Abstract Body: Introduction: Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition after which patients are at risk for vasospasm and delayed cerebral ischemia (DCI). Nimodipine, a calcium channel blocker, is used to reduce the risk of DCI. Despite its widespread application, the specific effects on cerebral hemodynamics and cortical activity are poorly characterized. It remains unknown whether this potent therapy may have unintended harmful consequences in some patients, which could potentially be mitigated or avoided. This study aims to characterize the effects of nimodipine on cerebral autoregulation, brain blood flow, and quantitative electroencephalography (qEEG).

Methods: Nimodipine-associated blood pressure (BP) reductions were quantified as percent change between median BP in the hour before nimodipine administration and the minimum BP in the hour following nimodipine. Autoregulatory function was measured by analyzing changes in near-infrared spectroscopy-derived tissue oxygenation (a surrogate for cerebral blood flow) in response to changes in mean arterial pressure (MAP). The resulting autoregulatory index was utilized to determine the limits of autoregulation in each patient. Cortical EEG activity was measured by computing percent changes in each qEEG frequency band in the anterior and middle cerebral vascular regions after artifact reduction and feature extraction.

Results: We identified 124 occurrences of nimodipine administration with simultaneous recording of continuous EEG and physiologic data among 13 aSAH patients (median age 59 ± 11 years, Hunt Hess 3.0 ± 1.0, modified Fisher 4.0 ± 0.6). Of these, 89 episodes (71.7%) showed a BP drop of 10% or greater, with a median MAP reduction of 25.6 mmHg. Blood pressure reductions were correlated with an increased time below the lower limit of autoregulation (p < 0.001). Nimodipine-associated BP reductions led to an average increase in time below the lower limit of autoregulation of 19.5 ± 24.1% (p < 0.001); a >5% increase was seen in 58.9% (56/89) of episodes. However, only 28 out of 89 episodes (31%) showed a >5% change in alpha-delta ratio.

Conclusions: Nimodipine-associated BP reductions are common and frequently lead to cerebral hypoperfusion with BP reduction below the lower limit of autoregulation. These episodes did not exhibit a consistent qEEG signature, suggesting that other factors may interact with or compensate for the decline in BP. Further exploratory analyses are on-going.