At our institute I do not think anything else is done. If anyone gives an advise it has to be very informal.

Ophthalmologist, Dr Ed Kondrot, Florida is working with homeopathy, syntonics and microcurrent therapies www.healingtheeye.com might be worth contacting him

I would check 24-hr IOP and would be interested in mean IOP changes. Another important issue will be evaluation of perfusion pressure in the progressing low IOP cases. This will establish a basis to collaborate with an internist. Other than these, we do not employ anything else,such as complimentary medicine.

Neuroprection with pharmacologic agents may be beneficial. PEDF, produced by the retinal pigment epithelium, has recently been shown to be neuroprotective. PEDF is increased by retinal laser treatment. New forms of harmless retinal laser treatment may thus be potential glaucoma treatments via neuroprotection.

If the patient plays a wind instrument, I advise them that there is some evidence that playing such an instrument increases IOP and that they may want to cut down their playing time (musicians, both pros and amateurs, don't like this advice - they are usually passionate about their music). I take care not to imply that their music has caused their glaucoma. And as far as i know, there is no evidence that stopping playing will stop glaucoma progression.

That ~ funny, but true. The famous principal tuba player for the Chicago Symphony, Arnold Jacobs, had bad glaucoma and there was quite a controversy over whether his tuba playing aggravated the condition. I am a trumpet player (see itunes) - higher risk due to the higher register - and have glaucoma. Haven't stopped playing. Yet. But this applies to very, very few with glaucoma...glass-blowers, balloon artists, etc.

I ask them to avoid YOGA that needs them to stand upside down.

I think neuroprotection can help in some situation

I am not a Ophthalmologist and I don't advise them to do anything. But I think lowering intraocular pressure is useful

Lowering the intraocular pressure to less than the target IOP , neuroprotection , and increasing the optic nerve vasculature is need

The most proven and broadly accepted therapy for glaucoma is to lower intraocular pressure. So called, pressure independent / neuroprotective therapies are exciting but there value remains somewhat controversial.

There are, however, helpful things that can be considered:

- searching for evidence of poor perfusion by measuring 24 hr BP. This is especially valuable in patients with NTG that are taking systemic BP medicines who are more likely to have nocturnal hypotension. Working with the physician to change BP medicines to eliminate hypotension / hypoperfusion may be useful. These concepts are supported by studies suggesting that treating HTN (and perhaps inducing hypotension / hypoperfusion) may be a risk factor for glaucoma (Mitchell et al, J Glaucoma, Open-angle glaucoma and systemic hypertension: the blue mountains eye study, 2004) - as described above by Dr Irkec.

- avoiding behaviors that might elevate IOP (i.e. head standing in Yoga and perhaps playing some musical instruments) As described above as well.

- the data for neuroprotective effects of brimonidine have long been debated and some of the data is quite weak. however, one recent study by Krupin et al., AJO, A randomized trial of brimonidine versus timolol in preserving visual function: results from the Low-Pressure Glaucoma Treatment Study (2011) suggests that brimonidine may have some pressure-independent effects in protecting from glaucoma damage.

- there is interest in studies of supplements such as gingko and curcumin. but the data are not overwhelming.

In low pressure glaucoma that are worsening despite therapy I tend to: search for diurnal IOP variation and low BP. If low BP is found, I work with the patients general physician to consider changing BP meds to maintain adequate perfusion pressure. In these patients I tend to avoid beta-blocker eye drops and I also tend to use brimonidine more often than I would in other patients.

There are exciting studies of the genetic causes of low pressure glaucoma (i.e. mutations in the OPTN or TBK1 genes) that have led to animal models of glaucoma that occurs without elevated IOP. New therapies may be identified in the future by studying these animals!!

Hope this is helpful.

John

For all the music friends

Graefes Arch Clin Exp Ophthalmol. 2011 Jun;249(6):895-901. doi: 10.1007/s00417-010-1600-x.

