eMedicine Specialties > Ophthalmology > Intraocular Pressure

Glaucoma, Primary Open Angle

Author: Jerald A Bell, MD, Staff Physician, Department of Ophthalmology, Billings Clinic; Glaucoma Director, Leadership Council Member, Physician Advocate for Personal Service Excellence Committee
Contributor Information and Disclosures

Updated: Nov 10, 2008

Introduction

Background

The definition of glaucoma has changed drastically since its introduction around the time of Hippocrates (approximately 400 BC). The word glaucoma came from the ancient Greek word glaucosis, meaning clouded or blue-green hue, most likely describing a patient having corneal edema or rapid evolution of a cataract precipitated by chronic elevated pressure. Over the years, extensive refinement of the concept of glaucoma has continued, accelerating, especially in the last 100 years, to the present date.

Glaucoma is currently defined as a disturbance of the structural or functional integrity of the optic nerve that causes characteristic atrophic changes in the optic nerve, which may also lead to specific visual field defects over time. This disturbance usually can be arrested or diminished by adequate lowering of intraocular pressure (IOP). Nevertheless, some controversy still exists as to whether IOP should be included in the definition, as some subsets of patients can exhibit the characteristic optic nerve damage and visual field defects while having an IOP within the normal range. The generic term glaucoma should only be used in reference to the entire group of glaucomatous disorders as a whole, because multiple subsets of glaucomatous disease exist. A more precise term should be used to describe the glaucoma, if the specific diagnosis is known.

Primary open-angle glaucoma (POAG) is described distinctly as a multifactorial optic neuropathy that is chronic and progressive with a characteristic acquired loss of optic nerve fibers. Such loss develops in the presence of open anterior chamber angles, characteristic visual field abnormalities, and IOP that is too high for the continued health of the eye. It manifests by cupping and atrophy of the optic disc, in the absence of other known causes of glaucomatous disease.1,2  Note that the definition of POAG is not synonymous or solely defined by the presence of elevated IOP, but that increased IOP is a risk factor associated with the development of the disease, and is not the disease itself. Patients could develop optic neuropathy of glaucoma in the absence of documented elevated IOP. This condition has been termed normal-tension or low-tension glaucoma.

People who maintain elevated pressures in the absence of nerve damage or visual field loss exist. They are considered at risk for glaucoma and have been termed glaucoma suspects or ocular hypertensives (see Ocular Hypertension). POAG is a major worldwide health concern, because of its usually silent, progressive nature, and because it is one of the leading preventable causes of blindness in the world. With appropriate screening and treatment, glaucoma usually can be identified and its progress arrested before significant effects on vision occur.

See related CME at Glaucoma.

Pathophysiology

The exact cause of glaucomatous optic neuropathy is not known, although many risk factors have been identified, to include the following: elevated IOP, family history, race, age older than 40 years, and myopia.

Elevated IOP is the most studied of these risk factors because it is the main clinically treatable risk factor for glaucoma. Multiple theories exist concerning how IOP can be one of the factors that initiates glaucomatous damage in a patient. Two of the major theories include the following: (1) onset of vascular dysfunction causing ischemia to the optic nerve, and (2) mechanical dysfunction via cribriform plate compression of the axons.

In addition to vascular compromise and mechanically impaired axoplasmic flow, contemporary hypotheses of possible pathogenic mechanisms that underlie glaucomatous optic neuropathy include excitotoxic damage from excessive retinal glutamate, deprivation of neuronal growth factors, peroxynitrite toxicity from increased nitric oxide synthase activity, immune-mediated nerve damage, and oxidative stress. The exact role that IOP plays in combination with these other factors and their significance to the initiation and progression of subsequent glaucomatous neuronal damage and cell death over time is still under debate; the precise mechanism is still a hot topic of discussion.

However, IOP is the only clinical risk factor that has been able to be successfully manipulated to date. Categorizing and managing patients based on their IOP and when IOP should be treated to prevent optic nerve damage became the forefront issue of glaucoma management for most of the last half of the 20th century.

Several studies over the years have shown that as IOP rises above 21 mm Hg, the percentage of patients developing visual field loss increases rapidly, most notably at pressures higher than 26-30 mm Hg. A patient with an IOP of 28 mm Hg is about 15 times more likely to develop field loss than a patient with a pressure of 22 mm Hg. Therefore, a patient population of those with elevated IOP should not be thought of as homogeneous. Furthermore, before initiating treatment of a patient based on a specific IOP measurement, the following factors should be considered regarding that IOP level obtained:

  • Variability of tonometry measurements per examiner (usually found to be about 10%, or 1-2 mm Hg)
  • Effect corneal thickness has on accuracy of IOP measurements (see Other Tests)
  • Diurnal variation of IOP (often highest in the early morning hours, but maximum IOP can be at any time of day in some patients)
  • In addition, remember that while normal eyes have a diurnal variation of approximately 3-4 mm Hg, glaucomatous eyes have even higher variation (>10 mm Hg). Note: Multiple readings should be taken over time and should be considered with correlative evidence of visual field and optic nerve examination before any diagnosis or therapy is rendered.

Other points of importance when considering a diagnosis of POAG are described below.

Disc cupping and nerve fiber layer losses of up to 40% have been shown to occur before actual visual field loss has been detected. Therefore, visual field examination cannot be the sole tool used to determine when a patient has begun to sustain undeniable glaucomatous damage, and it should not be used in isolation as the benchmark for treatment.

In cases where POAG is associated with increased IOP, the cause for the elevated IOP generally is accepted to be decreased facility of aqueous outflow through the trabecular meshwork. Occurrence of this increase in resistance to flow has been suggested by multiple theories, to include the following:

  • An obstruction of the trabecular meshwork by accumulated material
  • A loss of trabecular endothelial cells
  • A reduction in trabecular pore density and size in the inner wall endothelium of the Schlemm canal
  • A loss of giant vacuoles in the inner wall endothelium of the Schlemm canal
  • A loss of normal phagocytic activity
  • Disturbance of neurologic feedback mechanisms

Other processes thought to play a role in resistance to outflow include altered corticosteroid metabolism, dysfunctional adrenergic control, abnormal immunologic processes, and oxidative damage to the meshwork.

Numerous other undetermined factors are considered to be at work in the pathogenesis of glaucoma. Basic and clinical science research continues to play a role in the search for such factors that contribute to the development and prognosis of the patient with POAG.

