The ESAS-score: A histological severity grading system of subarachnoid hemorrhage using the modified double hemorrhage model in rats

Mielke, Dorothee; Bleuel, Kim; Stadelmann, Christine; Malinova, Vesna

doi:10.1371/journal.pone.0227349

Cited by 5 publications

(4 citation statements)

References 30 publications

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“…Previous studies were able to demonstrate that this specific model facilitates the reliable induction of severe SAH with a high incidence of vasospasm, making it specifically suitable for the evaluation of this phenomenon. 17,18,31 In the present study, we found an overall high incidence of cerebral vasospasm on day 2 (65%) as well as on day 5 (86%), which again reflects the aforementioned benefits of this experimental SAH-model. Considering vasospasm severity, expectedly, severe vasospasm was seen more often on day 5 (49%) compared to day 2 (21%).…”

Section: Cerebral Vasospasm In Experimental Sah Modelssupporting

confidence: 79%

The impact of transcranial direct current stimulation on cerebral vasospasm in a rat model of subarachnoid hemorrhage

Malinova

Bleuel

Stadelmann

et al. 2021

J Cereb Blood Flow Metab

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Transcranial direct current stimulation (tDCS) has been shown to induce changes in cortical excitability and perfusion in a rat ischemic stroke model. Since perfusion disturbances are a common phenomenon, not only in ischemic but also in hemorrhagic stroke, tDCS might have a possible beneficial effect on cerebral perfusion in hemorrhagic stroke as well. We applied tDCS in a rat model of subarachnoid hemorrhage (SAH) and evaluated its impact on vasospasm. SAH was induced using the double-hemorrhage rat model. TDCS was applied on day 3 and 4. For vasospasm assessment magnetic resonance angiography was performed on day 1, day 2 and day 5. A total of 147 rats were operated, whereat 72 rats died before day 5 and 75 rats survived the whole experiment and could be analyzed. The cathodal group consisted of 26 rats, the anodal group included 24 rats. Thirteen rats served as controls without tDCS, and twelve rats underwent a sham operation. The cathodal group revealed the lowest incidence of new vasospasm on day 5 ( p = 0.01), and the lowest mean number of vasospastic vessels per rat ( p = 0.02). TDCS influences the vasospasm incidence in an SAH-model in rats, where cathodal-tDCS was associated with a lower vasospasm incidence and severity.

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Section: Cerebral Vasospasm In Experimental Sah Modelssupporting

confidence: 79%

The impact of transcranial direct current stimulation on cerebral vasospasm in a rat model of subarachnoid hemorrhage

Malinova

Bleuel

Stadelmann

et al. 2021

J Cereb Blood Flow Metab

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“…Regarding WFNS scoring and Fisher grading, the patients were examined as a dichotomy between low-grade and high-grade SAH presentation-WFNS grades 1 to 3 are considered low grade and 4 and 5 considered high grade; Fisher grades 1 and 2 as low grade and 3 and 4 as high grade. 6,7 All patients admitted to the hospital with nontraumatic SAH were treated with calcium channel blockade in the form of nimodipine.…”

Section: Methodsmentioning

confidence: 99%

Management and Outcomes of Delayed Cerebral Ischemia Associated with Vasospasm Post Nontraumatic Subarachnoid Hemorrhage: A Retrospective Cohort Study in the National Neurosurgical Center in Ireland

