Axel Masson1, Grégoire Boulouis2, Kevin Janot2, Denis Herbreteau2, Jean-Phlippe Cottier2, Richard Bibi2, Clara Cohen3, Sandra Obry2, Stéphane Velut4, Aymeric Amelot4, Héloïse Ifergan5. 1. Department of Diagnostic and Interventional Neuroradiology, Bretonneau Hospital, University of Tours, Tours, France. axel.masson92@sfr.fr. 2. Department of Diagnostic and Interventional Neuroradiology, Bretonneau Hospital, University of Tours, Tours, France. 3. Department of Diagnostic Neuroradiology, Orleans Hospital Center, Orleans, France. 4. Department of Neurosurgery, Bretonneau Hospital, University of Tours, Tours, France. 5. Department of Diagnostic and Interventional Neuroradiology, Bretonneau Hospital, University of Tours, Tours, France. ifergan.heloise@hotmail.fr.
Abstract
BACKGROUND: Delayed cerebral infarction (DCIn) following aneurysmal subarachnoid hemorrhage (aSAH) is a major cause of morbi-mortality; yet, the causes for DCIn remain incompletely understood. OBJECTIVE: We tested the hypothesis that acute hydrocephalus could be related to the occurrence of DCIn, independently of the occurrence and severity of vasospasm. METHODS: Radiological and clinical data of patients treated at a single large volume academic center for aSAH between 2017 and 2019 were retrospectively analyzed. DCIn was defined as imaging stigma of cerebral infarction visible on 6-week imaging follow-up after aSAH. Hydrocephalus was defined on baseline imaging as a relative bicaudate index above 1. Cerebral vasospasm was defined by reduction of artery diameter in comparison with initial diameter. We used uni- and multivariable models to test the associations between these variables, hydrocephalus and DCIn. RESULTS: Of 164 included patients, vasospasm occurred in 58 patients (35.4%), and DCIn in 47 (28.7%). Acute hydrocephalus was present in 85 patients (51.8%) on baseline CT. No relation was found between acute hydrocephalus and delayed cerebral infarction in our multivariate analysis (adjusted OR: 1.20 95% CI [0.43-3.37]; p = 0.732). Only vasospasm occurrence was independently associated with DCIn (adjusted OR: 10.97 95% CI [4.60-26.01]). CONCLUSION: Our study did not show an association between acute hydrocephalus and DCIn after aSAH, after adjustment for the presence and severity of cerebral vasospasm.
BACKGROUND: Delayed cerebral infarction (DCIn) following aneurysmal subarachnoid hemorrhage (aSAH) is a major cause of morbi-mortality; yet, the causes for DCIn remain incompletely understood. OBJECTIVE: We tested the hypothesis that acute hydrocephalus could be related to the occurrence of DCIn, independently of the occurrence and severity of vasospasm. METHODS: Radiological and clinical data of patients treated at a single large volume academic center for aSAH between 2017 and 2019 were retrospectively analyzed. DCIn was defined as imaging stigma of cerebral infarction visible on 6-week imaging follow-up after aSAH. Hydrocephalus was defined on baseline imaging as a relative bicaudate index above 1. Cerebral vasospasm was defined by reduction of artery diameter in comparison with initial diameter. We used uni- and multivariable models to test the associations between these variables, hydrocephalus and DCIn. RESULTS: Of 164 included patients, vasospasm occurred in 58 patients (35.4%), and DCIn in 47 (28.7%). Acute hydrocephalus was present in 85 patients (51.8%) on baseline CT. No relation was found between acute hydrocephalus and delayed cerebral infarction in our multivariate analysis (adjusted OR: 1.20 95% CI [0.43-3.37]; p = 0.732). Only vasospasm occurrence was independently associated with DCIn (adjusted OR: 10.97 95% CI [4.60-26.01]). CONCLUSION: Our study did not show an association between acute hydrocephalus and DCIn after aSAH, after adjustment for the presence and severity of cerebral vasospasm.
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