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Q: medical statistics ( Answered 4 out of 5 stars,   1 Comment )
Subject: medical statistics
Category: Health > Conditions and Diseases
Asked by: 37169650-ga
List Price: $100.00
Posted: 30 May 2006 16:05 PDT
Expires: 29 Jun 2006 16:05 PDT
Question ID: 733804
To Whom It May Concern;

		This is a medical question which I have researched as far as my
limited computer skills allow on the internet, also asking questions
of eye specialists, and in researching library references. First you
should be familiar with my background ---

		I inherited medium-large lower eyelid 'bags' which I felt made me
look much older. I figured I'd just age into them eventually and
decided to forget about it. By the time I turned 40, however, I really
didn't look any older otherwise so I decided to have the bags removed
by what's called a blepharoplasty operation, which was done from
inside the lid. Everything went well.

		People with larger fat deposits around their eyes usually have
ancestors that lived for many generations in cold climates and
evolution developed these fatty deposits to protect their eyes from
the cold. I live in Southern California, a semi-arid climate. Before
the blepharoplasty procedure my eyes always seemed to be too warm, and
I frequently used ice packs to cool them down. After the procedure,
however, I noticed my eyes were cool most of the time, downright cold
at night. I thought at the time that this was a bonus.

		8 years later I developed open-angle intraoccular pressure (IOP) in
both eyes, about 25-30mm on the pressure gauge. This is a precursor
for glaucoma (95% of people with untreated IOP start developing
glaucoma within 10 years). I started treating the condition with
prescription eyedrops right away, and 8 years later have suffered no
'cupping' of the optic nerve (the degenerative disease called
		 What actually happens in IOP is that the eye continues to produce
aqueous fluid at a continuous pace, but drainage is slower than normal
and pressure backs up. The prescription eye drops all work in 1 of 2
ways: they either act on the glands to produce less fluid, or they
speed up the enzymatic action that allows fluid to drain more quickly.
Sometimes people have to use both. However, the body eventually
developes an intolerance to any drug. I'm on my fifth drug now, with
only more aggressive treatments to look forward to as I get older. Not
only that, long term drug use has a clouding effect on the clarity of
the cornea (the clear tissue in front of the eye), so I would like to
cure this condition rather than just treat the symptoms.

		It seemed unusual to me that I had this problem in the first place,
as most people who develope it don't show signs untill they're over
70. No one in my family has had it either with the exception of my
mother, who didn't get it until she was in her nineties.

		After being diagnosed with IOP I began to wonder if the lower
temperature that I was experiencing in my eyes was slowing down the
actual physical process of draining fluid. Temporary IOP is a rare
complication following a blepharoplasty procedure, and that is the
closest reference I could ever find doing internet searches. I was
only able to find two related references through he UCLA medical
library, both master's theses: one was about heat transfer analysis in
the eyes of rabbits at UC Berkeley, and the other was a study of
cornel temperature under simulated arctic conditions at the University
of Oulu in Canada. They basically said that temperature was important
for proper eyeball functioning, and that the insullation eye lids
provided was important too, along with many other factors.

		The eye specialists I have talked to think I have an interesting
theory which deserves a study, but they all say there is no current
medical evidence to support my hypothesis. There is a medical
procedure for putting fat back into the lower lid, but it usually
requires multiple treatments because they don't readily take. Before
getting into something like that, I would like to find more evidence
that my hypothesis is right. In other words, my question is:

		"Is there a definite link between lower lid blepharoplasty and long
term intraoccular pressure?"

		 Ideally, I'd like to know epidemiologically what percentage of
people who have had lower &/or upper lid blepharoplasty go on to
develope IOP and how this compares to the general population to see if
their is a difference and if it's satistically significant. Also, the
average age IOP showed up in this group compared to the general
population (as people who get blepharoplasties tend to be in their
thirties & forties), and how long on average after the blepharoplasty
procedure was IOP first diagnosed (out of curiosity I'd like to see if
it's less than 10 years). Of course, any other related material that
you might find would be helpful.

	Thank you for your assistance with this problem.

Request for Question Clarification by crabcakes-ga on 31 May 2006 10:41 PDT
Hello 37169650,

   Because I can?t find the answer to all your questions, particularly
the statistics, let me share what I did find. I found that cold
decreases the blood supply to the optic nerve, which is undesirable in
increased IOP. I found no direct link to lower lid blepharoplasty and
increased IOP.

IOP is the intraocular pressure, that we all have. I?m going to assume
you are referring to increased open-angle intraocular pressure.

?Visual loss following blepharoplasty is well-described in the
literature, but the mechanism has not been completely understood. The
most likely factor is increased orbital pressure and vascular
impairment subsequent to hemorrhage or edema within the orbit induced
by operative manipulation(3-6). Total vascular insufficiency for
60-120 minutes produces permanent loss of vision(7). Increased
intraorbital pressure can produce a central retinal artery(8) or
vein(3) occlusion with ischemia of the anterior optic nerve or
angle-closure glaucoma in susceptible individuals(6)?

