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normal tension glaucoma — anyone out there?

Question:

Dr. Wright writes" "… think of the strength or weakness of the optic nerve and its supporting structures. A very strong nerve will be able to withstand high pressures, an average nerve will withstand normal pressures but be damaged by higher than average pressures and a weak nerve may sustain damage at pressures within the ‘normal range." and "Treatment of all glaucoma, regardless of type, is aimed at reducing the intraocular pressure to a level at which further damage if not sustained by the optic nerve." It seems to me that we haven’t gotten to the root of the matter.  In speaking about optic nerves that are more sensitive to lower IOPs, what made them more sensitive?  Often they were strong and then became weak.  What made them weak? If we knew perhaps we could stop them from weakening without reducing the IOP to subnormal levels. I believe that it is possible that there are people suffering eye damage labelled as "glaucoma damage" without IOP being part of the cause.  The cause was some eye blood circulation problem, disease, or something, but not IOP. I also wonder why the IOP is at whatever level it is.  The body sets the IOP pressure value.  What factors cause it to set it to a particular value? Perhaps there are times when the body sets a higher IOP pressure value for a good reason.  For example, a higher IOP could be useful in compensating for higher blood pressure that might burst the tiny blood vessels in the eye. Asking the right questions is more important than providing the right answers. Steve, (not an eye professional)

Response:

Katie wrote: >I was diagnosed with it in December 99, I am seeing one of the nation’s >best docs, , but I’d like to know if there’s anyone else out there with >NTG and what their profile and diagnosis  is, etc.. >Long story short, I don’t fit 95% the glaucoma profiles I’ve read about. >But NTG is different. >My "normal" eye  pressure is between 16-18.  I’m 47, below average >weight, no diabetes, no cardio problems and borderline high blood >pressure, and no history of any of the above. >Im on Xalatan, so far so good I guess. >Anyone?<

Although I do not have NTG, I have been interested in the topic–and in the variation in pressure readings from one individual to another. In one study, 31% of patients diagnosed with NTG did not in fact have the condition, but had Primary Open Angle Glaucoma. The misdiagnosis occurred because these patients had thinner than normal corneas, causing the pressure testing device to falsely indicate lower tension by as much as 9 mm. (See Archives of Ophthalmology, January 1999.) Therefore, a pressure of 18 could in fact be 27–high enough in some individuals to result in damage to the optic nerve. Add to this the normal variation in pressure throughout the day (diurnal) of up to 20 mm, and a person showing pressure of 18 with thin corneas "could" (under extreme conditions) have peaks of 47, certainly a high risk level. (I, by the way, have been caught with a pressure of 47, although no damage resulted.) Katie didn’t provide details of her diagnosis as to vision loss, cup-to-disk ratio, etc., which might suggest an underlying condition other than glaucoma. (Not a professional response)

Response:

Picking up on one section of Steve’s thought-provoking post: >It seems to me that we haven’t gotten to the root of the matter.  In speaking >about optic nerves that are more sensitive to lower IOPs, what made them more >sensitive?  Often they were strong and then became weak.  What made them >weak? >If we knew perhaps we could stop them from weakening without reducing the IOP >to subnormal levels.<

This may get into the newly popular area of neuroprotection, and my interest in the role of vitamin B-12 in health of the nervous system. My interest in this began with a relative who had the disease Shingles, which involves various nerves. At the time, one of the only treatments was B-12 injections due to its ability to rejuvenate nervous tissue. Another relative had pernicious anemia, which is a fatal degeneration of the nervous system which comes about by inability of the body to absorb B-12, and is also successfully treated by B-12 injection. I then noticed my often mentioned five -year study by Sakai in Glaucoma 1992:14:167-170 in which visual fields were stabilized or actually IMPROVED after usage of 1500 MICROgrams of B-12 daily. I have run across other mentions of B-12 and retinal/optic nerve associations. So perhaps this partially addresses Steve’s concerns in the above quote–"getting to the root of the matter", "what made (optic nerves) more sensitive," "what made them weak," etc. It would seem to me that it is very important for a person to know his/her B-12 nutritional status. This can be found through blood test B-12 assays, which may be expensive and which insurers may resist authorizing. There is, however, a backdoor way of getting to this information. Simply check your own records of laboratory tests for Hgb (hemoglobin), MCV, MCH, MCHC and look for low, or even low normal hgb, or high or high normals in the other three. If these conditions exist, you MAY have insufficient B-12 in your system due either to dietary insufficiency (a frequent finding among vegetarians) or an absorption problem (due to lack of the "intrinsic factor" in digestive secretions). I have tried to encourage the commissioning of a study of the relationship of B-12 levels to glaucoma and optic nerve/retina condition but have not been successful as yet. Even without a formal study, I am personally convinced that maintaining adequate B-12 is essential wherever there is any question about visual health. Note that B-12 supplements are  very difficult to absorb by mouth. An alternative is sublingually (under the tongue), or the preferred way, injection. HOWEVER, A COMPETENT PHYSICIAN SHOULD BE CONSULTED BEFORE ASSUMING THAT B-12 WOULD BE HELPFUL OR APPROPRIATE AS UNDER SOME CIRCUMSTANCES THERE COULD BE SERIOUS ADVERSE EFFECTS. One other thought that relates to the quoted section of Steve’s post–I have long suspected that "cholesterol deposits" could also occur in the vessels nourishing the eyes, affecting blood and fluid flow. This may be another factor to consider. (Not a professional response)

