Preface

In recent decades, a rapid expansion in our understanding of the physiology, epidemiology, and genetics of glaucoma has brought about the development of new diagnostic and therapeutic techniques. As a result, it has become increasingly difficult for clinicians to assimilate this mass of information and apply it to the care of their patients.

A comprehensive understanding of this leading cause of blindness encourages the physician to be familiar with all of these basic and clinical science advances. This text is primarily intended to provide the resident and general clinician with a single volume, clinically-oriented source that covers the full spectrum of glaucoma problems, including the pathophysiology, epidemiology, and genetics of the many specific types of glaucoma. The glaucoma specialist, too, will also find the information provided by the international group of contributors to be authoritative, well documented and clearly presented.

To build and reinforce this understanding, we have taken the logical, time-honored approach of presenting first the pertinent, basic knowledge, followed by clinical disease entities and then their treatment. This is accomplished in 7 sections, beginning with the epidemiology and genetics. These two rapidly advancing disciplines provide an excellent framework for understanding the importance of glaucoma, both for society and the individual. They also provide important insights for understanding potential mechanisms and future therapy of the major forms of glaucoma that are discussed later in the text.

The next two sections discuss the basic and clinical sciences of two topics that are common to all forms of glaucoma: intraocular pressure and the optic nerve. In each section, we include the basic anatomy and physiology of the involved structures, as well as methods for their clinical evaluation. For the optic nerve section, this includes a discussion of glaucomatous optic neuropathy, and encompasses the clinical aspects of optic nerve damage as well as considerations of its likely mechanisms.

Specific chapters deal with new methods of analysis of the optic nerve head and nerve fiber layer, followed by a thorough discussion of perimetry and its application to glaucoma.

The next section considers the major categories of the clinical forms of glaucoma. Although this primarily follows an etiologic approach to disease classification, several major forms of glaucoma are each discussed in their own chapter, rather than under a broader heading. This is in keeping with our primary goal of presenting readily accessible information that is essential for clinical recognition and treatment. Each of these chapters considers the background of the entity, its pathogenesis, clinical diagnosis, and differential diagnosis, followed by medical and surgical management. The final 3 sections of the book discuss the medical, laser, and surgical methods commonly used in the management of all forms of glaucoma.

All chapters are introduced by an overview to prepare the reader for the content that is to follow. Highlight boxes emphasizing pearls, pitfalls, controversial points and items of special consideration are used to call the reader’s attention to specific, important information. Tables are used throughout to provide a useful framework for understanding this information. This is to help the resident physician learn this material for the first time, and provide a quick reference useful to the busy clinical practitioner in need of a quick review.

Although this text is meant to be comprehensive, we have tried to present the most commonly encountered problems and the most important issues without providing an excess of information or detail. We recognize some information found in textbooks is quickly outdated by new information found in journals and presented at scientific meetings. This is certainly the case with the rapidly evolving fields of genetics and glaucoma therapy. Nevertheless, at the time of this publication the reader will find the information contained to be timely, current, and relevant.

We are indebted to the many contributors to this text, each of whom dedicated much time and effort to write one or more chapters reflecting their knowledge and expertise. We gratefully recognize the Casey Eye Institute photography department for giving us access to their considerable archives of excellent clinical photographs, with special thanks to Patrick Wallace for his aid with scanning this photographic material for publication. We thank Andrea

Seils who recruited us for this project and Esther Gumpert for guiding it to competition. We thank Owen Zurhellen, editorial assistant and Rebecca Dille, our production editor, for guiding this to a finished product.

We are expecially indebted to Doctors Bernard Becker and E. Michael Van Buskirk who, along with innumerable other mentors, provided us with our lifeline to ophthalmology and opthalmic research.

Glaucoma is the second leading cause of blindness in the world.1 As of the year 2000 66.8 million people are now estimated to have glaucoma, with 6.7 million bilaterally blind from this disease. Aside from its medical impact on the afflicted population, the total economic and social costs of glaucoma are virtually unknown.

In spite of many advances in the diagnosis and treatment of glaucoma, the fundamental causes of most glaucomas remain unknown. This hampers our ability to predict who will require treatment to prevent loss of vision. Generally, however, diseases do not occur at random; they instead present with specific patterns. The field

of epidemiology (Table 1–1) seeks to identify these patterns and gain insight into why certain individuals succumb to disease and others do not. This knowledge, in turn, helps us understand the mechanism of disease and guides screening and treatment toward specific populations and subpopulations.

