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GLAUCOMA AND INTRAMEDICAL PRESSURE
Nearly 150 Years of Deception in the Interest of Medical Greed 1993
Index:
History, definition, methodology and socio-economics
The recent literature from clinical and epidemiological studies
My personal experience with glaucoma treatment:
History, definition, methodology and socio-economics
A couple of decades ago, there were some movements by lay persons, in the United States, which challenged some of the self- centered, ineffective, overexpensive and unhealthful practices and methodology of organized American medicine. Today, our populace seems only bent upon finding some beneficent source to pay for the incredible cost of all this deviant medical elitism. Neither quality nor cost-containment of health care will be achieved until the public and the federal government hack into the over- moneyed, sacerdotal jungle of pseudoscience which is American medicine today. To be fairly stated, an account of the present situation should admit that not all of the impetus in this racket is attributable to conscious greed, but comes about as a result of an ingrown medical culture of believers who have taken great pains to avoid direct real-world feedback on their work product, as expressed in terms of common sense and non-profession- contaminated science. The definition, diagnosis and treatment of those deficits/ailments which are grouped under the term 'glaucoma' in this country and in many others today provide probably the best examples of what the public is presently sucking on from the profession which has claimed the domain of human-body repair and standardization. Today, whether it should come from a health-care practitioner or a layperson, almost always any mention of the term 'glaucoma' is followed by reference to raised intraocular pressure- with at least the implication that most of what is called 'glaucoma', and consists of certain reported patterned gaps or distortions of sightfulness in the visual field of one or both of the complainer's eyes, correlating to atrophy of some of the final- stage, retina-attached neurons of the optic nerve trunk(s) of the affected eye(s), particularly as observed at the rim(s) of the so-called optical disk(s) where this trunk feeds through the rear of the eyeball(s), results from the action of whatever pressure of the aqueous humor should be found within the affected eyeball(s)-- even when this pressure sits only slightly above what it was before any damage to the nerves, or even sits at the very same value it had before the damage! Some persons also still include, under the term 'glaucoma', conditions where this pressure is raised to some degree above normal but where there is no detectable subjective visual deficit or objective physiological damage--conditions otherwise known as ocular hypertension). This word game then leads into dictating that, where there is damage but no pressure rise, the normal pressure must be lowered to prevent further damage to the affected tissues, a move which seldom has measurable success. Almost never is the prime cause of the damage assigned to a defect in the affected tissues. Why so unscientific an analysis, and one which flies in the face of common sense? Lay it to history, indolence and greed. Feedback in medicine is minimal: lack of successful results from a treatment has little deterrent effect where no phenomenal success is apparent by other means. If one wants to analyze the physical world for the purpose of predictably synthesizing something within it (create an operational model)--in health care, to modify to species standard, to repair, or to limit further degeneration--one must perceive and conceive entities based on their functional relevance to the physical world. If health care is to relieve suffering--or prevent the onset of same through scientific detection of specific preceding indicative signs or symptoms--and we're to initiate a legitimate business transaction where the customer (sufferer or sufferer-to-be), dubbed 'patient', or his/her third party, pays a fee to obtain relief or prevention of the suffering he/she defines at the first level of analysis--we ought to, in the case of glaucoma, pretty much restrict our analysis to a complaint of vision loss, or to scientific prediction thereof, over all or part of the visual field (as reported either in respect to function or from subfunctional testing) and to the correlate characteristic defects in the optic nerve head(s) (as visually instrumentally detected). No causal step should be seen in this simple, subjective/objective dual definition of glaucoma, devoid of reference to any causation assignable to pressure or anything else. This definition of glaucoma has become fairly common, but numerous practitioners tend to hang onto contorted definitions of glaucoma which retain the not-necessarily etiological factor of raised intraocular pressure (IOP)--in order to save their holy mental spaces, cultural/historical disease-variety dichotomies and treatment methodologies, if not their whole ineffective or destructiveclinical practices. Much of the history and rationale for the distorted etiology, terminology and even ontology of gaucomatous eye damage is outlined in Sommer 1989 and Van Buskirk 1992 [see References below]. A good deal of what is basically a nearly cause/effect reversal, in regard to IOP and tissue damage, seems to have stemmed merely from the facts that 1) fairly accurate and convenient tonometry appeared before the ophthalmoscope and 2) it is easier to measure IOP than to properly examine a nerve head with a scope or to get an accurate subjective report of a subject's loss of vision. Such a Scylla and Charybdis is stereotypical of the guiding lights that medical "experts" have time and again relied upon to keep their ineffective and expensive ships afloat. The technique equates to: regardless of having lost your watch in a dark alley, always look for it only within the convenient cone of light from an arterial street lamp (particularly if you can get someone to pay you for your time).
The recent literature from clinical and epidemiological studies
Alfred Sommer, a well-known researcher, in his 1989 editorial in the American Journal of Ophthalmology makes the following observations:
1) Increased IOP and glaucomatous nerve damage have been "inexorably. ..generally assumed to [stand in] a [respective] cause-and-effect relationship."