Intraocular pressure fluctuations in professional brass and woodwind musicians during common playing conditions.

http://www.ncbi.nlm.nih.gov/pubmed/21234587

For the sport friends

J Glaucoma. 2012 Aug;21(6):421-5. doi: 10.1097/IJG.0b013e31821826d0.

Walking for a short distance at a brisk pace reduces intraocular pressure by a clinically significant amount.

http://www.ncbi.nlm.nih.gov/pubmed/21499122

very nice Dicussion. i want to add one thing more, which is still missing. a study has been done in Pakistan in which it was proved that tight neck-tied are associated with glacomatous changes . in addition it is documented that mild to moderate exercise can lower the intraocular pressure

Yes!

Bob Ritch published a paper in BJO in 2003 about neckties as a potential cause of elevated IOP.

The answer to the question “Do you recommend anything besides lowering intraocular pressure for your glaucoma patients” is complex. Glaucoma is a misunderstood disease. Until we fully understand the disease we can’t cure it. Even the role of lowering of IOP is questionable especially in NTG, why to worry about adjuncts to lowering of IOP until we fully understand this disease. We can’t treat a disease unless we fully understand it. In glaucoma we don’t even know what actually is happening to the nerve fibers. Are the nerve fibers really being atrophied in glaucoma? All we hear is that nerve fibers are being damaged in glaucoma. But word damage is very broad. What kind of damage we are talking about? Are the nerve fibers being compressed, crushed, sliced, severed or anything else. With all the recent technology we even can’t answer with certainty above basic question of glaucoma.

Lowering of the IOP in glaucoma may be slowing the disease at its best but surely unable to halt it. Therefore, it appears we are following a wrong path in glaucoma. We are following a 150 –year old paradigm of cupping without even fully understanding the phenomenon of cupping or excavation occurring in the glaucomatous disc. Ironically, we are using the term cupping to describe both physiological as well as pathological cupping. It is unheard of using the same parameter in describing both the healthy and disease state of an organ in other branches of medicine as we do in glaucoma. No wonder why the term cupping and cup/disc ratio has produced a conundrum in the glaucoma diagnosis.

Glaucoma is defined as optic neuropathy implying that nerve fibers are being atrophied in glaucoma. Optic neuropathy is big umbrella term which includes hundreds of diseases in which optic atrophy is occurring. Is glaucoma also an optic neuropathy? We must not ignore the very important fact that glaucomatous field defects reveal that nerve fibers are always being destroyed in a specific sequence starting with peripheral fibers, then arcuate and ending with central. It is unlikely that raised IOP acting directly or via ischemia would always cause atrophy of nerve fibers in a specific pattern and not destroy the nerve fibers haphazardly. If we believe that RGC’s are the primary site of injury in glaucoma then this scenario becomes even more puzzling. How is it possible that raised IOP or in fact any pathology directly or indirectly will always destroy systematically those RGC”s first which serve the peripheral vision and not occur randomly? I have been puzzled by aforementioned question in my entire professional career spanning over 50 years. But now I may have answer to this puzzling question at least to my satisfaction.

I learned very interesting things by comparing the morphology and histology of the glaucomatous disc with the non-glaucomatous optic atrophy such as due to multiple sclerosis. Morphology and histology of the glaucomatous and non-glaucomatous optic atrophy are distinctively different. Glaucomatous disc is excavated whereas the non-glaucomatous atrophic disc is non-excavated and flat. Blood vessels are sloping/ kinking at the disc margin in glaucomatous disc but not in the non-glaucomatous optic atrohies. Wedge shaped defects in the retina are present in glaucoma but not in non-glaucomatous optic atrophies. Histology of end-stage glaucomatous disc resembles an empty bean-pot devoid of nerve fibers, whereas in non-glaucomatous optic atrophies the nerve fibers though shrunken are still present.

