OBJECTIVE: To investigate the relationship between idiopathic intracranial hypertension (IIH) and transverse sinus stenosis through experiments performed on a validated mathematical model. METHODS: A mathematical model of intracranial pressure (ICP) dynamics has been extended to accommodate venous sinus compression through the introduction of a Starling-like resistor between the sagittal and transverse sinuses. RESULTS: In the absence of this type of resistor, the sinuses are rigid, and the model has only a unique, stable steady state with normal pressures. With resistance a function of the external pressure on the sinus, a second stable steady state may exist. This state is characterized by elevated ICP concurrent with a compressed transverse sinus. Simulations predict that a temporary perturbation that causes a transient elevation of ICP can induce a permanent transition from the normal to the higher steady state. Comparisons to clinical data from IIH patients provide supporting evidence for the validity of the model's predictions. Simulations suggest a possible clinical diagnostic technique to determine if an individual has a compressible transverse sinus and is at risk for developing IIH. CONCLUSIONS: Results of the model experiments suggest that the primary cause of IIH may be a compressible, as opposed to rigid, transverse sinus, and that the observed stenosis is a necessary characteristic of the elevated pressure state.
OBJECTIVE: To investigate the relationship between idiopathic intracranial hypertension (IIH) and transverse sinus stenosis through experiments performed on a validated mathematical model. METHODS: A mathematical model of intracranial pressure (ICP) dynamics has been extended to accommodate venous sinus compression through the introduction of a Starling-like resistor between the sagittal and transverse sinuses. RESULTS: In the absence of this type of resistor, the sinuses are rigid, and the model has only a unique, stable steady state with normal pressures. With resistance a function of the external pressure on the sinus, a second stable steady state may exist. This state is characterized by elevated ICP concurrent with a compressed transverse sinus. Simulations predict that a temporary perturbation that causes a transient elevation of ICP can induce a permanent transition from the normal to the higher steady state. Comparisons to clinical data from IIH patients provide supporting evidence for the validity of the model's predictions. Simulations suggest a possible clinical diagnostic technique to determine if an individual has a compressible transverse sinus and is at risk for developing IIH. CONCLUSIONS: Results of the model experiments suggest that the primary cause of IIH may be a compressible, as opposed to rigid, transverse sinus, and that the observed stenosis is a necessary characteristic of the elevated pressure state.