Ocular Hypertension Clinical Presentation

  • Author: Jerald A Bell, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Feb 22, 2012
 

History

The initial patient interview is extremely important in the evaluation of ocular hypertension to detect frank glaucoma or other ocular diseases secondarily causing elevated IOP (see the image below). Detail 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, and vascular occlusions; previous ocular surgery (including photocoagulation or refractive procedures); or ocular/head trauma[21, 22]
  • 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[23]
  • Risk factors for glaucomatous optic neuropathy[24]
    • Strongly implicated risk factors
      • History of elevated IOP, advanced age (particularly persons >50 y), 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]), and myopia
      • Be specific when asking family history - Which family members? Did actual visual loss from glaucoma occur? Did other causes of visual field loss occur? Are they under control on one or more medications? Did they require surgery for adequate control?
    • Possibly implicated risk factors - Systemic cardiovascular disease, diabetes mellitus, migraine headache, systemic hypertension, and vasospasm[25]
  • Anecdotal risk factors - Obesity, smoking, alcohol, and history of stress or anxiety (no definitive link to ocular hypertension)Flowchart for evaluation of a patient with suspectFlowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy of Ophthalmology.
Next

Physical

Screening of the general population for ocular hypertension and POAG is similar, being most effective if targeted toward those at high risk, such as African Americans and elderly persons, especially if the screening consists of IOP measurements combined with assessment of optic nerve status.

Screening should be performed 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, evaluation/monitoring should be performed on a more frequent basis, as appropriate.

A standard comprehensive eye examination, such as that outlined in the American Academy of Ophthalmology (AAO) Preferred Practice Patterns, should be performed on the initial visit.[26, 27] If there are any visual field or optic nerve changes consistent with early glaucoma, then the patient should be diagnosed as having such and should no longer be referred to as ocular hypertensive.[28, 29]

Emphasis during the examination should be on the following points to rule out early POAG or secondary causes of glaucoma:[30]

  • Visual acuity: Compare visual acuity with previous known acuities (if declining, rule out frank POAG or secondary causes of vision loss, whether from cataracts, age-related macular degeneration [ARMD], ocular surface disorders [eg, dry eye], or adverse effects from topical medications [especially if using miotics]).
  • Pupils: The presence/absence of afferent pupillary defect (Marcus-Gunn) should be seen.
  • Slit lamp examination of the anterior segment
    • Cornea: Look for signs of microcystic edema (found only with a sudden elevation of IOP); keratic precipitates; pigment on endothelium (Krukenberg spindle); and congenital anomalies.
    • Anterior chamber: Examine for cell or flare, uveitis, hyphema, and angle closure.
    • Iris: Transillumination defects, iris atrophy, synechiae, rubeosis, ectropion uveae, iris bombé, difference in iris coloration bilaterally (eg, Fuchs heterochromic iridocyclitis), or pseudoexfoliation (PXF) material may be observed.
    • Lens: Examine for cataract progression (ie, phacomorphic glaucoma, PXF, phacolytic glaucoma with a Morgagnian cataract).
    • Optic nerve/nerve fiber layer: Stereoscopically examine for evidence of glaucomatous damage, including 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 the 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.[31] See the images below. Illustration of progressive optic nerve damage. NoIllustration 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. 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.
    • 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: Obtain baseline stereo fundus photographs for future reference/comparison; if unavailable, record representative drawings.
  • Tonometry (see also 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, possibly more so in ocular hypertensives.
    • When checking IOP, record all of the following: measurements for both eyes, the method used (Goldmann applanation is the criterion standard), and the time of the measurement.
    • Review previous tonometry readings, if available (eg, Is the reading reproducible? What method was used to obtain the reading? What was the time of day? Where does it fall on the diurnal pressure curve? Do both the eyes have similar measurements?).
    • In patients who are obese, consider the possibility of a Valsalva movement causing an increased IOP when measured with the slit lamp by Goldmann 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 a greater likelihood of glaucoma. Expect an average of 10% difference between individual measurements. Repeat the measurements on at least 2-3 occasions before deciding on a treatment plan. Take the measurement 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 strongly suspected when a steadily increasing IOP is present.[30]
    • Pachymetry affects applanation tonometry values and, therefore, should be checked on the initial examination.
  • Gonioscopy: Gonioscopy should be performed to rule out angle-closure or secondary causes of IOP elevation, such as angle recession, pigmentary glaucoma, and PXF.
  • Pachymetry: Pachymetry is used to measure central corneal thickness (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).[32, 33] Ocular hypertension study (OHTS). Percentage of paOcular 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. See the image 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), as well as the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields.
    • If the patient is unable to perform automated testing, Goldmann testing may be substituted.
  • Remember the following caveats regarding visual field analysis (see Other Tests):
    • New-onset glaucomatous defects in an individual with previously diagnosed ocular hypertension are found most commonly as an early nasal step, temporal wedge, or a 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 in those diagnosed as ocular hypertensive.[34, 35] If the Humphrey visual field testing results are normal, SWAP should be considered to help detect visual field loss earlier. Studies suggest that 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 ocular hypertension.[36] 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.[37, 38]
    • Examination results must take into account that visual field defects may not be apparent until more than 40% loss of the nerve fiber layer has occurred. Therefore, base the therapy on the overall clinical picture and not on visual field testing alone (see Treatment).
    • Document the pupil size at each testing session, as constriction can reduce retinal sensitivity and mimic progressive field loss.
    • The risk factors, specifically for the development of glaucomatous field loss in ocular hypertension, have 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 found to be of significance 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 ocular hypertension 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.[39, 40] In follow-up, if there is a low risk of onset of glaucomatous damage, then repeat testing may be performed once a year. If there is a high risk of impending glaucomatous damage, then testing may be adjusted to as frequent as every 2 months.
Previous
Next

Causes

See Pathophysiology.