Sloping/kinking of blood vessels at disc margin in the glaucomatous disc, prior to any change in contour of physiological cup, suggests that optic disc may be sinking in glaucoma. Excavation or empty spaces occurring in the glaucomatous disc can only be explained due to severance of the nerve fibers, not due to their atrophy. End-stage glaucomatous disc may not be 100% cupped atrophic disc but a crater left over after severance of all nerve fibers. Wedge shaped defects in the retina and arcuate field defects in glaucoma can only be explained by severance of the arcuate fibers, not by their atrophy. Progressive thinning of the RNFL can only be explained by continuous severing of the nerve fibers in the glaucomatous disc and it is not occurring in non-glaucomatous optic atrophies. In view of aforementioned I hypothesize that nerve fibers are being severed in glaucoma due to sinking disc. If true, then glaucoma is in fact a herniation of the disc in the scleral canal, a mechanical failure. In this regard the lowering of IOP may be too late. Lowering of IOP may serve as a prophylactic treatment but not an ultimate treatment if disc has started sinking and glaucoma has been initiated. We may have to find ways to stop the further sinking of the disc. Analogy: statins would prevent the build up of plaques but if the plaques have already formed then cardiologists would either break the plaques or bypass them by surgery. Thank you.

A very good review of nutritional supplements

Surv Ophthalmol. 2008 Sep-Oct;53(5):479-505. doi:

The potential value of natural antioxidative treatment in glaucoma.

http://www.ncbi.nlm.nih.gov/pubmed/18929760

and about ginko

Mol Vis. 2012;18:390-402. Epub 2012 Feb 9.

Ginkgo biloba: an adjuvant therapy for progressive normal and high tension glaucoma.

http://www.ncbi.nlm.nih.gov/pubmed/22355250

in my experience may help multivitamin complexes including lipoic acid and unsaturated fatty acid that usually I include as supporting therapy in late stage of glaucomatous optic atrophy. in some stadies I add also citicolin in high doses to obtain a neuroprotective effect

Main problem is not only to lower IOP but increase optic nerve blood flow.

Adequate blood pressure control and monitoring is an important issue to minimize optic nerve damage, in glaucoma.

Gareth Pryce Can you please post the reference. I am curious to look into the details.

Low vision rehabilitation to help patients cope with functional seeing deficits! While ther have been tremendous advancements in the diagnosis and treatment of glaucoma-related vision loss, some vision loss is inevitable. Before patting yourself on the back concerning the vision that your intervention has saved, you must acknowledge and deal with any vision that was lost. Acting as if such changes are inconsequential and therefore unworthy of your clinical attention is shallow and unrealistic. If low vision care is outside your legitimate professional capability and/or interest, refer your patient to a colleague who takes rehabilitation more seriously. This is in your patient's best interest.

Low vision care is precisely what the attached document is all about.

It is a simple research idea that would be extremely low cost. However, the benefits for patients with tunnel vision may well be impressive.

The document is quite short, however, there are a number of diagrams inserted for clarity.

The approach has attracted the interest of an eye surgeon - Camilo Tobon - who runs a clinic in Columbia. He is willing to provide patients for a study and to conduct the research. I think he wants me to provide funding for the study.

I have absolutely no skills when it comes to clinical studies and, in addition, I am not associated with a research institution. - This is a problem.

Will somebody please take a look at the attached proposal and either, give me some advice as to how to proceed, or else explain to me why the idea will not work.

Thanks Guys.

one potential adjunct beside IOP lowering in glaucoma may be the (oral) supplemantation with IDEBENONE. This Q10 derivate has shown in a study, where Primary human ONHA were investigate, significant cytoprotective effects regarding Ox stress in the context of glaucoma!

further effect of CoQ10 is that inhibits production of ET-1 vasoactive peptide involved in modify th ONH circulation in glaucoma patients.

moreover in very advanced cases I suggest the use of rehabilitation. rehabilitative strategies with biofeedback may lead to a better use of fixation reducing the disabilities and increasing visual performances and quality of vision

Whatever you are saying may work as a prophylactic like use of statins to prevent the build up of plaques. But if glaucoma has already started and the disc has started sinking (herniating in the scleral canal) , then it becomes a mechanical problem and we may have to find ways to re-anchor the sinking disc. Analogy: cardiologist would not keep on giving statins if plaques have already build up and interfering with circulation. They would do angioplasty or bypass surgery. I think same should apply to glaucoma.

