Primary Open-Angle Glaucoma Treatment & Management

  • Author: Jerald A Bell, MD; Chief Editor: Hampton Roy Sr, MD   more...
 
Updated: Jan 11, 2012
 

Medical Care

Major drug classes for medical treatment of POAG include the following: alpha-agonists, beta-blockers, carbonic anhydrase inhibitors, miotic agents, and prostaglandin analogs.

Basic science research continues on other possible pharmacologic sites of action, including nitric oxide and cannabinoid pathways, although no topical product has been evaluated in US FDA trials of yet.

Medical marijuana is not indicated for glaucoma treatment, as marijuana lowers IOP minimally and its duration of action is very short. In the future, topical derivatives that affect cannabinoid M receptors governing aqueous dynamics may be effective, but this is still under early investigation.

The other drug classes mentioned above have much more documented duration of action and efficacy without the systemic cannabinoid adverse effects. Furthermore, other options to treat ocular pain from end-stage glaucoma have arisen (eg, trans-scleral or endoscopic cyclophotocoagulation, absolute alcohol [ethanol] or chlorpromazine retrobulbar injections), which directly and more effectively alleviate the problem than in the past when marijuana was used for eye pain from end-stage glaucoma.

Legal justification of glaucoma as an indication for systemic medical marijuana use is scientifically and medically improper, as well as unethical; education of the public and legislators is needed on this subject.

Some physicians incorrectly treat all elevated IOPs over 21 mm Hg with the above topical medications. Other physicians do not treat unless evidence of optic nerve damage exists, although nerve fiber layer loss of up to 40% may occur before visual field defects occur, so do not treat based on visual field testing alone. Most physicians select and treat those patients thought to be at greatest risk for POAG damage and/or progression (most common approach). See History for a list of risk factors for glaucomatous field loss.

In any case, the goal of treatment is reduction of the pressure before it causes progressive loss of vision. Considering the high average monthly cost of glaucoma medication, along with the possible risks of adverse effects or toxic reactions from drugs, inconvenience of use, and incidence of noncompliance, a strong reason not to treat indiscriminately exists.

Several questions should be asked when considering treatment, to include the following: Is the elevated pressure significant? Will this patient develop visual loss if left untreated? Is the treatment worth the risk of adverse effects of the medications?

One should consider treatment more strongly if the patient reliability or the consequences of missing field loss is an issue (eg, poor reliability on visual field examination, 1-eyed patient, poor availability for follow-up care, younger patient, patient whose optic nerve is difficult to visualize, history of vascular occlusion).

Treatment is highly recommended if signs of damage consistent with glaucomatous optic neuropathy (eg, disc hemorrhage; visible nerve fiber layer defects; notching or vertical ovalization of the cup; asymmetric cupping, especially if >0.7) are observed.

Progressive cupping, even in the absence of visual field loss, can be glaucoma and should be treated as such, although systemic and neurologic workup/correlation for other disorders, including possible neuroimaging studies, should be considered, particularly if there are other nonophthalmologic symptoms. Otherwise, it depends on the assessment of risk factors and benefit of therapy to the patient, as to whether therapy should be initiated.

Discussion with the patient about the pros and cons of treatment versus observation should be completed. Individualization of therapy is the key; an ideal pressure in one patient may cause glaucomatous damage in another patient. Risk factors, systemic conditions, life expectancy of the patient, quality of life issues, and the patient's desire for therapy should be weighed when considering treatment.

Due to the high risk of optic nerve damage, most ophthalmologists treat if pressures are consistently above 28-30 mm Hg. If treatment is based on a high IOP only, then it should be ensured that the risks of treatment do not exceed the risk of the disease. Other reasons to treat include such symptoms as halos, blurred vision, or pain, or recent elevation of IOP, with continuing elevation on successive visits.

Initiation of a monocular trial (see Medication) may be useful in helping to decide whether or not to treat (ie, if the medication is effective in achieving good pressure reduction without adverse effects, which may argue in favor of treatment, instead of just observation).

Considering all of the above, no consensus exists on what is the appropriate medical treatment for preventing or delaying the damage due to POAG when a patient has only elevated IOP and no other signs of POAG. To date, no one has been able to define conclusively which subgroups will develop damage if left untreated, as opposed to those who will not sustain damage even if not treated.

The question of medical therapy versus observation in patients with solely elevated IOP is being addressed in the OHTS, an ongoing multicenter randomized clinical trial.