Frequency

United States

Multiple population studies (eg, Framingham, Beaver Dam, Baltimore, Rotterdam, Barbados, Egna-Neumarkt) have been performed to estimate the prevalence of eye disease, including that of POAG and those individuals with ocular hypertension (OHT) who are at risk for POAG.

Estimates of the prevalence of glaucoma in studies involving only the United States suggest the following: glaucoma is a leading cause of irreversible blindness, second only to macular degeneration; only one half of the people who have glaucoma may be aware that they have the disease; and more than 2.25 million Americans aged 40 years and older have POAG.

More than 1.6 million have significant visual impairment, with 84,000-116,000 bilaterally blind in the United States alone. These statistics emphasize the need to identify and closely monitor those at risk of glaucomatous damage.

In the United States, 3-6 million people, including 4-10% of the population older than 40 years, are currently without detectable signs of glaucomatous damage using present-day clinical testing, but they are at risk due to IOP of 21 mm Hg or higher. Roughly 0.5-1% per year of those individuals with elevated IOP will develop glaucoma over a period of 5-10 years. The risk may be declining to less than 1% per year, now that ophthalmoscopic and perimetric techniques for detecting glaucomatous damage have improved significantly.

International

Glaucoma is the second leading cause of blindness in the world (surpassed only by cataracts, a reversible condition). More than 3 million people are bilaterally blind from POAG worldwide, and more than 2 million people will develop POAG each year.

Mortality/Morbidity

  • Over a 5-year period, several studies have shown the incidence of new onset of glaucomatous damage in previously unaffected patients to be about 2.6-3% for IOPs 21-25 mm Hg, 12-26% incidence for IOPs 26-30 mm Hg, and approximately 42% for those higher than 30 mm Hg.
  • The Ocular Hypertension Treatment Study (OHTS) found that the overall risk for patients with IOPs ranging from 24-31 mm Hg but with no clinical signs of glaucoma have an average risk of 10% of developing glaucoma over 5 years, with that risk being cut in half if patients are preemptively started on IOP-lowering therapy. Significant subsets of higher and lower risk exist when pachymetry (central corneal thickness [CCT]) is taken into account (see Media file 11).
  • Some patients' first sign of morbidity from elevated IOP can be presentation with sudden loss of vision due to a central retinal vein occlusion (CRVO), the second most common risk factor for CRVO behind systemic hypertension.
  • See References for additional resources.

Race

Prevalence of POAG is 3-4 times higher in blacks than in Caucasians; in addition, blacks are up to 6 times more susceptible to optic disc nerve damage than Caucasians. A higher prevalence of larger cup-to-disc ratios exists in the normal black population as compared with white controls.

Glaucoma is the most common cause of blindness among people of African descent. They are more likely to develop glaucoma early in life, and they tend to have a more aggressive form of the disease.

  • The Barbados Eye Study over 4 years showed a 5 times higher incidence of developing glaucoma in a group of black ocular hypertensives as compared with a predominantly white population.
  • Some population studies have found the mean IOP in blacks to be higher than Caucasian controls. Other studies (eg, Baltimore) found no difference. Consequently, further study needs to be conducted to clarify this issue.
  • Furthermore, the OHTS has suggested that black patients overall may have a thinner average central corneal thickness, thereby leading to underdiagnosis of elevated pressure, and consequently, exposure to higher risk of developing glaucoma. Therefore, pachymetry measurement is particularly important in establishing a baseline for African-American patients who are glaucoma suspects.

Sex

Reports on sex predilection also differ. Although some age-controlled studies have reported significantly higher mean IOP values in women than in men, others have failed to find such a difference, while others have even shown males to have a higher prevalence of glaucoma.

Age

Age older than 40 years is a risk factor for the development of POAG, with up to 15% of people affected by the seventh decade of life.

  • Consequently, glaucoma is found to be more prevalent in the aging population, even after compensating for the fact that mean IOP slowly rises with increasing age.
  • However, the disease itself is not limited to only middle-aged and elderly individuals.

Clinical

History

The initial patient interview is extremely important in the evaluation for POAG or other ocular diseases secondarily causing elevated IOP.

Because of the silent nature of glaucoma, patients will not usually present with any symptoms or visual complaints until late in the disease course, particularly with POAG. However, narrow/closed angle glaucoma and secondary glaucomas can cause rapid closure of the trabecular meshwork, with an equally rapid rise in IOP, which is usually symptomatic, particularly when IOP is equal to or greater than 35 mm Hg.

Significant attention should be given to the following:

  • Past ocular history
    • History of eye pain or redness
    • Multicolored halos
    • Headache
    • Previous ocular disease, including cataracts
    • Uveitis
    • Diabetic retinopathy
    • Vascular occlusions
    • Previous ocular surgery, including photocoagulation or refractive procedures
    • Ocular/head trauma
  • Past medical history - Any surgeries or pertinent vasculopathic systemic illnesses
  • Current medications, including any hypertensive medications (which may indirectly cause fluctuation of IOP) or topical/systemic corticosteroids
  • Risk factors for glaucomatous optic neuropathy
    • Strong implications are as follows:
      • History of elevated IOP; advanced age, particularly after 50 years; African American descent; positive family history of glaucoma (first-degree relative, especially correlative if present in a sibling; relative risk 3.7-fold higher than if no family history of glaucoma); myopia
      • Be specific when asking family history (Which family members? Was there actual visual loss from glaucoma or other causes of visual field loss? Are they under control on one or more medications? Did they require surgery for adequate control?)
    • Possible implications are as follows:
      • Systemic cardiovascular disease
      • Diabetes mellitus
      • Migraine headache
      • Systemic hypertension
      • Vasospasm
    • Anecdotal risk factors
      • Obesity
      • Smoking
      • Alcohol
      • History of stress
      • Anxiety

