Close
New

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

 

Ocular Hypertension Medication

  • Author: Anne Chang-Godinich, MD, FACS; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: Mar 22, 2016
 

Medication Summary

The ideal drug for the treatment of ocular hypertension should effectively lower IOP, produce no adverse effects or systemic exacerbation of disease, be inexpensive, and have once-a-day dosing. Because no medicine currently possesses all of the above, these qualities should be prioritized based on the patient's individual needs and risks, and therapy should then be chosen accordingly.[59]

Older glaucoma medications such as cholinergics (ie, miotics, such as pilocarpine), osmotics, and nonselective adrenergic agonists have a limited role in the treatment of ocular hypertension. They should be considered only if contraindications prevent the use of preferred medications.

Newer products with neuroprotective effects (eg, memantine, an N -methyl-D-aspartate [NMDA] receptor antagonist) may be available in the future.[60, 61, 62, 63, 64]

Assessment

Follow-up assessment should be performed 3-4 weeks after beginning therapy.[28] Observe the patient for signs of allergy (eg, hyperemia, rash, follicular reaction). Query patients about the presence of any systemic adverse effects and symptoms. Continue the treatment if effective lowering of IOP has been achieved without adverse effects.[65] Reevaluate the treatment 1-6 months later, depending on the clinical picture.[28]

Modifications in therapy

Some patients do not respond to the chosen therapy, necessitating initiation of another medication with or without discontinuation of the initial medication. When changing therapies, keep in mind that many drugs have a washout period of up to 2-4 weeks (especially beta-blockers), during which time they may still have some IOP-lowering effect or residual systemic response. In addition, some medications (eg, brimonidine) may have an effect that plateaus at 6-8 weeks in some patients.[66, 67]

If the addition of a second agent has been decided, choose one that has a different mechanism of action, so that the 2 drug therapies have an additive effect. Usually, no additive effect is seen if 2 medications from the same drug class are used. When more than 1 topical ophthalmic drug is being used, instruct the patient to administer them at least 10 minutes apart.

Next

Antiglaucoma, Prostaglandin Agonists

Class Summary

These medications work by increasing uveoscleral outflow. Latanoprost, bimatoprost, travoprost, and tafluprost are examples of prostaglandin analogs that may help in IOP reduction.[68, 69, 70] Each of these drugs has its own set of characteristics that may be useful in the clinical setting.

Latanoprost (Xalatan 0.005%)

 

Latanoprost may decrease IOP by increasing the outflow of aqueous humor. Patients should be informed about possible cosmetic effects to the eye/eyelashes, especially if uniocular therapy is to be initiated.[71]

Bimatoprost ophthalmic solution (Lumigan, Latisse)

 

This agent is a prostamide analogue with ocular hypotensive activity. It mimics the IOP-lowering activity of prostamides via the prostamide pathway. Bimatoprost may achieve a large reduction in pressure in many patients, but it is known to cause significant conjunctival hyperemia.

Travoprost ophthalmic solution (Travatan Z)

 

This agent is a prostaglandin F2-alpha analogue. It is a selective FP prostanoid receptor agonist that is believed to reduce IOP by increasing uveoscleral outflow. Travoprost has been purported to achieve lower IOPs, particularly in African American patients, but these data are the subject of controversy. It may also cause significant conjunctival hyperemia.[72]

Unoprostone ophthalmic solution (Rescula)

 

This agent is a prostaglandin F2-alpha analogue. It is a selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Unoprostone has been shown to decrease pressure approximately 10-15% and may work partially through traditional outflow channels.[73] Unoprostone ophthalmic solution is used to treat open-angle glaucoma and ocular hypertension. It is available as an orphan drug.

Tafluprost (Zioptan)

 

Tafluprost is a topical, preservative-free, ophthalmic prostaglandin analogue indicated for elevated IOP associated with open-angle glaucoma or ocular hypertension. The exact mechanism by which it reduces IOP is unknown, but it is thought to increase uveoscleral outflow.

Previous
Next

Antiglaucoma, Beta-Blockers

Class Summary

These agents decrease aqueous production, possibly by blocking adrenergic beta receptors present in the ciliary body. The nonselective medications in this class can also interact with the beta-receptors in the heart and lungs, causing significant adverse effects.

Betaxolol ophthalmic (Betoptic-S)

 

This agent selectively blocks beta1-adrenergic receptors, with little or no effect on beta2 receptors. It lowers IOP by reducing the production of aqueous humor. The drug may have less effect on the pulmonary system. Its IOP-lowering effect is slightly less than that of nonselective beta-blockers. It may increase optic nerve perfusion and confer neuroprotection.

Carteolol 1%

 

Carteolol has an intrinsic sympathomimetic activity (partial agonist activity), with possibly less adverse effect on cardiac and lipid profiles.