?Draining the Fluid and Intraocular Pressure. The aqueous fluid is
continuously produced within the front of the eye, causing pressure
known as intraocular pressure (IOP). To offset the in-flowing fluid
and to maintain normal IOP, the fluid drains out between the iris and
cornea (an area known as the drainage angle). It does so through two
channels within this angle:

?The trabecular meshwork, a sponge-like, porous network, and its
connecting passageways are referred to as the "conventional" outflow
pathway. Most of the eye fluid outflow occurs in this region and flows
from the trabecular meshwork to a group of vessels encircling the
anterior chamber, called Schlemm's canal. From here, the fluid enters
collection chambers and then flows out into the general blood
circulatory system of the body.

?The uveoscleral pathway is located behind the trabecular meshwork and
is called the "unconventional" pathway. Up to 30% of the fluid flows
out through this channel.?

In glaucoma: ?Most people with glaucoma have the form called
primary-open-angle glaucoma (also called chronic open-angle glaucoma).
Open-angle glaucoma is essentially a plumbing problem.
The disease process may occur as follows:

?The drainage angle remains open, but tiny drainage channels in the
trabecular meshwork pathway become clogged. This pathway is
responsible for most aqueous humor fluid outflow. An imbalance then
occurs as fluid continues to be produced but does not drain out
efficiently. Experts have still not definitely determined the precise
area in the pathway where the blockage is most likely to occur. (In
rare instances the pressure is high because the eye produces too much
aqueous humor.)

?The fluid in the eyes anterior chamber builds up and increases
pressure within the eye. This is called intraocular pressure (IOP).
?The intraocular pressure exerts force on the optic nerve at the back of the eye.
?Over time, the persistent pressure or other factors irreversibly
damages the delicate long fibers of the optic nerve, called axons,
which convey images to the brain.
?As these axons die, the small cup-like head of the optic nerve may
eventually collapse into an enlarged irregular shape.
Optic nerve damage is the basic glaucoma condition. If it is
untreated, eventually the nerve deteriorates until a person loses
sight, first in the peripheral vision (the vision in the "corner of
the eyes"). If it becomes severe, the person loses central vision (in
the middle of the eyes), and may eventually become blind. (Blindness
is fortunately nearly always preventable with early treatment.)

Primary open-angle glaucoma tends to start in one eye but eventually
involves both. In about half of patients the damage in the eye is
diffuse, that is the nerve damage is generalized. In the other half
the disease is localized, causing wedge-shaped abnormalities in the
nerve fiber layers of the retina.?

?The intraocular pressures were 14 mmHg RE and 22 mmHg LE.?

?Normal intraocular pressure (IOP) ranges between 11 and 21 mm Hg:
however, this level may not necessarily be healthy for all people."?

?"Aqueous humor, which helps in lens metabolism and nourishes the lens
and cornea, maintains normal intraocular pressure (ie, normal IOP is
10 to 22 mm Hg) by the rate of its secretion and the resistance to
outflow by the trabecular meshwork."?

?The human eye is a delicate system which consists of a few components
that must be maintained at an optimum to ensure a production of an
undistorted image. These components are transparency, constancy of
form and smoothness of surface. The constancy of form of the ocular
bulb is maintained by the sclera and the IOP (Intraocular pressure).
This pressure is higher than that of the environment and is produced
by the flow of the aqueous humor.

The aqueous humor is a fluid produced by the active transport of
electrolytes. It flows through the anterior chamber and is drained
away every hour by the venous blood flow. If the drainage of the
aqueous fluid front he eye is sufficiently prevented by a physical
obstacle or production exceeds the outflow, then IOP builds up and a
condition known as glaucoma is developed.?

??researchers have determined: 1) that aqueous humor flows and serves
as a nutrient delivery system for the avascular cells in the cornea;
2) that the aqueous humor is pumped into the eye and eventually drains
into a vein; and 3) that the resistance of the drainage system leads
to an increased intra-ocular pressure (IOP), typically 15 mm Hg gauge
(2000 Pa). Higher IOP is necessary to maintain the curvature of the
cornea and thus proper eye function, but increased IOP can lead to
damage to the optic nerve.

?In recent years, emphasis has been given to adding lateral canthal
support as an important adjunct to lower lid blepharoplasty. Lower lid
malposition and ectropion are among the most feared complications
following lower lid blepharoplasty. Lateral canthoplasty and lateral
tarsal strip procedures were initially used to correct established lid
malposition; however, more recently, it has become an accepted and
useful prophylactic measure against lid malposition in cosmetic
blepharoplasty (Glat, 1997; Jelks, 1997; Fagien 1999).?

This site mentions increased  orbital pressure ? ?Postoperatively,
orbital hemorrhage is recognized by patient reports of pain, swelling,
and proptosis. Associated changes in light perception may also be
present. This condition is a true emergency that requires an emergency
evaluation by an ophthalmologist. Open the incision, evacuate clots,
and control bleeding. Usually, no one bleeding point is defined. If
increased orbital pressure is suspected, perform a lateral canthotomy
with lateral cantholysis. Control hypertension and consider osmotic

?Pulling fat forward may result in still-bleeding capsule vessels
slipping back into the orbit, and may be a principal cause of raising
the intraorbital pressure postoperatively.  Because of this risk,
muscle-septal splitting openings into the orbit should never be
sutured?and need not be, as they will close on their own once the
excess fat is removed.?
?The exact mechanism of the blindness is not clear (2): it may be due
to a build-up of pressure anywhere within the orbit which rapidly
involves the whole orbit and produces proptosis, which in turn leads
to the bulging eye becoming impacted between the tense, swollen lids.
This further raises the pressure both intraorbitally and intraocularly
until the retinal circulation is obliterated and sight is lost.

