Abstract WP283: Distinct Inflammatory Profiles in Angiography-Negative Subarachnoid Hemorrhage: A Focused Case Series

Introduction: The role of inflammation in predicting the subtype of hemorrhagic stroke has yet to be explored. While subarachnoid hemorrhage (SAH) is often linked to vascular malformations such as aneurysms, some patients have negative vascular imaging (angiography-negative SAH or anSAH). These patients are often managed like those with aneurysmal SAH (aSAH), but it remains unknown whether their inflammatory profiles differ. This focused case series examines the anSAH population to better understand its early inflammatory signature. Methods: Cytometric bead array was used to measure a panel of cytokines (interleukin-8 [IL-8], vascular endothelial growth factor [VEGF], C-C motif chemokine ligand 2 [CCL2], interleukin-6 [IL-6], and granulocyte-colony stimulating factor [G-CSF]) in cerebrospinal fluid (CSF) samples collected from hemorrhagic stroke patients between day 0 and 3 after symptom onset. Cytokine concentrations were log-transformed due to non-normal distribution. Logistic regression was used to assess the relationships between cytokine levels and (1) hemorrhage location (intracerebral hemorrhage [ICH] vs SAH) and (2) presence or absence of vascular malformation. Chi-squared tests were used to compare discharge Modified Rankin Score (mRS) dichotomized into (mRS≤4) and (mRS>4) between various hemorrhage subtypes. Results: CSF samples were collected from 36 ICH (n=29 primary ICH, n=7 arteriovenous malformation [AVM]) and 72 SAH patients (n=67 aSAH, n=5 anSAH). Compared to SAH, ICH CSF had significantly higher levels of IL-8 (p=0.004) and VEGF (p<0.001) and worse discharge functional status (p<0.001). Among SAH patients, anSAH CSF had higher levels of IL-8 (p=0.030) and VEGF (p=0.003) than aSAH, with no significant difference in discharge functional status. In patients without vascular malformations, anSAH had better discharge functional status than primary ICH (p=0.048), while cytokine levels did not differ significantly between the two groups. Within ICH, cytokine levels did not differ by vascular malformation status. Conclusion: The inflammatory profile of anSAH more closely resembles that of ICH than aSAH. While ICH patients had worse outcomes at discharge, anSAH resembled ICH in cytokine expression but fell between aSAH and ICH in clinical trajectory. Given the small sample size, these results should be interpreted as exploratory and hypothesis-generating but suggest that anSAH represents a unique clinical entity with a distinct inflammatory profile.