  • The OHTS is a multicenter, prospective, randomized, controlled, clinical trial studying over 1600 subjects to evaluate the safety and efficacy of medical treatment in preventing or delaying onset of visual field loss and/or optic nerve damage in patients with OHT who are at moderate risk for developing POAG.
  • Their medical therapy goal for the treated group is stepped therapy to reduce IOP by at least 20% from the average baseline IOP with its treated absolute value of 24 mm Hg or less.
  • So far, their results show a 10% risk over 5 years of developing glaucoma in those patients with baseline IOP of 24-31 mm Hg. This risk was reduced to 5% with medical therapy.
  • The OHTS has also revealed the importance of pachymetry as a diagnostic tool as well as in the workup.

Several sources agree on this initial goal of 20-25% reduction, while some specialists feel that more absolute numbers of less than 15 should be the goal of treatment. Keep in mind that the IOP goal must be set independently for each patient, depending on the risk factors, as an IOP level for one person with minimal risk factors may be far too high for a patient with multiple risk factors for sustaining glaucomatous damage.

Other regimens have been suggested, as follows: for minimal risk factors, consider lowering IOP by 20-30%; if moderate number of risk factors are present, lower by 30-40%; and in cases of numerous risk factors with markedly elevated pressures, reduction in the 40-60% range may need to be achieved to prevent neuronal loss.

If the patient is older than 65 years, consider treatment to keep IOP 25 mm Hg or less, secondary to 3% risk of vascular occlusion in OHT patients.

In any case, the target IOP should be reevaluated periodically, and regular review of IOP trends should be performed to determine whether the patient is consistently maintaining that goal.

Below is a suggested time guideline for therapy and follow-up based on initial IOP level. Adjust frequency of follow-up testing as needed based on the number of risk factors and clinical picture.

  • IOP 28 mm Hg or greater: Patients should be treated (see Medication), with follow-up care in 1 month to assess if treatment is effective and no adverse effects are present. If the goal is reached, then follow-up care should be performed every 3-4 months.
  • IOP 26-27 mm Hg: Follow-up care should be performed in 2-3 weeks to recheck pressure. If IOP is still within 3 mm Hg of the initial reading, then follow-up should be continued every 3-4 months with visual field and dilated optic nerve evaluation at least once a year. If IOP is lower, then a longer time should be considered between the pressure checks, making sure to recheck IOP at different times of the day on subsequent appointments.
  • IOP 22-25 mm Hg: Follow-up care should be performed 2-3 months later for recheck of IOP at different times of the day (ie, 8 am, 11 am, 1 pm, 4 pm). If it is still within 3 mm Hg of the initial reading at the second visit, then follow-up at 6 months with Humphrey visual field testing and dilated optic nerve evaluation, repeating it at least yearly.

Other caveats concerning follow-up care are as follows:

  • If a new visual field defect becomes apparent on testing, confirmation with repeat (possibly multiple) examinations during future office visits should be performed, before using it as a basis for the treatment of presumed progression of POAG.
  • Gonioscopy should be performed at least once every 1-2 years if a significant increase in IOP occurs, or if miotic therapy is instituted.
  • Optic disc photos should be repeated after the initial examination if a change in disc appearance is noted (or every 1-2 years if available).
    • Technologic and financial barriers, as well as increasing lack of trained ophthalmic staff, are making optic disc photos more difficult to obtain in many practices.
    • Whether nerve fiber layer imaging technologies (instead of recurring, serial optic disc photos) are sufficient for mainstream nontertiary ophthalmology practices is still under debate.

Retinal tomography, ocular coherence tomography, and/or laser polarimetry should be measured at baseline and then every 1-2 years. Results should be correlated with visual field results, IOP measurements, and examination findings.

Next

Surgical Care

Surgery is indicated when glaucomatous optic neuropathy worsens (or is expected to worsen) at any given level of IOP and the patient is on maximum tolerated medical therapy (MTMT).

MTMT varies considerably between individuals, and it may consist of medicines from 1 or several classes (including a beta-adrenergic antagonist, a prostaglandin agent, an alpha-agonist, and a topical carbonic anhydrase inhibitor). Some patients are observed to progress simply because compliance with the medical regimen becomes too difficult because of the following: high drug costs, inability to remember the schedule of multiple medications, inability to instill them in the eyes properly secondary to arthritis or other incapacitation (especially common among elderly patients or those with other chronic systemic conditions), or intolerable ocular and systemic adverse effects.

A brief mention of surgical options is listed below. Detailed information on surgical procedures, indications, and postoperative care is beyond the scope of this chapter.

