Pet Forum / Miscellaneous / Animal Health / January 2006

      Stress Induced Blindness - Effects Of Emotions On Glaucoma

HOWEDY People,

Blindness can be caused by STRESS and CHOKING
*(cite cate's hyperactive fear aggressive dog, Orson)

neckties tend to have MOORE glaucoma.

You can't be jerking and choking and scoldin your
dogs no MOORE

You're KILLIN and making your dogs go blind, to boot:

The most common precipitating events include illness,
emotional stress, trauma, intense concentration, and
pharmacologic pupillary dilation.[Sugar, 1941 #116; Lowe,
1961 #8957] The role of emotional stress in inducing acute
angle-closure should not be underestimated.[Inman, 1929
#190; Egan, 1955 #189; Cross, 1960 #188]

                       ==================

                   Death Producing Ulcers:
         "Emotional Influences On Health & Behavior"
                 Dr. George Von Hilsheimer

       Emotional Influences On Behavior

       Illness is directly related to depression and lack of
       adjustment, particularly to a new environment (Parens,
       McConville & Kaplan, 1966).

       A WIDE RANGE of PSYCHOSOMATIC or
       CORTICOVISCERAL DIS-EASES was surveyed
       by Wittkower (1965) to demonstrate the enormous
       importance of emotional factors in general health.

       Interview findings of emotional material (recently
       experienced hopelessness) pryor to biological
       examinations correctly identified 11 out of 19 with
       cervical cancer, and 25 of 32 who were cancer free
       even though psychological tests failed to discriminate
       these groups (Schmale & Iker, 1966)

       150 lung cancer patients showed significantly
       constricted expression of emotions. The had fewer
       childhood behavior problems, and lower neuroticism
       score than their cancer free controls. Heavy cigarette
       smokers who DO NOT INHALE are more apt to have LUNG
       CANCER. They, too, show LOWER neuroticism scores.
       Among heavy cigarette smokers poor emotional
       expression is as highly related to cancer as urban
       residence and is more important than a chronic cough
       or an air polluted environment (Kissen, 1966).

       A ten year observation of all the women who developed
       cancer in an isolated pupulation of 2,550 showed that
       they tended to be unstable or sub stable personalities
       characterized by melancholy and extraversion,
       especially marked with those of an undecided body
       build (Hagll, 1966). Personality dynamics effect both
       the development of cancer and it's SITE. Cancer
       may result from what appears to be a failure to grow--
       somatically, behaviorally and psychologically
       (Grinker, 1966).

       In 109 cases leukemia and lymphoma were associated
       with a number of losses or separations and with
       feelings of sadness, anxiety, anger or hopelessness.
       The PRIMARY FACTOR seems to be the shame and
       hopelessness of running out of psychological resources
       (Green, 1966). Cervical cancer patients are less
       emotionally responsive, more isolative, and less
       frequently diagnosed as having clinical neuroses than
       cancer free patients. There is NO CLEAR DIFFERENCE in
       their FEELINGS and ATTITUDES toward coitus (Rotkin,
       Qunk, & Couchman, 1965).

       Schmidt (1966) surveyed nearly 100 studies of
       behaviorally induced DIS-EASE in animals CONFIRMING
       and EXTENDING the DATA on PEOPLE. Behaviorally
       induced DIS-EASES tend to fall into two groups;
       (1) Hysteriform problems, which INCLUDE HYSTERICAL
       SEIZURES and FORMS of AGGRESSION as well as
       collective panic and epilepsies;

       (2) organic modifications, including functional
       difficulties and lesions affecting gastro intestinal,
       cardio vascular, respiratory, sexual, endocrine, skin,
       urinary, and neuro muscular systems.

       It is INTERESTING, and SLIGHTLY HORRIFYING, to note that
       the ONLY SCIENTIFIC RELEVANCE of the standard six hour
       school day that I have been able to detect in research
       is that Sawrey and Weisz quite by accident found that
       six hours on and six hour off of "EXECUTIVE  BEHAVIOR"
       in monkeys was the ONLY TIME STRUCTURE that INDUCED DEATH
       PRODUCING ULCERS.

                        -------------

       Stress Induced Blindness - Effects Of Emotions On Glaucoma

Subject: Re: UPDATE: Dog going blind, what can I do?
Date: 2003-09-28 18:21:31 PST

From: David Wright (djwri...@tesco.net)
Subject: Re: Effects of emotions on glaucoma
Newsgroups: alt.support.glaucoma
Date: 1999/07/01

The role of stress in glaucoma is difficult to establish but
anecdotal evidence from many doctors  suggests that it might
well play a role in glaucoma. As far as we know there are not
any clinical papers on the subject, indeed part of the problem
in investigating the relationship of stress to any condition
is that the investigation itself tends to be somewhat
stressful. However, the best advice would be to keep stress
levels as low as possible without raising them again by
worrying about it.

David Wright MSAE
Chief Executive, International Glaucoma Association

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.

----------
In article <7lfuf7$f5...@nnrp1.deja.com>,

m...@my-deja.com wrote:

From: ritch (r...@inx.inx.net)
Subject: Re: Cerebrospinal Pressure,Glaucoma, etc.
Newsgroups: sci.med.vision, alt.support.glaucoma
Date: 1996/01/26

2. Constant elevated IOP was shown to block axoplasmic
transport at the level of the lamina cribrosa a generation ago
by electron microscopic studies. However, it has more recently
been advocated that shear stress is just as important. In the
latter case, changes in IOP can cause sliding of the plates of
the lamina cribrosa over each other, twisting and damaging the
axons that pass through it.

=========================

Natural Eye Care, An Encyclopedia: Complementary
Treatments For Improving And Saving Your Eyes Marc
Grossman, O.D., L.Ac. & Glen Swartwout, O.D. Keats
Publishing/NTC/Contemporary Publishing Group, Inc.
4255 West Touhy Avenue, Lincolnwood, IL
60646 0-87983-704-7  $16.95

    As well as being practicing optometrists, Dr. Marc
Grossman and Dr. Glen Swartwout have been trained
in Chinese medicine, acupuncture,  and naturopathic
medicine.

