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CHAPTER 14
CORRELATION BETWEEN THE OPTIC NERVE HEAD
PARAMETERS MEASURED WITH THE HRT AND VISUAL
FIELD DEFECTS
14.1 Introduction
In the literature, the following authors have studied the correlation between comput-
erized perimetry and the HRT parameters: Burk and coworkers [1], with most parame-
ters; Zangwill and coworkers [2] and Lesk and coworkers [3] with the mean RNFL thick-
ness and cross sectional area; Lewis and coworkers [4], with the cup volume; Mikelberg,
Drance and coworkers [5], with the rim volume and cup shape measure; Berglff and
coworkers [6], with localized nerve fiber bundle defects; Lusky and coworkers [7], with
the rim volume and cup volume; and Eid and coworkers [8].
14.2 Parameters studied
The parameters chosen were those with the greatest reproducibility with the HRT
and with a minimum SEM, so that the variability in a normal population is small and the
parameter values of pathological cases immediately deviate from the normal range (table
14.1).
Figure 7.6 (chapter 7) shows the limits of the normal values of these parameters
(obtained with the mean and the standard deviation) studied in a group of 110 normal
eyes of volunteers.
PARAMETERS CORRELATED WITH COMPUTERIZED PERIMETRY
- RIM VOLUME
- MEAN RNFL THICKNESS- CROSS SECTION AREA
- CUP SHAPE MEASURE
- RIM AREA
- CUP AREA
- CUP VOLUME
Table 14.1
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14.3 Material
One hundred and ninety eyes belonging to glaucomatous patients were studied.
Some of them were undergoing the hypertensive period, others the preperimetric pe-
riod, and others the perimetric period.
In the hypertensive period, the only pathological sign is ocular hypertension, since
both, optic nerve and visual field are normal. In the preperimetric period there is ocular
hypertension and the optic nerve has glaucomatous damage, but the visual field remains
normal. The perimetric period is featured by ocular hypertension and glaucomatous
optic nerve and visual field damage (pathological MD and CLV values).
14.3.1 Exclusion criteria
The exclusion criteria were: refractive errors higher than 4 (positive or negative) di-
opters or astigmatisms higher than 3 diopters; transparent media opacities: cataracts(measured with the Opacity Lensmeter); fixation or behavioral problems; macular dis-
eases; previous surgeries; optic nerve or visual field damage caused by pathologies other
than glaucoma. Finally, those patients with low-tension glaucoma were also excluded.
14.4 Methods
Optic nerve tomography was performed with the HRT, software version 1.11. Three
images were acquired from each eye and those with a standard deviation higher than 30
m were excluded. The contour line was always drawn by the same experienced techni-
cian in order to eliminate interobserver variation. The parameters already mentioned in
table 14.1 were studied.
The visual field was examined with the Octopus 1-2-3 perimeter, program G1. Each
patient had at least three visual field examinations performed prior to the examination
used for this study. Cases with a reliability factor higher than 10 were excluded.
Of the visual field parameters, the mean defect (MD) and corrected loss variance
(CLV) were chosen.
The criterion for ocular hypertension was either a single spot check yielding an IOP
higher than 23 mmHg or a daily pressure curve with a mean higher than 19 mmHg and
with a standard deviation over 2.1 [9, 10, 11].
14.5 Results
With the values of the optic nerve and visual field parameters studied, we have built
the graph shown by figure 14.1, where each point on the abscissa represents each of the
190 eyes arranged from left to right and in a decreasing order according to rim volumevalues. The ordinate shows the MD values in decibels in an increasing order from top to
bottom.
The abscissa in figure 14.2 is the same as in the previous figure (rim volume values
in a decreasing order), while the values for the CLV, in decibels, appear on the ordinate.
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The visual field index with the highest correlation with the HRT parameters is MD
(mean defect). This is due to the fact that the CLV (corrected loss variance) starts to rise
with visual field progression, but when the defect turns homogeneous at the end of the
visual field evolution, this index decreases.
The sample was statistically representative of the population studied. Nevertheless,the correlation showed low values due to the fact that both damages (optic nerve and
visual field) do not occur simultaneously, but rather, there is a time interval between
them. It might be stated that there is a "linear correlation deferred in time". Should the
values be high for this correlation, the optic nerve damage would not precede the visual
field damage.
