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Updated: Jun 9, 2026

A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
Course of brain damage following malignant hypertension
Jean Sebastien Liegey1, Antoine Cremer2, Ludovic Lucas3
1Coronary and vascular diseases Department, Bordeaux university Hospital, Bordeaux, France. jean-sebastien.liegey@chu-bordeaux.fr.
Malignant hypertension crises can cause new strokes and hemorrhages, with brain MRI markers evolving over time. Follow-up imaging reveals persistent microvascular changes, impacting patient care.
Area of Science:
- Neurology
- Radiology
- Nephrology
Background:
- Malignant hypertension (MHT) crises cause significant brain microvascular damage.
- Limited data exists on the evolution of cerebral injuries after MHT management.
- Brain MRI markers are crucial for assessing acute and chronic changes.
Purpose of the Study:
- To investigate the changes in brain MRI markers following acute malignant hypertension crisis.
- To identify the incidence of new cerebrovascular events and microangiopathy post-MHT.
Main Methods:
- Retrospective analysis of brain MRI data from MHT patients (2008-2022).
- Inclusion criteria: at least one follow-up MRI.
- Analysis focused on PRES, stroke, hemorrhage, and microangiopathy markers.
Main Results:
- Follow-up MRIs in 47 patients showed new strokes (10.6%) and cerebral hemorrhages (4.3%).
- No cases of PRES were observed.
- Increased prevalence of chronic lacunar infarcts and microbleeds; stable Fazekas scores in 66%.
Conclusions:
- Malignant hypertension crises carry a risk of subsequent cerebrovascular events.
- Brain MRI markers dynamically change post-MHT, indicating ongoing microvascular impact.
- Findings support improved diagnosis, personalized treatment, and proactive care for MHT patients.
Related Concept Videos
Hypertension III: Clinical Manifestations and Diagnostic Studies
Hemorrhagic Stroke l: Introduction
Hemorrhagic Stroke ll: Pathophysiology
Increased Intracranial Pressure l: Introduction
Increased Intracranial Pressure ll: Pathophysiology
Cerebral Edema ll: Pathophysiology