Argon laser trabeculoplasty

  • Argon laser trabeculoplasty (ALT) uses a laser beam focused through a goniolens to treat at the border between anterior and posterior trabecular meshwork. A full treatment consists of 100 spots placed over the entire 360 degrees of the trabecular meshwork. This may be divided between 2 sessions consisting of 50 spots over 180 degrees.
  • Aqueous outflow improves after the procedure.
  • The specific mechanism of this improved outflow is unknown, but one hypothesis is up-regulation of trabecular endothelial cells.
  • IOP reduction obtained is usually in the 7-10 mm Hg range, and it may last up to 3-5 years following ALT.
  • A study by Heijl et al studied patients with low IOP levels before ALT. The study found that IOP before ALT significantly influenced the IOP reduction produced by ALT, in that a much larger decrease was observed in eyes with higher IOP before ALT.[14]
  • Unfortunately, the decrease in IOP is not usually permanent. Approximately 10% of treated patients will return to pretreatment IOP for each year following treatment.
  • Complications include a brief, but potentially significant, increase in IOP after the procedure (therefore, alpha-agonists often are used either preoperatively or postoperatively for prophylaxis of this occurrence); transient iritis or corneal opacities; peripheral anterior synechiae; and hyphema.
  • ALT usually is pursued after MTMT has been reached, but it may be performed sooner in the treatment algorithm if pseudoexfoliation or pigmentary glaucoma is present, or if the patient is of black ethnicity, because laser therapy may be most effective in these individuals.

Selective laser trabeculoplasty

  • Selective laser trabeculoplasty (SLT) uses a Q-switched 532 Nd:YAG laser to selectively target pigmented cells of the trabecular meshwork in a nonthermal manner, increasing fluid outflow and thereby lowering IOP.
  • The 3-nanosecond high-energy specific wavelength of light used induces the same cell replacement mechanism as traditional ALT but without the destructive burning and obliteration of structural support tissue in the meshwork. The short pulse of the laser does not allow time for heat to spread to other cells. SLT delivers just enough energy to the trabecular meshwork to target specific melanin-rich cells, without incurring collateral thermal damage and scarring to adjacent nonpigmented trabecular meshwork cells and underlying trabecular beams. When treated with SLT, a primarily biologic response is induced in the trabecular meshwork that involves the release of cytokines that trigger macrophage recruitment as well as other changes leading to IOP reduction.
  • The laser beam bypasses surrounding tissue leaving it undamaged by light. Unlike ALT, SLT can be repeated several times. Whereas patients treated with ALT can receive only 2 treatments in their lifetime, patients treated with SLT can receive 2 treatments a year.
  • SLT requires a specially designed laser, as follows:
    • A short pulse to allow for thermal relaxation
    • Precise wavelength for optimal melanin absorption
    • Sufficient energy to heat melanin to the point that it releases cytokines
    • Sufficient spot size to ensure full coverage at the trabecular meshwork

Trabeculectomy

  • Trabeculectomy surgery usually is performed after MTMT and ALT have failed to control IOP adequately. If IOP is so high that ALT and SLT are likely to be ineffective in reaching target IOP, then proceeding from MTMT to penetrating surgery may be indicated.
  • A superficial flap of sclera is dissected anteriorly to the trabecular meshwork, and a section of trabecular meshwork is removed underneath the flap.
  • This alternate outflow pathway is created to increase passage of aqueous from the anterior chamber to the subconjunctival space, creating a filtering bleb and, thereby, lowering IOP.
  • Either releasable sutures or laser suture-lysis may be used to control aqueous drainage and corresponding IOP postoperative. Alternatively, to maximize surgical success, antimetabolites (eg, 5-fluorouracil, mitomycin C) may be applied during or after surgery to decrease fibroblast proliferation and scar formation.
  • Risks and complications of filtering surgery include the following: hypotony, blebitis/endophthalmitis, hyphema, suprachoroidal hemorrhage or effusions, encapsulation of the bleb with resultant transient IOP elevation, loss of 1 or more lines of visual acuity, and increased risk of cataract formation.
  • With the risk of severe complications from trabeculectomy and the need for frequent postoperative follow-up care (ie, usually weekly for 2 months, initially), some patients with transportation, financial, or long-distance issues concerning postoperative follow-up care may be better served by tube shunt surgery instead. See the Tube versus Trabeculectomy Study below.
  • Vision loss may be a serious complication after trabeculectomy, with severe and ongoing unexplained loss ("snuff-out") experienced by as many as 2% of patients. Attendant risk factors such as split fixation on visual fields prior to surgery, preoperative number of quadrants with split fixation, and postoperative choroidal effusions with eventual resolution are possible.[15]