Increase in pressure may very rarely be due to a retrobulbar
hemorrhage, which is more likely to arise following accident trauma,
intraorbital injection, or manipulation of orbital fractures. It is
possible that unheralded loss of sight may be caused by spasm of the
retinal arteries, by optic nerve ischemia caused by preoperative
drug-induced hypotension, or by undue and prolonged pressure on the
eye during surgery.?

3.	?Why does a small linear increase in intraocular pressure occur
with age in the normal population, as shown in Image 1?
4.	Why does a parasympathomimetic medication, such as pilocarpine,
produce a dramatic decrease in intraocular pressure in patients with
ocular hypertension and POAG but only produce a minimal decrease in
intraocular pressure in healthy patients?
Increased aqueous inflow is not the cause of ocular hypertension or
POAG. Ocular hypertension and POAG are caused by a decrease in aqueous
outflow. Aqueous outflow is controlled predominantly by trabecular
meshwork pore size. Davanger examined the relationship of pore size to
intraocular pressure using a hydrodynamic model. He found that as pore
size decreases, intraocular pressure increases according to a
hyperbolic function, as shown in Image 2.?

?Because of the hyperbolic relationship of intraocular pressure to
pore size, the healthy patient experiences only a small increase in
intraocular pressure with age as the diameter of the trabecular pore
size decreases because of the age-related decrease in baseline tension
of the ciliary muscle (see Image 4). On the other hand, patients with
ocular hypertension or POAG have inherited small pores or a protein
that effectively makes the pore diameter smaller. Therefore, although
patients with ocular hypertension and POAG experience the same change
in pore size with age as healthy patients, because of the reduction in
baseline ciliary muscle tension, they are starting near the bend of
the hyperbola (see Image 4). The same age-related change in pore size
produces a dramatic increase in intraocular pressure in those patients
who have inherited smaller pores and results in ocular hypertension
and POAG.?

?The two main types of glaucoma are primary open angle glaucoma
(POAG), and angle closure glaucoma. These are marked by an increase of
intraocular pressure (IOP), or pressure inside the eye. When optic
nerve damage has occurred despite a normal IOP, this is called normal
tension glaucoma.?

?Some people with normal pressure may experience vision loss from
glaucoma, and many people with high IOP (sometimes called ocular
hypertension) do not develop glaucoma. However, the higher the IOP,
the more likely optic nerve damage will occur.?
?Primary open-angle glaucoma 
Primary open-angle glaucoma accounts for 60-70% of glaucoma cases in
the United States. In open-angle glaucoma, the aqueous humor is unable
to drain out of the eye. For unknown reasons, the trabecular meshwork
(i.e., eye’s filtration area) does not function normally, the pressure
in the eye increases, and the optic nerve is damaged.
Most people do not experience symptoms until their vision is
compromised and extensive damage to the optic nerve has been done.
Peripheral vision is affected before central vision.?

?There is evidence that altered optic nerve head (ONH) blood flow may
play a role in the development and progression of glaucoma. In the
present study, investigators examined the baseline characteristics in
a population participating in a clinical trial in which the ocular
hemodynamic effects of timolol and dorzolamide were compared. The
trial included 140 patients with primary open-angle glaucoma (POAG) or
ocular hypertension (OHT); their baseline parameters were compared
with those of a group of 102 age-matched control subjects. Researchers
used scanning laser Doppler flowmetry to measure blood flow in the
temporal neuroretinal rim and the cup of the ONH. They assessed
pulsatile choroidal blood flow by laser interferometric measurement of
fundus pulsation amplitude. They also calculated hemodynamic
parameters and mean arterial pressure in both groups.

All ocular hemodynamic parameters were significantly lower in the
POAG/OHT group compared with the control group. In addition, results
showed a significant positive correlation between laser Doppler
flowmetry readings and mean arterial pressure in patients with
glaucoma but not in healthy control subjects. Likewise, the
correlation coefficient between fundus pulsation amplitude and mean
arterial pressure was higher in patients with glaucoma than in healthy
control subjects.

This study indicates reduced ONH and choroidal blood flow and an
abnormal association between blood pressure and ocular perfusion in
patients with POAG or OHT, independent of topical antiglaucoma
medication. Hence, vascular dysregulation appears to be an early
manifestation in glaucoma that is not caused by pharmacologic

?The effects of exercise and water replacement on intraocular pressure
(IOP) have not been well established. Furthermore, it is not known
whether the temperature of the fluid ingested influences the IOP
response. In the present study we determined the effect of water
ingestion at three temperatures (10, 24 and 38ºC; 600 ml 15 min before
and 240 ml 15, 30 and 45 min after the beginning of each experimental
session) on the IOP of six healthy male volunteers (age = 24.0 ± 3.5
years, weight = 67.0 ± 4.8 kg, peak oxygen uptake (VO2peak) = 47.8 ±
9.1 ml kg-1 min-1).?
The effects of physical exercise on IOP have received some attention
since the beginning of the 20th century (2) and there have been
reports suggesting that IOP decreases during exercise (2-9). However,
these studies often failed to control for variables such as the type,
intensity and duration of exercise, or subject age and level of
fitness and possible tonometric errors (10). Thus, definite
conclusions concerning IOP changes due to exercise cannot be reached.
The metabolic muscular heat produced during exercise increases body
temperature and activates thermoregulatory mechanisms to dissipate
excess heat. In hot environments, sweat is the main mechanism for heat
loss during exercise, leading to weight loss. Sweat contains small
amounts of minerals such as sodium and potassium (1). Profuse sweating
may lead to changes in plasma osmolarity, which could affect IOP.

