Ординатура / Офтальмология / Английские материалы / Atlas of Glaucoma, Second Edition_Choplin, Lundy_2007
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172 Atlas of glaucoma
(e)
Figure 12.2 Continued.
have lower intraocular pressures and tend to be younger and are more often female (Figure 12.4).
Disc hemorrhages (Figure 12.5) have been frequently described as occurring more frequently in normal-tension glaucoma. Kitazawa et al.28 noted a prevalence of disc hemorrhage of 20.5% in individuals with normal-tension glaucoma. Recurrent disc hemorrhage occurred in 64% of these eyes, which was much higher than in the other groups they studied. Drance29, in his extensive review article, noted that disc hemorrhages were not rare events. The closer one follows the disc and records the disc appearance, the more hemorrhages will be noted. He estimated the prevalence to be about 20% in normal-tension glaucoma. In addition, he felt that there were possibly two groups of patients: those who hemorrhage and those who do not. Disc hemorrhages were also felt to precede retinal nerve fiber layer loss, topographic changes of the optic disc, and visual field loss. Hendrickx et al.30,
however, felt that the cumulative incidence of disc hemorrhages were similar in ocular hypertension, primary open-angle glaucoma, and normal-tension glaucoma. With treatment, however, they noted that the incidence of disc hemorrhages decreased in ocular hypertension and primary open-angle glaucoma, but not in normal-tension glaucoma. In addition, recurrent disc hemorrhages tended to be scattered all over the disc in normal-tension glaucoma, but tended to occur at the same site in primary open-angle glaucoma and ocular hypertension, perhaps implying a different etiology for the disc hemorrhage in the different conditions.
Peripapillary atrophy (Figures 12.5 and 12.6) also has been reported to occur more frequently in normal-tension glaucoma than in primary openangle glaucoma. Buus and Anderson31 concluded that peripapillary crescents correlated with disc damage and were therefore more common in normal-tension glaucoma than in ocular hypertension.
Normal-tension glaucoma 173
Peripapillary atrophy |
Loss of temporal rim |
Loss of rim |
Resolving disc hemorrhage |
Deep cupping |
Figure 12.3 Loss of inferotemporal rim. Low-tension glaucoma with greatest loss of temporal and inferior rim. Also note peripapillary atrophy.
Figure 12.5 Disc hemorrhage. Low-tension glaucoma with loss of temporal and inferior rim, with resolving disc hemorrhage and peripapillary atrophy.
Geijssen and Greve32 noted peripapillary atrophy in the entity of senile sclerotic glaucoma. However, Jonas and Xu33 felt that there were similar degrees of paripapillary atrophy between normal-tension glaucoma and primary open-angle glaucoma in their study population.
It therefore becomes problematic to define what if any features of the optic disc are characteristic of
Figure 12.4 Loss of inferotemporal rim. Loss of temporal and inferior rim with especially deep inferior cupping of the optic disc in normal-tension glaucoma.
Figure 12.6 Peripapillary atrophy. Peripapillary atrophy in normal-tension glaucoma (arrow). This change is typical of what has been termed ‘senile sclerotic glaucoma’.
174 Atlas of glaucoma
normal-tension glaucoma. Our inability to do so |
Subtle differences between visual fields of |
undoubtedly reflects on our inability to define what |
normal-tension glaucoma and high-tension glau- |
are likely to be the many entities which may result |
coma subjects appear to exist. Numerous studies |
in glaucomatous optic atrophy, the complexities of |
have compared the visual fields seen in normal- |
attempting to study and analyze the optic disc, and |
tension glaucoma with those seen in high-tension |
the tremendous physiological variability that is typi- |
glaucoma. Anderton and Hitchings35,36 as well as |
cal of the eye and optic nerve. |
Caprioli and Spaeth37 found a higher incidence |
|
of defects near fixation, especially superonasally, |
VISUAL FIELD DEFECTS |
in normal-tension glaucoma (Figures 12.7–12.9). |
Caprioli and Speath noted that visual field defects |
|
|
in normal-tension glaucoma had greater depth and |
The diagnosis of normal-tension glaucoma is made |
a steeper slope than the defects of high-tension |
on the basis of progressive visual field loss and/or |
glaucoma. Other studies, however, have not suppor- |
optic disc changes in the absence of elevated intra- |
ted these findings. Motolko and others38,39, and Greve |
ocular pressure. For the most part, visual field |
and Geijssen40 found no significant difference in |
defects in normal-tension glaucoma are similar |
the proximity of field defects near fixation between |
to defects found in high-tension glaucoma34. Nasal |
the normal-tension and high-tension glaucoma |
steps, paracentral scotomas and arcuate defects |
groups. King et al.41 even found that defects in high- |
predominate. |
tension glaucoma tended to be closer to fixation. |
Figure 12.7 Superonasal defect near fixation. This typical low-tension glaucoma defect involves loss of inferotemporal nerve fibers. It is very dense and comes close to fixation.