Physical

  • Screening the general population for POAG is most effective if targeted toward those at high risk, such as African Americans and elderly individuals, especially if the screening consists of IOP measurements combined with assessment of optic nerve status.
  • Perform screening at least every 3-5 years in asymptomatic patients aged 40 years or younger and more often if the person is African American or older than 40 years. For those with multiple risk factors, evaluate and monitor on a more frequent basis, as appropriate.
  • Perform a standard comprehensive eye examination, such as that outlined in the American Academy of Ophthalmology (AAO) Preferred Practice Patterns, on the initial visit. If any visual field or optic nerve changes consistent with early glaucoma are present, then diagnose the patient as having such.
  • Emphasize the following points during the examination to distinguish POAG from either secondary causes of glaucoma or from OHT in patients with only elevated IOP and no damage.
    • Compare visual acuity with previous known acuities. If declining, rule out secondary causes of vision loss, whether it is from cataracts, age-related macular degeneration (ARMD), ocular surface disorders (eg, dry eye), or adverse effects from topical medications (especially if using miotics).
    • Pupils - Test for presence/absence of afferent pupillary defect (Marcus Gunn pupil).
    • Slit lamp examination of the anterior segment
      • Cornea - Signs of microcystic edema (found only with acute elevation of IOP); keratic precipitates, pigment on endothelium (Krukenberg spindle); congenital anomalies
      • Anterior chamber - Cell or flare, uveitis, hyphema, angle closure
      • Iris - Transillumination defects, iris atrophy, synechiae, rubeosis, ectropion uveae, iris bombe, difference in iris coloration bilaterally (eg, Fuchs heterochromic iridocyclitis), pseudoexfoliation (PXF) material
      • Lens - Cataract progression (ie, signs of phacomorphic glaucoma, pseudoexfoliation, phacolytic glaucoma with a Morgagnian cataract)
      • Optic nerve/nerve fiber layer - Stereoscopically examine for evidence of glaucomatous damage, including the following: cup-to-disc ratio in horizontal and vertical meridians (describe by color and slope, and diagram, if needed); appearance of disc; progressive enlargement of the cup; evidence of nerve fiber layer damage with red-free filter; notching or thinning of disc rim, particularly at superior and inferior poles (because nerve fibers at the superior and inferior poles of the disc can often be affected first); pallor; presence of hemorrhage (most common inferotemporally); asymmetry between discs; parapapillary atrophy (possible association with development of glaucoma); or congenital nerve abnormalities.
      • Fundus - Other abnormalities that could account for any nonglaucomatous visual field defects or vision loss present (eg, disc drusen, optic pits, retinal disease), vitreous hemorrhage, or proliferative retinopathy.
  • Baseline stereo fundus photographs for future reference/comparison; if unavailable, record representative drawings.
  • Tonometry (see also Other tonometric methods in Other Tests)
    • IOP varies from hour-to-hour in any individual. The circadian rhythm of IOP usually causes it to rise most in the early hours of the morning; IOP also rises with a supine posture.
    • When checking IOP, measurements for both eyes, the method used (Goldmann applanation is the criterion standard), and the time of the measurement should all be recorded. 
    • Previous tonometry readings, if available, should be reviewed (eg, Is the reading reproducible? What method was used to obtain the reading? What time of the day was it? Where does it fall on the diurnal pressure curve? Do both eyes have similar measurements?).
    • In obese patients, the possibility of a Valsalva movement causing an increased IOP should be considered when measured in the slit lamp by Goldman applanation. Measurement should be tried via Tono-Pen, Perkins, or pneumotonometer with the patient resting back in the examination chair.
    • A difference between the 2 eyes of 3 mm Hg or more indicates greater suspicion of glaucoma. An average of 10% difference between individual measurements should be expected. The measurements should be repeated on at least 2-3 occasions before deciding on a treatment plan. The measurement should be completed in the morning and at night to check the diurnal variation, if possible. (A diurnal variation of more than 5-6 mm Hg may be suggestive of increased risk for POAG.) Early POAG is suspected strongly when a steadily increasing IOP is present.
    • Pachymetry affects applanation tonometry values and, therefore, should be checked on the initial examination (see also Pachymetry and Other tonometric methods in Other Tests). 
  • Perform gonioscopy to rule out angle-closure or secondary causes of IOP elevation, such as angle recession, pigmentary glaucoma, and PXF.
    • Check the peripheral contour of the iris for plateau iris, and examine the trabecular meshwork for peripheral anterior synechiae, as well as neovascular or inflammatory membranes.
    • The Schlemm canal may be seen with blood refluxing through the canal into the posterior trabecular meshwork. This possibly could indicate elevated episcleral venous pressure, with such conditions as carotid-cavernous fistula, Graves orbitopathy, or Sturge-Weber syndrome needing to be ruled out.
  • Pachymetry: Pachymetry is used to measure CCT. According to the OHTS, pachymetry is now the criterion standard for every baseline examination in patients who are at risk for or suspected of having glaucoma (see Media file 11).
  • Visual field testing
    • Perform automated threshold testing (eg, Humphrey 24-2) to rule out any glaucomatous visual field defects.
    • If the patient is unable to perform automated testing, Goldmann testing may be substituted.
  • Caveats about visual field analysis are outlined below (see also Other Tests).
    • New-onset glaucomatous defects are found most commonly as an early nasal step, temporal wedge, or paracentral scotoma (more frequent superiorly); generalized depression related to IOP level also can be found.
    • Swedish interactive thresholding algorithm (SITA)-based software algorithms may decrease testing time and boost reliability, especially in older patients.
    • SWAP (short wavelength automated perimetry or blue-yellow perimetry) may provide a more sensitive method of detecting visual field deficits, especially in those previously labeled as ocular hypertensive. If the Humphrey visual field testing results are normal, SWAP should be considered to help detect visual field loss earlier. Recent studies suggest SWAP may detect visual loss/progression up to 3-5 years earlier than conventional perimetry, as well as in 12-42% of patients previously diagnosed with only OHT. Because the testing time may be lengthened, it may be tiring for some patients. However, new SITA-SWAP algorithm software may speed up the testing time and thus improve reliability.
    • Frequency doubling perimetry (also called frequency doubling technology or FDT, which is enhanced with MATRIX software) is a newer technology that projects an alternating pattern of gridlines onto a screen and stimulates specific neurons that may be damaged early in OHT or POAG.  As in SWAP, this may also be able to help detect nerve fiber layer loss at an earlier stage in the glaucomatous disease process, thereby screening out more people who are currently misdiagnosed as having OHT instead of early POAG. Current sensitivities and specificities are continually improving, but continued baseline data is needed to determine in what setting this newer technology will prove to be most useful.
    • Examination results must take into account that visual field defects may not be apparent until over 40% loss of the nerve fiber layer has occurred. Therefore, the therapy should be based on the overall clinical picture and not on visual field testing alone (see Treatment).
    • The pupil size should be documented at each testing session, as constriction can reduce retinal sensitivity and mimic progressive field loss.
    • Risk factors, specifically for the development of glaucomatous field loss in OHT, have recently been studied, and it was found that several presumed risk factors (ie, presence of hypertension, diabetes, refractive error, race, family history of glaucoma, gender, smoking or ethanol use, disc area) were not significant for prediction of eventual field loss.
    • Significant positive predictive factors of field loss included higher IOP, older age, presence of a disc crescent, larger cup-to-disc ratio, smaller rim-disc area ratio, and cup asymmetry. Consequently, the relationship of risk factors for OHT and POAG compared with that of actual field loss development is much more complex than has been previously presumed.
    • The initial visual field baseline may need to be repeated at least twice on successive visits, especially if initial testing shows low reliability indices. Newer glaucoma progression analysis (GPA) software can help identify reliable perimetric baselines, and probability-based analyses of subsequent fields can assist in determining if there is true progression over time versus artifact. In follow-up, if a low risk of onset of glaucomatous damage is present, then repeat testing may be performed once a year. If a high risk of impending glaucomatous damage is present, then testing may be adjusted (as frequent as every 2 mo).

