Acta neurochirurgica · 2010
Is ventriculomegaly in idiopathic normal pressure hydrocephalus associated with a transmantle gradient in pulsatile intracranial pressure?
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Eide Per Kristian, Saehle Terje
Аннотация
PURPOSE: In patients with idiopathic normal pressure hydrocephalus (iNPH) and ventriculomegaly, examine whether there is a gradient in pulsatile intracranial pressure (ICP) from within the cerebrospinal fluid (CSF) of cerebral ventricles (ICP(IV)) to the subdural (ICP(SD)) compartment. We hypothesized that pulsatile ICP is higher within the ventricular CSF.
METHODS: The material includes 10 consecutive iNPH patients undergoing diagnostic ICP monitoring as part of pre-operative work-up. Eight patients had simultaneous ICP(IV) and ICP(SD) signals, and two patients had simultaneous signals from the lateral ventricle (ICP(IV)) and the brain parenchyma (ICP(PAR)). Intracranial pulsatility was characterized by the wave amplitude, rise time, and rise time coefficient; static ICP was characterized by mean ICP.
RESULTS: None of the patients demonstrated gradients in pulsatile ICP, that is, we found no evidence of higher pulsatile ICP within the CSF of the cerebral ventricles (ICP(IV)), as compared to either the subdural (ICP(SD)) compartment or within the brain parenchyma (ICP(PAR)). During ventricular infusion testing in one patient, the ventricular ICP (ICP(IV)) was artificially increased, but this increase in ICP(IV) produced no gradient in pulsatile ICP from the ventricular CSF (ICP(IV)) to the parenchyma (ICP(PAR)).
CONCLUSIONS: In this cohort of iNPH patients, we found no evidence of transmantle gradient in pulsatile ICP. The data gave no support to the hypothesis that pulsatile ICP is higher within the CSF of the cerebral ventricles (ICP(IV)) than within the subdural (ICP(SD)) compartment or the brain parenchyma (ICP(PAR)) in iNPH patients.
METHODS: The material includes 10 consecutive iNPH patients undergoing diagnostic ICP monitoring as part of pre-operative work-up. Eight patients had simultaneous ICP(IV) and ICP(SD) signals, and two patients had simultaneous signals from the lateral ventricle (ICP(IV)) and the brain parenchyma (ICP(PAR)). Intracranial pulsatility was characterized by the wave amplitude, rise time, and rise time coefficient; static ICP was characterized by mean ICP.
RESULTS: None of the patients demonstrated gradients in pulsatile ICP, that is, we found no evidence of higher pulsatile ICP within the CSF of the cerebral ventricles (ICP(IV)), as compared to either the subdural (ICP(SD)) compartment or within the brain parenchyma (ICP(PAR)). During ventricular infusion testing in one patient, the ventricular ICP (ICP(IV)) was artificially increased, but this increase in ICP(IV) produced no gradient in pulsatile ICP from the ventricular CSF (ICP(IV)) to the parenchyma (ICP(PAR)).
CONCLUSIONS: In this cohort of iNPH patients, we found no evidence of transmantle gradient in pulsatile ICP. The data gave no support to the hypothesis that pulsatile ICP is higher within the CSF of the cerebral ventricles (ICP(IV)) than within the subdural (ICP(SD)) compartment or the brain parenchyma (ICP(PAR)) in iNPH patients.