Titre :

Experimental Models of Posterior Reversible Encephalopathy Syndrome: A Review From Pathophysiology to Therapeutic Targets.

Auteur(s) :

Largeau, Bérenger [Auteur]
CHU Trousseau [Tours]
Bergeron, Sandrine [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Auger, Florent [Auteur]
Plateformes Lilloises en Biologie et Santé - UAR 2014 - US 41 [PLBS]
Salmon Gandonnière, Charlotte [Auteur]
Centre Hospitalier Régional Universitaire de Tours [CHRU Tours]
Jonville-Béra, Annie-Pierre [Auteur]
MethodS in Patients-centered outcomes and HEalth ResEarch [SPHERE]
Ehrmann, Stephan [Auteur]
Centre d’Investigation Clinique [Tours] CIC 1415 [CIC ]
Gautier, Sophie [Auteur]
Lille Neurosciences & Cognition - U 1172 [LilNCog]
Bordet, Regis [Auteur]
Lille Neurosciences & Cognition (LilNCog) - U 1172

Titre de la revue :

Stroke

Nom court de la revue :

Stroke

Numéro :

55

Date de publication :

2023-12-22

ISSN :

1524-4628

Mot(s)-clé(s) en anglais :

animal
blood-brain barrier
brain edema
hypertension
posterior leukoencephalopathy syndrome

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological entity characterized by nonspecific symptomatology (eg, headache, visual disturbances, encephalopathy, and seizures) and classically cortical ...
Lire la suite >Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological entity characterized by nonspecific symptomatology (eg, headache, visual disturbances, encephalopathy, and seizures) and classically cortical and subcortical vasogenic edema predominantly affecting the parietooccipital region. PRES etiologies are usually dichotomized into toxic PRES (eg, antineoplastic drugs, illicit drugs) and clinical condition-associated PRES (eg, acute hypertension, dysimmune disorders). Although the pathophysiology of PRES remains elusive, 2 main pathogenic hypotheses have been suggested: cerebral hyperperfusion due to acute hypertension and cerebral hypoperfusion related to endothelial dysfunction. Research into the pathogenesis of PRES has emerged through the development of animal models in the last decade. The motivation for developing a suitable PRES model is 2-fold: to fill in knowledge gaps of the pathophysiological mechanisms involved, and to open new perspectives for clinical assessment of pharmacological targets to improve therapeutic management of PRES. All current models of PRES have a hypertensive background, on which other triggers (acute hypertension, inflammatory, drug toxicity) have been added to address specific facets of PRES (eg, seizures). The initial model consisted in inducing a reduced uterine perfusion pressure that mimics preeclampsia, a leading cause of PRES. More recently, a model of stroke-prone spontaneously hypertensive rats on high-salt diet, originally developed for hypertensive small vessel disease and vascular cognitive impairment, has been studied in PRES. This review aims to discuss, depending on the research objective, the benefits and limitations of current experimental approaches and thus to define the desirable characteristics for studying the pathophysiology of PRES and developing new therapies.Lire moins >

Langue :

Anglais

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

Université de Lille
Inserm
CHU Lille

Collections :

• Lille Neurosciences & Cognition (LilNCog) - U 1172

Date de dépôt :

2024-05-06T22:48:08Z
2024-05-27T12:23:31Z