Causes

  • The exact cause of elevated IOP in POAG is not certain, although the role of accumulating mucopolysaccharides in the trabecular meshwork beams continues to be a focus of research.
  • In general, the physiologic chain of events that leads to glaucomatous optic nerve damage from pressure or other secondary mechanisms is unknown, although various theories, as described below, have been proposed.
  • The disease affects the individual axons of the optic nerve, which may die by apoptosis, also known as programmed cell death.
    • There has been some laboratory data that shows glutamate may play a role in glaucoma-related apoptosis, via neurotransmitter excitatory toxicity.  However, so far, a human subject trial of the glutamate inhibitor (also referred to as an N-methyl D-aspartate [NMDA] inhibitor), memantine, has been unsuccessful in meeting its endpoints. To date, it has not been specifically approved by the US Food and Drug Administration (FDA) for the treatment of glaucomatous optic neuropathy.  It is available in the United States and is approved for the treatment of other neurodegenerative diseases, such as certain types of dementia.
    • As a whole, the subjects in the memantine trial did not show a significant difference in their rates of progression whether on memantine or placebo.  However, on further analysis of the different study population subgroups, those subjects with severe glaucomatous vision loss did possibly show a benefit on memantine. Future studies are needed to confirm, characterize, and quantify this potential benefit.
  • Other various theories (see Pathophysiology) have been advanced to explain the possible etiologic role of elevated IOP in glaucomatous optic neuropathy.
    • The mechanical compression theory suggests that elevated IOP causes a backward bowing of the lamina cribrosa, kinking the axons as they exit through the lamina pores. This may lead to focal ischemia, deprive the axons of neurotrophins, or interfere with axoplasmic flow, triggering cell death.
    • The vascular theories propose that cell death is triggered by ischemia, whether induced by elevated IOP or as a primary insult.
    • Other risk factors may play a role in the development of POAG, including a history of migraine headaches (a condition associated with vasospasm), cardiovascular disease, diabetes, systemic hypertension (leading to arteriosclerosis), and systemic hypotension (leading to decreased perfusion).
    • Genetic theories propose that cell death is triggered by genetic predisposition. Following the death of individual axons, substances may be released into the environment that causes a secondary triggering of apoptosis in neighboring cells, including glutamate (a neurotransmitter that may cause excitotoxicity), calcium, nitric oxide, and free radicals.
  • Glaucoma is not just a disease of IOP but rather a multifactorial optic neuropathy. However, patients with OHT who have IOP outside of the statistically normal range should continue to have periodic follow-up examinations, because they are always at risk for development of glaucoma.
    • Other causes for optic neuropathy should be considered in all patients with apparent normal-tension glaucoma, and appropriate lab or radiologic testing should be initiated if history and/or physical findings are suggestive.
    • Patients who do not have elevated IOP but glaucomatous optic discs or visual fields may have normal-tension glaucoma. It is a diagnosis of exclusion (after other causes for optic neuropathy, such as temporal arteritis, have been investigated and ruled out).
  • Several secondary causes of glaucoma must be considered before diagnosing POAG. These causes include the following (see also Differentials):
    • Exfoliation syndrome
    • Pigment dispersion syndrome (pigmentary glaucoma)
    • Lens-induced glaucoma
    • Ocular inflammatory diseases
    • Intraocular tumors
    • Raised episcleral venous pressure
    • Topical or systemic corticosteroid use
    • Syndromes (eg, Axenfeld-Rieger syndrome)

More on Glaucoma, Primary Open Angle

Overview: Glaucoma, Primary Open Angle
Differential Diagnoses & Workup: Glaucoma, Primary Open Angle
Treatment & Medication: Glaucoma, Primary Open Angle
Follow-up: Glaucoma, Primary Open Angle
Multimedia: Glaucoma, Primary Open Angle
References
[ CLOSE WINDOW ]

References

  1. Bathija R, Gupta N, Zangwill L, Weinreb RN. Changing definition of glaucoma. J Glaucoma. Jun 1998;7(3):165-9. [Medline].

  2. Van Buskirk EM, Cioffi GA. Glaucomatous optic neuropathy. Am J Ophthalmol. Apr 15 1992;113(4):447-52. [Medline].

  3. Chihara E. Assessment of true intraocular pressure: the gap between theory and practical data. Surv Ophthalmol. May-Jun 2008;53(3):203-18. [Medline].

  4. ElMallah MK, Asrani SG. New ways to measure intraocular pressure. Curr Opin Ophthalmol. Mar 2008;19(2):122-6. [Medline].

  5. Annette H, Kristina L, Bernd S, Mark-Oliver F, Wolfgang W. Effect of central corneal thickness and corneal hysteresis on tonometry as measured by dynamic contour tonometry, ocular response analyzer, and Goldmann tonometry in glaucomatous eyes. J Glaucoma. Aug 2008;17(5):361-5. [Medline].

  6. Kaufmann C, Bachmann LM, Thiel MA. Comparison of dynamic contour tonometry with goldmann applanation tonometry. Invest Ophthalmol Vis Sci. Sep 2004;45(9):3118-21. [Medline].

