after a period of time, perhaps only after several months, a rapid deterioration in the field, with optic atrophy, perhaps with still minimal pathologic cupping. In following up such patients with a relatively high tension and a normal disc, we have no clues as to when they will begin to lose field. By the time we recognize optic atrophy, they have already lost considerable field. In patients with a lower tension, we can
out damage, which it surely is. Yes, we may safely withhold treatment as
sion is referred to in other countries to some extent, we encounter the term most commonly in North America, and the term is relatively new in ophthalmologic literature. There is an implication that ocular hypertension is a relatively benign disease, whereas open-angle glaucoma is a serious disorder. Do we need the term ocular hypertension? In our opinion, we do not need this term. Let us call the condition early open-angle glaucoma with-
w^
we believe this is true. However, during a period of time, we often can make a prediction in these untreated patients as to which are more likely to develop loss of field and which are less likely to do so. If, in the period of our observation, we detect beginning glaucomatous changes in the disc, we can safely predict that these are the patients who are most likely to develop loss of field if we continue to
such
hand, if the disc remains completely normal and unchanged during our period of observation, we can conclude
recognize beginning glaucomatous changes in the disc before there is loss of field and we can treat the patient accordingly. Although the term ocular hyperten-
and
withhold treatment. On the other
that we can safely continue to withhold treatment for a further period, providing tension remains 30 or less. We believe treatment should not be withheld, even if the disc is completely normal, if tension is in the mid to high 30s. There may be some difference of opinion about this, but we believe there should be no difference of opinion if tension is in the 40s or higher. To be sure, one may see the disc remain normal and the field full for a period of time with tension in the 40s or higher, but we have seen in
'Ocular
cases
long
as
the disc remains
completely
normal, and the tension is not unduly elevated, but let us not withhold treatment when
we
have detected
a
begin'
ning glaucomatous change in the optic disc, even though there is as yet not the slightest defect in the visual field. and let
us
not withhold
treatment
if the disc is completely normal » the tension is considerably elevated. In cases where the disc is normal and the angle open, if tension is in the 20s, if one were to insist on using the term ocular hypertension, we mi)in call this a mild case of ocular hyper' tension. If tension is in the 30s, might call this a moderate case; » tension is in the 40s or higher, this should be called a severe case. But m all three instances, it is simply ope11' even
angle glaucoma. Regardless of terms. let us treat the case as we would an)' case of glaucoma with similar tension elevation. Paul A. Chandler, MD W. Morton Grant, MD Boston
Hypertension' vs Open-Angle
Glaucoma:
A Different View After reviewing the preceding editorial prior to publication, we find that we must disagree with much of the pessimistic thesis and many of the conclusions of the authors. We agree with the authors' definition of ocular hypertension as a "condition where the angle is open, and the disc and visual field are normal, but the tension is above the normal range." It is important to realize, however, that the "normal range" is purely a statistical definition\p=n-\itsrelationship to glaucoma is based on the fact that the
majority of patients with open\x=req-\ angle glaucoma have elevated intraocvast
ular pressures. In addition, the elevated intraocular pressure usually precedes glaucomatous damage to the optic nerve by a variable period of time. The fact that most patients with glaucoma have elevated intraocular pressure does not logically mean, however, that most patients with elevated intraocular pressure have
glaucomatous optic nerve damage, or will, in fact, ever develop such damage. On the contrary, available
data indicate just the opposite to be true. Numerous studies from North America, as well as every other part the world, during the past decade ° demonstrate that the prevalence ocular hypertension in the genera population is at least ten to 15 times greater than the prevalence of glaucoof
matous
optic
nerve
damage (as
of
fined by visual field loss). Similarly.in studies in which patients with ,'1' vated intraocular pressure but wit"
optic nerve damage (ie, ocuia hypertension) are followed up witho11
out
Downloaded From: http://archopht.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/26/2015
treatment,
the incidence of visual 'eld loss in periods up to ten years is a"out 5% to 7%. One must therefore include that most patients with °cular hypertension will not develop
8'ftucomatous optic
I
nerve
damage,
even if not treated. This is indeed '0rtunate and makes unnecessary the Pessimistic approach to the disease taken by Chandler and Grant. To the Paient, moreover, the term glaucoma °tten implies a disease that causes kindness unless treated. This fact a'°ne establishes a need for such a term as ocular hypertension. Compared with the prognosis of untreated
agreement with Chandler and Grant, we treat all patients with optic
In
damage, and those in whom the likelihood of developing optic nerve
nerve
damage is sufficiently great that the
risks of therapy are less than the risks of developing damage. This may be true when intraocular pressure is consistently high (eg, above 30 mm Hg), when there is asymmetry or progression of cupping, when the of patient has a strong family history glaucoma (especially a maternal family history, according to recent data), when diabetes mellitus is present, when accurate perimetry is not possi-
"Pen-angle glaucoma (with damage),
ble, etc.
benign
"regardless of terms let us treat the case [of ocular hypertension] as we would any case of glaucoma with
J^Ular
hypertension
¿8
a
relatively
disease."