PEARL… Epidemiology seeks to identify patterns of disease that can provide insights into why some people succumb to disease and others do not.

When glaucoma is broadly classified into primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG), our understanding of the epidemiology of glaucoma draws from both global and regional experiences. The distinct geographic tendencies of these entities throughout the world help guide public health resources dedicated to the diagnosis and treatment of glaucoma. This knowledge also helps individual practitioners as they evaluate and treat ever increasing numbers of patients from diverse ethnic backgrounds. These epidemiological evaluations rely on standardized definitions of both forms of glaucoma. This allows investigators to perform careful comparisons among different studies and draw meaningful conclusions.

Studies of the specific patterns of these diseases, or risk factors, are derived mostly from Europe, the United States, and Australia. Because PACG is less common in these regions, our understanding of its risk factors is limited, although some have been identified, such as age, gender, refractive error, and family history.

In contrast, POAG has been widely studied. Many population-based studies and clinical series now exist; they provide accurate information on the prevalence of this condition and its relationship to several risk factors, which, in turn, sheds light on the possible mechanisms of this disease. Among these risk factors, intraocular pressure (IOP), ethnicity, and age are well established. Diabetes mellitus, systemic hypertension, myopia, and migraine headaches seem more controversial.

PUBLIC HEALTH IMPACT OF GLAUCOMA

In the United States, were estimated to be 130,540 people blind from primary glaucoma in the year 2000.2 In Olmsted County, Minnesota, 9% of subjects aged 66 years when diagnosed with glaucomatous optic nerve damage or visual field loss were bilaterally blind at the 20-year fol- low-up, in spite of receiving treatment.3 Although it is easy to imagine the difficulties associated with living in today’s society with vision less than 20>400 or 3>60 in the better eye (World Health Organization’s criteria for blindness), many people do not understand the impact that loss of peripheral vision, depth perception, and contrast sensitivity can have on an individual’s life prior to blindness. Topical eye medications and glaucomatous visual field loss are associated with an increased risk of falls and fractures in the elderly.4 In addition, a diagnosis of glaucoma is an independent risk factor for injurious car crashes in subjects 55 to 87 years of age.5

Because the visual loss and medications associated with glaucoma affect the activities of daily living,6–10 the economic impact of glaucoma on society is essentially unknown. Although we can measure the cost of medically treating glaucoma,11 the costs of visual impairment and blindness are much more difficult to estimate.

CHAPTER 1 EPIDEMIOLOGY OF GLAUCOMA • 3

Glaucoma is not a single disease but many. It is often categorized into PACG, secondary angle-closure glaucoma, POAG, secondary open-angle glaucoma, congenital glaucoma, and juvenile glaucoma.

As Figure 1–1 shows, the most common type of glaucoma in one region of the world may differ from that in another region. PACG is more common in Asia, whereas POAG is more evenly distributed throughout the world.1 In the United States, Europe, and Australia, 75 to 95% of glaucoma in Caucasians is POAG,1,12 whereas PACG accounts for 70 to 90% of glaucoma in China and India.12–14 Most glaucoma in Japan is POAG, which includes normal-tension glaucoma.15 Unfortunately, very little is known about which type of glaucoma is most prevalent in Africa. However, this is most likely POAG because PACG is rare in African Americans.16 In South America and the Near East, clinical records suggest that POAG is the most common form of glaucoma, even though PACG is more prevalent there than in Caucasians in both the United States and Europe.1

This global perspective strongly suggests that people of certain ethnic groups are more likely to have either PACG or POAG. This helps the practitioner diagnose and treat the individual glaucoma patient. From a public health perspective, understanding the epidemiology of PACG and POAG helps us determine why certain individuals are more likely to develop these conditions, and can improve the screening, treatment, and prevention of blindness.

PRIMARY ANGLE-CLOSURE GLAUCOMA

(SEE ALSO CHAPTER 16)

DEFINITION OF PRIMARY ANGLE-CLOSURE

GLAUCOMA

The 1996 American Academy of Ophthalmology Preferred Practice Pattern defines PACG as “appositional or synechial closure of the anterior chamber angle caused by relative pupillary block in the absence of other causes of angle closure.”17 Because PACG is a relatively rare disease in Europe, the United States, and Australia, very little is known of its epidemiology. In addition, the diagnosis of PACG depends on gonioscopy. However, there is no universally accepted gonioscopic definition of angle closure, which complicates comparison of population-based studies on this condition.

