Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Primary Open-Angle Glaucoma Clinical Presentation

  • Author: Jerald A Bell, MD; Chief Editor: Inci Irak Dersu, MD, MPH  more...
 
Updated: Feb 20, 2014
 

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 patient's past ocular history and other factors.

Past ocular history includes the following:

  • History of eye pain or redness
  • Multicolored halos
  • Headache
  • Previous ocular disease, including cataracts
  • Uveitis
  • Diabetic retinopathy
  • Vascular occlusions

Other factors include the following:

  • 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 are as follows:

  • Obesity
  • Smoking
  • Alcohol
  • History of stress
  • Anxiety

Risk factors for rapid glaucoma progression

Patients with open-angle glaucoma who have a worse mean deviation to their visual field, a greater vertical cup-to-disc ratio at baseline, or who are older are significantly more likely to experience a rapid decay of their visual field, according to a recent study of 767 eyes from 566 participants in the Advanced Glaucoma Intervention Study.[7] Rapid progression was defined as a rate of changes in the visual field of at least 36% per year. Other factors associated with an increased risk for progression that did not reach significance included being male and having worse baseline visual acuity.[7]

Next

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.

A flowchart for evaluation of suspected glaucoma is shown below.

Flowchart for evaluation of a patient with suspect Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.

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

See the list below:

  • 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 (see the image below), 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.
    Illustration of progressive optic nerve damage. No Illustration of progressive optic nerve damage. Notice the deepening (saucerization) along the neural rim, along with notching and increased excavation/sloping of the optic nerve and circumlinear vessel inferiorly. Courtesy of M. Bruce Shields, MD.
    Optic nerve asymmetry in a patient with glaucomato Optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly (similar to Image 5). Courtesy of M. Bruce Shields, MD.
    Glaucomatous optic nerve damage, with sloping and Glaucomatous optic nerve damage, with sloping and nerve fiber layer rim hemorrhage at the 7-o'clock position. Hemorrhage is indicative of progressive damage, usually due to inadequate pressure control. Further notching and pallor corresponding to the area of hemorrhage usually is seen several weeks after resorption of the blood. Courtesy of M. Bruce Shields, MD.
  • 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).

Gonioscopy

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 the image below).

Ocular hypertension study (OHTS). Percentage of pa Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).

Visual field testing

Perform automated threshold testing (eg, Humphrey 24-2) to rule out any glaucomatous visual field defects. A Humphrey visual field is shown below.

Humphrey visual field, right eye, showing patient Humphrey visual field, right eye, showing patient with advanced glaucomatous field loss. Notice both the arcuate extension from the blind spot (Bjerrum scotoma) and the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields, MD.

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.

Short wavelength automated perimetry or blue-yellow perimetry (SWAP) 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 for progressive field loss included higher IOP, older age, presence of peripapillary atrophy, larger cup-to-disc ratio, smaller rim-disc area ratio, and cup asymmetry. A study by De Moraes et al found some of the same risk factors for visual field progression in treated glaucoma/POAG: female sex, African or Latin, exfoliation syndrome, older age, cornea thinner and decreased CCT, peak IOP 1.13 mm Hg higher, disc hemorrhage, and beta zone peripapillary atrophy.[8] 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).

The rate of progression of visual field loss, as measured by mean deviation, is related to the amount of visual field loss present at initial presentation; the rate is greater the more loss is initially present.[9] A study by Nouri-Mahdavi et al suggests that accelerating the frequency of visual field testing from annually to biannually increases the ability to detect progression of glaucoma.[10]

Previous
Next

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)
Previous
 
 
Contributor Information and Disclosures
Author

Jerald A Bell, MD Staff Physician, Department of Ophthalmology, Billings Clinic

Jerald A Bell, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc

Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience

Disclosure: Nothing to disclose.

Chief Editor

Inci Irak Dersu, MD, MPH Associate Professor of Clinical Ophthalmology, State University of New York Downstate College of Medicine; Attending Physician, SUNY Downstate Medical Center, Kings County Hospital, and VA Harbor Health Care System

Inci Irak Dersu, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society

Disclosure: Nothing to disclose.

Additional Contributors

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, Association for Research in Vision and Ophthalmology, American Glaucoma Society, California Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous coauthors, Robert J Noecker, MD, and Emily Patterson, MD, to the development and writing of this article.