Timolol 0.25%, 0.5% (Timoptic, Timoptic XE, Blocadren, Istalol)

 

Timolol may reduce elevated and normal IOP, with or without glaucoma, by reducing the production of aqueous humor. Timolol gel-forming solution (Timoptic XE) usually is administered at night, unless it is used concurrently with latanoprost therapy. Timoptic XE and Istalol (an aqueous solution) are administered daily. Timolol is also available as a combination medication with dorzolamide (Cosopt) and brimonidine (Combigan).

Levobunolol 0.25%, 0.5% (Betagan)

 

Levobunolol is a nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increasing the outflow of aqueous humor.

Metipranolol 0.3% (OptiPranolol)

 

Metipranolol is a beta-adrenergic blocker that has little or no intrinsic sympathomimetic effect and membrane-stabilizing activity. It also has little local anesthetic activity. The drug reduces IOP by reducing the production of aqueous humor.

Previous
Next

Antiglaucoma, Carbonic Anhydrase Inhibitors

Class Summary

By slowing the formation of bicarbonate ions, causing a reduction in sodium and fluid transport, these agents may inhibit carbonic anhydrase in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP. Carbonic anhydrase inhibitors typically have a weaker effect than beta-blockers.

Dorzolamide (Trusopt)

 

Dorzolamide is a reversible carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably, it slows bicarbonate ion formation, producing a subsequent reduction in sodium and fluid transport.

Systemic absorption can affect carbonic anhydrase in the kidney, reducing hydrogen ion secretion at the renal tubule and increasing renal excretion of sodium, potassium bicarbonate, and water.

Brinzolamide (Azopt)

 

Brinzolamide catalyzes a reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. It may be used concomitantly with other topical ophthalmic drug products to lower IOP. Brinzolamide is less stinging on instillation secondary to buffered pH.

Acetazolamide (Diamox, Diamox Sequels)

 

Acetazolamide is primarily used for the treatment of refractory POAG and secondary glaucomas. Because of an increased incidence of adverse effects, it is rarely indicated for ocular hypertension.

Methazolamide (Neptazane)

 

Methazolamide reduces aqueous humor formation by inhibiting the enzyme carbonic anhydrase, which results in decreased IOP.

Previous
Next

Antiglaucoma, Alpha Agonists

Class Summary

Within this class, the alpha2 selective agonist brimonidine is the most commonly used for the treatment of ocular hypertension.[66] Apraclonidine is another alpha2-selective agonist, but it is believed to have more of an allergic potential, so it rarely is used as a long-term medication. Less selective adrenergics, such as epinephrine and dipivefrin, can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, and cystoid macular edema. Because these less selective agents are used infrequently in treating ocular hypertension, they are not discussed here. Alpha2 adrenergic agonists work by decreasing aqueous production.

Brimonidine (Alphagan-P)

 

Brimonidine is a relatively selective alpha2 adrenergic-receptor agonist that decreases IOP by dual mechanisms, reducing aqueous humor production and increasing uveoscleral outflow. Brimonidine has minimal effect on cardiovascular and pulmonary parameters. A moderate risk of allergic response to this drug exists. Caution should be used in individuals who have developed an allergy to Iopidine. IOP lowering of up to 27% has been reported.

Alphagan-P contains the preservative Purite and has been shown to be much better tolerated than its counterpart, Alphagan.

Apraclonidine 0.5%, 1% (Iopidine)

 

Apraclonidine is a potent alpha-adrenergic agent that is selective for alpha2 receptors, with minimal cross-reactivity with alpha1 receptors. It suppresses aqueous production and reduces elevated, as well as normal, IOP, whether accompanied by glaucoma or not. Apraclonidine does not have significant local anesthetic activity. It has minimal cardiovascular effects.

Previous
Next

Antiglaucoma, Combos

Class Summary

A combination medication may decrease aqueous humor secretion more than each medication would if used independently as monotherapy and improves patient compliance.[74]

Brimonidine/timolol (Combigan)

 

This solution contains a selective alpha2 adrenergic-receptor agonist and a nonselective beta adrenergic-receptor inhibitor. Each drug decreases elevated IOP, whether or not it is associated with glaucoma.

Timolol/dorzolamide (Cosopt)

 

Timolol is a nonselective beta-adrenergic receptor blocker that reduces IOP by decreasing aqueous humor secretion. It may also slightly increase outflow facility.

Timolol and dorzolamide administered together twice daily may result in greater IOP reduction than either component would achieve alone. However, the reduction is not as much as it is when the drugs are taken concomitantly, with dorzolamide administered 3 times daily and timolol administered twice daily.

Brinzolamide/brimonidine (Simbrinza)

 

This combination product contains the carbonic anhydrase inhibitor brinzolamide and the alpha2 adrenergic receptor agonist brimonidine. It is indicated for reduction of elevated intraocular pressure in patients with ocular hypertension.

Previous
 
Contributor Information and Disclosures
Author

Anne Chang-Godinich, MD, FACS Clinical Associate Professor, Department of Ophthalmology, Baylor College of Medicine; Physician, 1960 Eye Surgeons, PA; Attending Surgeon, Veterans Affairs Medical Center of Houston

Anne Chang-Godinich, MD, FACS is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Society of Cataract and Refractive Surgery, Texas Medical Association

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, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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

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

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

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

  4. 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].