Both have also published previous books. Their joint
effort, Natural Eye Care, An Encyclopedia: Complementary
Treatments For Improving And Saving Your Eyes, draws
from the best of traditional and modern medicine for the
prevention and treatment of eye disorders.

    The authors say that their "primary goal is to offer a
practical approach to vision care based on an underlying
philosophy that emphasizes prevention rather than cure."

   They begin with a fascinating discussion of how the eye
functions, including information like "the entire blood volume
of the body passes through the eyes every 40 minutes or so."

    Although many of us don't realize it, our eyes are the
first to suffer when we feel physical or mental stress.  They
also cite studies showing that allergies in children improve
when their vision is enhanced through vision therapy.

    Dr. Grossman and Dr. Swartwout devote one chapter to a
explanation of the various natural treatments and how they are
used for treating vision disorders.

   They emphasize the "vision diet," which focuses on eating
lots of fresh foods and eliminating processed or refined foods.
They also discuss the role of Traditional Chinese Medicine (TCM),
acupressure, herbs, physical exercise, eye exercises, spinal
adjustments, and homeopathy in preventing and treating eye
diseases.

    Each of the following eye diseases have their own chapter:
glaucoma, cataracts, macular degeneration, dry eyes, sties,
floaters, and conjunctivitis (pink eye).  The authors provide a
description of the causes and symptoms of each disease, and a
summary of conventional treatment.

They then describe a healing program for those who
have each vision disorder, based on natural treatments.
Each chapter ends with a prevention program for those
who still have healthy eyes.

    An appendix provides acupressure directions.  They also
include an extensive reference section, and listing for resources
for those who can't obtain natural products locally.

    Dr. Grossman and Dr. Swartwout say that "the good news
is that we don't have to be passive victims of eye disease.  Eye
deterioration can often be stopped--and even reversed."

Readers will find Natural Eye Care, An Encyclopedia a
comprehensive and invaluable resource for the prevention
and treatment of vision disorders.  Paper.  196 pp.

FIGGER IT HOWET.

The Amazing Puppy Wizard. <{} ; ~  )   >

                  ---------------

Stress Induced Blindness - Effects Of Emotions On Glaucoma

From: Ray Bonar (b...@tiac.net)
Subject: Angle-closure Glaucoma - Clinical types
Date: 1997/12/27

Angle-closure Glaucoma - Clinical types

Robert Ritch
Ronald F. Lowe

The nomenclature for the various clinically distinct types and
modes of presentation of angle-closure glaucoma has been
inconsistently used by different investigators, by
investigators in different countries, and at different points
in time. As a result, there is a moderate amount of confusion
regarding terminology. This pertains in particular to the
terms intermittent, prodromal, and subacute; chronic and
creeping; and combined mechanism versus mixed mechanism.

Angle-closure glaucoma has long been divided by convention
into "primary" and "secondary" forms. Primary angle-closure,
or relative pupillary block, is the most common mechanism of
angle-closure glaucoma and studies of series of patients with
acute angle-closure have been based on this concept. It should
be recognized that publications dealing with characteristics
of patients with "angle-closure glaucoma" include not only
relative pupillary block but other mechanisms as well.
However, because relative pupillary block forms the greatest
proportion, the data should be regarded as not inordinately
skewed.

PRESENTATION
Angle-closure glaucoma can present with a spectrum of
symptomatology, from none at all to severe pain, blurred
vision, and nausea. The terminology is based upon the signs
and symptoms at the time of diagnosis, and these should not be
though of as specific "types" of angle-closure, but merely
descriptive phenomena which may vary with time in any
individual patient (see Fig. 38-1). For example, a patient
with a narrow angle and peripheral anterior synechiae (chronic
angle-closure) may have symptoms of intermittent angle-closure
attacks which, if not detected or diagnosed, can later present
as acute angle-closure glaucoma. The mode of presentation
depends on a combination of the percentage of the filtering
meshwork occluded by the iris, the rapidity with which the
occlusion occurs, and the ease of reversal of the
iridotrabecular block. Fourman[Fourman, 1989 #2738] has
published a useful flow chart to aid the ophthalmologist in
dealing with acute angle-closure glaucoma.

Intermittent angle-closure
Intermittent angle-closure defines repeated, brief episodes of
angle-closure with mild symptoms and elevated intraocular
pressure. These resolve spontaneously and ocular function is
normal between attacks. Intermittent angle-closure is often a
prelude to acute angle-closure. The intraocular pressure is
high enough to cause symptoms, but not as high as in a
full-blown attack. This may be due to partial angle-closure,
which could affect more the narrower superior part of the
angle,[Leighton, 1971 #184] or 360° of closure with just
enough functioning meshwork remaining above the level of
closure to allow some aqueous to escape, or perhaps to a
freely reactive pupil, which allows spontaneous reversal of
the symptoms once the triggering element is removed.

Intermittent attacks are most commonly associated with
fatigue, dim light, and using the eyes for near work (see
Table 38-1). They tend to recur under similar circumstances
and at about the same time of day or evening. The symptoms are
a dull ache in or around one eye and mildly blurred vision.
Halos around lights are often not seen unless the patient is
outdoors. Haloes are believed to result from stretching of the
corneal lamellae, causing the cornea to act as a diffraction
grating, producing a blue-green central halo and a yellow-red
peripheral one. Halos that are seen every night are caused by
cataracts, corneal disease, or persistently high intraocular
pressure. Transient monocular visual loss has also been
noted.[Ravitz, 1984 #185]

 The patient may recognize the cause and avoid or reduce the
activity, such as watching television or reading. The attacks
last for about a half hour after cessation of the inciting
activity. Sleep is so often recognized as beneficial that many
patients go to bed early or take a nap to obtain relief.
Amelioration of the attack is attributed to sleep-induced
miosis and possibly to decreased intraocular pressure
resulting from decreased aqueous humor secretion.[Reiss, 1984
#186] If the symptoms persist overnight, a true attack has
developed.

