Chat Highlights
Normal-tension Glaucoma
August 29, 2001
Norma Devine, Editor
On Wednesday, August 29, 2001, Dr.
Elliot Werner, a glaucoma specialist at Wills, and the
glaucoma chat group discussed "Normal-tension Glaucoma."
Moderator: Tonight
the topic is "Normal-tension Glaucoma ." Dr. Elliot Werner
is our guest. Dr. Werner is a glaucoma specialist
at Wills. He will be here the last Wednesday of every month,
starting tonight. Welcome back, Doctor Werner.
Dr. Elliot Werner: Thank
you. I am not the world's fastest typist, so be patient.
P: Doctor Werner,
I'm a normal 41-one-year-old woman. Why would I have normal-tension
glaucoma (NTG?)
Dr. Elliot Werner: Most
NTG in younger patients is genetic in origin. Do you have a family
history of glaucoma?
P: No.
Dr. Elliot Werner: Remember,
NTG is probably not a different disease from the garden variety
open-angle glaucoma. Most of these are probably genetic
in origin. As glaucomas go, NTG is actually a relatively
benign condition. Blindness is unusual in NTG, but that
is not much comfort to those who have significant vision loss
from the disease.
P: In what way
is NTG relatively benign compared to POAG (primary open-angle)
glaucoma? It seems harder to treat.
Dr. Elliot Werner: NTG
is more difficult to treat in the sense that it is more difficult
to lower the IOP. It is more benign in the sense that blindness
is less likely to occur.
Moderator: The
next question is from a busy mother of two, who could not be here
tonight: "I have normal tension glaucoma. My visual
field tests show loss in my central vision. I thought glaucoma
robbed people of their peripheral vision first. Why would
this occur with NTG? Is this uncommon?"
Dr. Elliot Werner: Loss
of central vision is unusual in early glaucoma, but common as
the disease progresses. Whether or not this woman's loss
of central vision is remarkable depends upon how advanced her
optic nerve damage is.
P: Is loss of
vision close to fixation common in NTG?
Dr. Elliot Werner: The
evidence for loss of vision close to fixation is statistical only.
It is more common in NTG, but it is not characteristic.
P: Is there a
connection between chronically low blood pressure and NTG?
Dr. Elliot Werner: There
is some association between chronically low blood pressure and
NTG.
Moderator: What
percentage of NTG patients have chronically low blood pressure?
Dr. Elliot Werner: I'm
not sure, but probably a significant minority have some abnormality
of blood pressure on the low side. The blood pressure of
many people drops when they sleep, and that may have an association
with NTG.
P: If an NTG patient
has mildly elevated blood pressure and is being prescribed medication
to lower it, wouldn't a calcium channel blocker be a good alternative
to a diuretic?
Dr. Elliot Werner:
I wouldn't comment on treatment of blood pressure, but the
use of calcium channel blockers is a double- edged sword, since
they can drop the blood pressure too low in some people with NTG
and make it worse.
P: Do about half
of glaucoma patients have NTG?
Dr. Elliot Werner: Probably
closer to about 1/4 to 1/3 of glaucoma patients have NTG.
P: Is it more
difficult to control NTG, since pressures are already "normal"?
Dr. Elliot Werner: Most
patients with NTG do not show significant progressive visual loss
over many years, and often do not need any treatment at all.
Moderator: Could
optic nerve damage in NTG patients be caused by something other
than IOP?
Dr. Elliot Werner: Most
recent evidence from the NTG Collaborative Treatment Trial and
studies involving patients with asymmetric NTG show that IOP is
still the main, but certainly not the the only, factor producing
damage. The other factors are largely unknown at present.
The NTG treatment trial showed that about two-thirds of NTG patients
do not progress after five years of follow-up, so probably about
two-thirds do not need treatment.
P: Might those
patients just have a very slow rate of progression?
Dr. Elliot Werner: Of
the NTG patients who do progress, I don't know of any evidence
they progress more slowly. Rates of progression are highly
variable in all forms of glaucoma.
Moderator: I don't
understand. NTG patients must have optic nerve damage.
Does the damage stop?
Dr. Elliot Werner: It
either stops after a while, or it progresses so slowly that it
is not clinically detectable for long periods of time.
P: If two-thirds
of NTG patients don't show progression, isn't that the same as
saying they've been misdiagnosed?
Dr. Elliot Werner: The
two-thirds who did not progress in the treatment trial were almost
certainly correctly diagnosed.
P: I didn't mean
that the two-thirds who did not progress did not have glaucoma,
but that at some point in the past it may have been high-tension
glaucoma, e.g., pigmentary dispersion.
Dr. Elliot Werner: That's
possible, but is usually ruled out during the work-up of the patient.
P: I have heard
that some NTG patients are misdiagnosed and might have papillorenal
syndrome, a genetic disease. Can you tell us more?
Dr. Elliot Werner: Some
patients with diseases other than glaucoma may be misdiagnosed
as having NTG. That should be uncommon in the hands of a
good clinician, because glaucoma usually looks like glaucoma.
If it doesn't look like glaucoma, you need to look for another
diagnosis.
P: So it seems
that NTG, far from being the "bad" glaucoma, is better than some
of the other kinds?
Dr. Elliot Werner: All
glaucoma is bad. Some are worse than others. Most
patients with NTG do fairly well, but some do terribly.
P: NTG is the
most common form of glaucoma in Japan. Do you know
if the Japanese have any different treatment regimes or any long-term
studies on progression?
Dr. Elliot Werner: There
are many NTG studies out of Japan. In Japan, there tends
to be less use of surgery and more systemic treatment, such as
calcium channel blockers.
P: What is the
theory about why the Japanese have a high percentage of
NTG patients?
Dr. Elliot Werner: Nobody
knows why NTG is more common in Asian populations.