Wiseman,

Power,

MacNally

et al. 2024

J Neuroanaesth Crit Care

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Background Delayed cerebral ischemia (DCI) is the leading cause of adverse outcome in patients who survive the initial phase of subarachnoid hemorrhage (SAH). While guidelines recommend induced hypertension as a first-line treatment for DCI, there is no high-level evidence confirming outcome benefit. Methods Patients admitted with nontraumatic SAH over 3 years period were identified. Demographics, clinical/radiological presentation, aneurysm repair method, and Glasgow outcome score (GOS) 3 months postdischarge were recorded. A subgroup of patients who suffered clinically significant vasospasm were identified, and their hypertensive therapy and outcomes were examined. Results A total of 532 patients were admitted with SAH; 68 developed vasospasm. The vasospasm subgroup was divided based on vasopressor treatment—norepinephrine alone (n = 27) versus norepinephrine plus vasopressin (n = 35). No correlation was found between percentage of days that mean arterial pressure (MAP) targets were met and GOS outcome. Patients treated with both agents had worse GOS outcomes at than those treated with norepinephrine alone. Conclusion In our study, 12.8% of patients SAH developed vasospasm. Twenty-seven patients were treated with norepinephrine alone and 35 were treated with norepinephrine plus vasopressin to achieve augmented MAP targets. There was no correlation between percentage of days that MAP targets were met and improved patient outcome. The 68 patients stayed a total of 783 days in ICU, with a mean length of stay of 11.5 days. Patients who required dual therapy to achieve MAP targets had significantly worse neurological outcomes.

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“…The sham group underwent identical procedures without the vascular perforation. The severity of SAH was blindly assessed at the time of sacrifice according to the previously described grading system [13]. Rats displaying SAH severity scores between 8-13 were used for further experiments [14].…”

Section: Sah Model Conducted By Means Of Endovascular Perforationmentioning

confidence: 99%

Dexras1 Induces Dysdifferentiation of Oligodendrocytes and Myelin Injury by Inhibiting the cAMP-CREB Pathway after Subarachnoid Hemorrhage

Xin

Chen

Zhang

et al. 2022

Cells

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White matter damage (WMD), one of the research hotspots of subarachnoid hemorrhage (SAH), mainly manifests itself as myelin injury and oligodendrocyte differentiation disorder after SAH, although the specific mechanism remains unclear. Dexamethasone-induced Ras-related protein 1(Dexras1) has been reported to be involved in nervous system damage in autoimmune encephalitis and multiple sclerosis. However, whether Dexras1 participates in dysdifferentiation of oligodendrocytes and myelin injury after SAH has yet to be examined, which is the reason for creating the research content of this article. Here, intracerebroventricular lentiviral administration was used to modulate Dexras1 levels in order to determine its functional influence on neurological injury after SAH. Immunofluorescence, transmission electron microscopy, and Western blotting methods, were used to investigate the effects of Dexras1 on demyelination, glial cell activation, and differentiation of oligodendrocyte progenitor cells (OPCs) after SAH. Primary rat brain neurons were treated with oxyhemoglobin to verify the association between Dexras1 and cAMP-CREB. The results showed that Dexras1 levels were significantly increased upon in vivo SAH model, accompanied by OPC differentiation disturbances and myelin injury. Dexras1 overexpression significantly worsened OPC dysdifferentiation and myelin injury after SAH. In contrast, Dexras1 knockdown ameliorated myelin injury, OPC dysdifferentiation, and glial cell activation. Further research of the underlying mechanism discovered that the cAMP-CREB pathway was inhibited after Dexras1 overexpression in the in vitro model of SAH. This study is the first to confirm that Dexras1 induced oligodendrocyte dysdifferentiation and myelin injury after SAH by inhibiting the cAMP-CREB pathway. This present research may reveal novel therapeutic targets for the amelioration of brain injury and neurological dysfunction after SAH.

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The ESAS-score: A histological severity grading system of subarachnoid hemorrhage using the modified double hemorrhage model in rats

Cited by 5 publications

References 30 publications

The impact of transcranial direct current stimulation on cerebral vasospasm in a rat model of subarachnoid hemorrhage

The impact of transcranial direct current stimulation on cerebral vasospasm in a rat model of subarachnoid hemorrhage

Management and Outcomes of Delayed Cerebral Ischemia Associated with Vasospasm Post Nontraumatic Subarachnoid Hemorrhage: A Retrospective Cohort Study in the National Neurosurgical Center in Ireland

Dexras1 Induces Dysdifferentiation of Oligodendrocytes and Myelin Injury by Inhibiting the cAMP-CREB Pathway after Subarachnoid Hemorrhage

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