Initially, intermittent attacks occur at intervals of weeks or
months, but eventually may occur almost nightly. They may
continue uneventfully for months or years. Usually only one
eye is involved, but bilateral attacks can occur. Because the
eyes appear normal between attacks except for a narrow angle,
the diagnosis is frequently missed, and even ophthalmologists
may be misled by the patient's self-diagnosis of migraine,
sinusitis, anxiety or eyestrain.

Examination reveals shallow anterior chambers, iris bombé,
narrow angles, and sometimes an enlarged or oval pupil.
Provocative testing may result in angle-closure, elevated
intraocular pressure, and reproduction of the patient's
symptoms.

The end result of intermittent angle-closure glaucoma usually
differs between whites and races with thick, heavily pigmented
irides. In whites the attacks are essentially benign and may
recur for years without causing damage. Attacks may be
accompanied by progressive PAS formation, leading to chronic
angle-closure. The greatest danger lies in the possibility of
sudden conversion to acute angle-closure glaucoma. Laser
iridotomy is definitive if the eye is otherwise normal and the
angle not occludable by mechanisms other than pupillary block.

In Asians the history may be consistent with intermittent
angle-closure glaucoma, but the intraocular pressure is often
elevated and the angle variably closed by PAS, depending on
the frequency and severity of the attacks. Asian eyes are more
prone to "creeping" angle-closure and PAS formation. Iridotomy
alone may be insufficient to control intraocular pressure.
Blacks also have a greater tendency to develop chronic
angle-closure, but it is our impression that the anterior
chambers are often deeper than those of Asians and that iris
bombé is much less frequent. Both intermittent and acute
attacks are less common in blacks than in Asians. Comparative
biometric studies would greatly help to increase our
understanding of angle-closure in these groups.

Subacute angle-closure glaucoma
Subacute angle-closure describes a stage in which attacks may
be more frequent and prolonged than in intermittent
angle-closure, but less so than in acute angle-closure. At
least in some cases, this is caused by less than total closure
of the angle.[Chandler, 1955 #187] Symptoms of blurred vision,
pain, and halos may be more marked than in intermittent
angle-closure. Attacks may occur over months or years, finally
leading to an acute attack. Subacute attacks are much more
common in Asians than in whites and can cause severe damage
without much inflammation. They tend to produce a chronically
dilated pupil, mild iris atrophy, PAS, and pigment on the iris
close to the inferior angle. Intraocular pressure levels and
glaucomatous disc and visual field damage vary according to
the severity and duration of the attacks.

Acute Angle-closure Glaucoma
Precipitating events
Acute angle-closure glaucoma can lead to irreversible damage.
Various stimuli may trigger an attack. Most attacks occur
during the evening, beginning mildly and rapidly increasing in
severity. Approximately one-third of patients describe
episodes of intermittent or subacute angle-closure having
occurred before the acute attack. The physiological factors
that convert relative pupillary block to absolute pupillary
block remain poorly understood, as are those that determine
whether an eye will develop acute or chronic angle-closure.
Although pupillary block is the common underlying mechanism,
the course of the disease depends on the degree and suddenness
of the block, the flaccidity and physiologic responses of the
iris, and the width and depth of the anterior chamber angle.

Absolute pupillary block is most commonly triggered when the
pupil is middilated, about 3.5 to 6 mm in diameter.[Chandler,
1952 #105] In this position, the combination of pupillary
block and relaxation of the peripheral iris, allowing its
forward displacement into the anterior chamber, are maximal.
Mapstone[Mapstone, 1968 #127] concluded that the posteriorly
directed forces of the dilator and sphincter muscles and the
stretching force of the sphincter during contraction are
greatest when the pupil is middilated.

The most common precipitating events include illness,
emotional stress, trauma, intense concentration, and
pharmacologic pupillary dilation.[Sugar, 1941 #116; Lowe, 1961
#8957] The role of emotional stress in inducing acute
angle-closure should not be underestimated.[Inman, 1929 #190;
Egan, 1955 #189; Cross, 1960 #188] A memorable example was a
patient who, after narrowly missing being injured by a grenade
thrown through his living room window as an expression of some
differences of opinion, immediately developed bilateral
attacks. Attacks rarely begin simultaneously in both eyes.
Minor differences in anterior chamber depth almost invariably
result in the eye with the shallower chamber being involved
first.

A multitude of other inciting factors have been presented in
case reports, including acute infectious disorders, acquired
immunodeficiency syndrome, tumors, and trauma. In many of
these cases, the mechanism either has not been delineated or
the block is posterior to the lens, due to uveal effusion.

Symptoms and signs
The symptoms of an acute attack result from the sudden, marked
elevation of intraocular pressure to as high as 80 mmHg.
Corneal edema results in blurred vision and intense pain and,
secondarily, in lacrimation and lid edema. These, in
combination with anxiety and fatigue, lead to nausea and
vomiting, whereas vasovagal responses cause bradycardia and
diaphoresis. Systemic symptoms may be so severe as to mislead
the nonophthalmologist, and some patients have actually
undergone unwarranted exploratory laparotomy. We saw one
patient whose ataxia, blurred vision, and diagnosis of
multiple sclerosis disappeared after laser iridotomy.

The diagnosis is usually straightforward (Fig. 38-2). Central
visual acuity is reduced and the intraocular pressure is
markedly elevated. The lids are swollen and there is
conjunctival hyperemia and circumcorneal injection. The cornea
is edematous and the pupil usually middilated and vertically
oval because of iris sphincter ischemia. The anterior chamber
is shallow but usually formed centrally, whereas the
midperipheral iris is bowed anteriorly and may touch the
cornea peripherally. An inflammatory reaction is present in
the anterior chamber. Hypopyon can occur in severe or
prolonged attacks.[Zhang, 1984 #8961; Friedman, 1972 #8966]

Corneal edema may initially limit gonioscopic and posterior
segment examination, even after the topical application of
glycerin. Inability to open the angle with indentation
gonioscopy at this stage does not mean that the angle will
remain sealed after iridotomy, nor does it accurately reflect
the presence or extent of PAS. Examination of the opposite eye
is particularly useful in differentiating acute angle-closure
glaucoma from neovascular, uveitic or phacolytic glaucoma, and
usually reveals a shallow anterior chamber and narrow angle.