RISK FACTORS FOR PRIMARY

ANGLE-CLOSURE GLAUCOMA

Ethnicity

Several population-based studies have found that individuals of Eskimo or Chinese descent are at increased risk of PACG. The prevalence of PACG is 20 to 40 times higher in Eskimos than in Caucasians.12 In addition,

a population-based survey from Singapore associated a history of Chinese descent with a greater risk for PACG.18 The increased risk in Eskimos probably results from a smaller eye size and more crowded anterior chamber.19 With the exception of a smaller corneal curvature, however, the axial length and anterior chamber depth of Taiwanese and Caucasian eyes are remarkably similar.20

Age

Older patients are more likely to develop PACG. This increased risk probably results from steady growth of the crystalline lens throughout life.21,22 In Eskimos, Chinese, and Caucasians, the anterior chamber shallows and the angles become progressively narrower as the lens thick- ens.19,23–26 Because this disease is more prevalent within and beyond the fifth decade of life, it is recommended that screening for PACG start at age 40.12

Gender

Several population-based surveys suggest that women are at increased risk for PACG.12,18,27 Whether this is because women have smaller eyes and anterior chambers than men is uncertain. In Eskimos, women have more shallow anterior chambers than men.19 In Chinese and Caucasians, however, these differences are not enough to explain why women are more likely to develop PACG than men.

Refractive Error

Among Caucasians, hyperopia is associated with PACG.27 In a population-based survey in Western Cape, South Africa, individuals of Southeast Asian descent with hyperopia were more likely to have PACG.28 A comparison of the refractive errors between subjects in the Baltimore Eye Survey and a small population-based sample in Taiwan, however, showed that Caucasians were more likely to have refractive errors of +2.00 diopters or more.20 In spite of this, PACG is more common in Chinese than in Caucasians.

Positive Family History

A family history seems to be a strong risk factor for PACG across several ethnic groups. One to 12% of first-degree relatives of Caucasians with PACG can develop PACG.12 In Eskimos, the prevalence of PACG in first-degree relatives of patients with this disorder may be 3.5 times higher than in the general population.19 A populationbased survey in China showed that any family history of glaucoma increased the risk of PACG sixfold.25

Environmental Factors

Some population-based studies have reported associations of PACG attacks with the weather, such as the number of hours of sunshine and the daily temperature. A study in Singapore reported more attacks on hotter

days, and suggested that angle-closure attacks are more likely on days with more hours of direct sunshine.18 In Israel,29 PACG attacks occurred more frequently in the summer and winter. On the other hand, in Finland such attacks were more frequent in autumn and winter, when there is less sun exposure.30 The association of acute PACG attacks with the number of sunspots is similarly controversial.18 Currently, we do not understand the exact role of the weather in acute PACG.

PRIMARY OPEN-ANGLE GLAUCOMA

(SEE ALSO CHAPTER 15)

DEFINITION OF PRIMARY OPEN-ANGLE

GLAUCOMA

The 1996 American Academy of Ophthalmology Preferred Practice Pattern defines POAG as a “chronic, generally bilateral and often asymmetrical disease, which is characterized (in at least one eye) by all of the following”:

1.Evidence of glaucomatous optic nerve damage from either or both of the following:

i.The appearance of the disc or retinal nerve fiber layers (e.g., thinning or notching of the disc rim, progressive change, nerve fiber layer defects)

ii.The presence of characteristic abnormalities in the visual field (e.g., arcuate defect, nasal step, paracentral scotoma, generalized depression) in the absence of other causes or explanations

2.Adult onset

3.Open, normal-appearing anterior chamber angles

4.Absence of known other (e.g., secondary) causes of open angle glaucoma31

Depending on the definition of POAG, the prevalence of this disease in population-based studies ranges from 0.4 to 8.8%15,23,32–42 (Table 1–2). The majority of these studies used the appearance of both optic nerve head and visual field as part of the diagnostic criteria.15,23,32–42 In the Blue Mountains Eye Study,41 there was a prevalence of 5.6% when optic nerve damage alone was deemed sufficient to satisfy the diagnostic criteria for POAG. However, including both optic nerve head and automated visual field criteria decreased the prevalence by more than half, to 2.4%.

