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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]


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.


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.


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.


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.


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.


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.

Contributor Information and Disclosures

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.


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

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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).
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