2) ". . .we have. . .invented terminology and sought alternative explanations for seeming inconsistencies: 'low tension' glaucoma for glaucomatous optic nerve damage in the absence of increased intraocular pressure and 'ocular hypertension' for increased intraocular pressure in the absence of glaucomatous nerve damage."
3)". . .A THIRD OR MORE 'GLAUCOMA' PATIENTS HAVE 'NORMAL' INTRAOCULAR PRESSURE."
4) good epidemiology "suggests our present confusion may stem from preconceived notions that obscure basic unifying principles."
5) the bulk of the population has 'lower' IOP, and therefore "a large proportion of" those having "glaucomatous damage" have 'lower' IOP; i.e., THERE IS NO CORRELATION OF SUCH DAMAGE TO RAISED IOP. This researcher then tends to cop out some in his last paragraph, apparently fearing that even the ivy-covered walls of Johns Hopkins University may not prevent his body from later being found in Chesapeake Bay.
E. Michael Van Buskirk, in the same journal in 1992, states:
1) "Because intraocular pressure is easy to assess and the optic nerve is not, glaucoma has been characterized as a disorder of aqueous humor dynamics."
2) Jaeger, in 1858--only 28 years after MacKenzie first measured intraocular pressure in 1830, and only 8 years after von Helmholtz introduced the ophthalmoscope--viewed glaucoma as an intrinsic optic neuropathy.
3) ". ..STUDIES REPORT THAT AS MANY AS HALF OF PATIENTS WITH GLAUCOMATOUS OPTIC NEUROPATHY HAVE NORMAL INTRAOCULAR PRESSURES WHEN A DIAGNOSIS IS FIRST MADE."
4) ". . .almost all modern methods of treatment are designed to reduce intraocular pressure only. Further, the pressure-dependent hypothesis forms the basis of nearly all glaucoma research."
5) "We tend to explain our observations in terms of intraocular pressure because of our historical perspective."
6) "The average intraocular pressure of blacks and whites are about the same, yet the prevalence of glaucomatous optic neuropathy damage [(GOND)] is four to five times higher in blacks."
7) while more high-IOP persons than low-IOP ones develop GOND, so do more blacks than whiles having the same IOP. Now, we don't claim dark skin or other common negroid characteristics are causes of GOND. The crux here is the difference between a cause and a risk factor. A risk factor is only anywhere from a first to a far-removed cousin to a cause i.e., anywhere from an immediate result of an immediate common cause out to a distant result of a distant common cause. A recognized negroid attribute only flags some other obscure negroid physical attribute preferentially conducive to GOND relative to the correlate caucasoid physical attribute. IOP, however, is actually a less rationally chosen flag than whatever are the appropriate negroid attributes, because it may actually be, in some cases, at least, purely a result of GOND itself, though it may be better considered, in most cases, as a result of a cause common to both it and GOND.
In Sommer and Quigley 1991, it is stated: "The continuous nature of the IOP-glaucoma relationship suggests little basis for distinguishing between so-called high- and low-tension glaucoma, least of all by IOP criteria alone. Tonometry by itself, is neither an effective nor an efficient screening tool."
Krakau 1981 states:
1) "Clearly, to select glaucoma cases on the criterion hypertension and then conclude that glaucoma is characterized by a high IOP is tautology."
2) "We note that in population studies there are about as many cases with a low (</=20 mmHg) as with a high IOP among the glaucoma cases, which seems to be in disagreement with the definition [at the time] of glaucoma."
3) "This ad hoc hypothesis [setting pressure norms specific to particular eyes, thus creating 'low-tension glaucoma (LTG)' and 'ocular hypertension (OHT)'] saves the pressure theory, which, however, is no longer open to falsification by population surveys."
4) As to a "glaucoma case with a controlled IOP": "Now the situation has become paradoxical: when functional defects can be detected, therapy may not stop progression, and as long as no such changes can be detected the diagnosis glaucoma cannot be established. The pressure theory obviously becomes 'immune to falsification',. . ."
5) "In the follow-up studies of glaucoma cases quoted [in Krakau 1981--i.e., Dalby study, etc.]. . .--IT HAS SO FAR NOT BEEN POSSIBLE TO FIND SUPPORT FOR THE THEORY THAT THE IOP IS A CAUSE AND NOT ONLY A SYMPTOM,"
6) "It may seem heresy to recall the opposite possibility: That the pressure reduction may be harmful and a slight hypertension favourable, a possibility which has by no means been refuted."
I'd be surprised if this daredevil author hasn't been gunned down by now and his brain shredded. This paper's claim that later population studies invalidated the Leydhecker 1959 report on a population study brought about a hilarious, logically defective rebuttal in the form of Leydhecker 1983.
In a discussion of this paper, Bengtsson states: 1) It can be concluded that there are twice as many LTG patients in Dalby, Sweden, as high-tension glaucoma (HTG) patients and that, according to Quigley's reasoning, these LTGs have likely lost about 50% of their nerve-head fibers; thus the need is primarily to prevent, detect and treat LTG. He notes that a study reported in David 1977 found a greater incidence of glaucoma in treated than in untreated OHT patients. He cites Daubs and Crick 1980 as claiming that, if all OHTs were corrected, 99% of glaucomatous vision loss would still remain.