Table 14.2 shows the correlation between the optic nerve parameters and the MD
and CLV. Table 14.3 shows the specificity and sensitivity in the correlation of the optic
nerve parameters with the visual field parameters.
Fig. 14.1
Fig. 14.2
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Although the correlation between CLV values and HRT parameters is not signifi-
cant, tables 14.2 and 14.3 show all the correlation, probability, sensitivity and specificity
values. None of the graphics show the correlation between the CLV values and the HRT
parameters because it is not statistically significant.
A correlation islinear
if the two variables under comparison vary in the same or op-posite direction, in the same fashion and at the same time. There is a non-linearcorrela-
tion if both variables vary in the same or different direction, in the same fashion, but not
at the same time. Therefore, if optic nerve damage appears before visual field defects do,
it is logical for the linearcorrelation to have low values, while the non-linearcorrelation
is more significant.
Based on the explanation above, and taking previous hypotheses like Leydheckers
and Goldmanns postulates (1959) [12] and Capriolis theoretical curve [13], we have
Table 14.2
Table 14.3
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plotted a theoretical curve where the optic nerve starts to deteriorate before visual field
damage develops (figures 14.3 and 14.4).
In figure 14.3, the abscissa shows from left to right the evolution of glaucoma, from
normality to pathology, both in the optic nerve and in the visual field. The ordinate shows
on the left the visual field defects and on the right the optic nerve damage. On the top of
the figure, there appear the three glaucoma periods: hypertensive, preperimetric andperimetric. The curve at the bottom of the figure shows how, from the beginning of the
disease, the optic nerve starts to deteriorate as manifested by the HRT parameters, while
the MD of the visual field (curve at the center) starts to become pathological later. The
curve at the top shows that the CLV also starts to become pathological late, but as the
defect becomes larger and the visual field becomes homogenious, the CLV starts to be-
come lower. This is the reason why this parameter is less helpful.
Figure 14.4 shows the same as the previous figure, but without the CLV. In the hy-
pertensive period there is neither optic nerve damage nor visual field defect; in the pre-
Fig. 14.3
Fig. 14.4
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perimetric period, the optic nerve is damaged, while the visual field remains normal;
finally, in the perimetric period, the visual field starts to deteriorate and the optic nerve
damage continues its evolution.
We will now proceed to study the correlation of each parameter with the mean de-
fect of the visual field. In the following graphs, the ordinate on the left bears the MD
values, and the one on the right the HRT parameter with which it is compared. The ab-
scissa, as always, shows the 190 eyes studied belonging to the hypertensive, preperi-
metric glaucomatous and perimetric glaucomatous periods.
Correlation between MD and rim volume (figure 14.5)
The rim volume is one of the first parameters to be altered in the evolution of glau-
coma and, therefore, this alteration widely precedes the occurrence of visual field defects.
It is pathological when it falls under 0.32 mm3.
Correlation between MD and mean RNFL thickness
Figure 14.6 shows that the mean RNFL thickness, like the rim volume, also lowers
early. Its normal minimum value is 170 m and, therefore, when it is under this value, the
optic disc is pathologically damaged.
Correlation between MD and RNFL cross section area
Figure 14.7 shows that the RNFL cross sectional area also falls before the visual
field defects appear, since this parameter is indirectly related to the nerve fiber volume.
Its decrease is related to both, diffuse defects and localized defects.Correlation between MD and cup shape measure
Figure 14.8 shows that the variation of the cup shape measure is related to the optic
disc shape and it accompanies the visual field curve, so it precedes visual field loss. It has
a steep fall at the end.
Fig. 14.5
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Fig. 14.6
Fig. 14.7
Fig. 14.8
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Correlation between MD and rim area
Figure 14.9 shows that the rim area falls to pathological values before visual field
defects start. Nevertheless, this decrease happens later than in other parameters, since it is
a surface measure (quadratic variable). Pathological values are lower than 1.37 mm2.
Correlation between MD and cup area
Figure 14.10 shows a fairly good correlation between cup area and MD. The cup
area becomes pathological late (higher than 0.60 mm2). Therefore, this parameter is not a
good index to detect early optic nerve changes preceding visual field damage.
