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Updated: Mar 23, 2026
Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging MRI
Published on: December 16, 2021
Evaluation of a filament perforation model for mouse subarachnoid hemorrhage using 7.0 Tesla MRI
Carl Muroi1, Yuto Kashiwagi2, Takemi Rokugawa2
1Institute of Aging and Brain Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka, Japan; Department of Neurosurgery, Kantonsspital Aarau, Aarau, Switzerland.
Abstract:
The filament perforation model (FPM) in mice is becoming increasingly popular to elucidate the molecular pathogenesis of neuronal injury after subarachnoid hemorrhage (SAH). We evaluated brain MRI in a mouse FPM. A total of 28 male C57Bl/6J mice were used. Seventeen animals underwent SAH induction by FPM. In two animals, transient middle cerebral artery occlusion (MCAo) was induced. Nine mice served as controls. T1-weighted images (T1WI), T2-weighted images (T2WI), T2(∗)-weighted images (T2*WI) and apparent diffusion coefficient maps were acquired at day 0 and at various time points following SAH (range: day 1-6 after SAH). Cerebral blood flow (CBF) analysis by (14)C-iodoamphetamine ((14)C-IMP) autoradiography was conducted in nine animals. Hemorrhage could be best confirmed using T2*WI. The degree of hemorrhage varied. All animals evaluated for ⩾2days were hydrocephalic, which was best seen on T2WI. T2-hyperintensity of the corpus callosum and external capsule, indicating white matter (WM) injury, was present after SAH. Ventricle and WM injury volumes were statistically significantly higher at day 3 compared to day 0. Territorial ischemia was detectable in MCAo but not in SAH. Markedly hypointense cortical veins were visible in the hyperacute and delayed phase after SAH on T2*WI. The (14)C-IMP analysis indicated decreased CBF after SAH. MRI is feasible and useful in evaluating pathophysiological changes over time. T2*WI seems best for SAH detection and grading. The chronological change of hydrocephalus and WM injury could be analyzed. T2*WI illustrated specific signal changes of cortical veins, possibly caused by increased oxygen extraction fraction due to decreased CBF.
Insights
Brain MRI effectively tracks neuronal injury after subarachnoid hemorrhage (SAH) in mice. T2-weighted imaging best detects hydrocephalus and white matter injury, while T2*-weighted imaging excels at identifying hemorrhage and cortical vein changes.
Area of Science:
- Neuroscience
- Radiology
- Pathophysiology
Background:
- Subarachnoid hemorrhage (SAH) poses significant neurological risks.
- The filament perforation model (FPM) is a key tool for studying SAH pathogenesis.
- Understanding SAH-induced brain injury requires advanced imaging techniques.
Purpose of the Study:
- To evaluate the utility of brain magnetic resonance imaging (MRI) in a mouse filament perforation model (FPM) of subarachnoid hemorrhage (SAH).
- To assess the chronological changes in hydrocephalus and white matter (WM) injury post-SAH.
- To correlate MRI findings with cerebral blood flow (CBF) alterations.
Main Methods:
- Filament perforation model (FPM) induced SAH in 17 mice; 2 underwent middle cerebral artery occlusion (MCAo); 9 served as controls.
- Brain MRI, including T1WI, T2WI, T2*WI, and ADC maps, was performed at baseline and up to 6 days post-SAH.
- Cerebral blood flow (CBF) was assessed using (14)C-iodoamphetamine autoradiography.
Main Results:
- T2*-weighted imaging (T2*WI) was optimal for hemorrhage detection; T2-weighted imaging (T2WI) best visualized hydrocephalus.
- Significant increases in ventricle and white matter (WM) injury volumes were observed by day 3 post-SAH.
- T2*WI revealed hypointense cortical veins in SAH, suggesting altered CBF, which was confirmed by (14)C-IMP analysis showing decreased CBF.
Conclusions:
- Brain MRI is a feasible and valuable tool for monitoring SAH-induced pathophysiological changes over time.
- T2*WI is highly effective for SAH detection and grading, while T2WI aids in assessing hydrocephalus and WM injury.
- MRI can reveal specific vascular changes related to reduced CBF in SAH, offering insights into disease mechanisms.
