The Investigation Of Brain Bridging Veins And Its Significance For Increased Intracranial Pressure

The classic Monroe-Kellie principle states that volume fluctuation can affect the homeostasis of intracranial pressure (ICP). Based on this principle, most clinical treatments targeting down-regulation of ICP are aimed at reducing the volume inside the inflexible cranial cavity by removal of a space-occupying lesion, alleviating edema by dehydration or inhibition of cerebrospinal fluid (CSF) secretion, etc. However, despite these treatments, deterioration in the condition of many patients still cannot be prevented, which can even eventually lead to death. This is why it is important to seek more efficient means to control ICP.Physiologically, the cranial cavity is occupied by brain tissue, CSF and blood. The brain tissue takes up the most volume in the cavity but is the least adjustable due to inelasticity. Cerebrospinal fluid accounts for the least occupancy and also is the least manipulable. Therefore, investigation of the relationship between the brain circulation system and ICP regulation has drawn more and more interest. Some researchers have tried to control ICP by manipulating the arterial and capillary systems, such as by decreasing blood inflow into the cranial cavity by controlling arterial pressure or promoting re-absorption of interstitial fluid through capillaries. These attempts have generated not only positive effects but also have caused serious complications or limitations because control of arterial pressure results in further reduction in the brain perfusion pressure which had been already reduced in response to high ICP. Although the re-absorption of interstitial fluid through capillaries can alleviate brain tissue edema, it abrogates the transportation of re-absorbed fluid. As a result, this kind of fluid shift does not reduce the intracranial volume or down-regulate ICP level effectively. Being the outflow part of the brain circulation system, the cerebral venous system (CVS) does not have an effect on decreasing the perfusion pressure nor does it affect the blood supply and metabolism. In addition, the blood volume in the CVS accounts for more than70%of the total intracranial blood volume and it is quite manageable. Therefore, the investigation of the volume response of the CVS under intracranial hypertension will be of great clinical importance.Quite a few research articles have reported the finding of ICP being associated with cerebral blood flow increase in animal models, and we postulated that this increase might be essential for preventing the bridging veins from collapsing. It is known that subsidable vein vessels can maintain their circular shape only if the inner pressure is higher than or equal to that of the outer tissue. However, if the transmural pressure decreases to below zero the venous vessels will collapse or even become entirely closed. Surprisingly, the intracranial veins are not caused to collapse by the outer pressure even under intracranial hypertension, indicating that the venous transmural pressure must have been increased in compliance with ICP elevation; but how the inner venous pressure responds to ICP remains largely unknown.Rosengarten et al reported that a sudden arterial pressure decrease caused the intracranial blood volume to increase despite decreased arterial inflow. They hypothesized that the increase in intracranial blood volume resulted from a relative decrease in venous outflow. Bateman reported that the inflow rate through the arterial system was higher than the outflow rate through veins in patients with idiopathic intracranial hypertension, and increased ICP in some idiopathic intracranial hypertension patients might be associated with increased extracranial resistance to cerebral venous outflow. In addition, some other studies have revealed a close relationship between achondroplasia-induced hydrocephalus and reduced flow in the superior sagittal sinus, and it has been proved that the diameter of cerebral veins is enlarged during intracranial hypertension and the extent of diameter enlargement is closely related to ICP level. These findings demonstrated the potential role of the CVS in ICP regulation. But the questions of how the CVS is involved in ICP regulation and to what extent this CVS involvement contributes to intracranial disorders with high ICP remain to be answered.Our previous findings proved that an unusual morphological structure exists between brain bridging veins (BBVs) and venous sinuses which might play an important role in regulating the venous drainage under increased ICP conditions. In the present study, this particular structure, the outflow cuff segment (OCS), was further confirmed in the outflow terminal of the human CVS. Under increased ICP, we investigated the hemodynamics of the CVS and found significant changes in obstruction of venous drainage, decrease of flow velocity and distension of vessel diameter. Based on previous and present results we put forward the hypothesis of concurrent "venogenic intracranial hypertension"(cVIH) in which we speculate that the CVS has an effect on ICP dysregulation by cVIH. In more detail, cVIH is intracranial hypertension resulting from both the congestion of cerebral venous blood and the initial intracranial hypertension. Since the hemodynamic changes of the CVS have been observed in multiple neurological disorders, we believe that the existence of cVIH and its synergistic effect on worsening the pre-existing high ICP circumstances through a vicious feedback loop is prevalent. Research on vein-activated cVIH will be of great clinical significance for managing intracranial diseases via regulation of ICP.