Under certain conditions, hyperthermia induced by physical exercise
may be hazardous to health and physical performance. To counteract the
effects of dehydration, sweat losses during exercise must be replaced
with adequate amounts of water (1).

In experimental studies on rabbits, severe hypothermia caused a
decrease in IOP, while hyperthermia caused an increase in IOP (10) and
a decrease in IOP was reported after exposing the cornea to cold air.
The literature shows that water ingestion affects IOP in humans. It
was observed that 78% of healthy volunteers showed an increase of 2.7
mmHg in IOP 10 min after drinking 1000 ml of water and progressive
increases in IOP during a period of 30 min, and a return to basal
levels within the next 30 min (11).

The water temperatures were selected to produce physical cooling
(10ºC), to simulate body temperature (38ºC) and to reach an
intermediate point (24ºC).
IOP was measured by the applanation tonometry method using a
Haag-Streit Goldmann tonometer, model R 900, prior to the intake of
600 ml of water, 10 min after the intake of 600 ml of water, just
after the end of each experimental session (exercising or resting),
and 15, 30 and 45 min after the end of each session.
There was a 3-day interval between the different experimental
conditions and each volunteer performed the sequence of experiments at
the same time of day.
The results were similar when the right eye and the left eye were
compared. A statistically significant increase in IOP was observed
between the first and the second, the first and the third, and the
first and the fourth measurements of IOP, in both exercising and
resting sessions. There were no significant differences in IOP between
the resting and exercising conditions
Certain inverse relationships have been found between osmolarity and
IOP (5.8) and these changes in IOP have been attributed to serum
lactate or blood pH by some authors (5,6,8).

The loss of water and electrolytes that occurs during exercise may
affect plasma osmolarity and volume, which could cause changes in IOP.
In the present study, heart rate, blood lactate, mean skin
temperature, oxygen consumption, carbonic gas extraction, and
hydration status were consistently different between rest and
exercise, but no significant differences in IOP were found between
exercising and resting conditions. Furthermore, the temperature of the
water ingested by the volunteers during the different experimental
treatments did not influence the IOP results.

The variations in IOP - an initial increase followed by a return to
basal values (Figure 1) - were similar during exercise and rest and
were probably due to the ingestion of water, a result previously
reported in the literature (11).
We may conclude that metabolic changes induced by exercise under
conditions of water ingestion or the temperature of the ingested water
had no significant effects on IOP. In fact, only a transient increase
in IOP was observed, related to the ingestion of water.?
© 2006  Brazilian Journal of Medical and Biological Research

Av. Bandeirantes, 3900
14049-900 Ribeirão Preto SP Brazil
Tel. / Fax: +55 16 3633-3825

The above are only snippets of the entire article.(Copyrighted) You
may be able to access the entire article through your public library?s
First Search subscription.
Braz J Med Biol Res, January 2002, Volume 35(1) 121-125 (Short Communication)
Effects of submaximal exercise with water ingestion on intraocular
pressure in healthy human males
M.A. Moura1, L.O.C. Rodrigues2, Y. Waisberg1, H.G. de Almeida1 and E.

I found the article above without need for a library!

?Glaucoma is often associated with an increase in the intraocular
pressure (IOP) [11]. The regulation and increase of IOP is not fully
understood but it has been suggested that the trabecular meshwork (TM)
cells are important. One gene proposed as a candidate gene for
glaucoma is the Oculomedin (OCLM) or Trabecular meshwork-Inducible
Stretch Response gene (TISR). The function of the gene is unknown, but
it is induced by cyclic stretching in TM cells. The TM is located in
the iridocorneal angle which is the principal site of aqueous outflow
from the eye. It is proposed that the trabecular cells sense the
intraocular pressure and regulate the aqueous outflow. The gene is
expressed in the TM and retina, but not in other tissues. Oculomedin
translates into a small protein containing 44 amino acids. The gene
has homology to neuromedin K and an ALU repeat in the 5' UTR [12]. It
is a valid candidate for glaucoma by the analogy to the TIGR/MYOC

?The increased IOP could lead to the tissues, and thereby the cells,
in the eye undergoing stress in the form of mechanical stretching. The
discovery of a gene product induced by cyclic stretching in the tissue
involved in regulation of intraocular pressure was interesting, since
mutations in such a gene could very well give a phenotype that
involves elevated pressure in the eye?

In rabbits:?Circadian rhythms of IOP and body temperature were present
under the regular light-dark cycle and in constant dark. As did
pupillary enlargement, IOP rose sharply at the beginning of the
subjective dark phase and peaked shortly thereafter. Body temperature,
however, increased gradually and peaked in the late subjective dark
phase. In rabbits with unilaterally decentralized ocular sympathetic
nerves, the circadian rhythm of pupil size was present only in the
intact eye. In addition, the circadian IOP elevation in the
decentralized eye was reduced significantly. CONCLUSIONS: In
light-dark entrained rabbits, basal pupil size changes in a circadian
pattern and peaks at the beginning of the dark phase. The circadian
pupillary rhythm disappears after ocular sympathetic decentralization.
There are similar characteristics in the circadian rhythm of IOP. The
increase of basal pupil size in the early dark phase is not related to
the nocturnal increase of body temperature.?