Drainage implant (ie, seton/tube/shunt) surgery

  • Generally, this procedure is performed after multiple attempts at successful trabeculectomy have failed.
  • A tube is placed in the anterior chamber to shunt aqueous to an equatorial reservoir, and then posteriorly to be absorbed in the subconjunctival space.
  • Types of implants include Molteno, Baerveldt, Ahmed, and Krupin.
    • Most shunts function by allowing passive drainage of aqueous from the anterior chamber.
    • The Molteno implant consists of a silicone drainage tube, which is connected to 1 or 2 acrylic plates that are sutured to the sclera.
    • The Baerveldt implant is available with larger plates with increased reservoir size. The seton (tube) connected to the reservoir usually is tied off with an absorbable suture, allowing flow to initiate 4-6 weeks postoperative once some conjunctival wound remodeling has taken place, thereby reducing the risk of immediate postoperative hypotony.
    • The Ahmed and Krupin implants have 1-way valves, which are designed to maintain pressure above 8 mm Hg. These implants may reduce the risk of hypotony, a complication of nonvalved shunts in the early postoperative period.
  • Because of less numerous postoperative visits, tube shunts may be indicated as primary surgery when patients are unable to come as frequently for follow-up care (because of transportation, financial, or long-distance issues). This can be a particular concern in rural areas that cover large distances.
  • A valved shunt may also be indicated as primary surgery if a patient has a strenuous job or other activities that require strenuous exertion. Severe exertion may cause a significant Valsalva maneuver, significantly increasing venous pressure postoperatively, which could result in a delayed suprachoroidal hemorrhage and possible severe loss of vision.
  • The Tube versus Trabeculectomy Study has been undertaken to see if glaucoma tube shunt surgery may actually be a viable first-line alternative to (or even surpass) trabeculectomy surgery. Some training programs have removed trabeculectomy training from their residency program curricula, with only fellows performing trabeculectomy (not a general trend).
  • One-year data have shown nonvalved tube shunt surgery was more likely to maintain IOP control and to avoid persistent hypotony or reoperation for glaucoma than trabeculectomy at 1 year, although both procedures produced similar IOP reduction.
  • Less supplemental medical therapy has been needed so far in the trabeculectomy group.
  • The incidence of postoperative complications at 1 year was higher in the trabeculectomy group.
  • Serious complications resulting in reoperation and/or vision loss occurred with similar frequency in both groups at 1 year.

Ciliary body ablation

  • Postoperative pain and inflammation are common complaints. Loss of 1 or more lines of visual acuity has been reported. Phthisis is a concern after this procedure, although it has not been reported as of yet after the diode laser method of cycloablation.
  • This procedure is indicated as a last resort for patients who have failed medical management and other surgeries or for those patients who have limited visual potential (often 20/200 or less).
  • By destroying a portion of the nonpigmented ciliary epithelium, aqueous humor production is limited.
  • The ciliary body epithelium can be destroyed by cyclocryotherapy, diathermy, ultrasound, transscleral Nd:YAG or diode laser (known as cyclophotocoagulation), or a newer endoscopic laser (EndoOptiks, Inc).[16]

Several of the newer surgical procedures are promising, but many ideas have been tried before and few have stood the test of time. Generally, the less complications, the less effective in lowering IOP. There is the possibility that visual loss can be better prevented, with fewer complications, and treatment can be tailored to the individual patient. If simple, safe procedures become available, surgery could be performed earlier in the disease process and adherence to medications could become less problematic.

The ideal glaucoma procedure would use the healthy portions of the outflow system and bypass the diseased portions; control IOP without infection and other risks of a thin-walled bleb; reduce the risk of hypotony during the perioperative period, with less postoperative care management and complications, as compared with trabeculectomy and setons; and provide adequate IOP control for the life of the patient.

Many innovative glaucoma surgical techniques and devices are on the horizon. Interest in this new frontier is because of the lack of an existing, ideal glaucoma procedure despite decades of research. Many devices are not yet approved by the FDA for use in the United States.

Newer techniques

  • Deep sclerectomy/viscocanalostomy/with or without collagen implant – This is probably not as effective as trabeculectomy and is technically more difficult, but it is associated with less complications.
  • 360-degree suture canaloplasty (iScience) – This is a useful alternative in infants (with congenital glaucoma or juvenile glaucoma) to trabeculotomy. In adults, suture under tension left in the Schlemm canal to further open the trabecular meshwork (similar mechanism to miotics).