  7. Reichert, Inc. The Ocular Response Analyzer. Available at http://www.ocularresponseanalyzer.com/. Accessed 2008.

  8. Ziemer Ophthalmology. The Pascal Dynamic Contour Tonometer. Available at http://www.ziemergroup.ch/home/products/pascal.html. Accessed 2008.

  9. Chen TC, Ahn Yuen SJ, Sangalang MA, Fernando RE, Leuenberger EU. Retrobulbar chlorpromazine injections for the management of blind and seeing painful eyes. J Glaucoma. Jun 2002;11(3):209-13. [Medline].

  10. Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL. Treatment outcomes in the tube versus trabeculectomy study after one year of follow-up. Am J Ophthalmol. Jan 2007;143(1):9-22. [Medline].

  11. Jamil AL, Mills RP. Glaucoma tube or trabeculectomy? That is the question. Am J Ophthalmol. Jan 2007;143(1):141-2. [Medline].

  12. Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of refractory glaucoma. J Glaucoma. Apr-May 2008;17(3):238-47. [Medline].

  13. Allen RC, Netland PA, eds. Glaucoma Medical Therapy: Principles and Management. American Academy of Ophthalmology; 1999.

  14. Alward WL. The genetics of open-angle glaucoma: the story of GLC1A and myocilin. Eye. Jun 2000;14 (Pt 3B):429-36. [Medline].

  15. American Academy of Ophthalmology. Preferred Practice Patterns: Primary Open Angle Glaucoma Suspect and POAG. 1995-1996.

  16. Ang GS, Bochmann F, Townend J, et al. Corneal biomechanical properties in primary open angle glaucoma and normal tension glaucoma. J Glaucoma. Jun-Jul 2008;17(4):259-62. [Medline].

  17. Ashaye AO, Adeoye AO. Characteristics of patients who dropout from a glaucoma clinic. J Glaucoma. Apr-May 2008;17(3):227-32. [Medline].

  18. Aung T, Chew PT, Yip CC, et al. A randomized double-masked crossover study comparing latanoprost 0.005% with unoprostone 0.12% in patients with primary open-angle glaucoma and ocular hypertension. Am J Ophthalmol. May 2001;131(5):636-42. [Medline].

  19. Azuara-Blanco A, Burr JM. Assessment of glaucoma imaging technology. Ophthalmology. Jul 2008;115(7):1266-7; author reply 1267-8. [Medline].

  20. Bakri SJ, McCannel CA, Edwards AO, et al. Persisent ocular hypertension following intravitreal ranibizumab. Graefes Arch Clin Exp Ophthalmol. Jul 2008;246(7):955-8. [Medline].

  21. Beckers HJ, Schouten JS, Webers CA, et al. Side effects of commonly used glaucoma medications: comparison of tolerability, chance of discontinuation, and patient satisfaction. Graefes Arch Clin Exp Ophthalmol. Oct 2008;246(10):1485-90. [Medline].

  22. Bengtsson B. A new rapid threshold algorithm for short-wavelength automated perimetry. Invest Ophthalmol Vis Sci. Mar 2003;44(3):1388-94. [Medline].

  23. Bengtsson B, Heijl A. Normal intersubject threshold variability and normal limits of the SITA SWAP and full threshold SWAP perimetric programs. Invest Ophthalmol Vis Sci. Nov 2003;44(11):5029-34. [Medline].

  24. Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. May 2008;115(5):763-8. [Medline].

  25. Berisha F, Feke GT, Hirose T, et al. Retinal blood flow and nerve fiber layer measurements in early-stage open-angle glaucoma. Am J Ophthalmol. Sep 2008;146(3):466-472. [Medline].

  26. Bramley T, Peeples P, Walt JG, et al. Impact of vision loss on costs and outcomes in medicare beneficiaries with glaucoma. Arch Ophthalmol. Jun 2008;126(6):849-56. [Medline].

  27. Brandt JD. Corneal thickness in glaucoma screening, diagnosis, and management. Curr Opin Ophthalmol. Apr 2004;15(2):85-9. [Medline].

  28. Brandt JD, Beiser JA, Gordon MO, et al. Central corneal thickness and measured IOP response to topical ocular hypotensive medication in the Ocular Hypertension Treatment Study. Am J Ophthalmol. Nov 2004;138(5):717-22. [Medline].

  29. Brandt JD, Beiser JA, Kass MA, et al. Central corneal thickness in the Ocular Hypertension Treatment Study (OHTS). Ophthalmology. Oct 2001;108(10):1779-88. [Medline].

  30. Brubaker RF. Mechanism of action of bimatoprost (Lumigan). Surv Ophthalmol. May 2001;45 Suppl 4:S347-51. [Medline].

  31. Bruhn RL, Stamer WD, Herrygers LA, et al. Relationship between Glaucoma and Selenium Levels in Plasma and Aqueous Humor. Br J Ophthalmol. Jun 12 2008;[Medline].

  32. Brusini P, Salvetat ML, Zeppieri M, et al. Comparison of ICare tonometer with Goldmann applanation tonometer in glaucoma patients. J Glaucoma. Jun 2006;15(3):213-7. [Medline].

  33. Cantor L. Section 10: Glaucoma. In: Basic and Clinical Science Course. American Academy of Ophthalmology; 1996-1997.

  34. Chaudhry I, Wong S. Recognizing glaucoma. A guide for the primary care physician. Postgrad Med. May 1996;99(5):247-8, 251-2, 257-9, Pass;M. [Medline].

  35. Chauhan BC. Endothelin and its potential role in glaucoma. Can J Ophthalmol. Jun 2008;43(3):356-60. [Medline].

  36. Cheung W, Guo L, Cordeiro MF. Neuroprotection in glaucoma: drug-based approaches. Optom Vis Sci. Jun 2008;85(6):406-16. [Medline].

  37. Chihara E. Assessment of true intraocular pressure: the gap between theory and practical data. Surv Ophthalmol. May-Jun 2008;53(3):203-18. [Medline].

  38. Cioffi GA, Latina MA, Schwartz GF. Argon versus selective laser trabeculoplasty. J Glaucoma. Apr 2004;13(2):174-7. [Medline].

  39. Colton T, Ederer F. The distribution of intraocular pressures in the general population. Surv Ophthalmol. Nov-Dec 1980;25(3):123-9. [Medline].

