Abstract
INTRODUCTION: Pseudotumor cerebri is characterized by elevated intracranial pressure (ICP) without ventricular dilation. The pathophysiology of pseudotumor is traditionally viewed as chronic cerebrovenous hypertension which causes impaired cerebrospinal fluid (CSF) resorption. Increased resistance to CSF absorption results in ventriculomegaly in obstructive hydrocephalus. In pseudotumor, however, lack of ventriculomegaly cannot be explained by this mechanism. In this study, we model the cerebral windkessel as a CSF pulsation absorber. We hypothesize that inability to absorb CSF pulsation diverts pulsatile energy to ventricles, causing ventriculomegaly, whereas effective CSF pulsation absorption leaves ventricles normal in size. METHODS: Cerebral windkessel is a band-pass filter considering arterial blood pressure (ABP) as input and ICP as output. We used a tank circuit with parallel inductance and capacitance to model windkessel and compare with the transfer function between ABP and ICP in normal dogs. Normal CSF dynamics were simulated by setting circuit parameters to correlate physiological recordings from dogs: frequency for heart rate, input and output voltages for ABP and ICP, and CSF and capillary resistance for resistance to pulsatile and pulseless flow, respectively. CSF path resistance was increased to simulate CSF space narrowing in hydrocephalus. Capillary resistance was increased to simulate impaired venous flow in pseudotumor. RESULTS: The circuit output shows agreement with physiological recordings, in which ICP pulse precedes ABP pulse. Windkessel is most effective at a given pulse frequency. In hydrocephalus, increased resistance to CSF flow disrupts cerebral windkessel, leading to ineffective pulse dampening and increased ICP phase lead. In pseudotumor, increased capillary resistance does not change cerebral windkessel effectiveness or ICP phase lead. CONCLUSION: The cerebral windkessel is a CSF pulsation absorber. An ineffective windkessel in hydrocephalus inhibits CSF pulsation absorption and diverts pulsatile energy to dilate ventricles, whereas an effective one in pseudotumor leaves ventricles normal. Our model of CSF dynamics emphasizes that ventricular dilation is a result of ineffective windkessel and decreased CSF pulsation absorption. This model provides a novel perspective on the pathophysiology of abnormal CSF dynamics and offers new directions for future research.
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