Abstract
The fine balance between the secretion, composition, volume and turnover of cerebrospinal fluid (CSF) is strictly regulated. However, during certain neurological diseases, this balance can be disrupted. 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. Yet, the exact cellular, molecular and physiological mechanisms that contribute to altered hydrodynamic pathways in these diseases are poorly defined or hotly debated. 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. 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. Undoubtedly CSF secretion, absorption and drainage are important aspects of brain fluid homeostasis in maintaining a stable ICP. Traditionally, pharmacological interventions or CSF drainage have been used to reduce ICP elevation due to over production of CSF. However, these drugs are used only as a temporary solution due to their undesirable side effects. 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.
Highlights
Elevation 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 [1]
This review summarises our current understanding of Cerebrospinal fluid (CSF) dynamics with a focus on effects on ICP during neurological diseases, and highlights some of the discrepancies within the field
Some evidence suggests the involvement of aquaporin 1 (AQP1) at the choroid plexus [83], and more recent discoveries implicate the molecular transfer of water via NKCC1 in CSF secretion [70]; these insights may provide targets for therapeutic control of CSF in conditions of excessive secretion and elevated ICP
Summary
Elevation 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 [1]. Cerebrospinal fluid (CSF) is an important component of maintaining a stable ICP, and disruptions to secretion or drainage can lead to ICP elevations [2]. CSF 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 [3]. It serves as a critical mechanism for transporting nutrients and hormones from one area to another [3–5].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
