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Determination of the Optic
Disc Cupping in Glaucoma
Syed S. Hasnain M.D.
560 W. Putman Ave # 6
Porterville CA 93257, U.S.A.
www.hasnaineye.com
Email:[email protected]
Author has no financial interest in this presentation.
Purpose
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The term cupping implies that the physiological cup begins
enlarging in glaucoma.
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The terms cupping and simple glaucoma have been
synonymous since the 1850’s.
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This presentation is to determine whether or not cupping is
occurring. If it is not cupping, then what may be
occurring to the physiological cup?
The methods section discusses three puzzling questions and
how their answers by deductive reasoning and photographic
evidence led to the conclusion that the optic disc may not be
cupping, but instead sinking in its entirety.
Methods: Three Puzzling Questions
in Glaucoma
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Question 1: Why do some patients develop
glaucoma at a normal IOP such as 15mmHg,
while others do not at a high IOP such as
30mmHg?
Question 2: Why are the arcuate fibers
selectively destroyed first, whereas the
macular fibers last until the end stage of
glaucoma?
Question 3: Why can’t we halt glaucoma in
spite of maximally lowering of IOP with
treatment?
Answers to the above questions are discussed in this presentation.
Discussion: Puzzling Question #1
Why do some patients develop glaucoma at a normal IOP such
as 15mmHg (NTG), while others don’t at a high IOP such as
30mmHg (Ocular Hypertension)?
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Medical history revealed that HTG patients were usually in good
health, whereas the NTG patients had cardio-pulmonary and
circulatory problems. Furthermore, about 70% of NTG patients were
smokers.
Findings suggest that NTG may be a systemic disease and glaucoma
a multifactorial disease. Glaucoma being a multifactorial disease
may be the answer to question # 1. More the risk factors present,
higher the likelihood of development of glaucoma.
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This raises another question: If HTG is an ocular disease, whereas
NTG a systemic disease, then why are the arcuate field defects
present in both cases? If glaucoma is a multifactorial disease, then
there should be a common site of injury somewhere in the course of
pathogenesis of both HTG and NTG.
Since arcuate fibers are destroyed in both HTG and NTG, the pursuit
of their pathogenesis may lead to a common site of injury.
Discussion: Puzzling Question # 2
Can the arcuate fibers in the disc or in retina be selectively
destroyed by any pathology ?
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Not likely. How is it possible that high IOP, or any other
pathology, can selectively and precisely destroy only the arcuate
fibers among the one million or so densely packed nerve fibers in
the optic disc? If this is not possible, then the optic disc may not
be the primary site of injury.
How is it possible that high IOP, or any other pathology, can
selectively and precisely destroy only the arcuate fibers of the
retina? If this is not possible, then the retina may not be the
primary site of injury.
Regarding apoptosis: How is it possible that apoptosis in
glaucoma will initiate selectively with only those ganglion cells
of retina which serve the arcuate fibers? If this is not possible,
then apoptosis of the ganglion cells may not be occurring.
If the disc or retina is not the primary site of injury, then what
may be the primary site of injury? We are left with the circular
border tissue which we will discuss in next slide.
Discussion: Can the border tissue be the
common site of injury?
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Circular border tissue lies between the optic disc and scleral rim and
secures the disc in the scleral opening.
Border tissue is exclusively supplied by short posterior ciliary
arteries (ciliary circulation). Ciliary circulation is a low pressure
system due to its multiple branches as compared to the CRA which
mainly remains solitary from its origin.
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IOP and arterial pressure are opposing forces.
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Normally, IOP should be lower than the arterial pressure of the
border tissue for its healthy maintenance.
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The above circulatory balance would be reversed due to either an
increase in IOP or decrease in arterial pressure resulting from poor
systemic circulation. In the latter scenario, even normal IOP would
become high for that particular eye and would compress the already
weak circulation of the border tissue. This would result in chronic
ischemia and atrophy of border tissue and thus sinking of optic disc.
Discussion: Can the arcuate fibers be
selectively destroyed if optic disc is sinking?
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Likely. As the border tissue atrophies, the optic disc would
become loose and begin to sink.
Since the optic disc usually has an oblique entry in the globe,
the temporal part is more closer to the scleral edge (rim).