  40. Cox JA, Mollan SP, Bankart J, et al. Efficacy of antiglaucoma fixed combination therapy versus unfixed components in reducing intraocular pressure: a systematic review. Br J Ophthalmol. Jun 2008;92(6):729-34. [Medline].

  41. Craven ER, Walters TR, Williams R, et al. Brimonidine and timolol fixed-combination therapy versus monotherapy: a 3-month randomized trial in patients with glaucoma or ocular hypertension. J Ocul Pharmacol Ther. Aug 2005;21(4):337-48. [Medline].

  42. Deokule S, Weinreb RN. Relationships among systemic blood pressure, intraocular pressure, and open-angle glaucoma. Can J Ophthalmol. Jun 2008;43(3):302-7. [Medline].

  43. Dhaliwal JS, Mason BF, Kaufman SC. Long-term use of topical tacrolimus (FK506) in high-risk penetrating keratoplasty. Cornea. May 2008;27(4):488-93. [Medline].

  44. Doughty MJ, Zaman ML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol. Mar-Apr 2000;44(5):367-408. [Medline].

  45. ElMallah MK, Asrani SG. New ways to measure intraocular pressure. Curr Opin Ophthalmol. Mar 2008;19(2):122-6. [Medline].

  46. Eskridge JB. Ocular hypertension or early undetected glaucoma?. J Am Optom Assoc. Sep 1987;58(9):747-69. [Medline].

  47. Filippopoulos T, Rhee DJ. Novel surgical procedures in glaucoma: advances in penetrating glaucoma surgery. Curr Opin Ophthalmol. Mar 2008;19(2):149-54. [Medline].

  48. George MK, Emerson JW, Cheema SA, et al. Evaluation of a modified protocol for selective laser trabeculoplasty. J Glaucoma. Apr-May 2008;17(3):197-202. [Medline].

  49. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. Jun 2002;120(6):714-20; discussion 829-30. [Medline].

  50. Gordon MO, Kass MA. The Ocular Hypertension Treatment Study: design and baseline description of the participants. Arch Ophthalmol. May 1999;117(5):573-83. [Medline].

  51. Greenfield DS, Girkin C, Kwon YH. Memantine and progressive glaucoma. J Glaucoma. Feb 2005;14(1):84-6. [Medline].

  52. Greenfield DS, Weinreb RN. Role of optic nerve imaging in glaucoma clinical practice and clinical trials. Am J Ophthalmol. Apr 2008;145(4):598-603. [Medline].

  53. Grus F, Sun D. Immunological mechanisms in glaucoma. Semin Immunopathol. Apr 2008;30(2):121-6. [Medline].

  54. Grus FH, Joachim SC, Wuenschig D, et al. Autoimmunity and glaucoma. J Glaucoma. Jan-Feb 2008;17(1):79-84. [Medline].

  55. Gupta N, Weinreb RN. New definitions of glaucoma. Curr Opin Ophthalmol. Apr 1997;8(2):38-41. [Medline].

  56. Halkiadakis I, Kipioti A, Emfietzoglou I, et al. Comparison of optical coherence tomography and scanning laser polarimetry in glaucoma, ocular hypertension, and suspected glaucoma. Ophthalmic Surg Lasers Imaging. Mar-Apr 2008;39(2):125-32. [Medline].

  57. Hernandez R, Rabindranath K, Fraser C, et al. Screening for open angle glaucoma: systematic review of cost-effectiveness studies. J Glaucoma. Apr-May 2008;17(3):159-68. [Medline].

  58. Hitchings RA. Glaucoma: current thinking. Br J Hosp Med. Mar 20-Apr 2 1996;55(6):312-4. [Medline].

  59. Hodapp EA, Anderson DR. Treatment of early glaucoma. In: Focal Points. Vol 4. 1986.

  60. Holz HA, Lim MC. Glaucoma lasers: a review of the newer techniques. Curr Opin Ophthalmol. Apr 2005;16(2):89-93. [Medline].

  61. Hoskins HD Jr. The management of elevated intraocular pressure with normal optic discs and visual fields. II. An approach to early therapy. Surv Ophthalmol. May-Jun 1977;21(6):479, 489-93. [Medline].

  62. Inatani M, Iwao K, Inoue T, et al. Long-term relationship between intraocular pressure and visual field loss in primary open-angle glaucoma. J Glaucoma. Jun-Jul 2008;17(4):275-9. [Medline].

  63. Jacobi S, Dubielzig RR. Feline primary open angle glaucoma. Vet Ophthalmol. May-Jun 2008;11(3):162-5. [Medline].

  64. Johnson TD, Zimmerman TJ. Ocular hypertension, glaucoma suspect, preglaucoma, or glaucoma? Synopsis of views. Ann Ophthalmol. Nov 1986;18(11):313-4. [Medline].

  65. Juzych MS, Chopra V, Banitt MR, et al. Comparison of long-term outcomes of selective laser trabeculoplasty versus argon laser trabeculoplasty in open-angle glaucoma. Ophthalmology. Oct 2004;111(10):1853-9. [Medline].

  66. Kahook MY, Noecker RJ. Comparison of corneal and conjunctival changes after dosing of travoprost preserved with sofZia, latanoprost with 0.02% benzalkonium chloride, and preservative-free artificial tears. Cornea. Apr 2008;27(3):339-43. [Medline].

  67. Kass MA. When to treat ocular hypertension (with discussion). Surv Ophthalmol. 1980;28(Supp.):229-234.

  68. Kass MA, Hart WM Jr, Gordon M, et al. Risk factors favoring the development of glaucomatous visual field loss in ocular hypertension. Surv Ophthalmol. Nov-Dec 1980;25(3):155-62. [Medline].

  69. Kiekens S, Veva De Groot, Coeckelbergh T, et al. Continuous positive airway pressure therapy is associated with an increase in intraocular pressure in obstructive sleep apnea. Invest Ophthalmol Vis Sci. Mar 2008;49(3):934-40. [Medline].

  70. Krupin T, Liebmann JM, Greenfield DS, et al. The Low-pressure Glaucoma Treatment Study (LoGTS) study design and baseline characteristics of enrolled patients. Ophthalmology. Mar 2005;112(3):376-85. [Medline].

  71. Ku JY, Danesh-Meyer HV, Craig JP, et al. Comparison of intraocular pressure measured by Pascal dynamic contour tonometry and Goldmann applanation tonometry. Eye. Feb 2006;20(2):191-8. [Medline].