The optic nerve head may be hyperemic and edematous early in
the attack. With prolonged attacks or cases in which
unrecognized chronic angle-closure glaucoma precedes an acute
attack, pallor and cupping, along with visual field damage,
may be present. Central retinal vein occlusion may occur as a
result of an acute attack[Tornquist, 1958 #195; Sonty, 1981
#2801] or may precipitate one.[Bloome, 1977 #630; Grant, 1973
#631; Hyams, 1972 #632; Mendelsohn, 1985 #633; Weber, 1987
#634; Segal, 1986 #2796]

Visual field changes associated with acute pressure elevation
usually show nonspecific generalized or upper field
constriction.[McNaught, 1974 #191] Early loss of central
vision, enlargement of the blind spot, and nerve fiber bundle
defects may be found.[Douglas, 1975 #204; Horie, 1975 #635]
After normalization of intraocular pressure, the visual fields
may also normalize, or patients may be left with reduced color
vision, generalized decreased sensitivity, or specific
defects. These may be exaggerated by cataract formation or
progression.

An attack may terminate spontaneously if iris atrophy from
tissue necrosis allows aqueous humor to percolate through the
iris stroma, equivalent functionally to a spontaneous
iridotomy.(Fig. 38-4) However, this occurs more frequently as
a result of suppression of aqueous secretion by the high
pressure. Spontaneous termination may also be facilitated by a
change in the position of the lens-iris contact, or segmental
iris constriction with peaking of the pupil.[Phillips, 1963
#192]

Chronic Angle-closure Glaucoma
Chronic angle-closure refers to an eye in which portions of
the anterior chamber angle are permanently closed by PAS.
Variable and sometimes conflicting terminology has been used
to describe somewhat differently appearing forms. The approach
to therapy is similar in all of them. The terminology used in
this section is an attempt to differentiate the two pathways
by which chronic angle-closure can develop.

In the first, iris bombé from relative pupillary block may
appositionally close the angle. Prolonged apposition or
repeated subacute attacks lead to gradual PAS formation. These
usually begin in the superior angle, which is narrower than
the inferior angle,[Bhargava, 1973 #142; Mapstone, 1977 #636]
as pinpoint synechiae reaching to the midtrabecular meshwork
and then gradually expanding in width. In early cases, in
which appositional closure is present but PAS have not yet
formed, we prefer the term chronic appositional closure. This
condition can lead to elevated intraocular pressure and
glaucomatous disc and visual field damage without PAS
formation.[Foulds, 1957 #637]

Eyes with progressive PAS formation may eventually develop an
acute attack of angle-closure when pupillary block results in
closure of the remaining portions of the angle unaffected by
PAS. Many cases, however, develop elevated intraocular
pressure and glaucomatous damage in the absence of symptoms.
The presentation is similar to that of open-angle glaucoma,
with progression of glaucomatous cupping and visual field
loss. This is the situation most commonly associated in the
United States with chronic angle-closure glaucoma. However,
eyes with the same appearance but normal intraocular pressure
merely constitute an earlier stage.

PAS may also form during an acute attack, remaining after
iridotomy has opened the unaffected portions of the angle.
These PAS are usually high and broad. When first observed at
this stage, it is impossible to determine whether the PAS
formed before or during the attack, or at both times.

In eyes with darker irides, a second mechanism of progressive
angle-closure is more common. The closure is circumferential
and begins in the deepest portion of the angle. Closure occurs
more evenly in all quadrants, so that the angle progressively
becomes more shallow. The appearance over time is of a
progressively more anterior iris insertion. Lowe[Lowe, 1964
#194] has termed this creeping angle-closure. The PAS
gradually creep up the ciliary face to the scleral spur and
then to the trabecular meshwork.

Insertion of the iris at or anterior to the scleral spur is
rare in young individuals, and in many eyes with angle-closure
glaucoma that have such an insertion, creeping angle-closure
is the underlying reason. Creeping angle-closure is uncommon
in whites but much more prevalent in Asians, in whom it ranks
high as a cause of blindness. Black patients with
angle-closure also tend to have this form. It occurs in eyes
with slightly deeper, though still shallow, anterior chambers
than are found in acute angle-closure. The gradual shortening
of the angle in the presence of iris bombé brings the
peripheral iris close to the external angle wall more and more
anteriorly, narrowing the gap between the iris and the
trabecular meshwork. Eventually, an acute attack may supervene
(more commonly in Asians), or the PAS may permanently occlude
the trabecular meshwork and lead to elevated intraocular
pressure and glaucomatous damage (more commonly in black
patients).

The intraocular pressure in eyes with chronic angle-closure
may be normal or elevated. As PAS formation progresses in the
absence of intermittent attacks, the pressure rises gradually
as less and less functional trabecular meshwork becomes
available. In eyes with intermittent attacks, the pressure
rises more rapidly relative to the extent of PAS formation
caused by recurrent damage to the trabecular meshwork by the
transient angle-closure.

Dispersed pigment granules collect in the iridocorneal angle
where the peripheral iris is in contact with the cornea. Dense
blotches of pigment on the meshwork, particularly in the
superior angle, or deposits of black pigment in the angle of a
lightly pigmented iris, are highly suggestive of previous
appositional closure. If the angle opens, this deposited line
of pigment shows the extent of previous angle closure and can
sometimes be a helpful diagnostic feature.

The anterior chamber is quiet and usually deeper than in eyes
with acute angle-closure glaucoma. The pupil is normal. The
gradual elevation of intraocular pressure does not result in
corneal endothelial decompensation, and edema is rare. The
intraocular pressure is usually less than 40 mmHg and does not
reach the levels found in acute angle-closure glaucoma.
Symptoms are absent until the pressure rises high enough to
affect the cornea or until extensive visual field damage has
occurred. Although iridotomy will eliminate the pupillary
block, intraocular pressure often remains elevated, and
further medical treatment or surgery is required.