Studies such as reported in Chauhan and Drance 1989 and in ditto 1990 conclude that the nerve damage of lower-IOP subjects have more localized damage than do those having higher IOPs.
Bengtsson 1981 (Dalby study) states as to the pressure theory:
1) "Eyes are thought to differ in pressure-sensitivity but this imaginary variable has not been defined and cannot be measured. The absolute level of the IOP can, therefore, no longer be used for predictive purposes. It does not matter if the notion of a 'too high' IOP in glaucoma is essentially right or wrong--the pressure theory has lost most of its meaning and has become almost completely useless (Krakau 1981). . . . What remains is mainly, a therapeutic tradition--apparently well-tried but based on obsolete ideas and, as a matter of fact, never shown to be justified by any positive effect of the desired object, which is always the same--a lowering of the IOP (Cochrane et al. 1968)."
2) Disc hemorrhages are both sensitive and specific to manifest glaucoma.
3) ". . .why are they [low-tension glaucoma cases] so often overlooked? The first part of the answer is that ophthalmoscopy and manual perimetry are severely biased by tonometry readings. The second part of the answer is that high pressures, concentrically constricted isopters, expanded blind spots and enlarged optic cups continue to attract so much attention that deep scotomas, polar notches and disc haemorrhages are missed."
4) routine tonometry was abandoned in Dalby, Sweden , in 1971.
5) No association of manifest glaucoma was found with diabetes, vascular diseases, hemodynamic crisis or antihypertensive medication.
6) glaucoma is independent of systemic blood pressure and refraction.
7) The distribution of IOPs of manifest glaucoma subjects is displaced only 5 mmHg upward in persons </=70 yr old.
8) "Tonometry must not be used to exclude the possibility of a manifest glaucoma and should not be allowed to bias judgments based on ophthalmoscopy and perimetry."
9) It is proposed that "THE INCREASE OF THE INTRAOCULAR PRESSURE IS AN EFFECT RATHER THAN THE CAUSE OF GLAUCOMA." Bengtsson 1987 states 1) ". . .high intraocular pressure is an unreliable symptom at and an unusual finding 5-10 yr before the detection of glaucomatous visual field defects. . ." 2) "common clinical experience may seem to tell a different tale [than population studies] but is, of course, irrelevant in so far as it remains biased by routine tonometry and pressure limits."
Eddy 1983 notes that 9% of persons over 40 have </=22 mmHg IOP and 1 out of 50 of those has glaucoma, but that about 50% of those of the general population having glaucoma will be undetected by selecting only persons with such IOPs. This paper states that: "From the available evidence it does not appear that earlier diagnosis makes a substantial difference in the patient's outcome. . . . Screening with tonometry does not appear to be warranted."
Chauhan and Drance 1992 states: 1) ". . .intraocular pressure alone cannot separate these two groups of patients [those with stable glaucomatous field loss and those with progressive same]."
2) ". . .the range of. . .pressure. . .under which progressive field damage occurs is impressive. . . The range under which the fields of glaucoma patients remain stable is equally impressive."
3) ". . .factors quite independent of intraocular pressure may be responsible for progression in glaucoma."
Schulzer and Drance 1990 found, in a study of a group of glaucoma patients 55% of whom were of the "low-tension" variety (LTG), and wherein which study multivariate analysis of 51 bodily physicobiochemical variables was performed, that:
1) Two patient groups separated out on an axis of blood-flow variables.
2) The smaller of these groups, consisting of only 25% of the patient base, related to vasospastic finger blood-flow measurements and showed a high correlation between field loss and highest IOP, while the patients in the 75% group showed the disturbed coagulation and biochemical measurements of vascular disease and did not show the IOP correlation of the other group.
Schulzer and Drance 1991 states: 1) "AT THE PRESENT TIME, THERE IS NO AGREEMENT ON WHETHER MEDICAL TREATMENT PREVENTS OR DELAYS THE ONSET OF GLAUCOMATOUS DAMAGE IN PATIENTS WITH ELEVATED IOP."
2) "The results of [our] study suggest that although the IOP was significantly lowered by the use of timolol, there was no significant difference in the incidence of glaucomatous field defects."
3) "Our study suggests that the pressure reduction obtained may not protect the susceptible individual from the development of localized visual field defects and possibly disc changes as well."
Panek 1989 states, ". . .AS MANY AS 30% TO 60% OF GLAUCOMA CASES MAY FALL INTO THIS CATEGORY [GLAUCOMA WITH 'NORMAL PRESSURES' (NTG)]." This summary paper on low-tension glaucoma then proceeds to discuss its subject based on the historical high-pressure causality of nerve damage.
Bojic` 1993 reports a double-blind study where subjects who had glaucomatous visual field loss were exposed on a daily basis to 2.0 bars of air pressure for 90 min. Sixty percent of the subjects engaged in an oxygen-breathing schedule, while the remainder breathed only air. The report summarizes: 1) "In the experimental group there was a significant improvement of visual fields (p<0.5), whereas there was no change in the subjects in the control group."