This article is not copy-able, but pp. 12-13 have some information on
IOP and glaucoma.

This is interesting, but please discuss any supplements you would
consider using, with your ophthalmologist first.
Q; Are there any natural alternatives to aid in the treatment of glaucoma? 

A: Yes, the key with glaucoma treatment is to increase circulation in
and around the eye. Ginkgo biloba 120 mg twice a day should help
increase overall circulation and Magnesium 500 mg, which I recommend
taking at bedtime when the eye is in repair and the IOP is highest.
Also recommended is the trifola formula made by my colleague, Alan
Tillotson, Ph.D. (302-994-0565, which works in
numerous ways to support eye health and reduce your stress in general.
The B vitamins, especially B 12, DHA, Vitamin E and alpha lipoic acid
all support nerve and photo receptor cell function.?

?Patients with glaucoma who had evidence of acral vasospasm, however,
were more likely to show deterioration in visual fields after cooling
than patients without acral vasospasm (P = 0.007). CONCLUSIONS:
Patients with glaucoma have an abnormal increase in plasma ET-1 after
the body cools. It is possible that at least in some patients,
increased levels of ET-1 in response to vasospastic stimuli may be
involved in the pathogenesis of glaucomatous damage.?

?The mechanisms that lead to the development of glaucomatous optic
neuropathy are still not completely understood. In at least some
patients, factors besides increased intraocular pressure (IOP)
probably play a role in the pathogenesis of the disease. Among these
other factors, vasospasm has been suggested to be causative by several
investigators, leading to decreased blood flow or a diminished
capacity to autoregulate blood flow to the optic nerve head.1?

Please visit each web site for complete information.

Regards, Crabcakes

Search Terms
temperature + increased IOP
postoperative complications + lower lid blepharoplasty
increased iop + lower lid blepharoplasty
Increased IOP + trabecular meshwork
ocular hypertension + lower lid blepharoplasty
trabecular damage + lower lid blepharoplasty
cold weather  + increased IOP
cold + effect   + increased IOP
cold + effect   + IOP
cold + effect   + glaucoma

Clarification of Question by 37169650-ga on 01 Jun 2006 16:02 PDT
Hi Crabcakes,
		Thank you for effort to date. I'm not sure what kind of
clarification you need, so I will elaborate on what you've found so

		My study of a paper on eskimo eyes that I mentioned in my
background, which is actually called, "The thermostatic theory of the
eye", indicated that temperature in the main body of the eyeball
pretty much remains close to the core temperature of the body. So I
don't think that my optic nerves are in jeopardy solely because of the
temperature condition that so concerns me.

		I would really need the statistics I alluded to to 'prove' my case,
if it is in fact true. However, you provided some information that
indicates to me that my theory may not be right:

	First, the hyperbolic relationship of IOP to inherited trabecular
meshwork pore size vs. the age-related decrease in baseline tension of
the ciliary muscle may more accurately define the cause of my
condition as it did occur simultaneously with the development of
presbyopia  in my late forties. This also dovetailed with a related
website article you provided on scleral expansion.

	Second, the experimental studies on rabbits which demonstrated a
decrease in IOP after exposure to severe hypothermia; and the other
experiment which showed no relationship between the circadian rhythm
of IOP and the nocturnal increase of body temperature. In addition,
another website reference stated that Asians and Eskimos have a higher
prevalence of POAG than all other ethnic groups. These are the people
who have the largest 'naturally' occurring eyelids; again indicating
that a colder temperature in the anterior chamber of the eyeball might
actually decrease IOP.

		There were some other interesting references. The loss of
electrolytes during exercise causing a temporary drop in IOP. The
effects of pilocarpine. The ongoing study of possible gene therapy
versus a stretching response within the eye.

		I tried ginkgo biloba and magnesium treatments but they had no
effect on me. There are some other esoteric compounds I haven't tried.
My next step right now is to undergo the SLT trabeculoplasty procedure
which just targets pigmentation cells in the meshwork that have
sloughed off the iris over a lifetime, but the effect is limited. A
future cure for presbyopia seems to be my best bet.

		This all leaves me with just one remaining nagging problem. To test
my theory on myself, I bought an insulated eye mask that doesn't touch
the eyes (no latent pressure) and tried wearing it every night between
my 4 month pressure checks. When I wore it, my eyes felt more relaxed
when I woke up in the morning and my pressure was always 2-3mm less
when I went in for a checkup. When I didn't wear it, my eyes felt
under pressure when I woke, and my pressure checks were always worse. 
I've repeated this test over several years now, always with the same
result. I don't know how to reconcile my personal experiment with the
provided data. I would appreciate it if you could address this somehow
before I release this "question" as answered. Thanks again.

			Sincerely,   Ron

Request for Question Clarification by crabcakes-ga on 01 Jun 2006 17:00 PDT
Thanks for your response. I will re-read it and dig around some more.
What an interesting theory however!