Response:

Thanks Steve for pointing our more clearly exactly what I was trying to say. You are completely correct in your point that we "haven’t gotten to the root of the matter" at present we simply don’t know, there are a lot of theories, but nothing has been established beyond doubt and there is increasing evidence that ocular blood flow may be part of the answer, as probably are many other factors some of which we are most likely unaware of even as possibilities. A tremendous amount of research is being carried out all over the world to establish the whole pathogenesis of glaucoma but it takes time and, for example, it is only recently that we have had the necessary instruments to begin to investigate ocular blood flow in the living eye. We at the IGA have recently instigated a programme whereby glaucoma patients can donate their eyes for research after their death, with the researchers having full access to their medical history visual field and IOP records. Because of logistical problems this scheme is limited to the London area at present, but we hope eventually to be able to provide the service across a much wider area. Steve also mentions that "it is possible that there are people suffering eye damage labelled as "glaucoma damage" without IOP being part of the cause". Perhaps there is a misunderstanding here, IOP is certainly the major modifiable factor in the treatment of glaucoma, but raised IOP is not part of the definition of glaucoma, despite the fact that the majority of glaucomas are associated with a raised pressure. One workable definition may be that the glaucomas are a group of conditions which exhibit a characteristic pattern of progressive visual field loss which may or may not be associated with a raised intraocular pressure. The characteristic nature of the loss refers to the scotoma which is commonly seen in glaucoma patients and progression is also important in order to differentiate glaucoma from some other forms of optic atrophy. The level of IOP varies throughout the day as part of a natural cycle which is partly why some people are misdiagnosed as having normal tension glaucoma when in fact they have the more common primary open angle glaucoma. The level of the IOP is determined by the balance of production of aqueous fluid and its drainage. The exact reason why some people experience a rise in the level of IOP to a pressure at which damage occurs to the optic nerve is not fully understood in all forms of glaucoma but it is generally considered to be a reduction in the efficiency of the drainage mechanism over time. This partly explains why glaucoma prevalence rises with age. Hope this helps. Incidentally, I am not a doctor, nor am I medically qualified in any other way. I have been trained to answer glaucoma questions over the last 18 years or so, but I would not wish anyone to be under the wrong impression. (MSAE is an association management qualification) — David Wright MSAE Chief Executive, International Glaucoma Association IGA Web Site – http://www.iga.org.uk/home.htm While we are pleased to offer the above information, it is not possible for the International Glaucoma Association to advise on an individual patient’s eye condition or treatment as this has to be the role of their own doctor or eye specialist who knows the full details of their particular case. Any comments above should therefore viewed as general observations. ———- In article <20000217001827.01140.00001…@ng-cb1.aol.com>, electr…@aol.com – Hide quoted text — Show quoted text -(ELECTRPOW) wrote: > Dr. Wright writes" > "… think of the strength or weakness of the optic nerve and its supporting > structures. A very strong nerve will be able to withstand high pressures, an > average nerve will withstand normal pressures but be damaged by higher than > average pressures and a weak nerve may sustain damage at pressures within > the ‘normal range." and "Treatment of all glaucoma, regardless of type, is > aimed at reducing the intraocular pressure to a level at which further damage > if not sustained by the optic nerve." > It seems to me that we haven’t gotten to the root of the matter.  In speaking > about optic nerves that are more sensitive to lower IOPs, what made them more > sensitive?  Often they were strong and then became weak.  What made them weak? > If we knew perhaps we could stop them from weakening without reducing the IOP > to subnormal levels. > I believe that it is possible that there are people suffering eye damage > labelled as "glaucoma damage" without IOP being part of the cause.  The cause > was some eye blood circulation problem, disease, or something, but not IOP. > I also wonder why the IOP is at whatever level it is.  The body sets the IOP > pressure value.  What factors cause it to set it to a particular value? > Perhaps there are times when the body sets a higher IOP pressure value for a > good reason.  For example, a higher IOP could be useful in compensating for > higher blood pressure that might burst the tiny blood vessels in the eye. > Asking the right questions is more important than providing the right answers. > Steve, > (not an eye professional)