An analogy with angle-closure glau-
coma may be used to
reemphasize the
above point. Almost all patients with acute angle-closure glaucoma have a"atomieally narrow angles prior to havinir an acute attack. The prevaetice of anatomically narrow angles, lowever, is far greater than the preva'ence of angle-closure glaucoma. Few would •Phthalmolpgists a"
suggest that
with narshould have surgery to
asymptomatic patients
0vv
angles Invent the possibility
closure.
of
angle-
^rs Chandler and Grant, in sug-
that the term ocular hyperpstinjr te"sion be eliminated, state "let
us
a'l the condition
sl&Ucoma
early open-angle
without damage, which it Purely is." On the contrary, the bulk of 'bical evidence indicates that most Stances of ocular hypertension are the upper end of the intraoc'ar pressure distribution curve and °t all "early open-angle glaucoma"! •8 true that the population of atients with ocular hypertension concis most of those patients with early glaucoma, but it is not true Pen-angle "at most patients with ocular hyper'"sion will develop glaucoma if ""treated. It is for just this reason at ocular hypertension is a useful .
"Jerely
ell"ical term.
'
the previous comments should not
*
as indicating that anything wrong or incorrect '"stituting therapy for glaucoma in ^e patients with ocular hyperten-
misinterpreted
Cre is
.
,
°n
in the absence of visual field loss.
Drs Chandler and Grant state that
similar
tension
elevation."
Here
again, we must disagree. If a patient has optic nerve damage, he is already demonstrating that the degree of
pressure elevation is sufficient to produce visual loss under the various genetic and vascular conditions existing in him and his eyes. Under these circumstances, every effort must be made to lower his intraocular pressure so that further damage will be prevented. This includes the use of topical and systemic medications, all of which may have serious side effects, and even surgery when necessary. We do not believe that patients with "similar tension elevation" but without optic nerve damage should be subjected to such intensive therapy, for the treatment itself may in many instances carry more risk and induce more damage than the likelihood of developing the disease. When a person has less than one chance in ten of developing field loss, why subject him to up to a 50% chance of developing cataracts from long-term use of cholinesterase inhibitors, or the renal colic, acidosis, and other systemic effects of long-term carbonic anhydrase inhibitors, or the ocular complications of surgery, merely to normalize a statistical number? Remember, this patient does not demonstrate that the degree of pressure elevation in his eyes will ever produce optic nerve damage. In summary, when the risk of damage is high, therapy is mandatory.
When the chance for damage is slight, the dangers of therapy may well outweigh the risk and must be carefully evaluated. Drs Chandler and Grant make an important point that during a period of time we often can make a prediction in untreated (ocular hyperten-
sive) patients,
as
to
which
are more
develop field loss and which are less likely to do so. Knowing that 10% or less of such patients will develop optic nerve damage makes early accurate identification of the patient with true glaucoma extremely important. We agree that evidence of beginning optic nerve damage makes treatment mandatory, but that is
likely
to
later than we would like to start therapy. New, exciting research offers hope that one can identify the true patient with glaucoma from among the patients with ocular hypertension more accurately and earlier than ever before. Identification of the relation-
ship between primary open-angle may glaucoma and HLA antigens an important link. In a such provide yet unpublished study, it is demonstrated that 41% of patients with ocular B7
or
hypertension
and either HLA-
HLA-B12 antigens develop
glaucomatous optic
nerve
damage in
five to ten years, while only 5% of similar patients without these antiof gens suffer such damage (and most Another study these were diabetics). presents the predictive value of isthe effects of topical epinephrine and to be published in the Archives. Of 34 patients with ocular hypertension whose intraocular pressure was reduced
by
more
treatment with
than 5
mm
epinephrine,
Hg after 17 (50%)
developed glaucomatous field loss in five to ten years, whereas only three ((5.5%) of 46 similar patients with
hypertension who were less responsive to epinephrine treatment offer the
ocular
lost visual field. Such studies primary optimistic promise that true soon be open-angle glaucoma may separable from the population of patients with ocular hypertension. Until such time, we believe the term
ocular hypertension serves a useful clinical purpose. Allan E. Kolker, MD Bernard Becker, MD
Downloaded From: http://archopht.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/26/2015
out damage, which it surely is. Yes, we may safely withhold treatment as
sion is referred to in other countries to some extent, we encounter the term most commonly in North America, and the term is relatively new in ophthalmologic literature. There is an implication that ocular hypertension is a relatively benign disease, whereas open-angle glaucoma is a serious disorder. Do we need the term ocular hypertension? In our opinion, we do not need this term. Let us call the condition early open-angle glaucoma with-