Absolute Glaucoma
Absolute glaucoma refers to an eye with no light perception
and a persistently elevated intraocular pressure. The angle
initially may be open or closed, but in phakic eyes an
intumescent cataract often develops and leads to an associated
angle-closure. The time required for a neglected angle-closure
attack to cause total blindness is variable and depends on the
severity of the acute attack, but appears to be an average of
1 to 2 years.

Treatment is palliative and intraocular surgery is
unwarranted. If corneal edema and pain are not relieved by
topical beta-adrenergic blocking agents, steroids, and
cycloplegics, noninvasive cycloablation may be performed. If
this is insufficient or if complications such as phacolytic
glaucoma develop, evisceration or enucleation may be
necessary. Phthisis bulbi is not an uncommon outcome.

PLATEAU IRIS
Plateau iris configuration refers to the anatomic structure
in which the iris root angulates forward and then
centrally.[Tornquist, 1958 #195] In many cases, the iris root
is short and is inserted anteriorly on the ciliary face, so
that the angle is shallow and narrow, with a sharp drop-off of
the peripheral iris at the inner aspect of the angle. The iris
surface appears flat and the anterior chamber is not unusually
shallow on slit-lamp examination.

Plateau iris syndrome refers to the development of
angle-closure, either spontaneously or after pupillary
dilation, in an eye with plateau iris configuration despite
the presence of a patent iridectomy or iridotomy. Some
patients may develop acute angle-closure glaucoma[Godel, 1968
#196; Lowe, 1968 #197; Lowe, 1981 #198; Wand, 1977 #199] The
risk of postoperative pupillary dilation after iridectomy or
iridotomy is infrequently realized.

Until recently, plateau iris syndrome was considered a rare
entity. We have differentiated two subtypes.[Lowe, 1989 #2841]
In the complete syndrome, which comprises the classic
situation and is rare, intraocular pressure rises when the
angle closes with pupillary dilation. In the incomplete
syndrome, intraocular pressure does not change. The important
factor differentiating the complete and incomplete syndromes
is the level of the iris stroma with respect to the angle
structures, or the "height" to which the plateau rises . If
the angle closes to the upper trabecular meshwork or
Schwalbe's line, intraocular pressure rises, whereas if the
angle closes partially, leaving the upper portion of the
filtering meshwork open, the pressure will not rise. This is a
far more common situation and is clinically significant as
these patients can develop PAS up to years after a successful
iridotomy produces what appears as a well-opened angle.

Plateau iris results from large and/or anteriorly positioned
ciliary processes holding up the peripheral iris and
maintaining its apposition to the trabecular meshwork
.[Pavlin, 1992 #240; Ritch, 1992 #1046; Wand, 1993 #3212] When
indentation gonioscopy is performed in such an eye, the
ciliary processes prevent posterior movement of the peripheral
iris. As a result, a sinuous configuration results (sine wave
sign), in which the iris follows the curvature of the lens,
reaches its deepest point at the lens equator, then rises
again over the ciliary processes before dropping peripherally.
Much more force is needed during gonioscopy to open the angle
than in pupillary block because the ciliary processes must be
displaced, and the angle does not open as widely. In a
morphometric study of the ciliary sulcus, Orgül et al.[Orgül,
1993 #2835] proposed that the displacement of the pars plicata
from the peripheral iris to the iris root during embryogenesis
may be incomplete in eyes of shorter axial length. Darkroom
gonioscopy is important in plateau iris as well as in
pupillary block, and an angle which appears open in the light
can close in the dark.

Patients with plateau iris tend to be female, younger (30s to
50s) and less hyperopic than those with relative pupillary
block, and often have a family history of angle-closure
glaucoma. Except in the rare younger patients (20s and 30s),
some element of pupillary block is also present. However,
because of the nature of the anatomic relationships of the
structures surrounding the posterior chamber, the degree of
relative pupillary block necessary to induce angle-closure is
less than that in primary angle-closure glaucoma; this seems
to account for the deeper anterior chamber and flatter iris
surface in eyes with angle-closure and plateau iris. Patients
with plateau iris who develop angle-closure glaucoma are also
somewhat younger than those with pupillary block angle-closure
glaucoma. As a general rule, the older the patient, the less
prominent the angulation of the peripheral iris and the
greater the element of pupillary block. Iridotomy is
successful at opening the angle when a component of pupillary
block is present, but periodic gonioscopy remains indicated,
as the angle can narrow further with age due to enlargement of
the lens.

If plateau iris was not diagnosed before iridotomy and
intraocular pressure is elevated postlaser, careful gonioscopy
should be performed. If the angle is open, secondary damage to
the trabecular meshwork or pigment liberation with dilation
are the most likely causes. If the angle is closed, the
differential diagnosis, besides plateau iris, should include
malignant glaucoma, in which the anterior chamber is extremely
shallow; PAS, which can be ruled out by indentation
gonioscopy; or incomplete iridectomy.

Although plateau iris syndrome is usually recognized in the
postoperative period, it may develop years later. Patients
with plateau iris configuration should not be assumed to be
permanently cured, even though plateau iris syndrome does not
develop immediately.

IRIDOSCHISIS
Iridoschisis is a separation of the anterior and posterior
iris stromal layers which occurs primarily in older women. It
is usually bilateral, but may be asymmetric. The amount of
stromal separation can sometimes be dramatic. Iridoschisis has
been associated in the literature with narrow angles and
angle-closure glaucoma.[Romano, 1972 #203; Salmon, 1992 #8638;
Loewenstein, 1948 #8969; Loewenstein, 1945 #8968; Haik, 1952
#8970; McCulloch, 1950 #8971; Mills, 1967 #8972; Rodrigues,
1983 #8973; Carter, 1953 #8974] Whether angle-closure requires
an eye with a preexisting narrow angle is unknown.

