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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
|Classification and external resources|
Glaucoma refers to a group of diseases that affect the optic nerve and involves a loss of retinal ganglion cells in a characteristic pattern. It is a type of optic neuropathy. Raised intraocular pressure is a significant risk factor for developing glaucoma (above Template:Convert/mmHgTemplate:Convert/test/Aon). One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressure for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.
Glaucoma can be divided roughly into two main categories, "open angle" and "closed angle" glaucoma. Angle closure can appear suddenly and is often painful. Visual loss can progress quickly but the discomfort often leads patients to seek medical attention before permanent damage occurs. Open angle, chronic glaucoma tends to progress more slowly and the patient may not notice that they have lost vision until the disease has progressed significantly.
Glaucoma has been nicknamed the "sneak thief of sight" because the loss of vision normally occurs gradually over a long period of time and is often only recognized when the disease is quite advanced. Once lost, this damaged visual field can never be recovered. Worldwide, it is the second leading cause of blindness. Glaucoma affects one in two hundred people aged fifty and younger, and one in ten over the age of eighty. If the condition is detected early enough it is possible to arrest the development or slow the progression with medical and surgical means.
There are rarely any symptoms in the early stages of the disease so regular eye checks by qualified professionals are important. Ophthalmologists and optometrists will diagnose glaucoma on the basis of intraocular pressure, visual field results and optic nerve head appearance.
Patients will sometimes notice patchy loss of peripheral vision or reduced contrast sensitivity and these people may benefit from a review by an eye specialist.
Symptoms of angle closure glaucoma can include pain in or behind the eye ball, headache with nausea and vomiting and visual disturbances with halos around lights but sometimes there are no symptoms.
The major risk factor for most glaucomas and focus of treatment is increased intraocular pressure. Intraocular pressure is a function of production of liquid aqueous humor by the ciliary processes of the eye and its drainage through the trabecular meshwork. Aqueous humor flows from the ciliary processes into the posterior chamber, bounded posteriorly by the lens and the zonules of Zinn and anteriorly by the iris. It then flows through the pupil of the iris into the anterior chamber, bounded posteriorly by the iris and anteriorly by the cornea. From here the trabecular meshwork drains aqueous humor via Schlemm's canal into scleral plexuses and general blood circulation. In open angle glaucoma there is reduced flow through the trabecular meshwork; in angle closure glaucoma, the iris is pushed forward against the trabecular meshwork, blocking fluid from escaping.
The inconsistent relationship of glaucomatous optic neuropathy with ocular hypertension has provoked hypotheses and studies on anatomic structure, eye development, nerve compression trauma, optic nerve blood flow, excitatory neurotransmitter, trophic factor, retinal ganglion cell/axon degeneration, glial support cell, immune, and aging mechanisms of neuron loss.
The major types of glaucoma are discussed below.
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Please improve this article if you can. (April 2008)
Ocular hypertension (increased pressure within the eye) is the largest risk factor in most glaucomas, but in some populations only 50% of patients with primary open angle glaucoma actually have elevated ocular pressure. 
Those of African descent are three times more likely to develop primary open angle glaucoma. People who are older, have thinner corneal thickness, and myopia also are at higher risk for primary open angle glaucoma. People with a family history of glaucoma have about a six percent chance of developing glaucoma.
Many Asian groups, such as Mongolian, Chinese, Japanese, and Vietnamese, are prone to developing angle closure glaucoma due to their shallower anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Inuit also have a twenty to forty times higher risk than Caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers.
Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).
Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes at several loci . Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.
There is increasing evidence that ocular blood flow is involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.
A number of studies also suggest a possible correlation between hypertension and the development of glaucoma. In normal tension glaucoma, nocturnal hypotension may play a significant role.
There is no clear evidence that vitamin deficiencies cause glaucoma in humans. It follows then that oral vitamin supplementation is probably not useful in glaucoma treatment. 
Various rare congenital/genetic eye malformations are associated with glaucoma. Occasionally, failure of the normal third trimester gestational atrophy of the hyaloid canal and the tunica vasculosa lentis is associated with other anomalies. Angle closure induced ocular hypertension and glaucomatous optic neuropathy may also occur with these anomalies.  and modelled in mice .
Screening for glaucoma is usually performed as part of a standard eye examination performed by ophthalmologists and optometrists. Testing for glaucoma should include measurements of the intraocular pressure via tonometry, changes in size or shape of the eye, anterior chamber angle examination or gonioscopy, and examination of the optic nerve to look for any visible damage to it, or change in the cup-to-disc ratio and also rim appearance and vascular change. A formal visual field test should be performed. The retinal nerve fiber layer can be assessed with imaging techniques such as optical coherence tomography (OCT), scanning laser polarimetry (GDx), and/or scanning laser ophthalmoscopy also known as Heidelberg Retina Tomography (HRT3). Owing to the sensitivity of all methods of tonometry to corneal thickness, methods such as Goldmann tonometry should be augmented with pachymetry to measure central cornea thickness (CCT). A thicker-than-average cornea can result in a pressure reading higher than the 'true' pressure, whereas a thinner-than-average cornea can produce a pressure reading lower than the 'true' pressure. Because pressure measurement error can be caused by more than just CCT (i.e, corneal hydration, elastic properties, etc.), it is impossible to 'adjust' pressure measurements based only on CCT measurements. The Frequency Doubling Illusion can also be used to detect glaucoma with the use of a Frequency Doubling Technology (FDT) perimeter. Examination for glaucoma also could be assessed with more attention given to sex, race, history of drugs use, refraction, inheritance and family history.