2) "Hyperbaric oxygen did not have any influence on intraocular pressure."
3) ". . .the achieved visual field improvements [e.g., 30% less blind-spot area] remained stable for 3 months.. .
4) "Our study indirectly points to the role of a vascular mechanism in the pathogenesis of glaucoma."
Araie 1993, after noting that NTG is 3 times more frequent in Japanese than is HTG, refers to clinical findings of cases where GOND preceded a rise in IOP. The study found a difference in locations of field defects in NTG from those in HTG. It stated, "Prevalence of NTG may be much higher than previously thought, at least in Japan."
Sonnsjö and Krakau 1993 raises the following points: 1) 8-16 yr separates disc hemorrhages from appearance of visual field defects.
2) Most such hemorrhages occur in normal eyes.
3) The Dalby study came close to proving that all disc hemorrhagers become glaucomatous and that all those with glaucoma have hemorrhaged in their discs.
4) "Is there reason to believe that the vascular process is primary and manefests [sic] itself as both VO [vein occlusions], H [hemorrhages] and G [glaucoma]?"
5) "IS THE OCULAR HYPERTENSION IN G THEN AN EFFECT OF THE VASCULAR LESIONS, NOT THE CAUSE?"
6) "Separating the G into several groups is a modern trend which seems us to be of doubtful value except as a life-bouy [sic] for the pressure hypothesis,. . ." Need is mentioned for a good exercise of Occam's razor.
"THE VASCULAR AFFECTION WHICH OBSTRUCTS THE VESSELS WITH HINDRANCE OF THE BLOOD FLOW AND IMPAIRED NUTRITION OF NEURONAL TISSUE, MIGHT BE [READ 'IS'] THE PRIMARY CAUSE OF GLAUCOMA."
Quigley 1993 states: "In population-based surveys, between 25 and 50 percent of those with glaucomatous damage to the optic nerve have intraocular pressures in the normal range." Quigley, in this paper, however, exemplifies well the illogical thinking of the unbudgeable raised-IOP-etiology touters. This is particularly obvious in his conclusions about risk factors. He claims high IOP is the "most consistent risk factor" for development of glaucomatous vision loss (something hard to accept in itself, but OK,. . .. Then he says, "Since high intraocular pressure is a risk factor, it is logical that reducing it could have therapeutic benefit [!!!]." We'll overlook what he would do with the risk factor of certain negroid physiology as to glaucoma and proceed to a totally different problem in order to highlight the folly of this sort of logic: One might say that 18-wheelers are the most consistent risk factor for death in an auto accident. Auto accidents are a problem to society, as well as to individuals; therefore, to fix society we should remove all semis from the highways. Likewise, if gophers riddle an earthen dam, we should remove the water from its reservoir and use the dam with an empty reservoir, because water pressure has a long-time reputation for eroding earthen structures. Quigley is an excellent empirical data gatherer, but let him read my earlier discussion of the family tree of risk factors. You can't change your prospective offsprings' genes by modification of your siblings' genes.
Rojanapongpun and Drance 1993 reports that the age-adjusted peak mean-enveloped and diastolic blood velocities in the ophthalmic artery, as measured by Doppler ultrasound, were all significantly reduced in the "chronic open-angle (COAG)" and "normal-tension (NTG)" glaucoma subjects as compared to the normals in their test group. The NTG subjects also had significantly lower mean-enveloped velocities, than the COAG subjects. The study concludes that the significance of these results is unknown, but they would appear to support a vascular cause of glaucoma not involving the lamina cribrosa and that what's going on prior to sight loss is better seen in NTG subjects than in the "COAG" or HTG (whatever the angle closure) subjects.
Cartwright 1992 compared the reported "immune-related" diseases of NTG subjects (</=22 mmHg) versus those of ocular hypertension (OHT) subjects (IOP >22 mmHg and no GOND or VFL) and found that 30% of the NTGs reported at least one such disease, while only 8% of the OHTs did. The paper states: "Our results support an association between susceptibility to glaucomatous damage and immunoreactive tendencies." Cartwright 1993, a reply to letters responding to that paper, states: "Studies carried out some years ago do not. . .support associations of immune disease and high-tension glaucoma." While the conclusions to be validly drawn from this study are questionable, particularly as to their reliance on patient reports of their medical histories and on the quandary of what "diseases" should or should not be classified as "immune-related"--the indication is, again, that low to moderate IOPs don't figure into the cause of glaucoma--and may be only other results, appearing only in some patients, of a glaucoma- causing process resultant from the effects of immune-system problems on blood vessels supplying the optic-nerve head.
