BACKGROUND: The role of the cerebral venous system (CVS) in intracranial pressure (ICP) regulation remains largely unclear. In the present study, the interaction between ICP and the cerebral venous system and its possible mechanism were investigated with respect to the biological characteristics of the cerebral venous system and its hemodynamic response under increased ICP. METHODS: We created intracranial hypertension animal model, measured and calculated the venous flow velocity and diameter of the outflow terminal of the CVS with color ultrasonic system and recorded the vascular morphology by 3-dimensional anatomical microscopy. Patients who suffered from raised ICP underwent MRI and digital subtraction angiography (DSA) examination to show the length in the vertical direction of the wall of the bridging vein representing the diameter value. Pathological autopsy was performed from bodies of patients who had died from non-cerebral causes to observe the juncture part between the venous sinuses and tributary vertical brain veins. RESULTS: Under increased ICP conditions, venous drainage through the outlet cuff segment, a unique structure between the bridge vein and sinus, was obstructed and in turn venous blood became congested. Therefore, the increased blood volume worsened the pre-existing ICP according to the well-accepted theory regarding volume-pressure relationship. This phenomenon was described as concurrent "venogenic intracranial hypertension", which is characterized by intracranial venous blood stasis responsive to and together with the original increased ICP. CONCLUSIONS: The existence of this special pathophysiological process is prevalent, rather than rare, in various intracranial disorders. This finding would definitely provide new insight into the area of cerebral venous system research.
BACKGROUND: The role of the cerebral venous system (CVS) in intracranial pressure (ICP) regulation remains largely unclear. In the present study, the interaction between ICP and the cerebral venous system and its possible mechanism were investigated with respect to the biological characteristics of the cerebral venous system and its hemodynamic response under increased ICP. METHODS: We created intracranial hypertension animal model, measured and calculated the venous flow velocity and diameter of the outflow terminal of the CVS with color ultrasonic system and recorded the vascular morphology by 3-dimensional anatomical microscopy. Patients who suffered from raised ICP underwent MRI and digital subtraction angiography (DSA) examination to show the length in the vertical direction of the wall of the bridging vein representing the diameter value. Pathological autopsy was performed from bodies of patients who had died from non-cerebral causes to observe the juncture part between the venous sinuses and tributary vertical brain veins. RESULTS: Under increased ICP conditions, venous drainage through the outlet cuff segment, a unique structure between the bridge vein and sinus, was obstructed and in turn venous blood became congested. Therefore, the increased blood volume worsened the pre-existing ICP according to the well-accepted theory regarding volume-pressure relationship. This phenomenon was described as concurrent "venogenic intracranial hypertension", which is characterized by intracranial venous blood stasis responsive to and together with the original increased ICP. CONCLUSIONS: The existence of this special pathophysiological process is prevalent, rather than rare, in various intracranial disorders. This finding would definitely provide new insight into the area of cerebral venous system research.
Authors: Alain Goriely; Marc G D Geers; Gerhard A Holzapfel; Jayaratnam Jayamohan; Antoine Jérusalem; Sivabal Sivaloganathan; Waney Squier; Johannes A W van Dommelen; Sarah Waters; Ellen Kuhl Journal: Biomech Model Mechanobiol Date: 2015-02-26