Normal-tension glaucoma 175
Figure 12.8 Example of a visual field defect near fixation. Note the depth of the defect and the sharp drop-off between the defect and the surrounding points.
The assertion that normal-tension glaucoma field |
in the high-tension group. This finding is based on |
defects are ‘deep, steep, and creep’ towards fixa- |
the decreased overall sensitivity of the ‘spared’ |
tion in comparison to high-tension glaucoma fields |
hemifield (no local defect) in high-tension glau- |
is still being debated. Phelps et al.42 attribute the |
coma. Araie et al. concluded that, even in the late |
disparate findings of the various studies to the dif- |
stages of disease, diffuse depression may be more |
ferent methodologies used. |
common in high-tension glaucoma. Zeiter and oth- |
Most studies have found that the superior hemi- |
ers47 reported that localized defects in the inferior |
field and particularly the superonasal quadrant are |
hemifield may be more common in normal-tension |
the most frequent locations for normal-tension glau- |
glaucoma. |
coma defects. Furthermore, Araie et al.43,44 reported |
The difference between normal-tension and |
that the inferior hemifield just below fixation |
high-tension glaucoma with respect to diffuse ver- |
might be relatively spared. Inferior defects that |
sus local field loss may be attributable to the differ- |
do occur are also typically deep with steep slopes |
ence in intraocular pressure rather than some other |
(Figure 12.10). |
intrinsic difference between normal-tension and |
Other differences between normal-tension glau- |
high-tension glaucoma. Instead of comparing nor- |
coma fields and high-tension glaucoma fields have |
mal-tension with high-tension glaucoma groups, |
been shown. Several groups, including Drance |
several studies compared glaucoma subjects (both |
et al.45, Chauhan et al.46 and Araie et al.43,44, have |
low tension and high tension) having diffuse visual |
shown that diffuse visual field loss is more common |
field loss with those having localized field defects. |
176 Atlas of glaucoma
Figure 12.9 Another example of a defect near fixation. Note that the overall pattern is that of a nerve fiber layer defect.
Glowazki and Flammer48, Caprioli et al.49, and Samuelson and Spaeth50 all found significantly higher intraocular pressures in subjects with diffuse field loss than in subjects with localized field loss (Figure 12.11).
While these differences between normal-tension and high-tension glaucoma fields are no-doubt important to our scientific understanding of normaltension glaucoma, the clinical significance is less clear. Distinguishing between normal-tension and high-tension glaucoma is obviously not based on the visual field defects. However, we should be aware that defects near fixation might be quite common in persons with normal-tension glaucoma. Defects near fixation (Figure 12.12) are clearly more worrisome than more peripheral ones. In monitoring for the progression of disease, we must realize that the existing defects may deepen rather than enlarge, so particular attention should be paid to the total deviation at each point.
Several studies have addressed the rate of progression of visual field changes in normal-tension glaucoma. Two retrospective analyses found a rather alarming rate of progression. Glicklich et al.51 found progression in 53% at 3 years and 62% at 5 years. Noureddin et al.52 found progression in 37% of eyes with a mean follow-up of 28 months. A very high rate of progression was initially seen in the Collaborative Normal-tension Glaucoma Study53,54 in which a duplicate field determination was necessary to confirm a change. However, by statistical reanalysis of the field data, the study group found a very high false-positive rate for progression. The criteria for progression were revised to include two sets of duplicate fields (four total) spaced 3 months apart that showed the same change of at least 10 dB. This increased testing reduced the false-positive rate to only 2%. The estimated rate of progression by the revised criteria was only 1.3% per patient per 3-month period. In light of the findings of the
Normal-tension glaucoma 177
Figure 12.10 Inferior field defect. Although less common than superior defects, inferior defects also tend to be deep and steep and may be close to fixation.
Normal-tension Glaucoma Treatment Trial55, we may need to repeat visual field testing several times before concluding that progression has occurred in a person with normal-tension glaucoma.