The modern goals of glaucoma management are to avoid glaucomatous damage, preserve visual field and total quality of life for patients with minimal side effects. This requires appropriate diagnostic techniques and follow up examinations and judicious selection of treatments for the individual patient. Although intraocular pressure is only one of the major risk factors for glaucoma, lowering it via various pharmaceuticals and/or surgical techniques is currently the mainstay of glaucoma treatment. Vascular flow and neurodegenerative theories of glaucomatous optic neuropathy have prompted studies on various neuroprotective therapeutic strategies including nutritional compounds some of which may be regarded by clinicians as safe for use now, while others are on trial.
Intraocular pressure can be lowered with medication, usually eye drops. There are several different classes of medications to treat glaucoma with several different medications in each class.
Each of these medicines may have local and systemic side effects. Adherence to medication protocol can be confusing and expensive; if side effects occur, the patient must be willing either to tolerate these, or to communicate with the treating physician to improve the drug regimen. Initially, glaucoma drops may reasonably be started in either one or in both eyes.
Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.
Commonly used medicationsEdit
- Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow
- Topical beta-adrenergic receptor antagonists such as timolol, levobunolol (Betagan), and betaxolol decrease aqueous humor production by the ciliary body.
- Alpha2-adrenergic agonists such as brimonidine (Alphagan) work by a dual mechanism, decreasing aqueous production and increasing trabecular outflow.
- Less-selective sympathomimetics like epinephrine and dipivefrin (Propine) increase outflow of aqueous humor through trabecular meshwork and possibly through uveoscleral outflow pathway, probably by a beta2-agonist action.
- Miotic agents (parasympathomimetics) like pilocarpine work by contraction of the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of the aqueous humour.
- Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.
- Physostigmine is also used to treat glaucoma and delayed gastric emptying.
Compounds in researchEdit
Natural compounds of research interest in glaucoma prevention or treatment include: fish oil and omega 3 fatty acids, bilberries, vitamin E, cannabinoids, carnitine, coenzyme Q10, curcurmin, Salvia miltiorrhiza, dark chocolate, erythropoietin, folic acid, Ginkgo biloba, Ginseng, L-glutathione, grape seed extract, green tea, magnesium, melatonin, methylcobalamin, N-acetyl-L cysteine, pycnogenols, resveratrol, quercetin and salt.  Magnesium, ginkgo, salt and fludrocortisone, are already used by some physicians.
Studies in the 1970s showed that marijuana, when smoked, effectively lowers intraocular pressure. In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated that some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye. Many of these studies demonstrated that marijuana — or any of its components — could safely and effectively lower intraocular pressure more than a variety of drugs then on the market.
In 2003 the American Academy of Ophthalmology released a position statement which said that "studies demonstrated that some derivatives of marijuana did result in lowering of IOP when administered orally, intravenously, or by smoking, but not when topically applied to the eye. The duration of the pressure-lowering effect is reported to be in the range of 3 to 4 hours".
However, the position paper qualified that by stating that marijuana was not more effective than prescription medications, stating that "no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of marijuana use to treat glaucoma compared with the wide variety of pharmaceutical agents now available."
The first patient in the United States federal government's Compassionate Investigational New Drug program, Robert Randall, was afflicted with glaucoma and had successfully fought charges of marijuana cultivation because it was deemed a medical necessity (U.S. v. Randall) in 1976.
- Main article: Glaucoma surgery
Both laser and conventional surgeries are performed to treat glaucoma.
Surgery is the primary therapy for those with congenital glaucoma.
Generally, these operations are a temporary solution, as there is not yet a cure for glaucoma.
Canaloplasty is a nonpenetrating procedure utilizing microcatheter technology. To perform a canaloplasty, an incision is made into the eye to gain access to Schlemm's canal in a similar fashion to a viscocanalostomy. A microcatheter will circumnavigate the canal around the iris, enlarging the main drainage channel and its smaller collector channels through the injection of a sterile, gel-like material called viscoelastic. The catheter is then removed and a suture is placed within the canal and tightened. By opening the canal, the pressure inside the eye may be relieved, although the reason is unclear since the canal (of Schlemm) does not have any significant fluid resistance in glaucoma or healthy eyes. Long-term results are not available.
