Medication Summary
The ideal drug for treatment of ocular hypertension should have the following characteristics: (1) effectively lower IOP, (2) no adverse effects or systemic exacerbation of disease, and (3) inexpensive with once-a-day dosing. However, because no medicine possesses all of the above, these qualities must be prioritized based on the patient's individual needs and risks; then, therapy should be chosen accordingly.[72]
Older glaucoma medications, such as cholinergics (ie, miotics, such as pilocarpine) and osmotics, as well as nonselective adrenergic agonists, have a limited role in the treatment of ocular hypertension and should only be considered if adverse effects prevent the use of the above-described medications.
Newer products having possible neuroprotective effects (eg, memantine, which is an N-methyl-D-aspartate [NMDA] receptor antagonist), as well as new multiple-agent combinations, are likely to be available in the future.[73, 74, 75, 76, 77] Their role in the treatment of ocular hypertension will have to be studied as they become available for use.
Once a medication has been initiated, perform close follow-up care to assess its effect. Perform initial follow-up care 3-4 weeks after the beginning of therapy. Recheck IOP at the drug's peak and trough times to see if target IOP has been reached and is maintained throughout the day. Observe for signs of allergy to the medication (eg, hyperemia, skin rash, follicular reaction). Query patients about the presence of any systemic adverse effects and symptoms. Continue the treatment if a therapeutic trial has shown effective lowering of IOP without adverse effects.[78] Reevaluate 2-4 months later, depending on the clinical picture.
Consider a monocular therapeutic trial when first initiating the medical therapy, since IOP in the other eye can be used as a baseline control to gauge effect of a medication (particularly useful in patients with a widely fluctuating diurnal curve). A difference of more than 4 mm Hg between the 2 eyes after treatment is strongly suggestive of a clinical effect. However, some agents (especially beta-blockers) may have crossover effects on the other eye even with monocular treatment, and so clinical correlation must be kept in mind.[79] If monocular therapy is found to be effective, consider initiating binocular therapy.
Some medications (eg, latanoprost, brimonidine) may have an effect that plateaus at 6-8 weeks in certain patients; keep this in mind when scheduling further follow-up examinations.[80, 81] Other patients will be nonresponders to some therapies. If this occurs, discontinue the medication and initiate a new drug. While discontinuing or changing therapies, keep in mind that many drugs have a wash-out period of up to 2-4 weeks (especially beta-blockers), during which they may still have some IOP-lowering effect or residual systemic response.
If one medication is not adequate in reaching the target pressure, choose a second medication that has a different mechanism of action, so that the 2 drug therapies will have an additive effect. (Usually, no additive effect is seen if 2 medications from the same drug class are used.)
Administer a specific plan of pharmacotherapy only after the possible effects of the systemic medications (eg, beta-blockers, calcium channel blockers, ACE inhibitors) that a patient is taking have been taken into consideration.
See AAO's Ophthalmology monograph #13 for an in-depth description of particular drugs.
Carbonic anhydrase inhibitors (CAIs)
Class Summary
By slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport, it may inhibit carbonic anhydrase (CA) in the ciliary processes of the eye. This effect decreases aqueous humor secretion, reducing IOP. These agents typically have a weaker effect than beta-blockers. The more commonly used drug of this type for the treatment of ocular hypertension is in the combination medication Cosopt (which may be tried if single agent beta-blocker therapy has had suboptimal results).
Dorzolamide (Trusopt)
Reversible carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably, it slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Systemic absorption can affect carbonic anhydrase in the kidney, reducing hydrogen ion secretion at renal tubule, and increasing renal excretion of sodium, potassium bicarbonate, and water.
Less stinging on instillation, secondary to buffered pH.
Brinzolamide (Azopt)
Catalyzes reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. May use concomitantly with other topical ophthalmic drug products to lower IOP. If more than 1 topical ophthalmic drug is being used, administer drugs at least 10 min apart.
Acetazolamide (Diamox, Diamox Sequels)
Primarily used only for the treatment of refractory POAG and secondary glaucomas. Because of increased incidence of adverse effects, rarely indicated for treatment of ocular hypertension.