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

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

  3. Traynis I, De Moraes CG, Raza AS, Liebmann JM, Ritch R, Hood DC. Prevalence and nature of early glaucomatous defects in the central 10° of the visual field. JAMA Ophthalmol. 2014 Jan 9. [Medline].

  4. Laidman J. Early glaucoma damage sometimes missed by visual field test. Medscape Medical News. January 17, 2014. [Full Text].

  5. Costa VP, Jimenez-Roman J, Carrasco FG, Lupinacci A, Harris A. Twenty-four-hour ocular perfusion pressure in primary open-angle glaucoma. Br J Ophthalmol. 2010 Oct. 94(10):1291-4. [Medline].

  6. Czudowska MA, Ramdas WD, Wolfs RC, Hofman A, De Jong PT, Vingerling JR, et al. Incidence of Glaucomatous Visual Field Loss: A Ten-Year Follow-up from the Rotterdam Study. Ophthalmology. 2010 Sep. 117(9):1705-12. [Medline].

  7. McNamara D. Predictors of Rapid Glaucoma Progression Identified. Medscape Medical News. Available at http://www.medscape.com/viewarticle/805049. Accessed: June 11, 2013.

  8. De Moraes CG, Juthani VJ, Liebmann JM, Teng CC, Tello C, Susanna R Jr, et al. Risk factors for visual field progression in treated glaucoma. Arch Ophthalmol. 2011 May. 129(5):562-8. [Medline].

  9. Rao HL, Kumar AU, Babu JG, Senthil S, Garudadri CS. Relationship between Severity of Visual Field Loss at Presentation and Rate of Visual Field Progression in Glaucoma. Ophthalmology. 2011 Feb. 118(2):249-53. [Medline].

  10. Nouri-Mahdavi K, Zarei R, Caprioli J. Influence of visual field testing frequency on detection of glaucoma progression with trend analyses. Arch Ophthalmol. 2011 Dec. 129(12):1521-7. [Medline].

  11. Leung CK, Yu M, Weinreb RN, Lai G, Xu G, Lam DS. Retinal Nerve Fiber Layer Imaging with Spectral-domain Optical Coherence Tomography: Patterns of Retinal Nerve Fiber Layer Progression. Ophthalmology. 2012 Jun 5. [Medline].

  12. Leung CK, Liu S, Weinreb RN, et al. Evaluation of retinal nerve fiber layer progression in glaucoma a prospective analysis with neuroretinal rim and visual field progression. Ophthalmology. 2011 Aug. 118(8):1551-7. [Medline].

  13. Medeiros FA, Zangwill LM, Anderson DR, Liebmann JM, Girkin CA, Harwerth RS, et al. Estimating the Rate of Retinal Ganglion Cell Loss in Glaucoma. Am J Ophthalmol. 2012 Jul 26. [Medline].

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

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

  16. 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. 2008 Aug. 17(5):361-5. [Medline].

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

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

  19. Heijl A, Peters D, Leske MC, Bengtsson B. Effects of argon laser trabeculoplasty in the early manifest glaucoma trial. Am J Ophthalmol. 2011 Nov. 152(5):842-8. [Medline].

  20. Francis BA, Hong B, Winarko J, et al. Vision loss and recovery after trabeculectomy: risk and associated risk factors. Arch Ophthalmol. 2011 Aug. 129(8):1011-7. [Medline].

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

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

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

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

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

  26. 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. 2001 May. 131(5):636-42. [Medline].

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

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

  29. 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. 2008 Oct. 246(10):1485-90. [Medline].

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

  31. 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. 2003 Nov. 44(11):5029-34. [Medline].

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

  33. 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. 2008 Sep. 146(3):466-472. [Medline].

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

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

  36. 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. 2004 Nov. 138(5):717-22. [Medline].

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

  38. Brown T. FDA Approves Simbrinza for Glaucoma, Ocular Hypertension. Medscape Medical News. Available at http://www.medscape.com/viewarticle/803064. Accessed: May 2, 2013.

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

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

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

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

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

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

  45. 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. 2002 Jun. 11(3):209-13. [Medline].

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

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

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

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

  50. 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. 2008 Jun. 92(6):729-34. [Medline].

  51. 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. 2005 Aug. 21(4):337-48. [Medline].

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

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

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

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

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

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

  58. 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. 2007 Jan. 143(1):9-22. [Medline].