I agree entirely that besides lowering IOP we need to prescribe neuroprotective agents- calcium channel blocker or nicergoline in tabs

I advocate a healthy lifestyle with plenty of aerobic exercise, control of BP - especially nocturnal dippers, Gingko Biloba and or Co Q10 as neuroprotective agents, counselling on the proper use of their medication and the fact that this is a chronic sight threatening disease which should not be taken lightly. Healthy diet including fresh green leafed vegetables or supplements if the diet is poor, including ascorbic acid. Stop smoking and avoid secondary smoke. I am not sure what to make of Patrick Holford's homocystiene levels and its control or if it is beneficial in glaucoma practice? (Folate as well as Vitamin B6 & B12 apparently modulate homocystein levels)

Dr. Davia, you would want the patient to use a negative lens to decrease the size of the image into the retina, so most of the central visual field would be compressed into the remaining functioning retina, but the rest of the visual field, the more peripheral visual field, would also be "compressed", and distorted and might induce rays from spherical aberration to enter the central field, thus worsening the visual perception.

The thing is that using a negative lens would also make the patient hyperopic, so their near vision would suffer, and thing will look smaller, so yes, they would have trouble adapting to distance calculations. I am not sure I would like to try that, but maybe an empirical observation of patients that have become myopic after cataract surgery could be done, comparing visual fields just when they were operated and after a few months...

In low vision patients reducing image size may cause reduction in resolution power so that most of patients do not prefer to use negative power lens even in my experience patients with visual field los may benefit from double prism with juncted base. Either vertical or horizontal

In glaucoma patients with advanced disease, I recommend them to, if they have high (or in the upper normal limits) levels of blood cholesterol, suggest their general practitioner to prescribe simvastatin (if there is no contraindication). There is published evidence supporting its effect decreasing the rate of glaucomatous damage progression. To the best of my knowledge, it s the only "neuroprotective" drug with some clinical results published in good scientific journals. Although we do not have an evidence level A about it, at least it is the only drug (with no ocular hypotensive effect) with some evidence strongly sugestting it may work.

1- Simvastatin and Disease Stabilization in Normal Tension Glaucoma: A Cohort Study

Dexter Y. L. Leung, FRCS, DRCOphth, Felix C. H. Li, MRCS, Yolanda Y. Y. Kwong, MRCS, Clement C. Y. Tham, MA, FRCS, Stanley C. C. Chi, FRCS, Dennis S. C. Lam, MD, FRCOphth

Ophthalmology 2010;117:471–476

2- The Relationship Between Statin Use and Open-Angle Glaucoma

Joshua D. Stein, MD, MS,1 Paula Anne Newman-Casey, MD,1 Nidhi Talwar, MA,1 Bin Nan, PhD,2 Julia E. Richards, PhD,1,3 David C. Musch, PhD, MPH1,3

Ophthalmology 2012;119:2074–2081

Interesting points raised by Syed. The rational behing the theory of optic nerve herniation that you are suggesting remains the pressure balance between compatiments. Hernation will develop from high presure compatment to low pressure ones, unless you think about intussusception. If your theory stands, do you think that the lamina cribrosa is weaker in glaucoma patients than non glaucoma. In that case, IOP reduction and any means by which lamina cribrosa could be reinforced would be the cure. Wish things could be that simple....

Dear Oscar,

I am very pleased that you took the trouble to read the paper.

i will contemplate your concerns about the suggested procedure.

I am not a Dr, by the way.

Chris

Dear Paul,

If I have to describe my hypothesis in one sentence then it would be “ that the optic disc/ Lamina Cribrosa (LC) is detaching and sinking in the scleral canal- a mechanical failure. As a result the prelaminar nerve fibers prior to their entry into LC along with its vasculature are being severed. Lamina cribrosa is not the site of injury.

