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Cerebrospinal Fluid and Cerebral Blood Flows in Idiopathic Intracranial Hypertension
Cyrille Capel1,2,3, Marc Baroncini4, Catherine Gondry-Jouet5
1Neurosurgery Department, Hospital University Center of Amiens-Picardie, Amiens, France. capel.cyrille@chu-amiens.fr.
Insights
Idiopathic intracranial hypertension (IIH) is linked to increased cerebrospinal fluid (CSF) and arteriovenous flow. This study found higher CSF and vascular flow in IIH patients, suggesting a hydrodynamic disturbance.
Area of Science:
- Neurology
- Neurosurgery
- Radiology
Background:
- Cerebrospinal fluid (CSF) and blood flow dynamics are closely related during the cardiac cycle.
- Idiopathic intracranial hypertension (IIH) is suspected to involve hemodynamic and hydrodynamic disturbances.
Purpose of the Study:
- To investigate the interaction between CSF and blood flow in patients with IIH.
- To analyze cerebral hydrodynamic and hemodynamic parameters in IIH.
Main Methods:
- Retrospective analysis of phase-contrast MRI (PCMRI) data.
- Inclusion of 13 IIH patients and 16 control subjects.
- Measurement of arterial and venous flow parameters, arteriovenous flow, and CSF flow (peak flow and stroke volume).
Main Results:
- No significant differences were observed in arterial and venous flow parameters between IIH and control groups.
- IIH patients exhibited significantly higher arteriovenous peak flow (PFav) and vascular stroke volume (SVVASC).
- Cerebrospinal fluid peak flow (PFCSF) and stroke volume (SVCSF) were significantly elevated in the IIH group.
Conclusions:
- Despite normal arterial and venous flow, increased arteriovenous flow and CSF flow were detected in IIH.
- A potential phase shift in venous outflow may contribute to increased arteriovenous pulsatility and brain expansion.
- Elevated arteriovenous flow may lead to increased CSF displacement and intracranial pressure (ICP) in IIH.
Objectives:
Cerebrospinal fluid (CSF) and blood flows have a strong relationship during a cardiac cycle. Idiopathic intracranial hypertension (IIH) is a pathology that seems to present hemodynamic and hydrodynamic disturbance. The aim of this study was to establish CSF and blood interaction in IIH.
Material And Methods:
We retrospectively studied cerebral hydrodynamic and hemodynamic flows by phase-contrast MRI (PCMRI) in 13 IIH subjects (according Dandy's criteria) and 16 controls. We analyzed arterial peak flow, pulsatility index, and resistive index in arterial and venous compartments (PFart, PIart, RIart, PFvein, PIvein, RIvein) and measured arteriovenous and CSF peak flow and stroke volume (PFav, SVVASC, PFCSF, SVCSF).
Results:
We found no significant difference between IIH and control groups in arterial and venous parameters. Arteriovenous flow analysis showed higher PFav and SVVASC in the IIH group than in the control group (respectively 369 ± 27 mL/min and 286 ± 47 mL/min, p = 0.02; and 1085 ± 265 μL/cardiac cycle and 801 ± 226 μL/cardiac cycle, p = 0.007). PFCSF and SVCSF were higher in the IIH group than in the control group (respectively 206 ± 50 mL/min and 126.6 ± 24.8 mL/min, p = 0.04; and 570 ± 190 μL/cardiac cycle and 430 ± 100 μL/cardiac cycle, p = 0.0007).
Conclusion:
Although no significant change was found in arterial and venous flows, we showed that a small phase shift of venous outflow might cause an increase in the arteriovenous pulsatility and an increasing brain expansion during the cardiac cycle. This arteriovenous flow increase would result in an increase of CSF flushing through the foramen magnum and an increased ICP.
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