Thomas Metayer1,2, Cyrille Orset3, Carine Ali3, Jonathane Furon3, Nicolas Szabla3, Evelyne Emery4,3,5, Denis Vivien3,5,6, Thomas Gaberel4,3,5. 1. Department of Neurosurgery, University Hospital of Caen, 14000, Caen, France. thomas.metayer@neurochirurgie.fr. 2. Normandie Univ, UNICAEN, INSERM, U1237, PhIND "Physiopathology and Imaging of Neurological Disorders," Institut Blood and Brain at Caen-Normandie, Cyceron, 14000, Caen, France. thomas.metayer@neurochirurgie.fr. 3. Normandie Univ, UNICAEN, INSERM, U1237, PhIND "Physiopathology and Imaging of Neurological Disorders," Institut Blood and Brain at Caen-Normandie, Cyceron, 14000, Caen, France. 4. Department of Neurosurgery, University Hospital of Caen, 14000, Caen, France. 5. Medical School, University of Caen Normandy, 14000, Caen, France. 6. Department of Clinical Research, Caen-Normandie University Hospital, CHU, 14000, Caen, France.
Abstract
BACKGROUND: Subarachnoid hemorrhage (SAH) can lead to acute hydrocephalus (AH). AH pathophysiology is classically attributed to an obstruction of the arachnoid granulations by blood. Recent findings in rodents suggest that after intraventricular hemorrhage, AH is related to cerebrospinal fluid (CSF) hypersecretion by the choroid plexus (CP), as it can be reduced by intracerebroventricular (ICV) injection of bumetanide. OBJECTIVE: Here, we investigated if and how CSF hypersecretion and/or CSF outflow disorders contribute to post-SAH hydrocephalus. METHODS: Ninety-four Wistar rats were used. SAH was induced by the endovascular perforation technique. The presence of AH was confirmed by magnetic resonance imaging (MRI), and rats with AH were randomly assigned to 4 groups: control group, superior sagittal sinus (SSS) thrombosis to block CSF reabsorption, ICV injection of saline, and ICV injection of bumetanide to decrease CSF secretion. Clinical outcome was evaluated with a neuroscore. A second MRI was performed 24 h later to evaluate the ventricular volume. RESULTS: Fifty percent of rats that survived SAH induction had AH. Their ventricular volume correlated well to the functional outcome after 24 h (r = 0.803). In rats with AH, 24 h later, ventricular volume remained equally increased in the absence of any further procedure. Similarly, ICV injection of saline or SSS thrombosis had no impact on the ventricular volume. However, ICV injection of bumetanide reduced AH by 35.9% (p = 0.002). CONCLUSION: In rodents, post-SAH hydrocephalus is may be due to hypersecretion of CSF by the CP, as it is limited by ICV injection of bumetanide. However, we cannot exclude other mechanisms involved in post-SAH acute hydrocephalus.
BACKGROUND: Subarachnoid hemorrhage (SAH) can lead to acute hydrocephalus (AH). AH pathophysiology is classically attributed to an obstruction of the arachnoid granulations by blood. Recent findings in rodents suggest that after intraventricular hemorrhage, AH is related to cerebrospinal fluid (CSF) hypersecretion by the choroid plexus (CP), as it can be reduced by intracerebroventricular (ICV) injection of bumetanide. OBJECTIVE: Here, we investigated if and how CSF hypersecretion and/or CSF outflow disorders contribute to post-SAH hydrocephalus. METHODS: Ninety-four Wistar rats were used. SAH was induced by the endovascular perforation technique. The presence of AH was confirmed by magnetic resonance imaging (MRI), and rats with AH were randomly assigned to 4 groups: control group, superior sagittal sinus (SSS) thrombosis to block CSF reabsorption, ICV injection of saline, and ICV injection of bumetanide to decrease CSF secretion. Clinical outcome was evaluated with a neuroscore. A second MRI was performed 24 h later to evaluate the ventricular volume. RESULTS: Fifty percent of rats that survived SAH induction had AH. Their ventricular volume correlated well to the functional outcome after 24 h (r = 0.803). In rats with AH, 24 h later, ventricular volume remained equally increased in the absence of any further procedure. Similarly, ICV injection of saline or SSS thrombosis had no impact on the ventricular volume. However, ICV injection of bumetanide reduced AH by 35.9% (p = 0.002). CONCLUSION: In rodents, post-SAH hydrocephalus is may be due to hypersecretion of CSF by the CP, as it is limited by ICV injection of bumetanide. However, we cannot exclude other mechanisms involved in post-SAH acute hydrocephalus.
Authors: Sara Diana Lolansen; Nina Rostgaard; Dagne Barbuskaite; Tenna Capion; Markus Harboe Olsen; Nicolas H Norager; Frederik Vilhardt; Søren Norge Andreassen; Trine L Toft-Bertelsen; Fenghui Ye; Marianne Juhler; Richard F Keep; Nanna MacAulay Journal: Fluids Barriers CNS Date: 2022-08-10