Previous
Proceed to Differential Diagnoses
 
 
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.

Coauthor(s)

Judie F Charlton, MD  Director, Division of Glaucoma, Professor and Chair, Department of Ophthalmology, West Virginia University School of Medicine

Judie F Charlton, MD is a member of the following medical societies: American Academy of Ophthalmology

Disclosure: Nothing to disclose.

Specialty Editor Board

Bradford Shingleton, MD  Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Bradford Shingleton, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Ophthalmology

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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: Nothing to disclose.

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.

References

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

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

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

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

  5. Chandler PA, Grant WM. 'Ocular hypertension' vs open-angle glaucoma. Arch Ophthalmol. Apr 1977;95(4):585-6. [Medline].

  6. Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. 1992.

  7. Shields MB. Textbook of Glaucoma. 3rd ed. Lippincott Williams & Wilkins; 1992.

  8. 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].

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

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

  11. 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].

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

  13. 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].

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

  15. Annette H, Kristina L, Bernd S, et al. 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].

  16. 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].

  17. 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].

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

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

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

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

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

  23. 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].

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

  25. 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].

  26. American Academy of Ophthalmology. Preferred practice patterns: primary open angle glaucoma suspect and POAG. 1995-1996.

  27. Cantor L. American Academy of Ophthalmology. In: Section 10: Glaucoma. In: Basic and Clinical Science Course. 1996.

  28. Hodapp EA, Anderson DR. Treatment of early glaucoma. In: Focal Points. 1986;4(4).

  29. Lin SC, Singh K, Jampel HD, 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].

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

  31. 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].

  32. 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].

  33. 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].

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

  35. 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].

  36. 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].

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

  38. 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].

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

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

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

  42. 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].

  43. 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].

  44. 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].

  45. 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].

  46. 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].

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

  48. 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].

  49. 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].

  50. Pablo LE, Ferreras A, Schlottmann PG. Retinal nerve fibre layer evaluation in ocular hypertensive eyes using optical coherence tomography and scanning laser polarimetry in the diagnosis of early glaucomatous defects. Br J Ophthalmol. Jan 2011;95(1):51-5. [Medline].

  51. 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].

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

  53. 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].

  54. 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].

  55. 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].

  56. Kass MA. When to treat ocular hypertension. Surv Ophthalmol. Dec 1983;28 Suppl:229-34. [Medline].

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

  58. 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].

  59. 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].

  60. 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].

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

  62. 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].

  63. 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].

  64. 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].

  65. 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].

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

  67. 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].

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

  69. 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].

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

  71. 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].

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

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

  74. 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].

  75. 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].

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

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

  78. 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].

  79. 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].

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

  81. 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:S39-47. [Medline].

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

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

  84. 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].

  85. 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].

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

  87. 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].

  88. 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].

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

  90. 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].

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

  92. 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].

  93. 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].

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

  95. 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].

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

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

  98. 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].

  99. 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].

  100. Gedde SJ, Schiffman JC, Feuer WJ, et al. Treatment outcomes in the tube versus trabeculectomy study after one year of follow-up. Am J Ophthalmol. Jan 2007;143(1):9-22. [Medline].

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

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

  103. 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].

  104. 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].

  105. 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].

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

  107. 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].

  108. 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].

  109. 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].

  110. 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].

  111. 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].

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

  113. 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. Oct 2008;90(4):501-11. [Medline].

  114. 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].

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

  116. 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].

 
Previous
Next
 
Diagram of intraocular pressure distribution, with a visible skew to the right (somewhat exaggerated compared to the actual distribution). Note that, while uncommon, there can be field loss among individuals with pressures in the upper teens. Also, note how the average pressure among those with glaucoma 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.
Flowchart for evaluation of a patient with suspected glaucoma. Used by permission of the American Academy 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 those with normal pressures who still have damage from glaucoma (ie, normal tension glaucoma). (Diagram used by permission of M. Bruce Shields.) 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), as well as the loss nasally (nasal step), which often occurs early in the disease process. Courtesy of M. Bruce Shields.
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.
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. Humphrey visual field courtesy of M. Bruce Shields.
Example of optic nerve asymmetry in a patient with glaucomatous damage, left eye, showing optic nerve excavation inferiorly similar to Image 5. Used by permission of M. Bruce Shields.
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.
Advanced glaucomatous damage with increased cupping and substantial pallor of the optic nerve head. Courtesy of M. Bruce Shields.
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).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
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.