The epithelial cells surrounding the capillaries compose a blood-CSF barrier (BCSFB), which selectively controls the movement of solutes and water to regulate the composition of CSF. It is estimated that around 80–90% of CSF is secreted by the choroid plexus, a highly-vascularised structure of epithelial cells located in the ventricles of the brain. An assessment of how both ICP and CSF physiology are affected by pathology may offer us a potential target for attenuating ICP elevations in several conditions of the CNS.ĬSF secretion The choroid plexus as the primary site of CSF secretion Factors influencing secretion, flow and drainage are under investigation and are relevant in conditions of elevated ICP, as CSF contributes to the overall pressure of the CNS. While there is debate about the dynamics of CSF, studies have attempted to elucidate how our current hypotheses of CSF physiology may be influenced by neurological disorders or injury. Studies conducted in multiple animal species also point to lymphatic drainage of CSF in which CSF exits the cranium through the cribriform plate and spinal canal to reach the cervical and spinal lymph nodes. The traditional view of CSF drainage is that fluid flows from the subarachnoid space through the arachnoid villi and drains into the blood of the superior sagittal sinus (Fig. The exact mechanisms of CSF secretion, flow and reabsorption/drainage are debated however, it is understood that alterations to normal physiology can contribute to elevated ICP. Reduced CSF secretion as a function of aging contributes to increased protein aggregation and has links to increased beta-amyloid deposition in Alzheimer’s disease or phosphorylated tau protein in chronic traumatic encephalopathy. CSF also plays a role in protein clearance within the CNS by mechanisms hotly debated. It serves as a critical mechanism for transporting nutrients and hormones from one area to another. However, a cogent review of the involvement of CSF in the elevation of ICP in pathologic conditions of the CNS is currently lacking.ĬSF serves as a protective fluid to the brain and spinal cord, cushioning them from mechanical injury, and acts to reduce the brain’s effective weight-its actual mass is ~ 1500 g while the buoyancy provided by CSF reduces its net weight to 25–50 g. Cerebrospinal fluid (CSF) is an important component of maintaining a stable ICP, and disruptions to secretion or drainage can lead to ICP elevations. The deleterious consequences of unchecked ICP highlight the importance of maintaining ICP homeostasis within the central nervous system (CNS). Uncontrolled raised ICP can worsen outcomes, and several manoeuvres have been proposed to mitigate ICP elevations. Emerging evidence suggests that pharmacological targeting of aquaporins, transient receptor potential vanilloid type 4 (TRPV4), and the Na +–K +–2Cl − cotransporter (NKCC1) merit further investigation as potential targets in neurological diseases involving impaired brain fluid dynamics and elevated ICP.Įlevation of intracranial pressure (ICP) after a neurological injury has been reported in numerous conditions including hydrocephalus, idiopathic intracranial hypertension (IIH), oedema, traumatic brain injury (TBI), and stroke. However, these drugs are used only as a temporary solution due to their undesirable side effects. Traditionally, pharmacological interventions or CSF drainage have been used to reduce ICP elevation due to over production of CSF. Undoubtedly CSF secretion, absorption and drainage are important aspects of brain fluid homeostasis in maintaining a stable ICP. This review evaluates and summarises current hypotheses of CSF dynamics and presents evidence for the role of impaired CSF dynamics in elevated ICP, alongside discussion of the proteins that are potentially involved in altered CSF physiology during neurological disease. The traditional views and concepts of CSF secretion, flow and drainage have been challenged, also due to recent findings suggesting more complex mechanisms of brain fluid dynamics than previously proposed. Yet, the exact cellular, molecular and physiological mechanisms that contribute to altered hydrodynamic pathways in these diseases are poorly defined or hotly debated. A significant disruption to the normal CSF circulation can be life threatening, leading to increased intracranial pressure (ICP), and is implicated in hydrocephalus, idiopathic intracranial hypertension, brain trauma, brain tumours and stroke. However, during certain neurological diseases, this balance can be disrupted. The fine balance between the secretion, composition, volume and turnover of cerebrospinal fluid (CSF) is strictly regulated.
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