Leydhecker 1983 mentions Erdmann 1907 as inducing glaucoma signs in rabbits by impressing 60 mmHg IOP in them for 2 wk and Ishikawa 1930 doing the same to dogs with 80 mmHg IOP over 8-13 da. More recently experimenters have wrecked monkey's eyes. These experiments are supposed to bolster the pressure theory. Yeah, and AIDS can be transmitted in New York via I-V needles; that doesn't mean it's transmitted that way in equatorial Africa.Nor does damage to the knees from jumping out a second-story window onto concrete explain arthritis. Obviously, quite high IOP can cause a similar ischemic effect, via mechanical action of the lamina cribrosa or otherwise,but it doesn't follow that lower values operate the same mechanism, or that because quite high values of IOP can be causal, that the presence of only slightly raised values cannot be simply an additional result, of some other cause of glaucoma, which result then merely accompanies glaucomatous damage.
My personal experience with glaucoma treatment:
So there exists some agreement among most present glaucoma "expert" contenders that there is value to sticking in one bin, presumably for efficient treatment purposes, all somatic/sensory defects medically detectable as manifesting both 1) a certain range of ophthalmoscopically observable optic-nerve-head damage and 2) certain types of spatially chartable patient reporting of subnormal functioning of his/her field of vision, as achieved by automated perimeter or other means; and that it is historically palatable, in this era, to label this condition--which, in a given patient, either constitutes an existing complaint of vision limitation or can be expected almost invariably to develop into one--with the name 'glaucoma'. Such a definition is not etiological and includes a wide range of anatomical/physiological and vision-loss situations of quite significant differences--but it is restricted to designation of observed damage to the most distal neuron level of the optic-nerve trunk(s) or to designation of functional deficit based on reported data showing a pattern of visual-field loss characteristic of such damage.
Both my manifestation and my clinical experiences are in some ways typical and in some ways atypical of what is respectively medically seen today and what are the authentic clinical shamanistic dances in vogue today to ward off the evil demons that produce such ailments. My signs and symptoms are totally and severely asymmetric to date (age 63) (update, age 64--still true), detection (subjectively) of the defect having been made first by me, by noting a partial superior arcuate scotoma with nasal step in my left field of vision extending from only about 0.25 deg to 5 deg radially from my point of fixation, as I viewed a flat field of blue sky, at age 57 and at a time when I had never seen such a pattern and had no knowledge of glaucoma.
Two years previous, an optometrists' air-burst tonometer had read 9 mmHg in my right eye (OD) and 12 in my left (OS). Some 6 or 8 yr before that, the UCB Optometry Clinic, at the time of refracting for eyeglasses had first questioned my anterior-chamber angles in respect to glaucoma and then decided that, in my case, there was no problem. Prior to my observation of the scotoma, I had had no eye complaints or diagnoses other than presbyopia and astigmatism; however, the latter had developed much more severely OS up to the cylindrical power of +2.0 or so. I had never had any indication of disc hemorrhaging or other oculovascular anomalies. A couple of months after my observation of the scotoma, my pressure readings were 16 OD and 22 OS, and have remained on average at about 18 and 22, respectively, ever since, although a few readings of the OS ranged up to 30. I administered timolol or betaxylol topically to my left cornea for 2 yr, at which time I underwent a laser iridotomy OS and quit the medication. Clearly neither the medication nor the laser punctures changed either my IOPs or the progression of vision loss OS. The vision loss progressed as five sequential alternately inferiorly and superiorly accumulating scotomata, expanding and deepening, all eventually absolute, together with relative to absolute shapeless filling in of both of my nasal, and my inferior temporal, OS quadrants--until presently there remains only a quite small central inferior fixation-to- blind-spot crescent of sight of about 2 deg at its maximum width, together with the peripheral area of my superior temporal quadrant. There seems to have occurred a stasis in functional loss during the last year. [Update 1995: central scotoma only about 1.5 deg and narrowing] I do not see this optic nerve degeneration of mine as independent of prior nasal mucosal allergy, crusting and surgical intervention, although I cannot pin down a mechanism of causation from any of the latter, as a result of reading either the ophthalmological or rhinological literature or from discussion with "experts" in these fields. The allergies have been to cow's milk, beef, certain airborne molds and probably to some other foods, such as gluten. It is not clear that either an extensive endonasal reconstruction or a removal of half of a left middle turbinate, in my case, could have affected the vision in my left eye in a manner so as to cause damage to the anterior portion of the optic nerve trunk to it. Certainly, however, it is clear to me that raised IOP is not a cause in my case and that vascular/ischemic effects of similar nature have gone on in both my nasal epithelium and my optic nerve head, though these are not served by locally common blood vessels and though little manifestation of allergy occurs elsewhere in my body, though nearly all of such in my head is sinistral. I have no systemic diabetic, hematological or vascular problems. My medical attention during the duration of my glaucoma symptoms has been limited to that available to indigents. Prior to my laser iridotomy, some 6 mo of quite undirected topical beta- blocker