TREATMENT OF NORMAL-TENSION
GLAUCOMA
The treatment of low-tension glaucoma remains as much an enigma as the disease itself. In general, the accepted clinical treatment of low-tension glaucoma parallels that for primary open-angle glaucoma. Individuals are usually started on medical therapy designed to lower their intraocular pressure and may undergo laser or glaucoma filtering surgery with very low pressures as the target goal. The Collaborative Normal-tension Glaucoma study provided the most convincing evidence that lowering intraocular pressure does decrease the
rate of progression in this disease. With a target pressure lowering of 30%, the study found that treatment reduced the progression rate by about two-thirds compared to untreated controls. The Early Manifest Glaucoma Trial also found that pressure-lowering treatment reduced the rate of progression in its subset of subjects with normaltension glaucoma compared to untreated controls56,57.
While critically important, reduction of intraocular pressure may not be the only potential treatment for normal-tension glaucoma. Therapy for low-tension glaucoma is always being critically re-evaluated and novel approaches to therapy in some individuals are being considered. Based on studies that suggest a vascular autoregulatory dysfunction or vasospasm in normal-tension glaucoma, some individuals have recommended therapy specific for these proposed pathophysiological abnormalities58. In addition, interest is increasing to consider agents that may have neuroprotective effects.
178 Atlas of glaucoma
Figure 12.11 Superior hemifield loss. The ‘spared’ inferior hemifield exhibits minimal overall sensitivity loss.
While medical treatment for normal-tension glaucoma is generally similar to treatment for primary open-angle glaucoma, some potentially important variations should be considered. There have been some suggestions that the 1-antagonist, betaxolol, may improve blood flow or provide neuroprotective benefits to help preserve visual function and thus may be of benefit in low-tension glaucoma. However, long-term studies addressing the efficacy of betaxolol, although suggestive, are not complete. Non-selective beta blockers generally lower pressure more than a selective beta blocker; however, there are concerns regarding potential vasoconstriction related to the pharmacological properties of these agents. In fact, the Collaborative Normal-tension Glaucoma Study avoided beta blockers for this reason. Although direct evidence of clinically significant vasospasm in low-tension glaucoma has been suggested, the evidence for such an effect is still to be defined.
The development of neuroprotective agents has been a very active area of glaucoma research and normal-tension glaucoma patients may achieve the greatest benefit from this type of therapy. The highly selective 2-agonist, brimonidine tartrate, has shown neuroprotective effects in cell culture and in a variety of animal models. Brimonidine is also being evaluated as a neuroprotective agent in a large clinical trial59. Other compounds, some already available such as memantine, are being investigated as potential neuroprotective agents.
Newer therapeutic approaches directed at improving blood flow to the optic nerve have also been considered. Calcium channel blockers have received the most interest and study. Although some suggestive indirect evidence does exist that individuals on calcium channel blockers may have better visual field survival, these studies are open to criticism and there is still much work to be done. In addition, these agents can be associated with serious
Normal-tension glaucoma 179
Figure 12.12 Paracentral scotoma. The field defect has encroached on fixation and should be monitored closely for further deepening of the defect.
systemic side-effects, such as hypotension and a reported increased risk of heart attack. Other novel approaches to treating low-tension glaucoma are being investigated and will hopefully lead to more satisfactory medical approaches in the future.
Most clinicians agree that, in the face of progressive low-tension glaucoma, aggressive surgical therapy should be considered. Several studies have suggested that, with aggressive surgery and intraocular pressure lowering to the low teens or below, visual field progression can be slowed or halted in many individuals. When considering glaucoma filtering surgery for low-tension glaucoma, many clinicians and glaucoma specialists will consider the use of an anti-metabolite such as 5-fluorouracil or mitomycin C. Although the use of anti-metabolites
increases the likelihood of obtaining low intraocular pressures, one must also deal with the short-term complications of hypotony, choroidal effusions, and flat anterior chamber, as well as the potential long-term complications of cataract progression, bleb leaks, and endophthalmitis.
Unfortunately, despite what might be considered as optimal therapy for an individual with low-tension glaucoma, many of these individuals seem to progress. Our lack of understanding of the etiology of low-tension glaucoma undoubtedly contributes to our therapeutic failures. Further research is necessary to define the underlying causes that predispose to low-tension glaucoma so that future therapy may be directed at specific pathophysiological abnormalities.
180Atlas of glaucoma
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