LAUSR

BackgroundThis study investigated cerebrospinal fluid (CSF) hydrodynamics using cine phase-contrast MRI in the cerebral aqueduct and the prepontine cistern between three distinct groups: pre-shunt normal pressure hydrocephalus (NPH) patients, post-shunt NPH patients, and controls. We hypothesized that the hyperdynamic flow of CSF through the cerebral aqueduct seen in NPH patients was due to a reduction in cisternal CSF volume buffering. Both hydrodynamic (velocity, flow, stroke volume) and peak flow latency (PFL) parameters were investigated.MethodsScans were conducted on 30 pre-treatment patients ranging in age from 58 to 88 years along with an additional 12 controls. Twelve patients also received scans following either ventriculoatrial (VA) or ventriculoperitoneal (VP) shunt treatment (9 VP, 3 VA), ranging in age from 74 to 89 years with a mean follow up time of 6 months.ResultsSignificant differences in area, velocity, flow, and stroke volume for the cerebral aqueduct were found between the pre-treatment NPH group and the healthy controls. Shunting caused a significant decrease in both caudal and cranial mean flow and stroke volume in the cerebral aqueduct. No significant changes were found in the prepontine cistern between the pre-treatment group and healthy controls. For the PFL, no significant differences were seen in the cerebral aqueduct between any of the three groups; however, the prepontine cistern PFL was significantly decreased in the pre-treatment NPH group when compared to the control group.ConclusionsAlthough several studies have quantified the changes in aqueductal flow between hydrocephalic groups and controls, few studies have investigated prepontine cistern flow. Our study was the first to investigate both regions in the same patients for NPH pre- and post- treatment. Following shunt treatment, the aqueductal CSF metrics decreased toward control values, while the prepontine cistern metrics trended up (not significantly) from the normal values established in this study. The opposing trend of the two locations suggests a redistribution of CSF pulsatility in NPH patients. Furthermore, the significantly decreased latency of the prepontine cisternal CSF flow suggests additional evidence for CSF pulsatility dysfunction.