Yes, there are a lot of justifications for this action in favor of optic neuropathy, however, still the main treatment of glaucoma revolves around IOP reduction. We may argue that we are also using drugs to increase optic nerve head blood flow to counter ischemia but truly speaking, the maximum effort in treating glaucoma is in the vicinity of IOP reduction so much so that we even treat Normal Tension Glaucoma by further 30% reduction of IOP as a treatment measure.
Ref: Shah SIA et al: Concise Ophthalmology Text & Atals. 5th ed. Param B (Pvt.) Ltd. 2018: 67-73
IOP is added as a risk factor for glaucoma as it causes optic neuropathy , and visual field defect.
Dear Ramesh, the agony is the same thing you have mentioned but in a different way, probably you are young and I am above sixty years. In fact, IOP is not "added" as risk factor but it is dropped down from the position of "cause" to just a "risk factor".
Well said but we cannot underestimate importance of IOP . IOP is the only factor which we can monitor in almost every setting i.e other than tertiary care center.It is highlighted as important risk factor if high . It is important to realize that it may be misleading in Low tension/ normo tension glaucoma management in a setup where sophisticated tools like OCT etc not available.. So when ever we see disparity in IOP measurement and disc changes on clinical examination must go for Central corneal thickness to add or substract correction factor accordingly.
IOP is still our main diagnostic and therapeutic tool in glaucoma and the main risk factor for evolution of glaucoma. CCT measuring makes it more accurate and special characteristics which are found with IOP curve enligthen us more about the pathophysiology of glaucoma and aid our therapeutic plan. Nevertheless IOP is not considered any more as the only or main cause pf glaucoma. So the question to be answered now is: which are really the causes and risk factors of glaucoma which we dont't know or understand? If scientific research answer this question we'll be able to have more sophisticated tools for therapy to add to hypotonic meds and surgery. Neuroprotection is an interesting field.
Thanks Prof Farah, Dr. Sevasti Tsironi and Prof Aziz for your inputs.
There are situation where no there is no increase in iop but glaucoma still occurs. A like ntg. Its just a theory of susceptibility. My. Way of understanding is...
If you put a dot with a marker in balloons of different wall thickness.. But apply same pressure in all. The thinner walled are likely to stretch or distort the dot more.
The elevated intraocular pressure is the main factor for the development of glaucoma. Unilateral traumatic glaucoma in a healthy young subject is the proof that even a slightly elevated IOP over the time can cause total blindness. Normal-tension glaucoma is also due to normal range IOP but acting as an ‘elevated IOP’ in such subjects. Rest of the factors such as high myopia, sleep apnea, Raynaud’s disease and others are all secondary but by themselves can’t cause glaucoma.
The site of injury in glaucoma is the border tissue of Elschnig , not the lamina cribrosa. The arcuate field defects in glaucoma correspond fully with the arcuate arrangement of nerve fibers in the retina until they make a 90-degree turn in the ONH. Due to 90-degree turn the nerve fibers become vertically oriented turn thus the arcuate pattern is lost in the LC. On this basis alone the LC can’t be the site of injury, as any injury in the LC couldn’t produce arcuate field defects which are the pathognomonic feature of glaucoma. There are two main features of chronic glaucoma. (1) border tissue of Elschnig (not LC) is the primary site of injury (2) glaucoma is not an optic neuropathy but an optic axotomy.
For details: following link to the article. Pathogenesis of chronic glaucoma: A Two-Stage disease
https://www.ecronicon.com/ecop/pdf/ECOP-10-00450.pdf
Dear Anadi Khatri, whatever explanation or reasoning we utilize to satisfy ourselves but the fact remains clear that our main tool of treatment is still IOP lowering so much so that even in low tension glaucoma our handy tool is to "further reduce IOP to as much as 30%"
I agree with you Dr Syed Hasnain, you argument is based on scientific ground. Thanks.
I am totally on the same page with you Syed Imtiaz Ali Shah . Even though we monitor the progression of change in cup to disc ratio, bayonetting of the vessels, thickness of neuroretinal rim, change in visual field indices and pattern and other associated factors, the main goal of controlling the progression of glaucoma is lowering the IOP.
Most of all glaucoma medications and even the surgical interventions are designed lower the IOP.
It cannot be denied that there are glaucoma in which there is necessarily no increase in IOP like normal tension and low tension glaucoma but majority of the global glaucoma composed of primary open angle glaucoma.
Until we come with other solid and convincing mechanism of the progression of glaucoma, IOP should not be expelled from the important position of cause of glaucoma to just a risk factor.
Dear Imtiaz, I hope you are doing fine. I deeply appreciate your positive feedback regarding my views of glaucoma. I am sorry to say that we are wrong in glaucoma since 1850s. We are stuck up in a wrong paradigm (cupping of LC and neuropathy) and don’t seem to come out of it. The lamina cribrosa, although widely believed, can’t be the site of injury for a simple reason. Why? Glaucomatous arcuate field defects are horizontally oriented and correspond fully to the arrangement of NFs in the retina until they make a 90-degree turn in the ONH. After their 90-degree turn the NFs become vertically oriented so the horizontal arcuate pattern is lost in the LC.
Therefore any injury within the LC couldn’t produce arcuate field defects which are the salient feature of glaucoma, and the basis for doing perimetry in glaucoma. The same applies to ganglion cell layer: GCs are not arranged in any arcuate pattern so ganglion cells of the retina couldn’t be the primary site of injury in glaucoma due to any reason. In other words the site of injury to the NFs has to be in the retina or in the ONH (most likely ONH ) until the NFs make a 90-degree turn in ONH. Period.
If true, then the 160-year old concept of cupping will become wrong and all the research associated with cupping of LC will become redundant.
Regarding IOP being expelled as the cause of glaucoma? IOP is the main cause of glaucoma in both HTG and NTG so we can never throw it away. How can we answer that IOP of 24 mmHg can cause glaucoma but IOP of 18 couldn’t, since both HTG and NTG have similar signs and course of disease? In both cases the NFs are being destroyed in an orderly sequence over the years. This feat couldn’t be achieved by the direct effect of IOP (whether elevated or normal) on the NFs. It appears that the elevated IOP or the normal IOP acting as an ‘elevated IOP’ in that particular subject is destroying some important component of the ONH which then leads to the orderly loss of NFs over the years. Glaucoma is a two –stage disease as I hypothesized in my previous post. We will have to change the current paradigm in order to solve the mystery of glaucoma. I will humbly accept if someone can prove me wrong. Thanks
Hi,
High IOP remains itselft the most important risk factor in glaucoma. However, as far as we know, there is not a definite value acting as a “trigger” in the glaucoma develpment. There are patients showing progressive glaucoma despite a normal pressure.
The fact itself that we have a certain category of patients with glaucomatous damage, but with normal IOP, reflects that we have other actors playing as concauses.
One example is offered by vascular impairment, which seems to play a major role expecially in the normal tension glaucoma patients I mentioned before.
Please, feel free to direct message me if you have any further question.
Best,
Clemente
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