Timolol/dorzolamide (Cosopt)
Carbonic anhydrase inhibitor that may decrease aqueous humor secretion, causing a decrease in IOP. Presumably slows bicarbonate ion formation with subsequent reduction in sodium and fluid transport.
Timolol is a nonselective beta-adrenergic receptor blocker that decreases IOP by decreasing aqueous humor secretion and may slightly increase outflow facility.
Both agents administered together bid may result in additional IOP reduction compared with either component administered alone, but reduction is not as much as when dorzolamide tid and timolol bid are administered concomitantly.
Methazolamide (Neptazane)
Reduces aqueous humor formation by inhibiting enzyme carbonic anhydrase, which results in decreased IOP.
Adrenergic agonists
Class Summary
Of this class, the alpha2-selective agonist, brimonidine, is the most commonly used for the treatment of ocular hypertension.[80] Apraclonidine is an alpha2-selective agonist but 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, also can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, or cystoid macular edema (CME). Because these less selective agents are used infrequently in treating ocular hypertension, they are not discussed herein. Alpha2-adrenergic agonists work by decreasing aqueous production.
Brimonidine (Alphagan, Alphagan-P)
Relatively selective alpha2-adrenergic receptor agonist, decreases IOP by dual mechanisms. Reduces aqueous humor production and increases uveoscleral outflow. 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% reported.
The brand Alphagan-P contains the preservative Purite and has been shown to be much better tolerated than its counterpart Alphagan.
Apraclonidine 0.5%, 1% (Iopidine)
Potent alpha-adrenergic agent selective for alpha2-receptors with minimal cross-reactivity to alpha1-receptors. Suppresses aqueous production. Reduces elevated, as well as normal, intraocular pressure (IOP) whether accompanied by glaucoma or not. Apraclonidine is relatively selective alpha-adrenergic agonist that does not have significant local anesthetic activity. Has minimal cardiovascular effects.
Prostaglandin analogs
Class Summary
Newer class of medication that works by increasing uveoscleral outflow.
Unoprostone (Rescula), bimatoprost (Lumigan), travoprost (Travatan), and tafluprost (Zioptan) are examples of prostaglandins analogs that may help in IOP reduction.[82, 83, 84] All of these drugs are new alternatives in the armamentarium of medications to treat elevated IOP. Limited data are available on these drugs, but each has its own set of characteristics that may be useful in the clinical setting. Unoprostone has been shown to decrease pressure approximately 10-15% and may work partially through traditional outflow channels.[79] Bimatoprost may achieve a large reduction in pressure in many patients but has been known to cause significant conjunctival hyperemia. Travoprost has been purported to achieve lower IOPs, particularly in patients of African American descent, but these data are in doubt and the subject of controversy. It also may cause significant conjunctival hyperemia.[85]
Latanoprost (Xalatan 0.005%)
May decrease IOP by increasing outflow of aqueous humor. Patients should be informed on possible cosmetic effects to eye/eyelashes, especially if uniocular therapy is to be initiated.
Bimatoprost ophthalmic solution (Lumigan)
A prostamide analogue with ocular hypotensive activity. Mimics the IOP-lowering activity of prostamides via the prostamide pathway. Used to reduce IOP in open-angle glaucoma or ocular hypertension.
Travoprost ophthalmic solution (Travatan)
Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.
Unoprostone ophthalmic solution (Rescula)
Prostaglandin F2-alpha analog. Selective FP prostanoid receptor agonist believed to reduce IOP by increasing uveoscleral outflow. Used to treat open-angle glaucoma or ocular hypertension.
Tafluprost (Zioptan)
Tafluprost is a preservative-free, topical, ophthalmic prostaglandin analog 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.
Beta-adrenergic blockers
Class Summary
Decreases aqueous production, possibly by blocking adrenergic beta-receptors present in the ciliary body. Unfortunately, the nonselective medications in this class also interact with the beta-receptors in the heart and lungs, causing significant adverse effects.