ANGLE-CLOSURE GLAUCOMAS ASSOCIATED WITH DRUGS AND OTHER DISORDERS
Miotic-induced Angle-closure Glaucoma

Prolonged miotic treatment in eyes with open-angle glaucoma
and narrow angles may lead to pupillary block and
angle-closure glaucoma. We have seen chronic angle-closure
develop after several years of miotic therapy in eyes that
initially had wide open angles. In some eyes, zonular
relaxation occurs more readily than in others, so that
anterior lens movement and an increase in axial lens thickness
may facilitate pupillary block and angle-closure. In other
eyes, there is little change in the lens, but progressively
increasing pressure in the posterior chamber gradually pushes
the peripheral iris against the trabecular meshwork. It is our
impression that eyes with exfoliation syndrome are
particularly prone to develop miotic-induced angle-closure. In
these eyes, the iris is thicker and stiffer than normal due to
deposition of exfoliation material within the stroma. In
addition, zonular weakness allows the lens to move forward,
leading to pupillary block.

Less commonly, miotic therapy can have a pronounced effect on
lens position and trigger malignant glaucoma.[Gorin, 1966
#625; Levene, 1972 #638; Merritt, 1977 #639; Rieser, 1972
#626] Unequal anterior chamber depths, a progressive increase
in myopia, or progressive shallowing of the anterior chamber
are clues to the correct diagnosis.

Combined Mechanism Glaucoma
Combined mechanism glaucoma refers to situations in which both
open-angle and angle-closure components are present. A patient
may have open-angle glaucoma and either narrow angles with
superimposed intermittent angle-closure glaucoma or
miotic-induced angle-closure. The most common situation is
that in which angle-closure, either acute or chronic, is
eliminated by iridotomy and/or iridoplasty and intraocular
pressure still remains elevated, with or without the presence
of PAS of any extent. Another situation occurs in eyes with
exfoliation syndrome successfully treated for angle-closure
glaucoma, in which open-angle glaucoma can develop
independently years later with progressive blockage of the
trabecular meshwork. In all of these cases, the residual
open-angle component is treated as open-angle glaucoma.

Mixed Mechanism Glaucoma
This term is often used interchangeably with combined
mechanism glaucoma, creating additional confusion. It is
better to reserve this term to describe residual appositional
angle-closure by another mechanism (plateau iris,
phacomorphic, ciliary block) remaining after elimination of
pupillary block with partial opening of the angle.

Phacomorphic Glaucoma
Swelling of the lens may convert an anterior chamber of medium
depth into one that is markedly shallow and precipitate acute
angle-closure glaucoma. In countries in which cataracts are
prevalent and operations not readily available, acute
angle-closure glaucoma from swollen hypermature lenses is
common. Again, some element of pupillary block may also be
present. Phacomorphic glaucoma is often unresponsive to
medical therapy, and paradoxical reactions to pilocarpine are
common. Pilocarpine, even in elderly patients, increases axial
lens thickness and causes anterior lens movement, further
shallowing the anterior chamber.[Abramson, 1973 #89]

Slight lens subluxation in eyes of elderly patients, formerly
termed senile subluxation of the lens, is most commonly
associated with exfoliation syndrome. Mild iridodonesis may be
seen. In some cases, anterior lens movement may be sufficient
to cause angle-closure glaucoma, usually chronic. These eyes
are more susceptible to the development of miotic-induced
angle-closure during treatment for open-angle glaucoma.
Iridotomy usually suffices to eliminate pupillary block and
the angle-closure component.

In younger patients anterior lens movement is often
associated  with secondary causes or ciliary block. After
iridotomy, iridoplasty may be necessary to eliminate continued
appositional closure if cycloplegics are unsuccessful at
maintaining a more posterior lens position and an open angle.
This topic is discussed more fully in Chapter 58.

Malignant Glaucoma
Malignant (ciliary block) glaucoma[Levene, 1972 #638;
Shaffer, 1978 #640; Simmons, 1972 #641; Weiss, 1972
#642; Dueker, 1994 #4726] is a multifactorial disease in
which the following components may play varying roles: (1)
previous acute or chronic angle-closure glaucoma, (2)
shallowness of the anterior chamber, (3) forward movement
of the lens, (4) pupillary block by the lens or vitreous, (5)
slackness of the zonules, (6) anterior rotation and/or swelling
of the ciliary  body, (7) thickening of the anterior hyaloid
membrane, (8) expansion of the vitreous, and (9) posterior aqueous
displacement into or behind the vitreous. This topic is
covered in Chapter 39.

Swelling or anterior rotation of the ciliary body with forward
rotation of the lens-iris diaphragm and relaxation of the
zonular apparatus causes anterior lens displacement which in
turn causes direct angle-closure by physically pushing the
iris agains the trabecular meshwork.[Phelps, 1974 #643]
Accurate diagnosis and treatment are often more difficult when
the initiating event is posterior to the lens-iris diaphragm.

In predisposed eyes, miotic therapy can have a pronounced
effect on lens position and trigger malignant glaucoma.[Gorin,
1966 #625; Levene, 1972 #638; Merritt, 1977 #639; Rieser, 1972
#626] Unequal anterior chamber depths, a progressive increase
in myopia, or progressive shallowing of the anterior chamber
are clues to the correct diagnosis.

 Malignant glaucoma may occur following cataract surgery with
posterior chamber intraocular lens implantation.[Brown, 1986
#1255; Epstein, 1984 #1395; Lynch, 1986 #2773; Duy, 1987
#2729; Reed, 1990 #1054; Vajpayee, 1991 #2812; Tello, 1993
#1963] The differential diagnosis includes pupillary block,
choroidal hemorrhage, and ciliochoroidal effusion with
anterior rotation of the ciliary body and secondary angle
closure. Shallowing of the central anterior chamber occurs in
pseudophakic malignant glaucoma, but not in pupillary block.
Rupture of the anterior hyaloid face is usually curative and
allows aqueous to move into the anterior segment. We have
examined several patients with presumed aqueous misdirection
in whom an annular ciliary body detachment had caused anterior
movement of the ciliary body. Whether a posterior diversion of
aqueous flow is present in these disorders is unknown.
Some of the disorders that can lead to this picture are
covered in other chapters.  These include drug sensitivity
(e.g., sulfonamides, see Chapter 56); angle-closure after
panretinal photocoagulation, central retinal vein occlusion,
or scleral buckling procedures (see Chapters 50 and 51); uveal
effusion from posterior segment inflammation; ciliary body
swelling, inflammation, or cysts ; posterior segment tumors
(see Chapter 52). Aphakic and pseudophakic malignant glaucoma
are discussed in Chapter 61.