Correlation between MD and cup volume
Figure 14.11 shows the correlation between the MD and the cup volume. The cup
volume is the last parameter to change to pathological values and this happens immedi-
ately before visual field defects appear. Both curves are parallel throughout almost all the
Fig. 14.9
Fig. 14.10
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evolution of the disease. The cup volume is not a helpful parameter to predict visual field
damage. It becomes pathological when it is higher than 0.12 mm3. In congenital glau-
coma it behaves conversely.
Figures 14.12 and 14.13 include all the correlations explained above. In figure
14.12, the parameters related to nerve fiber volume appear. All these parameters form a
curve with an upwards concave pattern since they become pathological early and, in
their course, move away from the visual field evolution curve, the alteration of which
takes longer.
In figure 14.13, the parameters related to the cup show, conversely, an evolutioncurve with a downwards concave pattern, which is more similar to the visual field evo-
lution curve. This evidences that the changes in these parameters occur late in the evolu-
tion of the disease.
The cup shape measure fails to follow this rule, since its change occurs parallel to
that of the visual field, throughout the complete evolution of glaucoma. The cup shape
measure is an excellent parameter to follow the changes undergone by the optic nerve in
its progressive deterioration.
When correlating optic nerve damage with visual field defects, it is important to bear
in mind that both are part of a cause / effect phenomenon so they cannot be analyzed as
individual and independent phenomena.
Quigley showed in 1985 [14], in a paper on the subject where he has reported the re-
sults of a follow-up in a group of patients, that it is possible for a normal visual field to
belong to an eye with a severely damaged glaucomatous optic nerve. In the study de-
scribed this paper, Quigley followed the patients with perimetry. As some of the patients
died, their eyes were enucleated, and the degree of retinal nerve fiber loss in their optic
nerves was determined histopathologically. Quigley demonstrated that patients with nor-
mal visual fields at death had lost up to 50 % of their optic nerve fibers.
In normal optic nerves, the number of fibers is higher than necessary to preserve a
normal visual function. In the preperimetric period of glaucoma, the elevated IOP influ-
ences the optic nerve and the fibers start to deteriorate (mechanical or circulatory factors).
Fig. 14.11
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It is not until the number of damaged fibers is substantial, that the damage has an impact
at a functional level and thus, the visual field is altered (perimetric period).
In our study, we were able to measure the volume of fibers making up to neuroreti-
nal rim and we have found that the visual field damage appears when the rim volume
decreases down to 0.30 or 0.20 mm3
(the normal mean is 0.48 mm3, and the normal
maximum is 0.65 mm3
), i.e. the visual field damage appears when the rim volume de-creases by 50%.
Figure 14.14, which is similar to the previous figure, better explains the statements
above. It includes the study of the preperimetric and perimetric periods. The abscissa
represents the rim volume decrease in different evolution phases of the optic nerve: N:
normal; B: borderline; P1: phase 1; P2: phase 2; P3: phase 3; P4: phase 4. The rim vol-
ume, in 10-3 mm3, is shown below these phases. It is important to stress that visual field
damage occurs when the optic nerve is in phase 2. When the evolution continues, the
Fig. 14.12
Fig. 14.13
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optic nerve will reach phase 4 and the visual field will become terminal. In phase 4, the
rim volume is lower than 0.10 mm3, while in phase 2, it ranges from 0.30 to 0.20 mm
3.
Figure 14.15 shows the same evolution phases but with the pertinent computerized
tomographic image of each phase, where the flat neuroretinal rim appears is green, the
tilted neuroretinal rim apperas in blue, and the cup appears in red. It is clearly seen that,in phase 2 the neuroretinal rim is substantially reduced in its surface and, therefore, also
in its volume. In some cases, the neuroretinal rim in phase 2 disappears within a small
segment at the cup margin since there is a damaged fiber bundle leading to a scotomatous
defect. In phase 2, the cup is separated from the cup margin just by a thin neuroretinal
rim. In phase 4, the neuroretinal rim has disappeared completely or almost completely.
Fig. 14.14
Fig. 14.15
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14.6 Discussion
Glaucoma is a disease which goes through three periods in its evolution: the first one
is the hypertensive period, the second one the preperimetric period, and the third is the
perimetric period.