Betaxolol ophthalmic (Betoptic-S)
Levobetaxolol (Betaxon) -- Selectively blocks beta1-adrenergic receptors with little or no effect on beta2-receptors. Reduces IOP by reducing production of aqueous humor. May have less pulmonary effects. IOP-lowering effect is slightly less than nonselective beta-blockers. May increase optic nerve perfusion and confer neuroprotection.
Carteolol 1% (Ocupress)
Has an intrinsic sympathomimetic activity (partial agonist activity), with possibly less cardiac and lipid profile adverse effects.
Timolol 0.25%, 0.5% (Timoptic, Timoptic XE, Blocadren, Istalol)
May reduce elevated and normal IOP, with or without glaucoma by reducing production of aqueous humor. Timolol gel-forming solution (Timoptic XE) usually is administered at night, unless used concurrently with latanoprost therapy.
The brands Timoptic XE and Istalol are both administered qd. However, Timoptic XE is a gel-forming solution, while Istalol is an aqueous solution.
Levobunolol 0.25%, 0.5% (Betagan, AKBeta)
Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production and possibly increasing outflow of aqueous humor.
Metipranolol 0.3% (OptiPranolol)
Beta-adrenergic blocker that has little or no intrinsic sympathomimetic effects and membrane-stabilizing activity. Has little local anesthetic activity. Reduces IOP by reducing production of aqueous humor.
Less-selective sympathomimetics
Class Summary
These less-selective adrenergic drugs increase outflow of aqueous humor through the trabecular meshwork and possibly through the uveoscleral outflow pathway, probably by a beta2-agonist action. Up to one third of patients will not respond to these drugs.
Less-selective adrenergics, such as epinephrine, dipivefrin, and memantine also can have a significantly higher allergic component and other substantial adverse effects, such as exacerbation of hypertension, angina, palpitations, or cystoid macular edema (CME). These less-selective agents are used infrequently. Memantine, increases outflow of aqueous humor through the trabecular meshwork and possibly through the uveoscleral outflow pathway, probably by a beta2-agonist action.[86, 76]
Epinephrine (Epifrin)
Lowers IOP by increasing outflow and reducing production of aqueous humor. Used as adjunct to miotic or beta-blocker therapy. Combination of miotic and sympathomimetic will have additive effects in lowering IOP.
Dipivefrin (AKPro, Propine)
Prodrug converted to epinephrine in eye by enzymatic hydrolysis. Appears to act by decreasing aqueous production and enhancing outflow facility. Has same therapeutic effect as epinephrine with fewer local and systemic adverse effects. May be used as an initial therapy or as an adjunct with other antiglaucoma agents for the control of IOP.
Memantine (Namenda, Axura)
Indicated for moderate-to-severe Alzheimer disease; currently still in Phase 3 trial for possible neuroprotective systemic treatment of glaucoma, although as of now, this is a non-FDA approved off-label use of the drug. N-methyl-D-aspartate (NMDA) antagonist. NMDA receptor stimulation in the CNS by glutamate (an excitatory amino acid) is hypothesized to contribute to Alzheimer symptoms, as well as apoptosis (programmed cell death) and neuronal degeneration.
Beta-blocker / Alpha Agonist Combination
Class Summary
Combination solution may further decrease aqueous humor secretion compared to each solution used as monotherapy, while improving compliance.[87]
Brimonidine/timolol (Combigan)
Selective alpha-2 adrenergic receptor agonist with a nonselective beta-adrenergic receptor inhibitor. Each of them decrease elevated IOP, whether or not associated with glaucoma.
Bathija R, Gupta N, Zangwill L, et al. Changing definition of glaucoma. J Glaucoma. Jun 1998;7(3):165-9. [Medline].
Eskridge JB. Ocular hypertension or early undetected glaucoma?. J Am Optom Assoc. Sep 1987;58(9):747-69. [Medline].
Johnson TD, Zimmerman TJ. Ocular hypertension, glaucoma suspect, preglaucoma, or glaucoma? Synopsis of views. Ann Ophthalmol. Nov 1986;18(11):313-4. [Medline].
