Compartmentalized Cerebrospinal Fluid

Abstract

The brain, spinal cord, and the optic nerve are surrounded by and bathed in cerebrospinal fluid (CSF). CSF is produced mainly by the choroid plexus epithelium and ependymal cells of the ventricles from where it flows into interconnecting chambers-the cisterns and the subarachnoid spaces (SASs). 1,2 It is assumed that there is a free and constant circulation of fluid from the sites of production in the third, fourth, and lateral ventricles to the cisterns and SASs.The mechanism by which CSF is driven from its site of production to reabsorption is not yet fully understood, but CSF flow is influenced by the release of newly produced CSF (causing a pressure gradient), the ventricular pulsations, and the pulse pressure of the vascular choroid. The main site of resorption is at the arachnoid villi. Additional possible sites of absorption are the lymphatic capillaries in the dura of the optic nerve and in the area of the olfactory bulb, as well as the dura of the spinal roots. 3-5 A newly discovered mechanism for resorption of CSF acts by means of the meningoepithelial cells (MEC) that cover the arachnoid, the pia, and the trabecular meshwork as well as the septae in the SAS of the optic nerve. 6,7 MECs are found to be more abundant in patients with primary open-angle glaucoma than in normal subjects. 8 In addition, an in vitro study demonstrated MEC proliferation of up to 20% when MECs were exposed to extrinsic increased pressure. 6 Proliferation of MECs was also demonstrated in an animal model after ligation of the optic nerve close to the optic canal. 9 It may thus be postulated that an increase in both the number and volume of MECs will result in a narrowing of the SAS and potentially reduce free CSF flow.

Asymmetric Papilledema in Idiopathic Intracranial Hypertension

“…Despite our small sample, there is a definite relationship between the severity of papilledema and the cross-sectional area of the optic canal, suggesting that asymmetric papilledema may result from asymmetries in the bony optic canal. Our study lends further support to the concept of compartmentation of the peri-optic subarachnoid spaces developed by Killer et al (24) and suggests that the bony optic canal may be a “bottleneck” interfering with the CSF flow between the peri-optic subarachnoid spaces and the suprasellar cistern. However, whether the asymmetry in size of the optic canal is congenital or acquired requires further study.…”

“…Our data, along with that of other investigators (24), continue to challenge the concept of free circulation of the CSF. The concept of compartmentation of the peri-optic subarachnoid spaces (4,24,25), in which the peri-optic subarachnoid spaces are partially separated from the suprasellar cisternal spaces, appears more likely to explain asymmetric papilledema.…”

“…The concept of compartmentation of the peri-optic subarachnoid spaces (4,24,25), in which the peri-optic subarachnoid spaces are partially separated from the suprasellar cisternal spaces, appears more likely to explain asymmetric papilledema. Whereas the orbital portion of the peri-optic subarachnoid spaces is loose enough to distend under increased CSF pressure, the intracanalicular portion, the narrowest (4,19), is characterized by tight relationships between the bone and the optic nerve (24). Because of its unique anatomy, the region of the optic canal plays a crucial role in CSF flow dynamics between the suprasellar cistern and the peri-optic subarachnoid spaces.…”

Use of A-scan Ultrasound and Optical Coherence Tomography to Differentiate Papilledema From Pseudopapilledema

“…It could be that ocular measurements and lumbar puncture were performed at different times, and/or the perioptic pressure differs from the lumbar puncture opening pressure. 36 Previous studies have shown optic nerve sheath diameter to be correlated with simultaneous invasively-measured intracranial pressure in neuro-intensive care patients. 25 …”

Choroidal Folds in Astronauts

“…The second possible explanation, in some astronauts, is that these changes are the end result of localized events occurring at the level of the intraorbital ON with or without a rise in intracranial pressure. 2,3 In this scenario, prolonged microgravity fluid shifts may cause alterations in CSF flow dynamics in the intraorbital portion of the subarachnoid space (SAS) such that CSF enters the SAS but outflow may become impeded. Thus, CSF within the SAS of the ON may gradually become sequestered with a resulting local elevation of optic nerve sheath (ONS) pressures capable of producing the anatomic changes observed.…”