  5. Chandler PA, Grant WM. Ocular hypertension' vs open-angle glaucoma. Arch Ophthalmol. 1977 Apr. 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. Souzeau E, Burdon KP, Dubowsky A, Grist S, Usher B, Fitzgerald JT, et al. Higher prevalence of myocilin mutations in advanced glaucoma in comparison with less advanced disease in an Australasian disease registry. Ophthalmology. 2013 Jun. 120(6):1135-43. [Medline].

  9. 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].

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

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

  12. 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].

  13. 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].

  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. Sommer A, Tielsch JM, Katz J, et al. Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey. Arch Ophthalmol. 1991 Aug. 109(8):1090-5. [Medline].

  16. Varma R, Wang D, Wu C, et al. Four-year incidence of open-angle glaucoma and ocular hypertension: the los angeles latino eye study. Am J Ophthalmol. 2012 Aug. 154(2):315-325.e1. [Medline]. [Full Text].

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

  18. Higginbotham EJ, Gordon MO, Beiser JA, et al. The Ocular Hypertension Treatment Study: topical medication delays or prevents primary open-angle glaucoma in African American individuals. Arch Ophthalmol. 2004 Jun. 122(6):813-20. [Medline].

  19. Hoehn R, Mirshahi A, Hoffmann EM, Kottler UB, Wild PS, Laubert-Reh D, et al. Distribution of intraocular pressure and its association with ocular features and cardiovascular risk factors: the Gutenberg Health Study. Ophthalmology. 2013 May. 120(5):961-8. [Medline].

  20. Luntz MH, Schenker HI. Retinal vascular accidents in glaucoma and ocular hypertension. Surv Ophthalmol. 1980 Nov-Dec. 25(3):163-7. [Medline].

  21. Friedman DS, Wolfs RC, O'Colmain BJ, et al. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004 Apr. 122(4):532-8. [Medline]. [Full Text].

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

  23. 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].

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

  25. 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].

  26. 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].

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

  28. American Academy of Ophthalmology. Preferred Practice Pattern Guidelines: Primary Open-Angle Glaucoma Suspect PPP - October 2010. Ophthalmic News and Education Network. Available at http://one.aao.org/CE/PracticeGuidelines/PPP_Content.aspx?cid=e2387c8a-e51c-4c21-be20-c30fbf4f3260. Accessed: August 6, 2012.

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

  30. 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].

  31. 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. 2008 Aug. 17(5):361-5. [Medline].

  32. 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].

  33. 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].

  34. 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].

  35. 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].

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

  39. 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].

  40. 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].

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

  42. 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. 2007 Oct. 114(10):1937-49. [Medline].

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

  44. 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].

  45. 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].

  46. 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].

  47. Liu S, Lam S, Weinreb RN, et al. Comparison of standard automated perimetry, frequency-doubling technology perimetry, and short-wavelength automated perimetry for detection of glaucoma. Invest Ophthalmol Vis Sci. 2011 Sep. 52(10):7325-31. [Medline].

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

  49. 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].

  50. 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].

  51. Gyatsho J, Kaushik S, Gupta A, Pandav SS, Ram J. Retinal nerve fiber layer thickness in normal, ocular hypertensive, and glaucomatous Indian eyes: an optical coherence tomography study. J Glaucoma. 2008 Mar. 17(2):122-7. [Medline].

  52. Weinreb RN, Zangwill LM, Jain S, et al. Predicting the onset of glaucoma: the confocal scanning laser ophthalmoscopy ancillary study to theOcular Hypertension Treatment Study. Ophthalmology. 2010 Sep. 117(9):1674-83. [Medline].

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

  54. Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun. 120(6):701-13; discussion 829-30. [Medline].

  55. 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].

  56. 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].

  57. Baudouin C, Renard JP, Nordmann JP, Denis P, Lachkar Y, Sellem E, et al. Prevalence and risk factors for ocular surface disease among patients treated over the long term for glaucoma or ocular hypertension. Eur J Ophthalmol. 2012 Jun 11. [Medline].

  58. Kymes SM, Kass MA, Anderson DR, Miller JP, Gordon MO. Management of ocular hypertension: a cost-effectiveness approach from the Ocular Hypertension Treatment Study. Am J Ophthalmol. 2006 Jun. 141(6):997-1008. [Medline]. [Full Text].

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

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

  61. 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].

  62. 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].

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

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

  65. 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].

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

  67. 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:S39-47. [Medline].

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

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

  70. 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].

  71. Pacella F, Turchetti P, Santamaria V, Impallara D, Smaldone G, Brillante C, et al. Differential activity and clinical utility of latanoprost in glaucoma and ocular hypertension. Clin Ophthalmol. 2012. 6:811-5. [Medline]. [Full Text].

  72. 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].

  73. 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].

  74. 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].

 
Previous
Next
 
Diagram of intraocular pressure distribution. Used with 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 © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.