administration was managed as primary open-angle glaucoma (POAG) at the California Pacific Medical Center (CPMC) Lions Eye Clinic, by a quite decent but very limitedly trained resident of marginal aptitude, under the aloof "glaucoma expert" Dr. Maurice Lieberman, and was set to continue thus for another 4 mo, while the resident was to learn some more of what the specialty was all about. On checking through UCB Optometry, I was referred to Dr. Brandt at UCD Sacramento, whose examination of me claimed observation of trabecular-meshwork scarring and gave me an angle- closure diagnosis. Finally, on recommendation of Brandt, I let a Dr. Tark at the Oakland VA Clinic puncture my left iris, but it never even changed the IOP. Tark later admitted that he could not see any trabecular scarring. It may also be noted that Tark didn't, until later, advise me of the minor contrast-lessening side effect from the laser procedure that would result from uncontrollable light leakage through the added holes in the iris. Later at one or more of the mentioned treatment centers, there was interest in my trying pilocarpine, but lack of desire for its visual side effects and my rejection of the pressure hypothesis, at my OS 22-mmHg mean reading, brought about my refusal of this drug. Although I contemplated no problem with my right eye, I considered the possible life restrictions if glaucoma occurred also in it to any significant extent, and I pursued Dr. Harry Quigley's claims of retinal nerve-fiber layer (NFL) assessment's predetecting vision loss some 6 yr earlier than does perimetry, and asked him who might, on the West Coast, be available to make such assessment as to my right eye. Unbelievably he referred me to Dr. Lieberman, who at first refused to even speak to me and then argued against my doing anything but coming back to take drops under his resident's management. However, finally I thought I had an agreement with him where, if I submitted to another round of routine check-out of both my eyes by another of his residents, he would do such an NFL count. Well, not only did he back out, but his resident and he then outrageously told me I should have laser iridotomy performed on my good eye. Now you can see how the incredibly prolonged tonometrical mythology both promotes such recommendation, particularly inappropriate in my case, to do invasive procedures and allows a whole charity-supported racket to go on at CPMC for the purpose of dragged-out training of MDs in a ridiculously unscientific, obsolete collection of diagnostic and therapeutic rituals. One has to assume Lieberman's view was the mindless one that, in the case of tonometrically selected eyeball pairs, where one only measures above 22 mmHg, if that one develops glaucoma, the odds are that the other one soon will; and therefore, the sooner you do something that according to the pressure ideologues is supposed to reduce the normal IOP in the second eye, the less will be the progression of the glaucoma that is to develop in it. To such as Lieberman, who gets very rich from Lions Club members' blind charity (their monitor, Don Stanaway, cops totally to conservative MD ruses), it doesn't matter that 1) the pressure in my bad eye was not reduced by laser iridotomy, 2) my eyes were not brought into scrutiny by tonometry, 3) many single eyes develop glaucoma (secondary to discoverable reasons, without their fellows so degenerating, 4) there was found, in at least one abovementioned study, that less glaucoma can be found in certain unmedically and unsurgically altered fellow eyes than in those doctored up, and that 5) slightly raised IOP may be better for glaucomatous or glaucoma-susceptible eyes than "normal" IOP. Playing with lasers is a symbol of expertise, of course, and worthy of bucks, charitable or uncharitable. A year or so ago, I went back to UCB to see if, through Dr. Andy Adams, I could get a blue-on-yellow Humphrey visual-field test on my good eye, having read of his and Chris Johnson's work (UCD, Sacto) in this area. Though Dr. Adams had by then become school dean and was unreachable, I was able to get the test, and it gave no indication of any future trouble in my right eye. This test, however, would only give me about 1 additional year's notice over white-on-white perimetry, and if Sonnsjö and Krakau 1993 is at all right, this is only 1 year out of 8 to 16. Clearly, if Quigley's fiber tricks are legit, they would provide considerably earlier notice--not that less vision loss would likely result if defects were found in my OD NFLs, and whatever best measures taken--but that life planning might be better conducted. [Update 1995: No further visual-field testing or tonometry has been done, but no deficit whatsoever in the vision of my right eye has become noticeable through ordinary usage.] My prime health concern has remained my hourly nasal crusting an hyperviscous postnasal drainage problem, increasingly with irritation and/or aching. Any comparable life disruption by my eye problem (although the nerve head is neurologically over 90% shot) remains more in the future--if at all.
The conclusion, of course, is that glaucoma clinical specializing, within ophthalmological clinical specializing, can-- if you believe in and offer much verbiage to the gods of the almighty Pressure Hypothesis, and prevent your patients from reading heretical papers by trans-Prussian European pagans, and enough of your buddies don't defect--earn you really big bucks; because, given the thereby-impeded progression in the understanding of glaucoma, there will certainly remain much progression of this disease in the public eyeballs--all the more to fill your pocket book and provide you with Mercedeses, country-club memberships, Chinese art collections, yachts, world excursions, self-published books and all the other fine things that make MDs wallow in ecstacy. But you also must pay your AMA dues and write letters to the editor against medical reform, just to keep in shape.