w^
we believe this is true. However, during a period of time, we often can make a prediction in these untreated patients as to which are more likely to develop loss of field and which are less likely to do so. If, in the period of our observation, we detect beginning glaucomatous changes in the disc, we can safely predict that these are the patients who are most likely to develop loss of field if we continue to
such
hand, if the disc remains completely normal and unchanged during our period of observation, we can conclude
recognize beginning glaucomatous changes in the disc before there is loss of field and we can treat the patient accordingly. Although the term ocular hyperten-
and
withhold treatment. On the other
that we can safely continue to withhold treatment for a further period, providing tension remains 30 or less. We believe treatment should not be withheld, even if the disc is completely normal, if tension is in the mid to high 30s. There may be some difference of opinion about this, but we believe there should be no difference of opinion if tension is in the 40s or higher. To be sure, one may see the disc remain normal and the field full for a period of time with tension in the 40s or higher, but we have seen in
'Ocular
cases
long
as
the disc remains
completely
normal, and the tension is not unduly elevated, but let us not withhold treatment when
we
have detected
a
begin'
ning glaucomatous change in the optic disc, even though there is as yet not the slightest defect in the visual field. and let
us
not withhold
treatment
if the disc is completely normal » the tension is considerably elevated. In cases where the disc is normal and the angle open, if tension is in the 20s, if one were to insist on using the term ocular hypertension, we mi)in call this a mild case of ocular hyper' tension. If tension is in the 30s, might call this a moderate case; » tension is in the 40s or higher, this should be called a severe case. But m all three instances, it is simply ope11' even
angle glaucoma. Regardless of terms. let us treat the case as we would an)' case of glaucoma with similar tension elevation. Paul A. Chandler, MD W. Morton Grant, MD Boston
Hypertension' vs Open-Angle
Glaucoma:
A Different View After reviewing the preceding editorial prior to publication, we find that we must disagree with much of the pessimistic thesis and many of the conclusions of the authors. We agree with the authors' definition of ocular hypertension as a "condition where the angle is open, and the disc and visual field are normal, but the tension is above the normal range." It is important to realize, however, that the "normal range" is purely a statistical definition\p=n-\itsrelationship to glaucoma is based on the fact that the
majority of patients with open\x=req-\ angle glaucoma have elevated intraocvast
ular pressures. In addition, the elevated intraocular pressure usually precedes glaucomatous damage to the optic nerve by a variable period of time. The fact that most patients with glaucoma have elevated intraocular pressure does not logically mean, however, that most patients with elevated intraocular pressure have
glaucomatous optic nerve damage, or will, in fact, ever develop such damage. On the contrary, available
data indicate just the opposite to be true. Numerous studies from North America, as well as every other part the world, during the past decade ° demonstrate that the prevalence ocular hypertension in the genera population is at least ten to 15 times greater than the prevalence of glaucoof
matous
optic
nerve
damage (as
of
fined by visual field loss). Similarly.in studies in which patients with ,'1' vated intraocular pressure but wit"
optic nerve damage (ie, ocuia hypertension) are followed up witho11
out
Downloaded From: http://archopht.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/26/2015
treatment,
the incidence of visual 'eld loss in periods up to ten years is a"out 5% to 7%. One must therefore include that most patients with °cular hypertension will not develop
8'ftucomatous optic
I
nerve
damage,
even if not treated. This is indeed '0rtunate and makes unnecessary the Pessimistic approach to the disease taken by Chandler and Grant. To the Paient, moreover, the term glaucoma °tten implies a disease that causes kindness unless treated. This fact a'°ne establishes a need for such a term as ocular hypertension. Compared with the prognosis of untreated
agreement with Chandler and Grant, we treat all patients with optic
In
damage, and those in whom the likelihood of developing optic nerve
nerve
damage is sufficiently great that the
risks of therapy are less than the risks of developing damage. This may be true when intraocular pressure is consistently high (eg, above 30 mm Hg), when there is asymmetry or progression of cupping, when the of patient has a strong family history glaucoma (especially a maternal family history, according to recent data), when diabetes mellitus is present, when accurate perimetry is not possi-
"Pen-angle glaucoma (with damage),
ble, etc.
benign
"regardless of terms let us treat the case [of ocular hypertension] as we would any case of glaucoma with
J^Ular
hypertension
¿8
a
relatively
disease."