Retinopathy of prematurity
Angle-closure may occur in very young children with
retinopathy of prematurity due to forward shifting of the
lens-iris diaphragm (see also Chapter 44).[Cohen, 1964 #8926;
Hittner, 1979 #1894; Pollard, 1980 #5292; McCormick, 1971
#1898; Laws, 1994 #8928; Kushner, 1982 #1057] These children
do not respond to iridotomy. In young adults with this
condition, there appears to be a superimposed element of
pupillary block, and iridotomy may be successful.[Ueda, 1988
#8927; Smith, 1984 #1899]

Nanophthalmos
Nanophthalmos is a bilateral, often familial form of
microphthalmos unaccompanied by other congenital
malformations. It is characterized by hyperopia, small corneal
diameter, thick sclera, and narrow angles.[O'Grady, 1971
#8231] Angle-closure glaucoma usually appears between the ages
of 20 and 50 years. Although by definition, nanophthalmos
refers to an eye of axial length less than 20 mm, there is
obviously a gradient of hyperopic refraction, the degree of
hyperopia correlating inversely with axial length. There is an
inverse correlation between the degree of hyperopia and the
age of onset of angle-closure. The youngest reported patient
was 9 years old with 21 diopters of hyperopia.[Hatcher, 1952
#8962] However, acute angle-closure glaucoma can also develop
in the elderly.[Cross, 1976 #8964]

The sclera in nanophthalmic eyes is abnormally
thick.[Brockhurst, 1975 #2710] Electron microscopy reveals
disordered collagen bundles and fraying of collagen fibrils,
with absence of elastic fibers.[Trelstad, 1982 #5595; Stewart,
1991 #2804] In tissue culture, scleral fibroblasts of eyes
with nanophthalmos appear to have an abnormal glycosamine
metabolism, which might explain the abnormal packing of
collagen bundles and scleral thickening.[Shiono, 1992 #2798]
Uveal effusion is common, either spontaneously or after
surgical procedures, including filtration surgery or cataract
extraction.[Brockhurst, 1975 #2710; Ryan, 1982 #8963]
Associations with retinitis pigmentosa[Ghose, 1985 #8230;
MacKay, 1987 #1042] and Hallerman-Streiff syndrome[Stewart,
1991 #2804] have been reported.

Laser iridotomy for angle-closure is usually unsuccessful or
only temporarily successful. If successful initially, lens
enlargement with age can lead to appositional closure.
Iridoplasty (gonioplasty) to flatten the peripheral iris was
first reported in 1979 by Kimbrough et al.[Kimbrough, 1979
#1412] Combined iridotomy and iridoplasty often brings the
angle-closure under control.[Jin, 1990 #2759] Uveal effusions
have been reported after both laser iridotomy[Karjalainen,
1986 #1408] and trabeculoplasty.[Good, 1988 #2742] The risks
of surgical intervention include malignant glaucoma, expulsive
suprachoroidal hemorrhage, and retinal detachment.[Hyams, 1990
#8965] Posterior sclerotomy may or may not be successful at
preventing uveal effusion.[Calhoun, 1975 #8047; Jin, 1990
#2759] Vortex vein decompression for nanophthalmic uveal effusion
was described by Brockhurst,[Brockhurst, 1980 #5305] but the
technique is technically difficult. Partial thickness
sclerectomies and sclerostomies were reported in one patient
to achieve complete resolution of retinal and choroidal detachments,
suggesting impairment of transscleral protein transport as a primary
pathophysiologic mechanism in nanophthalmic uveal effusion.[Allen,
1988 #1921] Subsequently, Wax et al. described success with anterior
lamellar sclerectomy without sclerostomy.[Wax, 1992 #2820]

CLINICAL PATHOLOGY OF ANGLE-CLOSURE GLAUCOMA
When the angle totally occludes, aqueous outflow is blocked,
and intraocular pressure rises markedly. The effect of the
elevated pressure depends on the magnitude and rapidity of its
rise. At the same time the pupillary reaction to direct light
decreases. The pupil becomes partly dilated and tends to
assume a vertically oval shape, but may be oblique or even
horizontal.

Cornea
With very high intraocular pressure, corneal edema is severe.
Transient loss of sensitivity can occur.[Patel, 1988 #2787]
The cornea is cloudy and may be twice its usual thickness.
Endothelial cell density is reduced by as much as 33%
following an acute attack and is greater the longer the
duration of the attack.[Bigar, 1982 #644; Mapstone, 1985 #121;
Markowitz, 1984 #652; Brooks, 1991 #8958; Olsen, 1980 #3558;
Malaise-Stals, 1984 #8959] Corneal decompensation may occur in
eyes with preexisting endothelial compromise.[Krontz, 1988
#1932; Hyams, 1983 #8960] When the pressure is lowered, the
edema clears first at the periphery. Folds in Descemet's
membrane form. Following prolonged high pressure, corneal
edema and striate keratopathy may persist for some days. With
severe damage, chronic edema may persist, lipid is deposited,
and the cornea may become fibrosed and vascularized.

Iris
Partial necrosis of the iris stroma is the first sign of
damage from elevated intraocular pressure experimentally.
[Anderson, 1975 #200] At pressures over 60 mmHg, the pupil
becomes increasingly resistant to miotics, probably caused
by direct pressure on the sphincter muscle.[Charles, 1970
#201] The sphincter may respond to miotics after the pressure
has been lowered, but when intraocular pressure exceeds the
diastolic blood pressure, the iris around the pupil becomes
ischemic.[Charles, 1970 #201]

The sphincter muscle then loses its ability to contract even
if intraocular pressure is lowered, and patchy atrophy of the
iris occurs. The dilator muscle is less affected than the
sphincter, so that the instillation of 10% phenylephrine
usually causes increased pupillary dilation.