Certainly also, Allergan-Humphrey isn't too poor these days, with its near worldwide monopoly in automatic perimeters. Yes, such instruments are better detectors and monitors of glaucoma than are tonometers, but they still detect much too late to allow therapeutic intervention into the problem-- that is, if there were anything effective that could be done about it, which mostly there isn't. These machines are, most of the time, just a health-care cost increaser. And, although more sensitive than prior perimetry, they are much less accurate as to mapping of field loss than a careful subject can be in using a pencil, paper and Ambler grid. Also, glaucomatous loss is mostly a matter of loss of resolution, with loss of light sensitivity being secondary; the Swedes are ahead in recognizing that also, but who buys their "nonstandard" machines? Of course, in any financial transaction, there is a second side of the deal--the consumers'. I'm not sure theirs is fit to print here, but many of the glaucoma industry's consumers are too blind to read it if it were. Basically, as with any other part of health care, there is prevention, detection, diagnosis and treatment.
Well, as to the first, considering the state of the art in the case of glaucoma, we'll leave it with those who say not to masturbate, with maybe an additional caveat to stay away from doctors--because nobody seems to know anything functional about it.
As to the second, obviously, without regenerative capability of central-nervous-system neurons, of which the optic nerve head is composed, and given the redundancy of rods and cones and neural interconnections of the human eye, optic nerve and visual cortex in respect to most tasks--some respectable amount of nerve-head damage can be tolerated before detection becomes imperative in order not to lose significant sight, but delay in detection, even until the point that a series of normally subliminal subjective reports become recordable on something like a perimeter, is inadequate. Clearly, at such a time as medicine should have some useful means of arresting glaucoma that is prevalent at ordinary IOP, there should be a type of automated retinal-nerve detail assessor for detection of the malady. As few researchers or clinicians seem to want to follow Quigley into such tedious activity by humans, I presume there would be no jealousy, from practitioners, of machines which would do this, as long as they could bill handsomely for them. Get with it, Humphrey; you owe us something for your as-yet uncompensated inflation of health care.
Differential diagnosis should always be tied in closely with modes of therapy. Medical metaphysical ontologies prove nothing but confirmation of the tendency of physicians, as we know them, to be culture-bugs--not very sensitive to real scientific distinctions. (But then, with science comes economy, and that surely isn't what the medisinners are after.) The anatomy of the optic-nerve terminal neuron level is quite distinct from that of the retinal sensors and from that of the second-level optical- nerve-trunk neurons, and from anything else around those parts, and the correlate subjective scotoma patterns are quite distinct from those resulting from problems in neighboring parts of the optical signal path, so we should be in good shape with our present distinct labeling of the physical defects / functional limitations we choose to group under the name 'glaucoma' (IOP now being out of the definition). However, we cannot be very smug about limitation of the range of causal trains to these defects/limitations. As in all of medicine, there can be both localized treatment and more systemic treatment. The more locally specialized the treatment, of course, the less concern may be had for any disparity in the causal basis of different instances of the condition. That, of course, is the motive for pursuit of understanding of "the (local) glaucoma mechanism". However, if a fair range of instances of glaucoma manifestation is found to truly correlate to more systemic bodily imbalances, and the latter are found to have known convenient means of correction, then part of the glaucoma treatment problem is solved to some extent. It is doubtful that correlation of a broad, semi-metaphysical category such as "immune-related diseases" to glaucoma is of much help, but some means of arresting the sort of glaucoma inflicted via whatever means is present in my instance would seem to be in reach through refinement of this more peripheral mode of attack.
The papers I have discussed above essentially all deal with either prospective or retrospective clinical or epidemiological correlations of signs, symptoms, traumata and treatments. There is also quite to-the-point work going on in more direct active, coherently scientific cause-and-effect experiments in vitro on the pertinent histological matter--tissues that include fibrinectin and elastin collagens, but I haven't seen reported much in the way of useful or definitive results. Probably a lot more grubby, apolitical work in this nuts-and-bolts, back-room activity would be more productive than a lot of argument over clinical or population correlations. But pluggers don't get paid as much or write papers that directly turn on money sources for their activities--and success in such efforts as I suggest here would not make clinicians richer or more famous. Except in cases where the measured IOP is sufficiently high as to truly be a cause of already existent or imminent glaucoma, and surgical intervention without severe side effects is feasible and does significantly lower the pressure, not much actual curtailment of progressive glaucoma seems to be presently achievable; the cards are often merely cut to make it look like something progressive has occurred, and much money is exchanged. But sometimes outright resultant iatric worsening of an eye condition can't be repaired or even whitewashed from the public eye. Where such things are done in the case of an IOP under 30, it is tantamount to a crime. But crimes of the wealthy are seldom punished. A CALL FOR ACTION I would like to hear from anyone in a position to influence stipulations that could be attached to either public or private funds donated to support glaucoma research, which stipulations would set limitations on the direction of such research. Numerous sizable private donations are made every year to the Glaucoma Research Foundation in San Francisco without the realization that these are squandered on useless studies which start with the premise that all glaucoma not secondary to trauma or infection results from intraocular pressure. Clinical physicians who derive a large income from the contiuation of prolonged "treatment" of glaucoma patients, under the status quo of acceptable knowledge in the field, make sure these donations reach only research that will not disturb the IOP mythos. Also, all members of the Lions Club should take note that their donations to Lions Eye inculcate the raised- IOP hypothesis in treatment, and accomplish next to nothing in the advertised fight against blindness.