  72. Lacey J, Cate H, Broadway DC. Barriers to adherence with glaucoma medications: a qualitative research study. Eye. Apr 25 2008;[Medline].

  73. Landers JA, Goldberg I, Graham SL. Detection of early visual field loss in glaucoma using frequency-doubling perimetry and short-wavelength automated perimetry. Arch Ophthalmol. Dec 2003;121(12):1705-10. [Medline].

  74. Lasseck J, Jehle T, Feltgen N, et al. Comparison of intraocular tonometry using three different non-invasive tonometers in children. Graefes Arch Clin Exp Ophthalmol. Oct 2008;246(10):1463-6. [Medline].

  75. Latina MA, Gulati V. Selective laser trabeculoplasty: stimulating the meshwork to mend its ways. Int Ophthalmol Clin. 2004;44(1):93-103. [Medline].

  76. Latina MA, Tumbocon JA. Selective laser trabeculoplasty: a new treatment option for open angle glaucoma. Curr Opin Ophthalmol. Apr 2002;13(2):94-6. [Medline].

  77. Lebrun-Julien F, Di Polo A. Molecular and cell-based approaches for neuroprotection in glaucoma. Optom Vis Sci. Jun 2008;85(6):417-24. [Medline].

  78. Lee PP, Walt JW, Rosenblatt LC, et al. Association between intraocular pressure variation and glaucoma progression: data from a United States chart review. Am J Ophthalmol. Dec 2007;144(6):901-907. [Medline].

  79. Leske MC, Connell AM, Wu SY, et al. Distribution of intraocular pressure. The Barbados Eye Study. Arch Ophthalmol. Aug 1997;115(8):1051-7. [Medline].

  80. Levin LA, Peeples P. History of neuroprotection and rationale as a therapy for glaucoma. Am J Manag Care. Feb 2008;14(1 Suppl):S11-4. [Medline].

  81. Li HK, Tang RA, Oschner K, et al. Telemedicine screening of glaucoma. Telemed J. Fall 1999;5(3):283-90. [Medline].

  82. Liesegang TJ. Glaucoma: changing concepts and future directions. Mayo Clin Proc. Jul 1996;71(7):689-94. [Medline].

  83. Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of refractory glaucoma. J Glaucoma. Apr-May 2008;17(3):238-47. [Medline].

  84. Lin SC, Singh K, Jampel HD, Hodapp EA, Smith SD, Francis BA, et al. Optic nerve head and retinal nerve fiber layer analysis: a report by the American Academy of Ophthalmology. Ophthalmology. Oct 2007;114(10):1937-49. [Medline].

  85. Linner E. The natural course of ocular pressure in ocular hypertension. Surv Ophthalmol. Nov-Dec 1980;25(3):136-8. [Medline].

  86. Lipton SA. Possible role for memantine in protecting retinal ganglion cells from glaucomatous damage. Surv Ophthalmol. Apr 2003;48 Suppl 1:S38-46. [Medline].

  87. Liu J, Roberts CJ. Influence of corneal biomechanical properties on intraocular pressure measurement: quantitative analysis. J Cataract Refract Surg. Jan 2005;31(1):146-55. [Medline].

  88. Madadi P, Koren G, Freeman DJ, et al. Timolol concentrations in breast milk of a woman treated for glaucoma: calculation of neonatal exposure. J Glaucoma. Jun-Jul 2008;17(4):329-31. [Medline].

  89. Medeiros FA, Zangwill LM, Bowd C, et al. Comparison of the GDx VCC scanning laser polarimeter, HRT II confocal scanning laser ophthalmoscope, and stratus OCT optical coherence tomograph for the detection of glaucoma. Arch Ophthalmol. Jun 2004;122(6):827-37. [Medline].

  90. Memarzadeh F, Ying-Lai M, Azen SP, et al. Associations with intraocular pressure in Latinos: the Los Angeles Latino Eye Study. Am J Ophthalmol. Jul 2008;146(1):69-76. [Medline].

  91. Migdal C. Glaucoma medical treatment: philosophy, principles and practice. Eye. Jun 2000;14 (Pt 3B):515-8. [Medline].

  92. Miglior S, Casula M, Guareschi M, et al. Clinical ability of Heidelberg retinal tomograph examination to detect glaucomatous visual field changes. Ophthalmology. Sep 2001;108(9):1621-7. [Medline].

  93. Milla E, Duch S, Buchacra O, et al. Poor agreement between Goldmann and Pascal tonometry in eyes with extreme pachymetry. Eye. Mar 28 2008;[Medline].

  94. Minckler DS. Histology of optic nerve damage in ocular hypertension and early glaucoma. Surv Ophthalmol. Apr 1989;33 Suppl:401-2; discussion 409-11. [Medline].

  95. Naskar R, Dreyer EB. New horizons in neuroprotection. Surv Ophthalmol. May 2001;45 Suppl 3:S250-5; discussion S273-6. [Medline].

  96. Nouri-Mahdavi K, Nikkhou K, Hoffman DC, et al. Detection of early glaucoma with optical coherence tomography (StratusOCT). J Glaucoma. Apr-May 2008;17(3):183-8. [Medline].

  97. Phelps CD. The no treatment approach to ocular hypertension. Surv Ophthalmol. Nov-Dec 1980;25(3):175-82. [Medline].

  98. Poli A, Strouthidis NG, Ho TA, et al. Analysis of HRT images: comparison of reference planes. Invest Ophthalmol Vis Sci. Sep 2008;49(9):3970-5. [Medline].

  99. Quigley HA, Enger C, Katz J, et al. Risk factors for the development of glaucomatous visual field loss in ocular hypertension. Arch Ophthalmol. May 1994;112(5):644-9. [Medline].

  100. Qureshi IA. Effects of mild, moderate and severe exercise on intraocular pressure of sedentary subjects. Ann Hum Biol. Nov-Dec 1995;22(6):545-53. [Medline].

  101. Racette L, Sample PA. Short-wavelength automated perimetry. Ophthalmol Clin North Am. Jun 2003;16(2):227-36, vi-vii. [Medline].

  102. Reeder CE, Franklin M, Bramley TJ. Managed care and the impact of glaucoma. Am J Manag Care. Feb 2008;14(1 Suppl):S5-S10. [Medline].

  103. Reus NJ, Colen TP, Lemij HG. The prevalence of glaucomatous defects with short-wavelength automated perimetry in patients with elevated intraocular pressures. J Glaucoma. Feb 2005;14(1):26-9. [Medline].