As the disc sinks, all temporal fibers (superior, inferior
arcuate, and macular) would be stretched and severed at the
scleral rim. However, since the arcuate fibers are fewer in
number, they would be depleted earlier, giving rise to double
arcuate field defects, whereas the macular fibers being
abundant would last until the end stage of glaucoma. This
may be the answer to question #2: that why are the arcuate
fibers selectively destroyed?
Results: Optic disc may be sinking as it can
explain the production of arcuate field
defects
Temporal sinking would result in severing of the
macular and sup.& inf. arcuate fibers. However
since arcuate fibers (blue) are fewer in number
they would be depleted earlier, giving rise to
double arcuate field defects whereas the macular
fibers being abundant would last until the endstage.
Double arcuate field defect
on perimetry
Early and Late Stage Glaucomatous Discs
Patients A & B
Patient A: Early stage Right eye: No change in contour of the
physiological cup. Prominent scleral edge due to thinning of
RNFL from severing and depletion. Sloping of blood vessels
due to sinking disc. splinter hemorrhage at 7o’clock due to
severing of smaller blood vessel.
Patient B: Early stage Right eye: No change in the contour of
physiological
cup. Prominent scleral edge due to thinning of
P
RNFL.
Sloping of blood vessels due to sinking of disc.
a
Late stage left eye of same patient A: Physiological cup
is broken due to confluence of cup pallor with the pallor
produced by the destruction of nerve fibers in the
peripheral part. Marked kinking of blood vessels at disc
margin due to loss of underneath nerve fibers.
Late stage left eye of same patient B. Physiological cup is
obliterated. Marked kinking of blood vessels at disc margin
due to loss of underneath nerve fibers.
Analogy:
Sinking manhole cover to a glaucomatous disc
Normal: Manhole cover flush with the road. Blood
vessels are straight at the margin of the disc. If there is
no sloping or kinking of blood vessel at the margin, then
there is no sinking of the disc and probably no glaucoma.
Late stage glaucoma: Physiological cup is broken due to
confluence of cup pallor with pallor produced by the
destruction of nerve fibers in the peripheral part. Nasal
shifting of vessels from loss of anchorage due to earlier
thinning of temporal RNFL as compared to that of nasal
RNFL.
Early stage glaucoma: Physiological cup is still intact.
Splinter hemorrhage at 7 o’clock. Kinking and sloping of
the blood vessels. Arcuate field defect present. Temporal
part pale and sunken due to thinning of RNFL.
End stage glaucoma: Total loss of the optic disc due
to axotomy of the axons. Disc area becomes an
empty crater. Only the larger blood vessels remain.
What happens as the sinking of the disc
continues?
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360 degrees of retinal nerve fibers anchor the optic disc in
place as roots anchor a tree.
As the nerve fibers are being severed and depleted, the optic
disc would become more loose and sinks further, resulting in
severing of more nerve fibers. This is revealed by OCT –
progressive thinning of the RNFL.
Severing of the nerve fibers creates a self-propagating
cascade of loosening and sinking of the disc which would
continue until all the nerve fibers are severed at the edge.
This may be the answer to question # 3: that once glaucoma
is initiated it cannot be halted.
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At the end-stage, unlike any other disease, there is no optic
disc and no nerve fibers. This is revealed by the histology of
the end-stage glaucomatous disc – an empty crater.
Conclusion:
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Physiological cup may not be enlarging but breaking up
(obliterating). Cupping occurring concentrically can’t explain
arcuate field defects.
Fibers for the central vision are located in the central part of the
disc and superficial (closer to the vitreous). Therefore, if cupping
were occurring, then the central fibers should have been
destroyed first but this is not the case because the central vision
fibers are destroyed last in glaucoma.
In sinking, the peripheral fibers would be severed first because
they lie deeper in close proximity to the scleral rim, whereas the
central and superficial fibers last - this is what is occurring as
revealed in glaucomatous field defects.
Continuous severing of prelaminer fibers due to continuous
sinking of disc would result in progressive thinning of the RNFL–
this is what revealed by OCT.
At the end-stage, the disc area is replaced with an empty crater
due to severance (axotomy) of all the axons of the optic disc –
this is what revealed by end-stage histology.