P: Do you find
that most patients with NTG are nearsighted or farsighted?
Dr. Elliot Werner: Nearsightedness
is more common in NTG and POAG, and is a significant risk factor
for glaucoma. There are five significant risk factors for
glaucoma: IOP, age, race, nearsightedness, and family history.
P: I hear that
one of the treatments to be studied for glaucoma is supplying
growth factors to the retinal ganglion nerves. What might
some of those factors be?
Dr. Elliot Werner: I
am not an expert on growth factors. These are proteins that
are found in the body that support and nourish cells. There
is nothing I know of anywhere near human trials.
P: My father was
diagnosed with NTG in 1969, and was nearly blind when he
died in 1997. My grandfather was also blind when he
died, though there was no doctor or diagnosis involved in his
case. My oldest sister was diagnosed with NTG, and has severe
vision loss in her right eye, even after experimental surgery.
It seems that blindness in my family is a factor. Can you
comment on that?
Dr. Elliot Werner: Family
history and genetics play a major role in the occurrence and course
of NTG. Your family must carry a gene for a particularly
virulent type.
P: Is the initial
loss shown on the visual field tests of NTG patients different
from the loss shown on the tests of POAG patients?
Dr. Elliot Werner: The
initial loss of visual field in NTG is not really different, but
on average tends to be more localized and closer to fixation than
in POAG.
P: Is there a
possible connection between auto-immune conditions or circulation
problems that result in a loss of blood perfusion to the eyes
and the diagnosis of NTG?
Dr. Elliot Werner: There
is some experimental evidence that immune system abnormalities
are associated with NTG, but there are no large population studies
and no data that would affect treatment.
P: How about circulation?
Dr. Elliot Werner: There
is some evidence that blood flow to the eye may be less in NTG
than in normals, but the same is true of POAG, and the significance
of that is unknown.
P: What do you
suggest when a patient is successfully lowering IOP to the single
digits, but vision loss continues unabated?
Dr. Elliot Werner: This
is unfortunately very common. Many patients with advanced
disease continue to deteriorate despite very low IOP. Not
much can be done, and no treatment has been shown to be safe and
beneficial.
P: Some researchers
suggest that the problem in NTG lies at the level of the optic
nerve, not in the trabecular meshwork.
Dr. Elliot Werner: The
studies in the journals tend to disagree.
Moderator: Are
there studies of why some glaucoma patients get worse even with
low IOPs?
Dr. Elliot Werner: Yes,
there's a lot of research concerning mechanisms of nerve damage
in glaucoma -- neuroprotection, glutamate, nitric oxide,
free radicals. There's a lot of basic science research,
but nothing therapeutic yet.
P: I'm going blind
(quickly) for a reason; and it's definitely not my IOP, which
has never been higher than 16 mm Hg.
Dr. Elliot Werner: You
represent one of the great tragedies of glaucoma practice.
You are going blind for a reason, but we don't know enough to
figure out the reason.
P: If NTG field
losses aren't that much different from field losses in open-angle
glaucoma, does that mean the appearance of the optic nerve
in NTG isn't much different from that of open-angle glaucoma either?
And if so, how can the diagnosis of NTG be made without
the patient having been followed before the diagnosis of
NTG?
Dr. Elliot Werner: I
rarely use the term "normal-tension glaucoma" for that reason.
I think of open-angle glaucoma as a single diagnosis, regardless
of the level of IOP.
P: In my case
of NTG, I am working on a layman's theory about my extreme myopia.
My ocular length is much longer than normal, with a very thin
retina. According to the theory, my eyes have outgrown the
circulatory support. Treatment would be anything that keeps
IOP low and increases blood flow, such as Cosopt, ginkgo biloba,
exercise, etc.
Dr. Elliot Werner: All
of those can be tried. Sometimes they work; sometimes they
don't.
P: Either we try
these things or just wait to go blind.
Dr. Elliot Werner: You
can try anything in a patient who is failing. Just be sure
the treatment actually works and is not going to make you worse.
P: Yes, I remember:
"Above all, do no harm."
P: Does a very
low intraocular pressure cause macular degeneration?
Dr. Elliot Werner: Low
IOP causes a type of macular damage called hypotony maculopathy,
which is different from macular degeneration.
P: It is a little
frustrating to hear how blood flow, circulation, and low blood
pressure might be a factor in NTG, but eye doctors never consider
the whole body, just the eye. What's the deal?
Dr. Elliot Werner: The
emphasis is on "might." There is no good evidence that that
is true, and no treatment except lowering IOP has ever been shown
to be effective.
P: Do cataracts
contribute in any way to the NTG syndrome?
Dr. Elliot Werner: I
have not heard of any evidence of a relationship between
cataract and NTG.
P: Can astigmatism
affect pressure measurements?
Dr. Elliot Werner: The
amount of astigmatism has to be very large to affect the IOP measurement.
Moderator: Dr.
Werner before you leave, do you have a minute to tell us a little
about your training?
Dr. Elliot Werner: I
graduated from medical school at the University of Pennsylvania
in 1971. I received ophthalmology training at McGill University
in Montreal, and served a glaucoma fellowship with Dr. Stephen
Drance in Vancouver, British Columbia, Canada. My offices
are in downtown Philadelphia and Bala Cynwyd, a suburb of Philadelphia.
Moderator: I hope
we haven't scared you off from returning, doctor.
Dr. Elliot Werner: See
you all next month.
Moderator: Thanks,
doctor.
End of highlights for August 29, 2001.
On September 5, Dr. Wilson discussed "Inflammation and Glaucoma"
in the Chat room. Click here for highlights
of that meeting.
Click here for the most recent
glaucoma chat highlights and links to the chat archives.
Click here for
upcoming glaucoma chat events.
|