In the three periods, close IOP monitoring by means of single spot checks, and par-
ticularly, by daily pressure curves, is critical. The method for performing daily pressure
curves, as reported at the 7th Argentine Congress of Ophthalmology held in Rosario,
Argentina, in 1961 [10] consists of seven measurements within the same day, at 6 a.m.,
with the patient still in bed and no lights turned on (with a hand applanation tonometer)
and then at the office at 9 and 12 a.m. and at 3, 6, 9 and 12 p.m. with applanation to-
nometry on the slit-lamp. With these readings the mean and the standard deviation or
variability are calculated. The upper normal limit is 19 mmHg for the mean and 2.1
mmHg for the variability.A daily pressure curve is pathological (hypertension) when its mean is pathological
and the variability is normal, when the variability is pathological and the mean is normal,
or when both values are pathological [9, 15].
This monitoring of IOP is necessary to correlate it with optic nerve damage and to
evaluate the efficacy of medical therapy. If the daily pressure curve with maximum medi-
cal therapy is pathological and the optic nerve continues its deterioration, surgical therapy
is required.
During the first period, the hypertensive one, it is critical to monitor the intraocular
pressure with applanation tonometry closely, as well as to carry out confocal laser scan-
ning tomography after certain periods (6 months) in order to determine if the second pe-
riod has started by detecting possible pathological changes in the optic nerve. The visual
field examinations should be thoroughly checked every 6 months in order to detect visual
field defects.
In the preperimetric period, it is important to follow the evolution with confocal la-
ser scanning tomography of the optic nerve and with visual field examinations at differ-
ent intervals, in order to detect the start of the third period.
During the perimetric period, thorough control of optic nerve tomographies and
computerized visual field examinations is fundamental to study their evolution.
IOP should be closely monitored in all the three periods in order to indicate either
medical or surgical treatment.
Figure 14.16 is a sketch of these three periods.
Figure 14.17 is a chart of the evolution phases which have been printed on the top of
the first page of the clinical history forms for glaucoma.It is widely known that when a patient comes to the office for a follow-up examina-
tion, it is difficult to determine in which evolution stage his glaucoma disease is. The IOP
readings and the different visual field and optic nerve examinations should be gone
through and compared to each other in order to detect any variations or to find out if they
have stopped their deterioration.
With the aid of the chart in the clinical history, if properly ticked, the evolution stage
can be determined easily and quickly with no need to analyze any of the above mentioned
examinations.
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On the bottom of the chart in figure 14.17, each of the three periods, hypertensive,
preperimetric and perimetric, are separated by thick vertical lines.
In the rectangle for the hypertensive period, the IOP values appear on the ordinates
in mmHg, 10, 20, 30, 40, 50 mmHg. The maximum IOP reading the patient has had in his
evolution is encircled.
On the second field, for the preperimetric period, there are three columns. The first
column is ticked when the tomography yields an optic nerve in the borderline phase, and
the second column when it is in phase 1; the third column is for optic nerves in phase 2.
The visual field in this period in usually normal, so the letter "N" is printed.
The field belonging to the perimetric period has four columns. The "B" on the first
column means that the visual field is borderline. The other columns are for visual fields
in stages I, II or III, according to the classification of Octopus perimetry. In addition to
this information, on the top, it can be indicated whether the optic nerve, according to theHRT, belongs to phase 2, 3 or 4 (see chapter 10).
The procedure to fill in this chart is to register the maximum IOP reading and then,
to color or tick one of the boxes for the different optic nerve evolution phases and one of
those for the visual field evolution stages.
The study we have just explained in detail is a confirmation of two similar hypothe-
ses of different clinical papers which were postulated by Goldmann and Leydhecker in
1959 [12].
Fig. 14.16
Fig. 14.17
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These hypotheses state that glaucoma is a disease characterized by a first period
manifested as ocular hypertension, followed by a period in which the optic nerve starts to
deteriorate and nearly 10 years after this, visual field loss appears. The period elapsed
between the occurrence of hypertension and the development of visual field damage is
approximately 20 years (figure 14.18).
