OBJECTIVE: To determine acute intracranial hydrodynamic changes after subarachnoid hemorrhage (SAH) via phase-contrast MRI (PC-MRI) analysis of the CSF stroke volume in the aqueduct (SVaq) and the foramen magnum (SVfm). METHODS: A prospective PC-MRI study was performed on 34 SAH patients in the acute and late phase. Data on CSF flow and hemorrhage site were analyzed according to acute or chronic hydrocephalus (HC). RESULTS: In the acute phase, CSF analysis was performed for 31 patients, 12 of whom presented HC. All 12 had an abnormal SVaq; those with communicating HC (n = 7) had an elevated SV and those with noncommunicating HC (n = 5) had a nil SV. None of the patients with a normal SVaq (n = 11) developed acute HC. Intraventricular bleeding led to more cases of acute HC (P = .005), which was communicating in 58% of cases. In the chronic phase, CSF analysis was performed for 27 patients, 7 of whom presented HC. None of these 7 patients displayed a depressed SVaq. CONCLUSION: SAH led to changes in cerebrospinal fluid hydrodynamics in the majority of patients. Acute HC was communicating in most cases, even when there was intraventricular bleeding. In the late phase, all chronic HC were communicating and did not display aqueductal stenosis.
OBJECTIVE: To determine acute intracranial hydrodynamic changes after subarachnoid hemorrhage (SAH) via phase-contrast MRI (PC-MRI) analysis of the CSF stroke volume in the aqueduct (SVaq) and the foramen magnum (SVfm). METHODS: A prospective PC-MRI study was performed on 34 SAHpatients in the acute and late phase. Data on CSF flow and hemorrhage site were analyzed according to acute or chronic hydrocephalus (HC). RESULTS: In the acute phase, CSF analysis was performed for 31 patients, 12 of whom presented HC. All 12 had an abnormal SVaq; those with communicating HC (n = 7) had an elevated SV and those with noncommunicating HC (n = 5) had a nil SV. None of the patients with a normal SVaq (n = 11) developed acute HC. Intraventricular bleeding led to more cases of acute HC (P = .005), which was communicating in 58% of cases. In the chronic phase, CSF analysis was performed for 27 patients, 7 of whom presented HC. None of these 7 patients displayed a depressed SVaq. CONCLUSION:SAH led to changes in cerebrospinal fluid hydrodynamics in the majority of patients. Acute HC was communicating in most cases, even when there was intraventricular bleeding. In the late phase, all chronic HC were communicating and did not display aqueductal stenosis.