RISK FACTORS FOR OPEN-ANGLE GLAUCOMA

The risk factors for POAG generally break down into demographic and clinical categories. However, IOP, which may be closely connected to the mechanism of POAG, deserves special attention.

Intraocular Pressure

The American Academy of Ophthalmology definition31 of POAG does not include IOP. Several population-based

CHAPTER 1 EPIDEMIOLOGY OF GLAUCOMA • 5

studies (Table 1–2) include elevated IOP in their diagnosis of POAG. In an editorial in the American Journal of Ophthalmology, Sommer43 discussed how IOP may be a risk factor, even when the IOP is only 16 mm Hg. The prevalence of POAG in both whites and African Americans progressively increases with higher levels of screening IOP (Fig. 1–2; Table 1–3). In addition, people can satisfy criteria for POAG even when the IOP is less than 18 mm Hg. In the Baltimore Eye Survey, 47 out of 3571 eyes with an IOP of 16 to 18 mmHg (0.01%) met the definition for POAG.44 These statistical associations are all consistent with IOP as a risk factor for POAG. However, they do not prove that IOP causes POAG in all cases.

PEARL… Epidemiology can determine the role of intraocular pressure in glaucoma by inference, but cannot prove it.

Such proof of causation can be inferred but not directly observed. Even randomized studies must rely on the inference that chance alone does not explain their results. Epidemiological studies, which lack the standardization of randomized trials, require even stronger assumptions. One approach to this problem draws on the experience of the 1962 Advisory Committee to the Surgeon General on smoking and health.45 From this, we can determine several lines of evidence suggesting that IOP is a causal risk factor for POAG. This evidence satisfies the following criteria:

1.Consistency of association. The population-based studies in Wales,32 Framingham,23 Baltimore,35 Beaver Dam,36 Barbados,39 and Blue Mountains41 all showed a consistent association between IOP level and POAG.

2.Strength of association. The Baltimore Eye Study44 reported that the strength of this association increased with progressively higher IOPs. Compared to eyes with screening IOP less than or equal to 15 mm Hg, the relative risk of POAG in eyes with IOPs of 22 to 29 was 12.8, and 39.0 for eyes with screening IOPs of 30 to 3444 (Table 1–3).

3.Specificity of association. This refers to the extent that a cause can be identified as leading to an effect to the exclusion of other factors. For example, it seems plausible that elevated IOP by itself could induce POAG given that elevated IOP may cause vascular ischemia, decreased perfusion of the optic nerve head, mechanical compression of the lamina cribrosa, and decreased axoplasmic flow. All of these events may be important features of glaucomatous optic nerve damage.

4.Temporal relationship of association. This means that the cause precedes the disease. This clearly occurs in the nonhuman primate model of glaucoma46 and in human eyes with acute-angle closure glaucoma, where elevated IOP causes glaucomatous optic nerve damage. Further support comes from the report of Kass and coauthors47 that lowering IOP in ocular hypertensives

TABLE 1–3 PREVALENCE OF PRIMARY OPEN-ANGLE

GLAUCOMA IN RELATION TO SCREENING INTRAOCULAR PRESSURE

(Adapted, with permission, from Arch Ophthalmol 1991;109:1092. Copyright, 1991, American Medical Association.)

reduces their risk of developing POAG. This observation has recently been strengthened by results of the Ocular Hypertension Treatment Study,48 which showed that lowering IOP by 20% in eyes with elevated IOP reduced the probability of developing POAG to 4.4% after 5 years. This was significantly less 1P 6 .00012 than that seen in the untreated group.48

5.Coherence of the association. This means that the interpretation of causality does not conflict with what is known about the natural history and biology of the disease. Thus the treatment of glaucoma, to lower IOP to a level (the target IOP) where there is no further optic nerve damage or visual field loss,31 is coherent with a causal role for IOP.

IOP, mm Hg

FIGURE 1–2 Prevalence of primary open-angle glaucoma in eyes in relation to their screening intraocular pressure, comparing white subjects (open circles) to black subjects (closed circles). (Reproduced with permission from Arch Opthalmol 1991;109:1092. Copyright 1991, American Medical Association.)

