scholarly journals CrossTalk opposing view: NKCC1 in the luminal membrane of choroid plexus is outwardly directed under basal conditions and contributes directly to cerebrospinal fluid secretion

2020 ◽  
Vol 598 (21) ◽  
pp. 4737-4739 ◽  
Author(s):  
N. MacAulay ◽  
C. R. Rose
2016 ◽  
Vol 96 (4) ◽  
pp. 1661-1662 ◽  
Author(s):  
Darko Orešković ◽  
Milan Radoš ◽  
Marijan Klarica

It is generally accepted that meningeal reactions in patients with mumps are due to the direct involvement of the meninges by the mumps virus. With the development of mumps vaccines, this view was extended to vaccinated people, who are considered serious post-vaccine meningitis. In present article, the author states that these reactions are not due to inflammation of the meninges, but to the choroid plexus caused by virulent and vaccine strains. Inflammation leads to an increase in cerebrospinal fluid secretion, which increases intracranial pressure and is manifested by meningeal symptoms. In the presence of this evidence, the author considers that meningeal reactions are not meningitis, but meningisms, based on clinical data, experiments on monkeys and the glymphatic system.


2013 ◽  
Vol 93 (4) ◽  
pp. 1847-1892 ◽  
Author(s):  
Helle H. Damkier ◽  
Peter D. Brown ◽  
Jeppe Praetorius

The choroid plexus epithelium is a cuboidal cell monolayer, which produces the majority of the cerebrospinal fluid. The concerted action of a variety of integral membrane proteins mediates the transepithelial movement of solutes and water across the epithelium. Secretion by the choroid plexus is characterized by an extremely high rate and by the unusual cellular polarization of well-known epithelial transport proteins. This review focuses on the specific ion and water transport by the choroid plexus cells, and then attempts to integrate the action of specific transport proteins to formulate a model of cerebrospinal fluid secretion. Significant emphasis is placed on the concept of isotonic fluid transport across epithelia, as there is still surprisingly little consensus on the basic biophysics of this phenomenon. The role of the choroid plexus in the regulation of fluid and electrolyte balance in the central nervous system is discussed, and choroid plexus dysfunctions are described in a very diverse set of clinical conditions such as aging, Alzheimer's disease, brain edema, neoplasms, and hydrocephalus. Although the choroid plexus may only have an indirect influence on the pathogenesis of these conditions, the ability to modify epithelial function may be an important component of future therapies.


Brain Edema X ◽  
1997 ◽  
pp. 279-281
Author(s):  
Richard F. Keep ◽  
J. Xiang ◽  
L. J. Ulanski ◽  
F. C. Brosius ◽  
A. Lorris Betz

2017 ◽  
Author(s):  
Hannah Botfield ◽  
Maria Uldall ◽  
Connar Westgate ◽  
James Mitchell ◽  
Snorre Hagen ◽  
...  

2021 ◽  
Author(s):  
Pinar Kuru Bektaşoğlu ◽  
Bora Gürer

Cerebrospinal fluid is an essential, clear, and colorless liquid for the homeostasis of the brain and neuronal functioning. It circulates in the brain ventricles, the cranial and spinal subarachnoid spaces. The mean cerebrospinal fluid volume is 150 ml, with 125 ml in subarachnoid spaces and 25 ml in the ventricles. Cerebrospinal fluid is mainly secreted by the choroid plexuses. Cerebrospinal fluid secretion in adults ranges between 400 and 600 ml per day and it is renewed about four or five times a day. Cerebrospinal fluid is mainly reabsorbed from arachnoid granulations. Any disruption in this well-regulated system from overproduction to decreased absorption or obstruction could lead to hydrocephalus.


2017 ◽  
Author(s):  
Connar Westgate ◽  
Hannah Botfield ◽  
Michael O'Reilly ◽  
David Hodson ◽  
Alexandra Sinclair

2019 ◽  
pp. 41-46
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak

Papilledema is the cardinal clinical sign of increased intracranial pressure. In this chapter, we begin by reviewing the symptoms and signs of increased intracranial pressure. We next review potential causes of increased intracranial pressure, which include intracranial masses, obstruction of the ventricular system, obstruction of cerebral venous outflow, decrease in cerebrospinal fluid absorption, increase in cerebrospinal fluid secretion, cerebral edema, medications, and idiopathic intracranial hypertension. We then review the approach to the diagnostic evaluation of increased intracranial pressure, including the recommended neuroimaging studies and cerebrospinal fluid evaluation. Lastly, we discuss the basic management approach for the patient with symptoms and signs of increased intracranial pressure.


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