Leydhecker [16] analyzed the results of a study conducted in 1959 on 20,000 eyes of
subjects working at factories or offices. Four hundred hypertensive eyes out of the total
eyes were selected (the indicator of Schiotzs tonometer signaled three or more divisions
with the 5.5 gram weight). 33% of the selected eyes had visual field damage.In the same year, Goldmann analyzed the results obtained by Leydhecker and built a
graph [17] (figure 14.19). On the ordinates, the population is expressed as the logarithm
of the number of cases; the abscissa shows the age of the patients. The crosses represent
the glaucoma suspect cases, which form a curve indicative a poor correlation, i.e. among
these suspected cases, there are some non-glaucomatous ones. The black circles belong to
glaucoma cases whose diagnosis is accurate, with no visual field loss. The white circles
are glaucoma cases with visual field damage. The correlation is very good: the circles fall
on two parallel lines. This indicates that it is a function of body growth. Both lines area
separated from each other by a distance of 10 years. This parallelism demonstrates that
visual field defects are a consequence of elevated intraocular pressure.
In 1972, at the "First Cambridge Ophthalmology Symposium", Goldmann stated: "...
All these issues help promote the tendency, among ophthalmologists, to consider certain
IOP as glaucomatous only when there is well-established paracentral visual field loss ...
Therefore, there is great danger, since the concept of ocular hypertension has steadily
developed as a reality which is dramatically different from that of glaucoma, leading to
the belief that diagnosis of glaucoma is impossible, just at the moment when it should be
made, i.e., before visual field defects occur. There is a risk to go back to the situation of
50 years ago, with all its implications ..."
Fig. 14.18
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Niesels hypothesis [18] states that the time elapsed until visual field loss starts, de-pends on the optic disc irrigation and, therefore, it is an individual factor, which differs
among patients. He relates IOP, blood pressure, perfusion pressure of optic nerve and
capillary resistance. The higher the IOP values, the lower the perfusion pressure and the
higher the capillary resistance, the earlier the optic nerve damage and the visual field
defects take place.
Caprioli has recently studied the correlation between optic nerve damage and visual
field manifestations in glaucoma. In the initial stages, there is a increasing involvement of
the optic nerve head, there is usually also a diffuse thinning of the neural layer before
visual field damage occurs. It is not until later on that perimetry becomes more relevant.
In the same paper, Caprioli shows the curve of relative velocity of optic nerve and
visual field involvement from the moment hypertension takes place (figure 14.20).
The curves start together and become separated immediately. The superior curve,representing the visual field, starts to go down very late (inferior concavity curve),
whereas the curve representing the optic nerve goes down rapidly from its beginning
(superior concavity curve). They join back at the end of the evolution, when the optic
nerve is completely deteriorated as well as the visual field.
Many authors with a vast and long experience in glaucoma share these concepts, like
Gloor (1995) [19], Schwartz (1985) [20], Quigley (1982) [21], Odberg and Riise (1985)
[22], Airaksinen (1983 and 1985) [23, 24], Hoyt (1973) [25], Motolko and Drance (1981)
[26] and Sommer, Miller and Polack (1984) [27].
Fig. 14.19
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Our experience has clearly demonstrated that in the presence of ocular hypertension,
before visual field loss occurs, the optic nerve starts to deteriorate.
Thirty percent of glaucoma cases may have a localized fiber defect as the first sign,
the analysis of which is different from that for diffuse defects. It is important here to
mention the fiber distribution map plotted by Webber and Ulrich in 1985 [28], where the
fiber bundles coming into the optic nerve are related to the scotomatous defects in thevisual field (figure 14.21).
14.7 Conclusion
In a group of open angle glaucomas, optic nerve damage, according to the parame-
ters of confocal tomography, is correlated with visual field loss, revealed by the indices
mean defect and corrected loss variance of computerized perimetry.
Fig. 14.20
Fig. 14.21
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The optic disc parameters becoming pathological long before visual field loss occurs
are those related to nerve fiber volume, such as rim volume, RNFL thickness, RNFLcross sectional area, and third moment (cup shape measure). The remaining parameters,
such as rim area, cup area and cup volume, are less significant, because they become
pathological later on, much closer to the occurrence of visual field defects. In particular,
the cup volume is the least important parameter, since it becomes altered at the same time
as the onset of visual field loss. The most important parameter for the determination of
optic nerve damage and the follow-up of its evolution is the rim volume. Airaksinen and
coworkers [29], according to the results of a study, state that the rim volume is the best
parameter classifying patients into the different groups: normals, ocular hypertensives
with no abnormalities, ocular hypertensives with abnormal nerve fiber layer and early,
moderate or advanced glaucomas.
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