Regards, Crabcakes

Request for Question Clarification by crabcakes-ga on 05 Jun 2006 21:35 PDT
Hello again,

  I've found nothing supportive of your theory still. I found just
small snippets of the effect of cold on IOP. I'm afraid I can't find a
definite answer for you.Perhaps another researcher will e more

" In order to perform surgery, it is necesary previously to cool all
fluids to be used in the operation to around 4 %, except for the
povidone drops, which should be at normal temperature for optimum
Before the operation, an eye mask of cold gel is placed over the eye
for about ten minutes (Figure 2), which will afford a degree of
analgesia to the eyelids, facilitating the insertion of the lid
We carry out ocular asepsia before surgery with 5 % povidone drops.
Next, a drop of cold methylcellulose is instilled into the eye before
placing the ophthalmic drape to isolate the eyelids. The cold
methylcellulose reduces the stinging sensation of the providone"

Drops to lower IOP
Dorzox-T  is comprised of two components: dorzolamide hydrochloride
and timolol maleate. Each of these two components decreases elevated
intraocular pressure, whether or not associated with glaucoma, by
reducing aqueous humor secretion. Elevated intraocular pressure is a
major risk factor in the pathogenesis of optic nerve damage and
glaucomatous visual field loss. The higher the level of intraocular
pressure, the greater the likelihood of glaucomatous field loss and
optic nerve damage."

"He also cools the eye first by applying a gel-containing mask for 10
minutes to reduce lid sensitivity and facilitate insertion of the lid
speculum. Cold methylcellululose is instilled in the eye after
placement of 5% povidone drops to reduce the stinging sensation caused
by the antiseptic agent.Next, the eye is irrigated with cool BSS prior
to create the paracentesis. A cool, high-density viscoelastic is
injected into the anterior chamber and a clear cornea incision is made
using a 3.2mm phaco knife, while the ocular surface is cooled with BSS
and the eye stabilised using a lens manipulator or spatula."

"There are two primary mechanisms for lowering eye pressure: 1)
Decrease the amount of aqueous humor coming into the eye i.e. reduce
the production of aqueous, and 2) Increase the amount of aqueous
leaving the eye i.e. increase the outflow of aqueous. Some medications
decrease the production of aqueous humor whereas others increase the
outflow. Aqueous humor flows out of the eye using two pathways: one
that is sensitive to eye pressure (the trabecular meshwork pathway)
and one that operates independently of eye pressure (the uveoscleral

"Exercise and Eye Pressure
Isokinetic exercises cause considerable reduction in intraocular
pressure and may be helpful in glaucoma (Ophthalmologica
1999;213:290-4). Aerobic exercise also lowers intraocular pressure
(IOP) and short-term studies show it may improve blood flow to the
retina and optic nerve as well. Eye pressure can be lowered by
exercise that raises the pulse just 20-25% --that could be a brisk
walk -- for 20 minutes, a minimum of four times a week or Aerobics
(Quigley H, in 2002, vol.19 newsletter).
In normal eyes of sedentary subjects who engage in moderate to heavy
exercise for 3 months, a consistent decrease in IOP occurs (on the
order of 1?2 mm Hg). The effect is diminished in physically fit
subjects. If one stops exercising, the effect wears off in 3 weeks.
Exercise may not be effective in lowering IOP in everyone. In one
study IOP was lowered by at least 2 mm Hg by exercise in 34%. However,
57% had no change in IOP, while 9% had an IOP elevation"

"Dr. Rick Wilson:   An abnormal pressure in the veins around the eye
leads to an immediate increase in IOP.  If the flow is above normal,
but not at a higher pressure, I am not sure that it would raise your


P:   Are cold feet considered to be a systemic blood flow problem?  


Dr. Rick Wilson:  Yes, cold hands and feet are often a sign of
impaired circulation that may also be present in the optic nerves. The
body regulates blood flow, depending upon the needs of the tissue in
question.  If you exercise or use an organ, the blood flow should
increase.  If it does not, that is a sign of dysregulation. Patients
with glaucoma do not seem to be able to adjust their blood flow to the
optic nerves as normally as most people."

Not closely related, but interesting:

I'm wondering if the cold mask simply causes tissue fluid and swelling
to decrease, thus making your eyes feel better and lowering IOP as
well. We  may never know!

Sincerely, Cracakes

Sincerely, Cracakes

Request for Question Clarification by crabcakes-ga on 07 Jun 2006 13:56 PDT
Hello again,

   The "B" key on my keyboard has been sticking lately! I noticed I
made several typos on my last clarification.

  How would you like me to proceed on this answer now?

  The Google Answers notification process apparently is still not
working, so you won't be notified when I post. I'd suggest you check
back every once in a while untill we resolve this issue.

  Sincerely, Crabcakes

Clarification of Question by 37169650-ga on 09 Jun 2006 12:15 PDT
Hi Crabcakes,
		Thanks for your note. I was surprised at the beginning of this
service not to get email notification from Google on your responses,
and I have been very busy this week as far as checking in is

		First off, I must have confused you about the insulated mask. The
mask has thermal insulation, not a cool gel. My hypothesis is that the
extra warmth, perhaps what was lost from removing the insulating fat
with the blepharoplasty procedure, speeds up the process of fluid

		Higher temperatures make fluids less dense, thereby easing their
flow. I was surprised to read some of the material you provided which
demonstrated the possibility that cold temperatures actually seem to
decrease IOP. My own experience is that my eyes feel better and I get
lower IOP readings when I wear the mask at least 5 hours/night
whenever the ambient temperature is less than about 57*F. Perhaps
sub-zero temperatures cause the fluid to contract to the point where
IOP is reduced, also?