Excavation (empty spaces), whitish pallor, sloping/kinking of blood vessels, splinter hemorrhages, progressive thinning of the RNFL, and finally histology of end-stage glaucoma disc(ESGD) revealing an empty crater all point in the direction that the nerve fibers are being severed in glaucoma. Researchers may approve or reject my hypothesis. Severing of the nerve fibers have answered all my unanswered question in glaucoma and I am certain it would answer my colleague’s questions as well.

https://www.facebook.com/pages/Glaucoma-Paradigm-Shift-Project/516804278413418

Besides using antiglaucoma medications that decrease IOP, we can do something to prevent systemic hypotension that puts the Optic Nerve at risk. Nocturnal systemic hypotension has been mentioned as one of the risk factors for glaucomatous damage. Also, if we are somehow able to increase Optic Nerve Head perfusion, then we can prevent some damage. Also alcohol helps decrease IOP, as based on this fact, when a patient presents with higher levels of IOP and there is no such medication, then the person is asked to drink alcohol, or force-fed alcohol.

I do recommend my patients to control co-morbid conditions like DM and hypertension aggressively. Moreover I do advise them to take a nutritional supplement which has magnesium and vitamin E in recommended doses. we have recently published extensively the role of magnesium in cataractogenesis and retinal ganglion cell apoptosis. Based on the literature review and our studies I have started advocating these supplements.However we do not have enough clinical data to support the routine use of these supplements. In future we are planning to conduct clinical studies on the effect of magnesium supplementation on glaucomatous neuropathy.

I would be careful in aggressively lowering hypertension. It is well documented that hypotension is implicated in glaucoma. If hypotension is the cause of glaucoma then hypertension should be protective for glaucoma as it may provide more perfusion to the disc. Moreover, we can't start giving supplements without knowing why we are doing so. We have to first agree on what is occurring to the individual nerve fibers in glaucoma then we should worry about finding treatment. All the evidence, like notching in the disc, wedge shaped empty spaces in retina and sharply defined arcuate fields defects, is pointing that the nerve fibers are being severed, not atrophied. Ganglion cells may be dying secondary to severance of nerve fibers,, not primarily due to apoptosis. Glaucoma may not be an optic disc neuropathy but an optic disc axotomy.

I fully agree with you on the issue of lowering blood pressure aggressively. However there is enough scientific evidence that in primary glaucomas ganglion cell apoptosis is the major mechanism of nerve fiber loss.If you can share any research that the severence of axons is the primary mechanism please share it.

Dear Puneet, would like to mention the most crucial aspect of glaucoma which is often ignored: that the nerve fibers or their RGCs are being destroyed in an orderly fashion starting from the peripheral fibers and ending with the central and never being destroyed randomly as in neurodegenerative diseases.

If glaucoma happens to be due to apoptosis or in other words due to programmed suicide of the RGCs, then our RGCs would have to fulfill two requirements. First, the RGCs would have to predict impending glaucoma so that they would have time to program themselves to start committing suicide in an orderly and tandem fashion starting with those serving the peripheral vision and ending with the central RGCs. I don’t believe our RGCs are smart enough to commit suicide in an orderly tandem fashion. If the nerve fibers are being destroyed in an orderly fashion in glaucoma, then we should expect the mechanism for their destruction to be an orderly one too—which can’t occur in a neurodegenerative disease. The apoptosis always occurs randomly. On this basis alone, I can't convince myself that the apoptosis of RGCs is occurring in glaucoma.

Regarding my hypothesis that severance of nerve fibers, not atrophy occurring in glaucoma we have ample proof but we have to look differently (gestalt switch). Sloping/kinking of blood vessels at disc margin in the glaucomatous disc, prior to any change in contour of physiological cup, suggests that the optic disc may be sinking in glaucoma. Excavation or empty spaces occurring in the glaucomatous disc can only be explained due to severance of the nerve fibers, not due to their atrophy. Wedge shaped defects in the retina in glaucoma can only be explained by severance and thus disappearance of the arcuate fibers, not due to their atrophy.

