GLAUCOMA AND INTRAMEDICAL PRESSURE:
Nearly 150 Years of Deception in the Interest of Medical Greed
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, 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="" change="" in="" no="" p="" the="" there="" was="" whereas="">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 to
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 Sonnsj? 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 and
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.
Conclusion
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.
raych@tsoft.net
Related article
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