An analogy with angle-closure glau-
coma may be used to
reemphasize the
above point. Almost all patients with acute angle-closure glaucoma have a"atomieally narrow angles prior to havinir an acute attack. The prevaetice of anatomically narrow angles, lowever, is far greater than the preva'ence of angle-closure glaucoma. Few would •Phthalmolpgists a"
suggest that
with narshould have surgery to
asymptomatic patients
0vv
angles Invent the possibility
closure.
of
angle-
^rs Chandler and Grant, in sug-
that the term ocular hyperpstinjr te"sion be eliminated, state "let
us
a'l the condition
sl&Ucoma
early open-angle
without damage, which it Purely is." On the contrary, the bulk of 'bical evidence indicates that most Stances of ocular hypertension are the upper end of the intraoc'ar pressure distribution curve and °t all "early open-angle glaucoma"! •8 true that the population of atients with ocular hypertension concis most of those patients with early glaucoma, but it is not true Pen-angle "at most patients with ocular hyper'"sion will develop glaucoma if ""treated. It is for just this reason at ocular hypertension is a useful .
"Jerely
ell"ical term.
'
the previous comments should not
*
as indicating that anything wrong or incorrect '"stituting therapy for glaucoma in ^e patients with ocular hyperten-
misinterpreted
Cre is
.
,
°n
in the absence of visual field loss.
Drs Chandler and Grant state that
similar
tension
elevation."
Here
again, we must disagree. If a patient has optic nerve damage, he is already demonstrating that the degree of
pressure elevation is sufficient to produce visual loss under the various genetic and vascular conditions existing in him and his eyes. Under these circumstances, every effort must be made to lower his intraocular pressure so that further damage will be prevented. This includes the use of topical and systemic medications, all of which may have serious side effects, and even surgery when necessary. We do not believe that patients with "similar tension elevation" but without optic nerve damage should be subjected to such intensive therapy, for the treatment itself may in many instances carry more risk and induce more damage than the likelihood of developing the disease. When a person has less than one chance in ten of developing field loss, why subject him to up to a 50% chance of developing cataracts from long-term use of cholinesterase inhibitors, or the renal colic, acidosis, and other systemic effects of long-term carbonic anhydrase inhibitors, or the ocular complications of surgery, merely to normalize a statistical number? Remember, this patient does not demonstrate that the degree of pressure elevation in his eyes will ever produce optic nerve damage. In summary, when the risk of damage is high, therapy is mandatory.
When the chance for damage is slight, the dangers of therapy may well outweigh the risk and must be carefully evaluated. Drs Chandler and Grant make an important point that during a period of time we often can make a prediction in untreated (ocular hyperten-
sive) patients,
as
to
which
are more
develop field loss and which are less likely to do so. Knowing that 10% or less of such patients will develop optic nerve damage makes early accurate identification of the patient with true glaucoma extremely important. We agree that evidence of beginning optic nerve damage makes treatment mandatory, but that is
likely
to
later than we would like to start therapy. New, exciting research offers hope that one can identify the true patient with glaucoma from among the patients with ocular hypertension more accurately and earlier than ever before. Identification of the relation-
ship between primary open-angle may glaucoma and HLA antigens an important link. In a such provide yet unpublished study, it is demonstrated that 41% of patients with ocular B7
or
hypertension
and either HLA-
HLA-B12 antigens develop
glaucomatous optic
nerve
damage in
five to ten years, while only 5% of similar patients without these antiof gens suffer such damage (and most Another study these were diabetics). presents the predictive value of isthe effects of topical epinephrine and to be published in the Archives. Of 34 patients with ocular hypertension whose intraocular pressure was reduced
by
more
treatment with
than 5
mm
epinephrine,
Hg after 17 (50%)
developed glaucomatous field loss in five to ten years, whereas only three ((5.5%) of 46 similar patients with
hypertension who were less responsive to epinephrine treatment offer the
ocular
lost visual field. Such studies primary optimistic promise that true soon be open-angle glaucoma may separable from the population of patients with ocular hypertension. Until such time, we believe the term
ocular hypertension serves a useful clinical purpose. Allan E. Kolker, MD Bernard Becker, MD
Downloaded From: http://archopht.jamanetwork.com/ by a University of Arizona Health Sciences Library User on 05/26/2015
