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Following aneurysmatic subarachnoid haemorrhage (SAH), complex pathophysiological processes take place which result in ischaemia, dysfunction of the blood-brain barrier and the clinical development of vasospasms and delayed cerebral ischaemia (DCI). The aim of this study was to present a biomarker panel that can be used for temporal assignment in the pathophysiological process after haemorrhage, a prediction of vasospasm, DCI or outcome. In a prospective multicentre approach, complex laboratory chemistry tests were used to determine the value of the biomarkers S100B, Claudin-5, Interleukin (IL) -10, Triggering receptor expresses on myeloid cells (TREM)-1 and TREM-2, and neurofilament light chain (NfL) as well as IgG and IgM in plasma and Cerebro-spinal-fluid (CSF) in SAH patients. The predictive power of mentioned biomarkers with regard to the occurrence of vasospasms, DCI and the outcome (Glasgow Outcome Scale) were defined by using sophisticated statistical methods with the level of significance at p ≤ 0.05. Mean age of the 12 patients included was 56 (SD:14) years with 67% female patients and that of the 11 control subjects was 74 (SD:3) years with 55% female subjects. S100B showed higher concentrations compared to the control patients on the first four days (p ≤ 0.0141). For IL-10, the CSF concentrations showed a continuous increase: day 2 (p = 0.0074), day 4 (p = 0.0012), and day 5 (p < 0.0001). Regarding the TREM1 and TREM2 balance, CSF concentrations of TREM1 increased until day eight (p ≤ 0.0055). TREM-2 plasma concentrations decreased below the levels of control patients and appeared unchanged for the further course. The greatest difference in the CSF concentration of NfL between the patients and the control group was seen on day 8 (p = 0.0104). The differentiation between patients with and without DCI showed different concentration curves of the TREM1 CSF-plasma index with increasing concentrations for patients with DCI. The TREM 2 CSF-plasma index showed higher concentrations for patients with DCI. Patients without DCI showed a decreasing concentration of the NfL CSF-plasma index compared to an increase when vasospasm was detected. NfL, TREM-1 and TREM-2 have the potential to be relevant biomarkers for SAH in the intermediate and delayed injury phase.
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http://dx.doi.org/10.1007/s12035-025-04889-3 | DOI Listing |
Pharm Dev Technol
September 2025
School of Pharmaceutical Engineering, Shenyang Pharmaceutical University, wenhua Road 103, Shenyang 110016, PR China.
Nimodipine (NMP), a poorly water-soluble small-molecule agent, demonstrates notable therapeutic limitations in addressing cerebral vasospasm secondary to subarachnoid hemorrhage (SAH). Owing to its inherent physicochemical properties characterized by low oral bioavailability, rapid elimination half-life, and extensive first-pass metabolism, conventional formulations necessitate frequent dosing regimens to sustain therapeutic plasma concentrations. These pharmacological challenges collectively result in suboptimal patient adherence, marked plasma concentration fluctuations, and recurrent vascular irritation.
View Article and Find Full Text PDFNeurocrit Care
September 2025
Department of Neurology and Neurosurgery, Division of Neurocritical Care, Emory University School of Medicine, Atlanta, GA, USA.
Acta Neurochir (Wien)
September 2025
Department of Neurosurgery, Kurume University School of Medicine 67, Asahimachi Kurume City, Fukuoka, 830-0011, Japan.
We report a 64-year-old woman who developed symptomatic vasospasm on postoperative day 7 after clipping of an unruptured right middle cerebral artery (MCA) aneurysm. Imaging revealed right MCA vasospasm, which resolved with oral antiplatelets and intravenous vasodilators. She was discharged without neurological deficits.
View Article and Find Full Text PDFNeurocrit Care
September 2025
Minnetronix Medical Inc., Saint Paul, MN, USA.
Brain Behav Immun
October 2025
Department of Physiology and Pharmacology, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA; Department of Anesthesiology, School of Medicine, Loma Linda University, Loma Linda, CA 92354, USA; Department of Neurosurgery, School of Medicine, Loma Linda University, Loma Linda, CA 9