1. Araie 1993 - Araie M, Yamagami J, Suzuki Y. Visual Field Defects in Normal-tension and high-tension Glaucoma. Ophth 1993; 100: 1808-1814
2. Bengtsson 1981 - Bengtsson B. Aspects of the Epidemiology of Chronic Glaucoma. Acta Ophth ;1981; Supp 146
3. Bengtsson 1987 - Bengtsson B. Further Follow-up of the Dalby Population. In: Krieglstein G. K. Glaucoma Update III (Springer-V) 1987; 1-48
4. Bojic` 1993 - Bojic` L, Racic" G, Gosovic S, Kovacevic` H. The effect of hyperbaric oxygen breathing on the visual field in glaucoma. Acta Ophth 1993; 315-319
5. Cartwright 1992 - Cartwright M J, Grajewski A L, Friedberg M L, Anderson D R, Richards D W. Immune-Related Disease and Normal-Tension Glaucoma. Acta Ophth 1992; 110: 500-502
6. Cartwright 1993 - Same in reply to letters. Acta Ophth 1993; 111: 23-24
7. Chauhan and Drance 1989 - Chauhan B C, Drance S M, Douglas G R, Johnson C A. Visual Field Damnage in normal-Tension and high- Tension Glaucoma. Am J Ophth 1989; 108: 636-642
8. Chauhan and Drance 1990 - Chauhan B C, Drance S M. The Influence of Intraocular Pressure on Visual Field Damage in patients With Normal-Tension and High-Tension Glaucoma. Investig Ophth & Vis Sci 1990; 31:2367-2372
9. Chauhan and Drance 1992 - Chauhan B C, Drance S M. The relationship between intraocular pressure and visual field progression in glaucoma. Graefe's Arch Ophth 1992; 230: 521- 526
10. Cochrane et al. 1968 - Cochrane A L, Graham P A, Wallace J. Glaucoma. In: Cohen R H L, et al. Screening in medical care. (Oxford) 1968; 81-88
11. Daubs and Crick 1980 -
12. David 1977 -
13. Eddy 1983 - Eddy D M, Sanders L E, Eddy J F. The Value of Screening for Glaucoma With Tonometry. Surv Ophth 1983; 28: 194-205
14. Erdmann 1907 - Erdmann P. Über experimentelles Glaukom nebst Untersuchungen am glaukomatösen Tierauge. Graefes Arch Klin Exp Ophth 1907; 66: 325-435
15. Ishikawa 1930 - Ishikawa F. Experimentelles Glaukom beim Hunde mit besondere Rücksicht auf Sehnervenerkrankungen. Graefes Arch Klin Exp Ophth 1930; 124: 387-443
16. Krakau 1981 - Krakau C E T. Intraocular Pressure Elevation - Cause or Effect in Chronic Glaucoma? Ophthalmologica 1981; 182: 141-147
17. Leydhecker 1959 - Leydhecker W. Zur Verbreitung des Glaucoma simplex in der scheinbar gesunden, augenärztlich nicht behandelten Bevölkerung. Doc Ophth 1959; 13: 359-388
18. Leydhecker 1983 - Leydhecker W. Is Glaucoma Therapy Useless? In: Glaucoma Update II (Springer-V) 1983; 95-102
19. Panek 1989 - Panek W C, Lee D A, Christensen, R E. Low- Tension Glaucoma. Glaucoma 1989; 11: 99-107
20. Quigley 1993 - Quigley H A. Open-Angle Glaucoma. NEJM 1993; 328: 1097-1106
21. Rojanapongpun and Drance 1993 - Rojanapongpun P, Drance S M, Morrison B J. Ophthalmic artery flow velocity in glaucomatous and normal subjects. Brit J Ophth 1993; 77: 25-29
22. Schulzer and Drance 1990 - Schulzer M, Drance S M, Carter C J, Brooks D E, Douglas G R, Lau W. Biostatistical evidence for two distinct chronic open angle glaucoma populations. Brit J Ophth 1990; 74: 196-200
23. Schulzer and drance 1991 - Schulzer M, Drance S M, Douglas G R. A Comparison of Treated and Untreated Glaucoma Suspects. Ophthalmology 1991; 98: 301-307
24. Shin 1976 -
25. Sommer 1989 - Sommer A. Intraocular Pressure and Glaucoma. Am J Ophth 1989; 107: 186-188
26. Sommer and Quigley 1991 - Sommer A, Katz J, Quigley H A, Miller N R, Robin A L, Richter, R C, Witt K A. Clinically Detectable Nerve Fiber Atrophy Precedes the Onset of Glaucomatous Field Loss. Arch Ophth 1991; 109: 778-83
27. Sonnsjö and Krakau 1993 - Sonnsjö B, Krakau C E T. Arguments for a vascular glaucoma etiology. Acta Ophth 1993; 71: 433-444
28. Van Buskirk 1992 - Van Buskirk E M, Cioffi G A. Glaucomatous Optic Neuropathy. Am J Ophth 1992; 113: 447-452
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