Can Cerebrospinal fluid pressure influence Optic nerve head neuropathy in Normal Tension Glaucoma?

Optom
Normal Tension Glaucoma is a type of Glaucoma without the common classical sign of Glaucoma pathogenesis- increased intraocular pressure (IOP). Increase in the pressure within the eyeball is the single most important factor that could indicate Glaucoma but it often times not enough to predict all types of Glaucomas. In Normal Tension Glaucoma, Optic nerve head neuropathy is the single most important sign of a pathology. The intraocular pressure (IOP) looks 'normal' but other signs like the dilation of the pupil & its apparent inability to react to light or acccomodation can be appreciated, especially when the disease has stayed for sometime...
Then comes the almighty question, why does the pupil becomes fixed & dilated when there is no 'high' IOP which should have compressed the Edinger Welpher pathway? Or how does the lamina cribosa death and optic nerve fibre appoptosis becomes possible in the presence of what appears to be 'normal' pressure?
Lets take a tour! The Optic nerve head tranverses through the the Optic disk via the lamina cribosa & terminates at the Optic chiasm. The lamina cribosa is the weakest portion of the sclera located at the posterior pole of the eyeball and perforated by the many fibres of the optic nerve. The optic nerve fibres @ this point (Optic disk area) is loosely attached to each other because of the absence of the cells of Muller. The weakness of the lamina cribosa area and the absence of the Muller cells in this position makes the optic disk head very vulnerable to inflamation and changes in pressure through the optic and neural pathways! The IOP of the eye is actually the pressure difference between the cornea and the atmospheric pressure. It is known as the transcorneal pressure. On the other hand, the pressure in the cranium and in the spinal cord is known as intracranial pressure (ICP). The later is a pressure difference between the atmosphere and the cranial compartments- the cranium and the vertebra.
Aqueous humor and the cerebrospinal fluid both similar in origin (a filtration substance) determines the IOP and ICP respectively. IOP should always be slightly higher than the ICP hence giving the optic disk head its classical depression. There is a homostatic arrengement as felt on the lamina cribosa and it is known as translaminar pressure, a pressure difference between the eyeball and the cranium and the spinal cord. Translaminar pressure has been attributed as the single most important phenomenon that discribes the stetching and subsequent atrophy of the lamina cribosa.
Translaminar pressure as felt on the lamina cribosa is calculated as (IOP-ICP). If the ICP is higher than the IOP a pseudo-tumor celebri or papilloedema or papillitis results. On the other hand, a very high IOP & low ICP results in Glaucomatous changes. It is attributed that the so called 'normal' tension glaucoma is as a result of the cushioning effect of the ICP on the lamina cribosa. The apparently 'high' IOP is cushioned by a not-too-low ICP causing a strain on the lamina cribosa to the point of nerve fibre cell apoptosis.
The average IOP is 16mmHg while the average ICP is 12mmHg, hence giving us a 4mmHg difference on the lamina cribosa. This gives the optic disk head a depression equivalent to the tranlaminar pressure difference of 4mmHg.
Even though glaucoma is not fully understood, I believe that ICP plays a role in normal tension glaucoma. It therefore becomes important to put such in consideration in diagnosis and management of this single most important silent thief of sight!
Thanks,
Dr Victor Ezebuiroh.
N/B: This article draws no financial interest anywhere.