cerebral ischemia and poor outcomes. We hypothesize that EEG can characterize the neuronal deterioration that occurs when patients fall outside their personalized LLA.

Objective

To determine if changes in systemic blood pressure (BP) upon nimodipine administration and the subsequent deviation from limits of autoregulation are associated with any electroencephalography (EEG) changes after aneurysmal subarachnoid hemorrhage (aSAH).

Design/Methods We assessed 8 patients with moderate-to-severe SAH (Hunt-Hess score 3-5 or modified Fisher score 3-4) and analyzed a total of 44 events with drops in BP below LLA after nimodipine administration. For each event, continuous EEG recorded between one hour before and after nimodipine were extracted and spectral features (FFT spectrogram and suppression ratio) were computed using Persyst 14. We performed event-based normalization for EEG features by subtracting the corresponding median value before nimodipine administration and computed summary statistics (mean, 95% confidence interval).

Results By manually reviewing EEG changes after nimodipine intervention, we identified 33 (75%) events with observable changes following 3 different patterns: 1) delta slowing measured by an increase in delta power [n=17, 0.74±0.39] and an associated decrease in suppression ratio [-0.85±1.04], 2) a decrease in alpha power [n=3, -0.44±0.41], and 3) a decrease in total power [n=13, -1.38±0.77] and associated increase in suppression ratio [1.14±1.38], resulting in a flatter EEG. 12 events had no change in EEG with BP reduction, suggesting other compensatory mechanisms maintain neurophysiologic function.

Conclusions

In this study, we provide evidence that EEG is a sensitive tool in capturing the neurologic consequences of BP reductions below the personalized LLA in patients with SAH. These events have potential to increase secondary brain injury after SAH.

Authors/Disclosures
Ilayda Top (Yale University) PRESENTER	Ms. Top has nothing to disclose.
Yilun Chen (Yale University)	Ms. Chen has nothing to disclose.
David Bartolome (Yale University School of Medicine)	Mr. Bartolome has nothing to disclose.
Amedeo Rapuano (Yale New Haven Hospital)	No disclosure on file
Emily J. Gilmore, MD (Yale University School of Medicine)	Dr. Gilmore has received personal compensation in the range of $5,000-$9,999 for serving as a Consultant for carpl.ai. Dr. Gilmore has received personal compensation in the range of $0-$499 for serving as a Consultant for AAN. Dr. Gilmore has received research support from NIH.
Kevin N. Sheth, MD, FAAN (Yale UniversityDivision of Neuro and Critical Care)	Dr. Sheth has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Ceribell. Dr. Sheth has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Zoll. Dr. Sheth has received personal compensation in the range of $10,000-$49,999 for serving on a Scientific Advisory or Data Safety Monitoring board for NControl. Dr. Sheth has received stock or an ownership interest from Astrocyte. Dr. Sheth has received stock or an ownership interest from Alva. The institution of Dr. Sheth has received research support from Biogen. The institution of Dr. Sheth has received research support from Novartis. The institution of Dr. Sheth has received research support from Bard. The institution of Dr. Sheth has received research support from Hyperfine. Dr. Sheth has received intellectual property interests from a discovery or technology relating to health care.
Charles Matouk	No disclosure on file
Nils Petersen, MD (Yale University)	Dr. Petersen has received research support from NIH.
Jennifer A. Kim, MD (Yale University School of Medicine)	Dr. Kim has nothing to disclose.