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A Lumped Parameter Modelling Study of Cerebral Autoregulation in Normal Pressure Hydrocephalus: Does the Brain choose to be Ischemic?
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Abstract
Background
It is well known that normal pressure hydrocephalus (NPH) is associated with a reduction in cerebral blood flow and, therefore, a relatively ischemic metabolic state. It would be expected that ischemia should exhaust the available autoregulation in an attempt to correct the metabolic imbalance. However, there is some evidence to suggest that although blunted, there is retained autoregulation reserve in NPH. The aim of this study is to model the cerebral autoregulation in NPH to discover a solution to this apparent paradox.
Methods
A lumped parameter model was developed utilizing the known limits of autoregulation in man obtained from the literature. The model was tested by predicting the cerebral blood volume changes which would be brought about by the changes in the resistance for each segment modeled. NPH and the post shunt state were then modeled using the known constraints provided from the literature.
Results
The model successfully predicted the cerebral blood volume changes brought about by both increasing and decreasing the cerebral perfusion pressure to the limit of autoregulation. The model suggests that NPH is associated with a balanced increase in resistance within the arterial and venous outflow segments. The arterial segment resistance decreases following shunt insertion, indicating a retained autoregulation reserve existed pre-shunt insertion.
Conclusions
The model suggests that the cerebral blood flow is actively limited in NPH by arteriolar constriction. This may occur to minimize the rise in ICP by reducing the apparent CSF formation rate.
Title: A Lumped Parameter Modelling Study of Cerebral Autoregulation in Normal Pressure Hydrocephalus: Does the Brain choose to be Ischemic?
Description:
Abstract
Background
It is well known that normal pressure hydrocephalus (NPH) is associated with a reduction in cerebral blood flow and, therefore, a relatively ischemic metabolic state.
It would be expected that ischemia should exhaust the available autoregulation in an attempt to correct the metabolic imbalance.
However, there is some evidence to suggest that although blunted, there is retained autoregulation reserve in NPH.
The aim of this study is to model the cerebral autoregulation in NPH to discover a solution to this apparent paradox.
Methods
A lumped parameter model was developed utilizing the known limits of autoregulation in man obtained from the literature.
The model was tested by predicting the cerebral blood volume changes which would be brought about by the changes in the resistance for each segment modeled.
NPH and the post shunt state were then modeled using the known constraints provided from the literature.
Results
The model successfully predicted the cerebral blood volume changes brought about by both increasing and decreasing the cerebral perfusion pressure to the limit of autoregulation.
The model suggests that NPH is associated with a balanced increase in resistance within the arterial and venous outflow segments.
The arterial segment resistance decreases following shunt insertion, indicating a retained autoregulation reserve existed pre-shunt insertion.
Conclusions
The model suggests that the cerebral blood flow is actively limited in NPH by arteriolar constriction.
This may occur to minimize the rise in ICP by reducing the apparent CSF formation rate.
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