In the segments in which the stroma is not obviously atrophic,
the pupillary margin is thick, rolled, and bunched with radial
folds. At the margins of the atrophic area, the stromal fibers
run obliquely to the periphery behind the edges of the
atrophic area, thus producing a twisting of this border zone
of the stroma[Winstanley, 1961 #202]. In severe and prolonged
attacks, diffuse iris atrophy occurs.

Sometimes a sector of the iris stroma will be disrupted and
look like iridoschisis[Romano, 1972 #203]. This may occur with
slow progressive atrophy months or years after the acute
attack. The pigment epithelium and dilator muscle can be
patchily affected and areas may transilluminate. Posterior
synechiae may be minimal or extensive. After iridectomy
aqueous humor flowing into the anterior chamber can
bypass the pupil, favoring formation of postoperative posterior
synechiae.

Ciliary Body
In 1973, Kerman et al.[Kerman, 1973 #645] reported that the
ciliary processes may be inserted more anteriorly than normal
and extend to the peripheral posterior iris in eyes with
angle-closure. With the discovery that plateau iris is caused
by large and/or anterior ciliary processes, it is now becoming
evident that there is a spectrum of ciliary body size and
position. The ciliary body itself does not appear to be
adversely affected by acute angle-closure glaucoma.

Lens
Lens damage can occur as: (1) glaukomflecken, (2) anterior
capsular cataract, (3) pigment deposition, posterior
synechiae, and fibrosis, (4) cortical cataracts, and (5)
nuclear sclerosis.

Glaukomflecken ("glaucoma flakes"), or disseminated anterior
subcapsular cataracts of acute glaucoma, are the most
characteristic signs of lens damage from sudden severe rises
of intraocular pressure. They are thought to be caused by
pressure necrosis of anterior lens fibers and do not occur at
the posterior pole.

When intraocular pressure is very high, the lens damage
simulates a thin, gray deposit of exudate on the lens
surface.[Jones, 1959 #646] With a fall in pressure, the sheet
becomes thinner in some places and more condensed in others.
Holes develop within it, so it may appear as a coarse,
irregular, white net.[Lowe, 1965 #647] Later these flakes
become more discrete and appear as small, irregular,
blue-white plaques. They tend to follow suture lines of the
lens, suggesting necrosis of the tips of the lens fibers.

Gradually, the flakes diminish and usually become relatively
sparse. As new lens fibers grow from the equator, they overlie
the flecks, which sink deeper into the lens and persist as
permanent evidence. Glaukomflecken occur almost entirely
within the pupil according to its size at the time of the
attack.[Sugar, 1946 #648]

Glaukomflecken are rare apart from acute angle-closure
glaucoma, but have been seen after contusion and chemical
burns and also when the anterior chamber has remained flat
postoperatively with the cornea and lens in contact for some
days.

Occasionally, small white plaques resembling glaukomflecken
may persist in the anterior surface of the lens. These are
anterior capsular cataracts. Anterior cortical lens opacities
commonly follow severe attacks of angle-closure glaucoma and
may persist as faint irregular streaks that almost invariably
progress.

The first sign of nuclear sclerosis is a myopic refractive
change, which may stabilize or progress. Following severe
glaucomatous iritis with extensive posterior synechiae,
fibrosis may extend from the iris onto the anterior lens
surface.

Zonules
The zonules can be damaged, so with surgery the lens may move
forward with the development of malignant (ciliary block)
glaucoma. Occasionally, the opaque lens may slowly dislocate
over the years and sink below the pupil.

Choroid Kubota et al.[Kubota, 1993 #2833] reported decreased
choroidal thickness in 12 eyes with angle-closure glaucoma
associated with malignant melanoma of the ciliary body. The
decreased thickness was primarily due to decreased choroidal
vessel diameter, suggesting decreased choroidal perfusion.

Retina and Optic Nerve

In intermittent angle-closure glaucoma, even after many
attacks, the optic disc is typically unaffected. During the
initial states of an acute attack, the disc may appear normal,
congested, or edematous with retinal venous congestion and
retinal hemorrhages near the disc. When intraocular pressure
is acutely elevated in owl monkeys, damage to the nerve fiber
layer and ganglion cells precedes damage to most other tissues
except the iris.[Anderson, 1975 #200]

Douglas et al.[Douglas, 1975 #204] found pallor without
cupping following acute attacks, and pallor and cupping in
patients with chronic angle-closure. Acutely elevated intraocular
pressure in monkeys leads to optic disc congestion lasting
several days before pallor and cupping develop.[Zimmerman,
1967 #650] Large retinal hemorrhages near the disc can occur
with sudden lowering of intraocular pressure as after hyperosmotic
or carbonic anhydrase inhibitor therapy. Retinal function is
depressed with raised intraocular pressure.[Uenoyama, 1969
#649] Abnormalities of visual evoked potentials have been
reported.[Mitchell, 1989 #1906]

In a histological study of 21 eyes with secondary angle-closure
glaucoma,Jonas et al.[Jonas, 1992 #1051] found the lamina cribrosa
significantly thinner, the optic cup deeper and wider,
and the corpora amylacea count lower than in controls.

Parapapillary atrophy was significantly greater and
occurred more frequently in glaucomatous eyes and the
parapapillary retina was significantly thinner.[Jonas, 1992
#1052] A significantly decreased photoreceptor, but not
retinal pigment epithelial, cell count was reported in eyes
with angle-closure following penetrating trauma.[Panda, 1992
#2786]

The final effects will depend on severity and duration of the
attack. Recovery may be complete or there may be contraction
of isopters and nerve fiber bundle defects.[Douglas, 1975
#204; Lowe, 1973 #624] Pallor without cupping was found to be
characteristic of discs after acute angle-closure glaucoma,
whereas both pallor and cupping occurred in chronic
angle-closure.[Douglas, 1975 #204] In prolonged attacks, when
treatment is delayed, glaucomatous damage may progress to the
point at which vision is reduced to perception of hand
movements or light. In chronic angle-closure glaucoma, the
visual field defects and optic disc cupping progress similarly
to those of open-angle glaucoma.