A recently developed model of communicating hydrocephalus suggests that ventricular dilation may be related to the redistribution of pulsations in the cranium from the subarachnoid spaces (SASs) into the ventricles. Based on this model, the authors have developed a method for analyzing flow pulsatility in the brain by using the ratio of aqueductal to cervical subarachnoid stroke volume and the phase of cerebrospinal fluid (CSF) flow, which is obtained at multiple locations throughout the cranium, relative to the phase of arterial flow.
Flow data were collected in a group of 15 healthy volunteers by using a series of images acquired with cardiac-gated, phase-contrast magnetic resonance imaging.
The stroke volume ratio was 5.1 ± 1.8% (mean ± standard deviation). The phase lag in the aqueduct was −52.5 ± 16.5° and the phase lag in the prepontine cistern was −22.1 ± 8.2°. The flow phase at the level of C-2 was +5.1 ± 10.5°, which was consistent with flow synchronous with the arterial pulse. The subarachnoid phase lag ventral to the pons was shown to decrease progressively to zero at the craniocervical junction. Flow in the posterior cervical SAS preceded the anterior space flow.
Under normal conditions, pulsatile ventricular CSF flow is a small fraction of the net pulsatile CSF flow in the cranium. A thorough review of the literature supports the view that modified intracranial compliance can lead to redistribution of pulsations and increased intraventricular pulsations. The phase of CSF flow may also reflect the local and global compliance of the brain.
Abbreviations used in this paper:BA = basilar artery; CA = carotid artery; CSF = cerebrospinal fluid; FOV = field of view; MR = magnetic resonance; NPH = normal-pressure hydrocephalus; SAS = subarachnoid space; SNR = signal-to-noise ratio; SD = standard deviation; SSS = superior sagittal sinus; Venc = encoding velocity.
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