Today, epidemiologists do not use a checklist of criteria to infer causation, but instead evaluate competing causal theories by how well they conform to crucial observations. In this manner, the observation that eyes with a higher screening IOP have a larger relative risk for POAG44 supports the possibility that IOP can cause POAG. Similarly, subjects with asymmetric glaucomatous optic nerve damage usually have the larger cup in the eye with the higher IOPs.49,50 Even more support comes from the Collaborative Normal-Tension Glaucoma Study, which found that reducing IOP by at least 30% significantly decreases vision loss, compared with control eyes without similar IOP reductions.51

C O N T R O V E R S Y

Although the role of intraocular pressure in the pathogenesis of glaucoma has been controversial, it remains an important risk factor for this disease.

Demographic Risk Factors for POAG

Age

Every population-based study has shown a statistical association between age and the prevalence of POAG.15,23,32–42 As an individual gets older, the risk for POAG increases. In the Baltimore Eye Survey, 35 the prevalence of glaucoma in whites was 3.5 times higher for individuals 70 to 79 years old (2.89%) as compared with those in their 40s (0.82%). In African Americans, the corresponding ratio was 7.4. Although age is clearly a risk factor for POAG, glaucoma can still occur in individuals younger than 40.

CHAPTER 1 EPIDEMIOLOGY OF GLAUCOMA • 7

Currently, we do not know why POAG is more prevalent in the elderly. Because nearly all chronic diseases are more common in older individuals, however, age may be a proxy for any of a number of possible underlying genetic, biological, or environmental factors.

Gender

Population-based studies disagree on the association between gender and POAG. Although males had higher rates of POAG in Framingham23 and Barbados,39 studies from Sweden,34 St. Lucia,40 and the Blue Mountains41 all reported higher rates in females. Both results were statistically significant. However, studies in Wales,32 Baltimore,35 Beaver Dam,36 and Melbourne42 found no such statistical associations. Gender is not usually considered a risk factor for POAG.

Ethnicity

Several population-based studies show that individuals of African heritage have an increased risk of developing POAG. In the Baltimore Eye Survey, African Americans were 3.7 times more likely to have glaucoma than whites, with an age-adjusted prevalence rate of 4.74% for African Americans and 1.29% for whites.35 Although in Jamaica the estimated prevalence of POAG in blacks aged 35 years or older was only 1.4%,33 rates in other parts of the Caribbean were even higher than those observed in Baltimore, 8.8% (ages over 30) in St. Lucia40 and 6.6% (ages 40 to 84) in Barbados.43 The prevalence of open angle glaucoma in Hispanic adults living in Arizona is intermediate between the reported values for whites and African Americans. It increased from 0.5% in Hispanic individuals age 41 to 49 years to 12.63% in those 80 years and older.51a

The cause of this higher prevalence of glaucoma in those of African or Hispanic origin is currently unknown. Although African Americans have larger cup-to-disc ratios than whites,52 they also have larger discs and more nerve fibers. Some investigators theorize that the increased disc area is associated with increased mechanical stress, putting the African American optic nerve at greater risk for glaucomatous damage.53 In support of this hypothesis, the Baltimore Eye Survey showed that the prevalence of POAG in African Americans compared with whites was higher at each specific level of IOP, even though they had a similar distribution of IOPs44 (see Fig. 1–2).

PEARL… Optic nerve characteristics, such as disc hemorrhage or asymmetric cupping, are not considered risk factors for glaucoma because they are part of the definition of glaucomatous optic nerve damage.

8 • SECTION I EPIDEMIOLOGY AND GENETICS OF GLAUCOMA

Clinical or Other Potential Risk Factors

Positive Family History and/or “Glaucoma Genes”

Several population-based studies support an association between a positive family history for glaucoma and POAG. The Baltimore Eye Survey revealed an age–race adjusted odds ratio of 2.85 for an association between POAG and a history of glaucoma among first-degree relatives.54 This association was strongest in siblings (ageadjusted odds ratio = 3.69) and weakest in the children of study subjects (age-adjusted odds ratio = 1.12). In the Barbados Eye Study,55 previously undiagnosed subjects were more likely to develop glaucoma if they had a history of glaucoma in one or more siblings (odds ratio = 4.5). The population-based familial aggregation study in Rotterdam56 showed that the lifetime risk of glaucoma in siblings and offspring of glaucoma patients was 9.2 times higher than in those of controls. Chapter 2 discusses the genetics of POAG and other forms of glaucoma.