The occurrence of notching in the superior and inferior part of the physiological cup may be due to severance and depletion of the arcuate fibers at the point of their entrance in the disc. Splinter hemorrhages at the disc margin, characteristic whitish pallor and absence of smaller vessels around the glaucomatous disc may be due to severance of smaller blood vessels, a fate similar to that of nerve fibers. Nasal shifting of the central vessels appears to be due to loss of anchorage due to severance of temporal fibers. The end-stage glaucomatous disc (ESGD) is totally devoid of nerve fibers, vasculature, and even the LC (cupped or otherwise) which has received much blame for glaucoma. Where did all these structures disappear which were once beautifully arranged in the normal disc? The total disappearance of all these structures can only be explained by their severance, not atrophy. For the severance causing orderly destruction of nerve fibers you may like to read my articles on this forum or internet. . Severance of nerve fibers have been confirmed by an article with following link. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3792954/

Many thanks for your interest in my hypothesis.

We have written a review article regarding the pathophysiology in Glaucoma. This article has been cited many times .Current concepts in the pathophysiology of glaucoma. Indian J Ophthalmol. 2009 Jul-Aug; 57(4): 257–266.

doi: 10.4103/0301-4738.53049

PMCID: PMC2712693

Very interesting what contributed by Syed Hasnain. then denaturation vitreous humor would be interesting to study

Dear Syed ,I read your hypothesis of optic nerve severence as the probable cause of glaucomatous optic neuropathy. However your discussion of progression of field defects in glaucoma is fallacious. I am pasting the paragraph from Becker and Schaffers Glaucoma textbook to refute your assertion that peripheral nerve fibres are the first affected in Glaucoma.

In the human eye the distribution of the nerve fibers from the

peripheral retina toward the optic nerve is such that axons from

peripheral ganglion cells are progressively overlayered by axons

derived from cell bodies closer to the optic nerve (Fig. 12–2).5

These peripheral fibers remain peripheral as they enter the disc; central fibers enter centrally, adjacent to the physiologic cup. This

topographic arrangement correlates with the clinical progression

of the glaucomatous visual field: paracentral scotomas appear early

in the disease as the cup enlarges, and the peripheral field remains

until the peripheral axons in the nerve are affected.6. ( Chapter 12 page 143)

Would you reconsider your hypothesis based on the anatomical and clinical data which is well documented.

Dear Puneet,

Thank you for introducing me following paragraph from Beckers & schaffer’s “ In the human eye the distribution of the nerve fibers from theperipheral retina toward the optic nerve is such that axons from peripheral ganglion cells are progressively overlayered by axons derived from cell bodies closer to the optic nerve (Fig. 12–2).5

As I understand the statement in above paragraph implies, that the fibers originating closest to the disc lie most superficial (closest to the vitreous) and exit from the central most part of the disc. Let us now discuss ‘cupping’ in view of aforementioned arrangement of nerve fibers.

The term cupping implies that the physiological cup start enlarging concentrically in glaucoma. If this is true then the central most fibers (originating closest to the disc) should be destroyed first and the peripheral fibers originating farthest from the disc and lying deepest (closest to sclera) at the end.

In the cupping scenario, the visual fields should reveal gradual concentric enlargement of the blind spot all the way to the peripheral limits of fields, engulfing the macular fibers in the very early stages of glaucoma. Thus, glaucoma subjects would have become totally blind much sooner due to total loss of macular fibers, but in actuality the central vision is preserved until the end-stage contradicting the concept of cupping in glaucoma.

The nutshell of my hypothesis: the nerve fibers (along with vasculature) are being severed, not atrophied in glaucoma. Analogy: Leg is amputated, not atrophied. I would welcome if you can prove the severance of nerve fibers wrong so I would abandon my hypothesis.