Alward WL. The genetics of open-angle glaucoma: the story of GLC1A and myocilin. Eye. Jun 2000;14 (Pt 3B):429-36. [Medline].
Chandler PA, Grant WM. 'Ocular hypertension' vs open-angle glaucoma. Arch Ophthalmol. Apr 1977;95(4):585-6. [Medline].
Ritch R, Shields MB, Krupin T, eds. The Glaucomas. 2nd ed. 1992.
Shields MB. Textbook of Glaucoma. 3rd ed. Lippincott Williams & Wilkins; 1992.
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].
Grus F, Sun D. Immunological mechanisms in glaucoma. Semin Immunopathol. Apr 2008;30(2):121-6. [Medline].
Grus FH, Joachim SC, Wuenschig D, et al. Autoimmunity and glaucoma. J Glaucoma. Jan-Feb 2008;17(1):79-84. [Medline].
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].
Minckler DS. Histology of optic nerve damage in ocular hypertension and early glaucoma. Surv Ophthalmol. Apr 1989;33:401-2; discussion 409-11. [Medline].
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].
Linner E. The natural course of ocular pressure in ocular hypertension. Surv Ophthalmol. Nov-Dec 1980;25(3):136-8. [Medline].
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].
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].
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].
Colton T, Ederer F. The distribution of intraocular pressures in the general population. Surv Ophthalmol. Nov-Dec 1980;25(3):123-9. [Medline].
Chihara E. Assessment of true intraocular pressure: the gap between theory and practical data. Surv Ophthalmol. May-Jun 2008;53(3):203-18. [Medline].
Chihara E. Assessment of true intraocular pressure: the gap between theory and practical data. Surv Ophthalmol. May-Jun 2008;53(3):203-18. [Medline].
Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of refractory glaucoma. J Glaucoma. Apr-May 2008;17(3):238-47. [Medline].
Lin SC. Endoscopic and transscleral cyclophotocoagulation for the treatment of refractory glaucoma. J Glaucoma. Apr-May 2008;17(3):238-47. [Medline].
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].
Van Buskirk EM, Cioffi GA. Glaucomatous optic neuropathy. Am J Ophthalmol. Apr 15 1992;113(4):447-52. [Medline].
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].
American Academy of Ophthalmology. Preferred practice patterns: primary open angle glaucoma suspect and POAG. 1995-1996.
Cantor L. American Academy of Ophthalmology. In: Section 10: Glaucoma. In: Basic and Clinical Science Course. 1996.
Hodapp EA, Anderson DR. Treatment of early glaucoma. In: Focal Points. 1986;4(4).
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].
Spaeth GL. Early primary open-angle glaucoma: diagnosis and management. Preface. Int Ophthalmol Clin. Spring 1979;19(1):vii-ix. [Medline].
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].
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].
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].
Racette L, Sample PA. Short-wavelength automated perimetry. Ophthalmol Clin North Am. Jun 2003;16(2):227-36, vi-vii. [Medline].
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].
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].
Bengtsson B. A new rapid threshold algorithm for short-wavelength automated perimetry. Invest Ophthalmol Vis Sci. Mar 2003;44(3):1388-94. [Medline].
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].
ElMallah MK, Asrani SG. New ways to measure intraocular pressure. Curr Opin Ophthalmol. Mar 2008;19(2):122-6. [Medline].
ElMallah MK, Asrani SG. New ways to measure intraocular pressure. Curr Opin Ophthalmol. Mar 2008;19(2):122-6. [Medline].
Azuara-Blanco A, Burr JM. Assessment of glaucoma imaging technology. Ophthalmology. Jul 2008;115(7):1266-7; author reply 1267-8. [Medline].
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].
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].
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].
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].
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].
Brandt JD. Corneal thickness in glaucoma screening, diagnosis, and management. Curr Opin Ophthalmol. Apr 2004;15(2):85-9. [Medline].
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].
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].
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].
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].