Response:

Normal tension glaucoma is not uncommon although in a significant number of cases, when phasing is carried out (repeated pressure tests over a period of time) it is found that there are peeks of pressure at higher levels). In essence normal tension glaucoma is a form of primary open angle glaucoma and forms part of the continuum between ocular hypertension (high pressure with no optic nerve damage) through primary open angle glaucoma (high pressure with optic nerve damage) to normal tension glaucoma (low pressure with optic nerve damage). The easiest way to understand these differences is to think of the strength or weakness of the optic nerve and its supporting structures. A very strong nerve will be able to withstand high pressures, an average nerve will withstand normal pressures but be damaged by higher than average pressures and a weak nerve may sustain damage at pressures within the ‘normal range. That is not of course the whole story and there may be other factors to do with circulation or structure which affect the optic nerve, but it works in terms of the rational for treatment. Treatment of all glaucoma, regardless of type, is aimed at reducing the intraocular pressure to a level at which further damage if not sustained by the optic nerve. This applies to normal tension glaucoma as much as to any other form, although it can sometimes be more difficult to achieve the necessary pressure reduction with medical therapy than with other higher pressure forms of glaucoma. There is of course a limit as to how low the pressure can be taken, but it is generally agreed that the significant factor is the percentage pressure reduction rather than the raw number of mm Hg the pressure is reduced. Therefore for a person with normal tension glaucoma, a pressure reduction of 4 mm Hg may be highly significant whereas for a high pressure glaucoma case it may be much less beneficial. Nevertheless, if one accepts the notion of a relatively weak nerve, then good compliance with the treatment regime prescribed is relatively much more important because a small pressure rise due to a missed or late drop, may result in greater damage than would be the case for higher pressure glaucoma. It is also worth discussing the possibility of using other agents to improve perfusion at the optic nerve head with the ophthalmologist. Many now consider the use of low dose aspirin a worthwhile treatment. Its effect on the optic nerve has not been sufficiently investigated to be confirmed as a beneficial treatment, but logic in terms of its known effects elsewhere in the body make its use in those patients who can tolerate it without undue side effects considered worthwhile in some cases. Every case of glaucoma is different and every optic nerve can withstand different levels of pressure, but provided the condition is detected early in its progression, the prospects for the long term retention of useful sight are generally considered good. — David Wright MSAE Chief Executive, International Glaucoma Association IGA Web Site – http://www.iga.org.uk/home.htm While we are pleased to offer the above information, it is not possible for the International Glaucoma Association to advise on an individual patient’s eye condition or treatment as this has to be the role of their own doctor or eye specialist who knows the full details of their particular case. Any comments above should therefore viewed as general observations. ———- In article <38A9F5B7.C6DED…@execnet.com>, Katie McAleenan – Hide quoted text — Show quoted text -<k…@execnet.com> wrote: > Does anyone out there have normal tension glaucoma (NTG)??? > I was diagnosed with it in December 99, I am seeing one of the nation’s > best docs, , but I’d like to know if there’s anyone else out there with > NTG and what their profile and diagnosis  is, etc.. > Long story short, I don’t fit 95% the glaucoma profiles I’ve read about. > But NTG is different. > My "normal" eye  pressure is between 16-18.  I’m 47, below average > weight, no diabetes, no cardio problems and borderline high blood > pressure, and no history of any of the above. > Im on Xalatan, so far so good I guess. > Anyone?

Response:

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