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

  60. 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. 2002 Jun. 120(6):714-20; discussion 829-30. [Medline].

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

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

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

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

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

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

  67. 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. 2008 Mar-Apr. 39(2):125-32. [Medline].

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

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

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

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

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

  73. 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. 2008 Jun-Jul. 17(4):275-9. [Medline].

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

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

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

  77. 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. 2004 Oct. 111(10):1853-9. [Medline].

  78. 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. 2008 Apr. 27(3):339-43. [Medline].

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

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

  81. Kawasaki R, Wang JJ, Rochtchina E, Lee AJ, Wong TY, Mitchell P. Retinal vessel caliber is associated with the 10-year incidence of glaucoma: the Blue Mountains Eye Study. Ophthalmology. 2013 Jan. 120(1):84-90. [Medline].

  82. 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. 2008 Mar. 49(3):934-40. [Medline].

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

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

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

  86. 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. 2003 Dec. 121(12):1705-10. [Medline].

  87. 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. 2008 Oct. 246(10):1463-6. [Medline].

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

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

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

  91. 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. 2007 Dec. 144(6):901-907. [Medline].

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

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

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

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

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

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

  98. 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. 2007 Oct. 114(10):1937-49. [Medline].

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

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

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

  102. 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. 2008 Jun-Jul. 17(4):329-31. [Medline].

  103. 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. 2004 Jun. 122(6):827-37. [Medline].

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

  119. 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. 2008 Mar. 19(2):102-6. [Medline].

  120. Roach L. Narrow retinal vessels raise risk for open-angle glaucoma. Medscape Medical News. January 9, 2013. Available at http://www.medscape.com/viewarticle/777428. Accessed: March 11, 2013.

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

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

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

  124. 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. 1996 Nov. 41 Suppl 1:S39-47. [Medline].

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

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

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

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

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

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

  131. 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. 2008 May 25. [Medline].

  132. 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. 1997 Dec. 115(12):1503-8. [Medline].

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

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

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

  136. 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. 2001 Jun. 42(7):1499-504. [Medline].

  137. 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. 2008 Mar-Apr. 39(2):133-6. [Medline].

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

  139. 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. 2007 Jun. 48(6):2653-60. [Medline].

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

 
Previous
Next
 
Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields, MD.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, field loss among individuals with pressures in the upper teens can occur. Also, note that the average pressure among those with glaucomas is in the low 20s, even though most individuals with pressures in the low 20s do not have glaucoma. Used by permission from Survey of Ophthalmology.
Diagram showing the relative proportion of people in the general population who have elevated pressure (horizontally shaded lines) and/or damage from glaucoma (vertically shaded lines). Notice that most have elevated pressure but no sign of damage (ie, ocular hypertensives), but there are also those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). Courtesy of M. Bruce Shields, MD.OHT = horizontal lines only NTG = vertical lines only POAG and other glaucomas with both elevated intraocular pressure and damage = overlapping horizontal and vertical lines
Humphrey visual field, right eye, showing patient with advanced glaucomatous field loss. Notice both the arcuate extension from the blind spot (Bjerrum scotoma) and the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields, MD.
Illustration of progressive optic nerve damage. Notice the deepening (saucerization) along the neural rim, along with notching and increased excavation/sloping of the optic nerve and circumlinear vessel inferiorly. Courtesy of M. Bruce Shields, MD.
Example of progressive visual field loss over time (from top to bottom) in a patient with glaucoma. Notice the early appearance of an inferior nasal step and arcuate loss, with progressive enlargement and increasing density of the scotomata over time. Courtesy of M. Bruce Shields, MD.
Optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly (similar to Image 5). Courtesy of M. Bruce Shields, MD.
Glaucomatous optic nerve damage, with sloping and nerve fiber layer rim hemorrhage at the 7-o'clock position. Hemorrhage is indicative of progressive damage, usually due to inadequate pressure control. Further notching and pallor corresponding to the area of hemorrhage usually is seen several weeks after resorption of the blood. Courtesy of M. Bruce Shields, MD.
Correction values according to corneal thickness.
Ocular hypertension study (OHTS). Percentage of patients who developed glaucoma during this study, stratified by baseline intraocular pressure (IOP) and central corneal thickness (CCT).
Intraocular pressure measurements. Adapted from Reichert Ophthalmic Instruments, Ocular Response Analyzer, How does it work Web page.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.