Katharina Sophie Seyfried

Ms. Katharina Sophie Seyfried


Research Focus & Metrics

Academic Career Length

2Years (2025-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Journal Article
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KSKatharina Sophie Seyfried
Katharina Sophie Seyfried
BKBenedikt Kremer
Benedikt Kremer
CCCatharina Conzen
Catharina Conzen
MVmännlich Veldeman
männlich Veldeman
UBUlf Bertram
Ulf Bertram
AHAnke Höllig
Anke Höllig
Despite extensive research on aneurysm treatment and neurocritical care, aneurysmal subarachnoid hemorrhage (SAH) is still a life-threatening disease, often leaving survivors with lasting neurological and cognitive impairments. Early brain injury (EBI) and delayed cerebral ischemia (DCI) are the main contributors to brain damage, with neuroinflammation being a critical shared pathophysiological process. While numerous inflammatory markers and their temporal profiles in cerebrospinal fluid (CSF) have already been identified, comparisons with age- and sex-matched controls are limited. This study analyzed CSF from 17 SAH patients requiring an external ventricular drain (EVD) due to symptomatic hydrocephalus, sampled on days 4 and 10 post-ictus. An age- and sex-matched control group included 17 cerebrovascularly healthy patients requiring lumbar drains during aortic surgery. Chemokines and cytokines were quantified using immunoassays. Significantly elevated markers in SAH patients across both time points included MCP-1, CXCL-13, Eotaxin-1, CXCL-10, IL-8, and MIF. MIP-1α and MIP-1β showed significant differences at particular time points, indicating a distinct temporal profile for each parameter. These findings highlight neuroinflammation’s key role in intracranial and systemic pathophysiology following SAH, emphasizing its complexity and individual variability. Knowing demographic factors impact the specific manifestations of pathophysiological processes, the comparison with an age- and sex-matched control group is meaningful.

27 September 2025 in Journal of Clinical Medicine
Verified
Journal Article
Open access
PDF file
MVmännlich Veldeman
männlich Veldeman
TSTobias Philip Schmidt
Tobias Philip Schmidt
KSKatharina Sophie Seyfried
Katharina Sophie Seyfried
CWCharlotte Sabine Weyland
Charlotte Sabine Weyland
KHKarlijn Hakvoort
Karlijn Hakvoort
CCCatharina Conzen
Catharina Conzen
Background: Aneurysmal subarachnoid hemorrhage (SAH) is over twice as common in females compared to males, who may also experience more severe hemorrhages and worse outcomes. Differences in SAH severity, susceptibility to delayed cerebral ischemia (DCI), and treatment responsiveness may underlie this disparity. This study evaluated sex-based differences in DCI timing, severity, treatment responsiveness, and outcomes after SAH. Methods: We analyzed 650 consecutive SAH patients admitted to RWTH Aachen University Hospital (2006–2021). SAH severity was assessed via the (World Federation of Neurological Surgeons) WFNS and modified Fisher scales. DCI-related infarction was defined as new infarcts on CT not present initially or within 48 h post-aneurysm occlusion. Endovascular rescue therapy (ERT) was used for treatment-resistant DCI. Outcomes were assessed at discharge and 12 months using the modified Rankin Scale (mRS). Generalized linear mixed-effects models adjusted for confounders. Results: Of 650 patients, 455 (70%) were female. DCI rates did not differ significantly between sexes (41.5% female vs. 36.4% male; p = 0.361). DCI-related infarction occurred in 19.4% of patients, with no sex-based differences in infarct volume (median 115 mL; p = 0.670) or location. ERT use was similar in females (22.4%) and males (23.9%; p = 0.825). Lower age, poor-grade SAH, and higher mFisher scores were associated with DCI and poor outcomes, but sex was not an independent predictor. Conclusions: Female sex was not associated with more severe SAH, a higher incidence of DCI, or more severe DCI manifestations. Although small effect sizes may become statistically significant in larger cohorts, our findings indicate that such effects are unlikely to be driven by differences in DCI timing, infarct size, or treatment responsiveness.