A lumped parameter modelling study of cerebral autoregulation in normal pressure hydrocephalus suggests the brain chooses to be ischemic

被引:4
|
作者
Bateman, Grant Alexander [1 ,2 ]
Bateman, Alexander Robert [3 ]
机构
[1] John Hunter Hosp, Newcastle Reg Mail Ctr, Dept Med Imaging, Locked Bag 1, Newcastle, NSW 2310, Australia
[2] Newcastle Univ, Fac Hlth, Callaghan Campus, Newcastle, NSW, Australia
[3] Univ New South Wales, Sch Mech Engn, Sydney, NSW, Australia
来源
SCIENTIFIC REPORTS | 2024年 / 14卷 / 01期
关键词
Autoregulation; Cerebral blood flow; Normal pressure hydrocephalus; Ischemia; CSF formation rate; INCREASED INTRACRANIAL-PRESSURE; CEREBROSPINAL-FLUID PRODUCTION; BLOOD-FLOW; HEMODYNAMIC-RESPONSE; OXYGEN UTILIZATION; VENOUS-PRESSURE; BRIDGING VEINS; SAGITTAL SINUS; VOLUME; RESISTANCE;
D O I
10.1038/s41598-024-75214-6
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Normal pressure hydrocephalus (NPH) is associated with a reduction in cerebral blood flow and an ischemic metabolic state. Ischemia should exhaust the available autoregulation in an attempt to correct the metabolic imbalance. There is evidence of some 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. A lumped parameter model was developed utilizing the known limits of autoregulation in man. The model was tested by predicting the cerebral blood volume changes which would be brought about by changes in resistance. NPH and the post shunt state were then modeled using the known constraints provided from the literature. The model successfully predicted the cerebral blood volume changes brought about by altering 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 resistance decreased after modelling shunt insertion. 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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收藏
页数:11
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