New devices

  • ExPress shunt (Optonol)
    • Erosion problems if used without scleral flap
    • Now mainly used underneath trabeculectomy flap to better regulate flow through sclerostomy
    • Easy to learn, appears effective, and otherwise has low complication rate
    • Awaiting long-term trials
    • May be especially useful for the ophthalmologist who only occasionally does glaucoma surgery
  • iStent (Glaukos)
    • Shunt device from the anterior chamber into the Schlemm canal
    • Internal placement approach
    • May need multiple devices placed
    • Still undergoing continuing research
  • Eyepass
    • Shunt device from the anterior chamber into the Schlemm canal
    • External placement approach
    • Inactive technology
    • Poor long-term IOP control
  • Solx gold suprachoroidal space microshunt (OccuLogix)
    • Shunts fluid from the anterior chamber into the suprachoroidal space via gold microchannels
    • External placement approach
    • Possibly titratable effect with titanium-sapphire laser to modify microchannel size
    • Needs further published series data
  • Trabectome (NeoMedix)
    • FDA approved
    • Ablates all of the trabecular meshwork for 90 degrees to 180 degrees via electrocautery and aspiration of the internal wall of the Schlemm canal
    • Similar idea to goniotomy but prevents rescarring of the Schlemm canal edges, as all tissue is removed
    • May have a place between trabeculoplasty and anterior filtering operations
    • Safer than trabeculectomy or tube shunt but may be less effective
    • Needs more long-term data on complication rate and persistence of effect
Previous
Next

Consultations

Neuro-ophthalmology consultation may have a role in those patients who are experiencing progressive visual loss that does not appear to follow a typical glaucomatous pattern or if there are systemic symptoms or complaints.

Previous
Next

Activity

Some studies show that a moderate amount of exercise can decrease IOP in both POAG patients and normal individuals. Whether it results in actual long-term IOP control and prevention of visual loss has yet to be determined.

Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

Neil T Choplin, MD  Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences

Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Association for Research in Vision and Ophthalmology, and California Medical Association

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.

Additional Contributors

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

References

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

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

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

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

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

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

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

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

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

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

  11. Annette H, Kristina L, Bernd S, Mark-Oliver F, Wolfgang W. Effect of central corneal thickness and corneal hysteresis on tonometry as measured by dynamic contour tonometry, ocular response analyzer, and Goldmann tonometry in glaucomatous eyes. J Glaucoma. Aug 2008;17(5):361-5. [Medline].

  12. 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].

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

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

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

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

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

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

  19. 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].

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

  21. 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].

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

  23. 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].

  24. 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].

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

  26. 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].

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

  28. 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].

  29. 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].

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

  31. 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].

  32. 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].

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

  34. 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].

  35. 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].

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

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

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

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

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

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

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

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

  44. 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].

  45. 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].

  46. 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].

  47. 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].

  48. 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].

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

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

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

  52. Gedde SJ, Schiffman JC, Feuer WJ, Herndon LW, Brandt JD, Budenz DL. Treatment outcomes in the tube versus trabeculectomy study after one year of follow-up. Am J Ophthalmol. Jan 2007;143(1):9-22. [Medline].

  53. 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].

  54. 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].

  55. 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].

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

  57. 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].

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

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

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

  61. 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].

  62. 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].

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

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

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

  66. 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].

  67. 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].

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

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

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

  71. 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].

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

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

  74. 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].

  75. 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].

  76. 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].

  77. 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].

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

  79. 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].

  80. 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].

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

  82. 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].

  83. 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].

  84. 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].

  85. 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].

  86. 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].

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

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

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

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

  91. Lin SC, Singh K, Jampel HD, Hodapp EA, Smith SD, Francis BA, et al. Optic nerve head and retinal nerve fiber layer analysis: a report by the American Academy of Ophthalmology. Ophthalmology. Oct 2007;114(10):1937-49. [Medline].

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

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

  94. 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].

  95. 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].

  96. 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].

  97. 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].

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

  99. 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].

  100. 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].

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

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

  103. 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].

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

  105. 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].

  106. 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].

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

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

  109. 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].

  110. 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].

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

  112. 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].

  113. 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].

  114. 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].

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

  116. 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 Suppl 1:S39-47. [Medline].

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

  118. 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].

  119. 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].

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

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

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

  123. 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. May 25 2008;[Medline].

  124. 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].

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

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

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

  128. 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].

  129. 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].

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

  131. 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].

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

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