PEARL… Intraocular pressure, age, African heritage, and family history are well-established risk factors for glaucoma.

Adult-Onset Diabetes Mellitus

Several case-control studies demonstrate statistical associations between diabetes and POAG.57–59 This may, however, result from selection bias. Because diabetics often undergo detailed eye examinations to rule out diabetic retinopathy, they have a greater opportunity to be diagnosed with POAG than nondiabetics. The Baltimore Eye Survey60 found no statistical association between diabetes mellitus and POAG (age-adjusted odds ratio of 1.03). However, a positive association did exist in individuals whose POAG had been diagnosed prior to the study, supporting the possibility that selection bias did influence the case-control studies. On the other hand, both the Beaver Dam61 and the Blue Mountains62 studies found that the odds of a diabetic having POAG were two times greater than those of a nondiabetic. In the Blue Mountains Eye Study,62 the association was even greater in individuals with previously diagnosed glaucoma.

Although diabetes mellitus may or may not be a risk factor for POAG, diabetics tend to have higher IOPs than nondiabetics, and this may explain a greater prevalence of POAG in this disease. However, the relationship between diabetes mellitus and POAG persisted in the Blue Mountains Eye Study62 even after controlling for IOP in the data analysis. This association could also result from the effect of diabetes on the small vessels of the eye and the optic nerve head, producing an increased susceptibility to IOP.

Systemic Hypertension

Case-control studies57,63 and population-based surveys provide mixed results on the statistical association between systemic hypertension and POAG. Although the Barbados64 and Baltimore65 studies did not find such an association, the study in Rotterdam66 did. For example, the Baltimore Eye Survey65 showed that systemic hypertension (defined as systolic and diastolic blood pressures greater than 160 mm Hg and 95 mm Hg, respectively, or current use of antihypertensive medications) was not a risk factor for glaucoma. On the other hand, this study did find that individuals with diastolic perfusion pressure (diastolic blood pressure minus IOP) less than 30 mm Hg were six times more likely to have POAG than those with a perfusion pressure of 50 mm Hg or more. The Barbados Eye Study64 reported a similar result (odds ratio = 3.29).

This association between diastolic perfusion pressure and POAG could result from autoregulation of optic nerve head blood vessels, which may protect the optic nerve head as long as perfusion pressure remains above 50 mm Hg. Below this level, due to either decreased blood pressure or elevated IOP, the autoregulatory response may degrade and increase the susceptibility of the optic nerve head to glaucomatous damage.67

Myopia

As with diabetes mellitus, there is concern that selection bias may label myopia a risk factor for POAG. Because myopes have more problems with their vision and need glasses, whereas emmetropes do not, they have greater opportunity to be diagnosed with POAG. However, one case-control study57 reported that patients with POAG were twice as likely to have myopia than controls. Perkins and Phelps68 reported that 27.4% of subjects with POAG were myopic versus 6.9% of the normal population. In addition, population-based studies in Casteldaccia69 and the Blue Mountains of Australia 69a showed a statistical association between POAG and myopia greater than or equal to 1.5 diopters.

Although it is still uncertain whether myopia is a risk factor for POAG, elevated IOP is statistically associated with myopia.70 Alternatively, the anatomy of the myopic disc may predispose it to glaucomatous optic nerve damage.71

C O N T R O V E R S Y

Investigators disagree on whether diabetes mellitus, systemic hypertension, myopia, and migraines are risk factors for primary openangle glaucoma.

Migraines

Several investigators have suggested that migraine headaches, or a vasospastic tendency, are also a risk fac-

tor for POAG. In one case-control study, Phelps and Corbett72 found a statistically significant relationship between headaches in low-pressure glaucoma subjects aged 70 years or older compared with controls. However, another study73 found no such association. Neither the Beaver Dam Eye Study74 nor the Blue Mountains Eye Study75 found a significant association between migraine headaches and POAG overall. However, the latter did show that, in the 70to 79-year age group, the odds of a typical migraine were 2.48 times greater in subjects with glaucoma than in those without glaucoma. Although the association between migraines and glaucoma remains controversial, vasospasm can theoretically encourage optic nerve damage by decreasing blood flow to the optic nerve head.

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CHAPTER 1 EPIDEMIOLOGY OF GLAUCOMA • 9

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