		The material you provided about trabecular meshwork pore size vs.
presbyopia was very interesting. To reiterate, when the ciliary
(focusing) muscle starts to lose elasticity as you get older, the lack
of pull on the trabecular meshwork reduces pore size. If you are
unlucky enough to already have smaller than average pore size, you
immediately enter a zone where IOP goes up. This sounds more like my
underlying problem. I suspect now that the drop in anterior chamber
temperature from the reduced insulation is just a contributing factor
and not the cause; therefore you have answered my question in as much
as I have decided not to undergo the additional procedures that would
be necessary to replace the lower lid insulating fat. Waiting for some
future cure to presbyopia seems to be my best long-term bet now,
although I will try the SLT trabeculoplasty which I wrote about

		I still don't have any concrete data to support my hypothesis. Maybe
now that I've clarified my position you can find something related to
heat and aqueous fluid flow? If not, I can terminate the question as
answered for all intents and purposes. Thanks again.
Subject: Re: medical statistics
Answered By: crabcakes-ga on 10 Jun 2006 20:58 PDT
Rated:4 out of 5 stars
Hello again Ron,

   Here is some additional material. At this point, I'm not sure I can
find exactly what you are seeking. The only tiny clue I found is the
fact that the argon laser heat does help flatten cilliary bodies...
perhaps the warmth of the mask flattens the cilliary bodies allowing
fluid to flow better. Maybe the warmth denatures proteins... I'm at a
loss. Thank you for accepting this answer, and if you have further
questions... or shoudl I say clues, please ask!

  "If the aqueous channels are blocked so that the fluid is trapped
inside the eye, then the pressure may build up to dangerous levels. In
many cases in Saudi Arabia, the eye is small and the iris (the brown
or blue part of the eye) blocks the channels (angle closure glaucoma).
This can happen suddenly with pain and immediate loss of vision, but
often develops slowly without pain or noticeable changes in sight. In
other parts of the world, open angle glaucoma is more common. These
aqueous channels appear normal but fail to allow the aqueous fluid to
pass through. The tendency to develop both kinds of blocked channels
is often inherited and may affect several members in one family. In
most patients, this blockage and high pressure is not related to the
blood or to anything one eats or drinks, although physical inactivity,
obesity and smoking can have an adverse affect on glaucoma."

"The trabecular meshwork can be cut with a laser, allowing the fluid
to move out of it more easily. Alternatively, a surgeon can remove a
piece of the eye wall and allow fluid to drain out under the
conjunctiva. Doctors can also insert tiny drainage tubes, similar to
those used for middle-ear problems, inside the eye to allow fluid
drainage to the outer layers of the eye. Lastly, laser, heat, or cold
can be used to destroy the ciliary epithelium, which secretes the
aqueous humor."

"The aging process itself lends to certain metabolic changes that may
predispose the lens to cataract development. Some of this occurs due
to low supply of oxygen and nutrients, which leave the eye open to
free radical damage. According to a 1983 report from the National
Academy of Science, cataracts are initiated by free-radical hydrogen
peroxide found in the aqueous humor. Free radicals such as hydrogen
peroxide oxidize glutathione (GSH), destroy the energy-producing
system of the eye, and allow leakage of sodium into the lens. Water
follows the sodium, and the edema phase of the cataract begins. Then,
body heat in the lens of the eye oxidizes (cooks) lens protein, and it
becomes opaque and insoluble (similar to egg protein)."
"Age-related losses of antioxidants increase physical stress on the
eye, and oxidative damage ensues.[7] For example, diminished
antioxidant activity in lacrimal (tear) fluid and blood plasma seems
to coincide with progression of glaucoma.[8] It?s also proposed that
the rate of crystalline damage increases as antioxidant capacity and
protease activity declines with age.[9]

In open-angle glaucoma, the common form of the disease, drainage of
the aqueous fluid is sluggish, so the backup causes the undue pressure
in the eye. The pressure pinches the blood vessels that feed the optic
nerve, causing the nerve to die over time, and leading to decreased
peripheral vision, tunnel vision and finally blindness. A rarer form
of glaucoma is called narrow-angle or congestive glaucoma, whereby the
flow of the aqueous liquid is blocked causing pressure to build up."

"Abstract. Long-term industrial exposure to low levels of infrared
radiation has for many years been associated with the development of
cataracts; the injury mechanism is widely held to be thermal. A finite
element model of the human eye is employed to calculate the
temperature rises experienced by the intraocular media when exposed to
infrared radiation. The model is used to calculate transient and
steady-state temperature distributions for various exposure times and
a range of incident irradiances. The effect of the eye's natural
cooling mechanisms on the heating is investigated. Specific absorption
rates in the infrared irradiated eye are presented. For a radiation
source of 1500 degrees C, absorption of radiant energy by the iris and
the lens combined with conduction of heat from the anterior regions is
found to be responsible for increases in the lens temperature of 1-2
degrees C, but under extreme exposure conditions the temperature rises
are found to be substantially higher."