  104. Ritch, Shields, Krupin, eds. The Glaucomas. 2nd ed. 1992.

  105. Rivera JL, Bell NP, Feldman RM. Risk factors for primary open angle glaucoma progression: what we know and what we need to know. Curr Opin Ophthalmol. Mar 2008;19(2):102-6. [Medline].

  106. Roizen A, Ela-Dalman N, Velez FG, et al. Surgical treatment of strabismus secondary to glaucoma drainage device. Arch Ophthalmol. Apr 2008;126(4):480-6. [Medline].

  107. Sahin A, Niyaz L, Yildirim N. Comparison of the rebound tonometer with the Goldmann applanation tonometer in glaucoma patients. Clin Experiment Ophthalmol. May-Jun 2007;35(4):335-9. [Medline].

  108. Schuman JS. Clinical experience with brimonidine 0.2% and timolol 0.5% in glaucoma and ocular hypertension. Surv Ophthalmol. Nov 1996;41 Suppl 1:S27-37. [Medline].

  109. Serle JB. A comparison of the safety and efficacy of twice daily brimonidine 0.2% versus betaxolol 0.25% in subjects with elevated intraocular pressure. The Brimonidine Study Group III. Surv Ophthalmol. Nov 1996;41 Suppl 1:S39-47. [Medline].

  110. Shields MB. Textbook of Glaucoma. 4th ed. Lippincott Williams & Wilkins; 1998.

  111. Shih CY, Graff Zivin JS, Trokel SL, et al. Clinical significance of central corneal thickness in the management of glaucoma. Arch Ophthalmol. Sep 2004;122(9):1270-5. [Medline].

  112. Siam GA, Gheith ME, de Barros DS, et al. Limitations of the Heidelberg Retina Tomograph. Ophthalmic Surg Lasers Imaging. May-Jun 2008;39(3):262-4. [Medline].

  113. Spaeth GL. Early primary open-angle glaucoma: diagnosis and management. Preface. Int Ophthalmol Clin. Spring 1979;19(1):vii-ix. [Medline].

  114. Stamper RL, Lieberman MF, Drake MV. Becker-Shaffers Diagnosis and Therapy of the Glaucomas. 7th ed. Mosby-Year Book; 1999.

  115. Sunaric-Megevand G, Leuenberger PM. Results of viscocanalostomy for primary open-angle glaucoma. Am J Ophthalmol. Aug 2001;132(2):221-8. [Medline].

  116. Svizenska I, Dubovy P, Sulcova A. Cannabinoid receptors 1 and 2 (CB1 and CB2), their distribution, ligands and functional involvement in nervous system structures - A short review. Pharmacol Biochem Behav. May 25 2008;[Medline].

  117. Tezel G, Kolker AE, Kass MA, et al. Parapapillary chorioretinal atrophy in patients with ocular hypertension. I. An evaluation as a predictive factor for the development of glaucomatous damage. Arch Ophthalmol. Dec 1997;115(12):1503-8. [Medline].

  118. Tezel G, Kolker AE, Wax MB, et al. Parapapillary chorioretinal atrophy in patients with ocular hypertension. II. An evaluation of progressive changes. Arch Ophthalmol. Dec 1997;115(12):1509-14. [Medline].

  119. Van Buskirk EM. Medicolegal aspects of glaucoma care. Surv Ophthalmol. Jul-Aug 1998;43(1):83-6. [Medline].

  120. Woodward DF, Krauss AH, Chen J, et al. The pharmacology of bimatoprost (Lumigan). Surv Ophthalmol. May 2001;45 Suppl 4:S337-45. [Medline].

  121. Yu DY, Su EN, Cringle SJ, et al. Comparison of the vasoactive effects of the docosanoid unoprostone and selected prostanoids on isolated perfused retinal arterioles. Invest Ophthalmol Vis Sci. Jun 2001;42(7):1499-504. [Medline].

  122. Yu JY, Kahook MY, Lathrop KL, et al. The effect of probe placement and type of viscoelastic material on endoscopic cyclophotocoagulation laser energy transmission. Ophthalmic Surg Lasers Imaging. Mar-Apr 2008;39(2):133-6. [Medline].

  123. Yucel YH, Gupta N. Paying attention to the cerebrovascular system in glaucoma. Can J Ophthalmol. Jun 2008;43(3):342-6. [Medline].

  124. Zangwill LM, Jain S, Racette L, et al. The effect of disc size and severity of disease on the diagnostic accuracy of the Heidelberg Retina Tomograph Glaucoma Probability Score. Invest Ophthalmol Vis Sci. Jun 2007;48(6):2653-60. [Medline].

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

primary open angle glaucoma, primary open-angle glaucoma, POAG, glaucoma, chronic open angle glaucoma, chronic open-angle glaucoma, COAG, chronic simple glaucoma, glaucomatous damage, intraocular pressure, IOP, ocular hypertension, OHT, optic neuropathy, optic nerve, open angle glaucoma, open-angle glaucoma, optic nerve damage, low tension glaucoma, low-tension glaucoma, normal pressure glaucoma, normal-pressure glaucoma, glaucomatous optic neuropathy, glaucoma surgery, trabeculectomy, cyclophotocoagulation, ciliary body, aqueous humor, trabecular meshwork, Schlemm's canal, Schlemm canal, trabeculoplasty, argon laser trabeculoplasty, ALT, selective laser trabeculoplasty, SLT, glaucoma meds, glaucoma medications, neuroprotection, neuro-protection, memantine, Namenda, tonometry, eye pressure, pachymetry, perimetry, visual field, peripheral vision loss, scotoma, blind spot

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Jerald A Bell, MD, Staff Physician, Department of Ophthalmology, Billings Clinic; Glaucoma Director, Leadership Council Member, Physician Advocate for Personal Service Excellence Committee
Jerald A Bell, MD is a member of the following medical societies: American Academy of Ophthalmology
Disclosure: Nothing to disclose.

Medical Editor

Neil T Choplin, MD, Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences
Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Association for Research in Vision and Ophthalmology, and California Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Martin B Wax, MD, Clinical Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Ophthalmology Research and Development, Head, Ophthalmology Discovery Research, Alcon Labs, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Society for Neuroscience
Disclosure: Alcon Labs Salary Employment

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.