Holz HA, Lim MC. Glaucoma lasers: a review of the newer techniques. Curr Opin Ophthalmol. Apr 2005;16(2):89-93. [Medline].
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].
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].
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].
Kass MA. When to treat ocular hypertension. Surv Ophthalmol. Dec 1983;28 Suppl:229-34. [Medline].
Phelps CD. The "no treatment" approach to ocular hypertension. Surv Ophthalmol. Nov-Dec 1980;25(3):175-82. [Medline].
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].
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].
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].
Migdal C. Glaucoma medical treatment: philosophy, principles and practice. Eye. Jun 2000;14 (Pt 3B):515-8. [Medline].
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].
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].
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].
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].
Filippopoulos T, Rhee DJ. Novel surgical procedures in glaucoma: advances in penetrating glaucoma surgery. Curr Opin Ophthalmol. Mar 2008;19(2):149-54. [Medline].
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].
Cioffi GA, Latina MA, Schwartz GF. Argon versus selective laser trabeculoplasty. J Glaucoma. Apr 2004;13(2):174-7. [Medline].
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].
Latina MA, Gulati V. Selective laser trabeculoplasty: stimulating the meshwork to mend its ways. Int Ophthalmol Clin. 2004;44(1):93-103. [Medline].
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].
Lacey J, Cate H, Broadway DC. Barriers to adherence with glaucoma medications: a qualitative research study. Eye. Apr 25 2008;[Medline].
Cheung W, Guo L, Cordeiro MF. Neuroprotection in glaucoma: drug-based approaches. Optom Vis Sci. Jun 2008;85(6):406-16. [Medline].
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].
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].
Lipton SA. Possible role for memantine in protecting retinal ganglion cells from glaucomatous damage. Surv Ophthalmol. Apr 2003;48 Suppl 1:S38-46. [Medline].
Naskar R, Dreyer EB. New horizons in neuroprotection. Surv Ophthalmol. May 2001;45 Suppl 3:S250-5; discussion S273-6. [Medline].
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].
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].
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].
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].
Brubaker RF. Mechanism of action of bimatoprost (Lumigan). Surv Ophthalmol. May 2001;45 Suppl 4:S347-51. [Medline].
Woodward DF, Krauss AH, Chen J, et al. The pharmacology of bimatoprost (Lumigan). Surv Ophthalmol. May 2001;45 Suppl 4:S337-45. [Medline].
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].
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].
Greenfield DS, Girkin C, Kwon YH. Memantine and progressive glaucoma. J Glaucoma. Feb 2005;14(1):84-6. [Medline].
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].
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].
Ashaye AO, Adeoye AO. Characteristics of patients who dropout from a glaucoma clinic. J Glaucoma. Apr-May 2008;17(3):227-32. [Medline].
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].
Allen RC, Netland PA, eds. American Academy of Ophthalmology. In: Glaucoma Medical Therapy: Principles and Management. 1999.
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].
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].
Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. May 2008;115(5):763-8. [Medline].
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].
Chauhan BC. Endothelin and its potential role in glaucoma. Can J Ophthalmol. Jun 2008;43(3):356-60. [Medline].
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].
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].
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].
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].
Jacobi S, Dubielzig RR. Feline primary open angle glaucoma. Vet Ophthalmol. May-Jun 2008;11(3):162-5. [Medline].
Jamil AL, Mills RP. Glaucoma tube or trabeculectomy? That is the question. Am J Ophthalmol. Jan 2007;143(1):141-2. [Medline].
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].
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].
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].
Li HK, Tang RA, Oschner K, et al. Telemedicine screening of glaucoma. Telemed J. Fall 1999;5(3):283-90. [Medline].
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].
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].
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].
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].
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].
Sunaric-Megevand G, Leuenberger PM. Results of viscocanalostomy for primary open-angle glaucoma. Am J Ophthalmol. Aug 2001;132(2):221-8. [Medline].
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].
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].
Yücel YH, Gupta N. Paying attention to the cerebrovascular system in glaucoma. Can J Ophthalmol. Jun 2008;43(3):342-6. [Medline].
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].
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