The article can be purchased for $5:
"Understanding Trabecular Meshwork Physiology: A Key to the Control of
Intraocular Pressure?

Artur Llobet, Xavier Gasull and Arcadi Gual

Laboratori de Neurofisiologia, Departament de Ciències Fisiològiques I
and Institut d?Investigacions Biomèdiques August Pi i Sunyer, Facultat
de Medicina, Universitat de Barcelona, 08036 Barcelona, Spain
The trabecular meshwork is a tissue located in the anterior chamber
angle of the eye, and it is a crucial determinant of intraocular
pressure values because of its resistance to the evacuation of aqueous
humor from the eye. Here we bring together classical and recent
discoveries on the function of the trabecular meshwork, keys to
understanding eye pathophysiology."

"CONCLUSIONS. Elevated IOP appears to cause a decrease in outflow
pathway resistance at 1 to 4 days, and this effect seems to disappear
with further time. In contrast, induction of TIGR/MYOC appears to be
strongest at 7 days. We speculate that this induction pattern might
indicate a stress-related, rather than a possible homeostatic, role
for the TIGR/MYOC protein."

"Contrary to what some people think, the laser does not burn a hole
through the eye. Instead, the heat causes some areas of the trabecular
meshwork to shrink, theoretically resulting in adjacent areas
stretching open and permitting aqueous humor to drain more easily. It
is also possible that the laser stimulates DNA synthesis, promoting
regrowth of trabecular cells."

You may find these articles useful

"Although effective in lowering IOP, ALT does produce some harmful
effects to the trabecular meshwork at a microscopic level. The argon
is a thermal laser, meaning that it generates heat when applied to
tissues. In ALT, heat damage occurs to the trabecular meshwork and the
surrounding structural collagen fibers. Because of these structural
changes (on a microscopic level) to the trabecular meshwork and the
surrounding tissue, the number of times that ALT can be performed is
limited?usually two or three times over a lifetime."

"Non-secretion of mutant proteins of the glaucoma gene myocilin in
cultured trabecular meshwork cells and in aqueous humor"
"Aqueous humor is made continuously by the ciliary body to provide
nutritive support for the avascular anterior tissues of the eye.
Aqueous humor exits the eye through the trabecular meshwork (TM), a
reticulated network of cell-lined extracellular matrix located at the
junction of the cornea and iris. In most forms of glaucoma, including
POAG, the efflux of aqueous humor from the eye is impaired leading to
the build-up of pressure inside the eye. The loss of vision in all
forms of glaucoma is due to the gradual death of ganglion cells in the
neural retina. This loss of retinal ganglion cells (RGCs) is
associated with distinct changes in the appearance of the optic nerve
head where the 1?1.5 million RGC axons exit the eye to form the optic

"RESULTS. IOP increased significantly with age in monkeys aged 3 to 29
years. AHF and anterior chamber volume were unchanged. Fu was
decreased, and trabecular outflow increased in monkeys aged 25 to 29
years compared with the remaining monkeys. Morphologically, there was
a significant increase in the thickness of the elastic fibers of the
trabeculum ciliare covering the anterior tips of the CM, and an
increase in extracellular material between the muscle tips. The number
of TM cells decreased with age, whereas the amount of fibrillar
material and sheath-derived plaques increased. This increase was less
pronounced in the middle filtering portion of the cribriform region
than in the anterior and posterior portions.

CONCLUSIONS. The decline in Fu in very old rhesus monkeys with normal
IOP parallels that seen in normotensive aging humans. This may be
correlated with thickening of the elastic fiber sheath in the CM tips
in addition to other morphologic changes. The TM findings are
analogous to those in the aging human eye and are consistent with the
age-related decrease in outflow facility reported in both humans and

"Prostanoid Receptor Gene Expression Profile in Human Trabecular
Meshwork: A Quantitative Real-Time PCR Approach"

The Effects of Protein Kinase C on Trabecular Meshwork and Ciliary
Muscle Contractility

"The aqueous humor inhibited the production of cytokines in a
dose-dependent manner. The inhibitory activity was heat labile. First
protein liquid chromatography showed at least four major peaks of
different molecular size, indicating that the aqueous humor contains
multiple immunosuppressive factors. Transforming growth factor-[beta],
[alpha]-melanocyte-stimulating hormone, and vasoactive intestinal
peptide did not suppress cytokine production. The inhibitory activity
was neutralized by monoclonal antibody to Fas ligand.

Conclusion. These data suggest that soluble Fas ligand is a candidate
suppressive factor in the aqueous humor.";jsessionid=GLDNzQBl2GJCXVnh6ZGscgm5dwQgvvJJsP2nnkCF1tMTnd2vQtYD!-818462210!-949856145!8091!-1

This looks interesting!

If nothing else, I hope this additional information has provided you
with interesting reading.

Sincerely, Crabcakes
37169650-ga rated this answer:4 out of 5 stars and gave an additional tip of: $25.00
A very good job in trying to answer a medical question that hasn't
been researched before.

Subject: Re: medical statistics
From: crabcakes-ga on 20 Jun 2006 16:47 PDT
Thank you for the generous tip! It is most appreciated.
Sincerely, Crabcakes

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