Laser trabeculoplasty may be used to treat open angle glaucoma. It is a temporary solution, not a cure. A 50 μm argon laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty utilizes a thermal argon laser. The procedure is called Argon Laser Trabeculoplasty or ALT. A newer type of laser trabeculoplasty exists that uses a "cold" (non-thermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure which uses a 532 nm frequency-doubled, Q-switched Nd:YAG laser which selectively targets melanin pigment in the trabecular meshwork cells, called Selective Laser Trabeculoplasty or SLT. Studies show that SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.
Nd:YAG Laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small full-thickness opening in the iris. This opening equalizes the pressure between the front and back of the iris correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork.
Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.
The most common conventional surgery performed for glaucoma is the trabeculectomy. Here, a partial thickness flap is made in the scleral wall of the eye, and a window opening made under the flap to remove a portion of the trabecular meshwork. The scleral flap is then sutured loosely back in place. This allows fluid to flow out of the eye through this opening, resulting in lowered intraocular pressure and the formation of a bleb or fluid bubble on the surface of the eye. Scarring can occur around or over the flap opening, causing it to become less effective or lose effectiveness altogether. One person can have multiple surgical procedures of the same or different types.
Glaucoma drainage implantsEdit
There are also several different glaucoma drainage implants. These include the original Molteno implant (1966), the Baerveldt tube shunt, or the valved implants, such as the Ahmed glaucoma valve implant or the ExPress Mini Shunt and the later generation pressure ridge Molteno implants. These are indicated for glaucoma patients not responding to maximal medical therapy, with previous failed guarded filtering surgery (trabeculectomy). The flow tube is inserted into the anterior chamber of the eye and the plate is implanted underneath the conjunctiva to allow flow of aqueous fluid out of the eye into a chamber called a bleb.
- The first-generation Molteno and other non-valved implants sometimes require the ligation of the tube until the bleb formed is mildly fibrosed and water-tight This is done to reduce postoperative hypotony—sudden drops in postoperative intraocular pressure (IOP).
- Valved implants such as the Ahmed glaucoma valve attempt to control postoperative hypotony by using a mechanical valve.
The ongoing scarring over the conjunctival dissipation segment of the shunt may become too thick for the aqueous humor to filter through. This may require preventive measures using anti-fibrotic medication like 5-fluorouracil (5-FU) or mitomycin-C (during the procedure), or additional surgery. And for Glaucomatous painful Blind Eye and some cases of Glaucoma, Cyclocryotherapy for ciliary body ablation could be considered to be performed. 
TR BioSurgical has commercialized a new implant specifically for veterinary medicine, called TR-ClarifEYE. The implant consists of a new biomaterial, the STAR BioMaterial, which consists of silicone with a very precise homogenous pore size, a property which reduces fibrosis and improves tissue integration. The implant contains no valves and is placed completely within the eye without sutures. To date, it has demonstrated long term success (> 1yr) in a pilot study in medically refractory dogs with advanced glaucoma 
Laser assisted non penetrating deep sclerectomyEdit
The most common surgical approach currently used for the treatment of glaucoma, is trabeculectomy, in which the sclera is punctured to alleviate inner eye pressure (IOP). Non-penetrating deep sclerectomy (NPDS) surgery is a similar but modified procedure, in which instead of puncturing the scleral wall, a patch of the sclera is skimmed to a level, upon which, percolation of liquid from the inner eye is achieved and thus alleviating IOP, without penetrating the eye. NPDS is demonstrated to cause a significantly less side effects than trabeculectomy.[How to reference and link to summary or text] However, NPDS is performed manually and requires great skill to achieve a lengthy learning curve.[How to reference and link to summary or text]
Laser assisted NPDS is the performance of NPDS with the use of a CO2 laser system. The laser-based system is self-terminating once the required scleral thickness and adequate drainage of the intra ocular fluid have been achieved. This self-regulation effect is achieved as the CO2 laser essentially stops ablating as soon as it comes in contact with the intra-ocular percolated liquid, which occurs as soon as the laser reaches the optimal residual intact layer thickness.
Major studies Edit
- Advanced Glaucoma Intervention Study (AGIS) - large American National Eye Institute (NEI) sponsored study designed "to assess the long-range outcomes of sequences of interventions involving trabeculectomy and argon laser trabeculoplasty in eyes that have failed initial medical treatment for glaucoma." It recommends different treatments based on race.
- Early Manifest Glaucoma Trial (EMGT) -Another NEI study found that immediately treating people who have early stage glaucoma can delay progression of the disease.
- Ocular Hypertension Treatment Study (OHTS) -NEI study findings: "...Topical ocular hypotensive medication was effective in delaying or preventing onset of Primary Open Angle Glaucoma (POAG) in individuals with elevated Intraocular Pressure (IOP). Although this does not imply that all patients with borderline or elevated IOP should receive medication, clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG."
- Blue Mountains Eye Study "The Blue Mountains Eye Study was the first large population-based assessment of visual impairment and common eye diseases of a representative older Australian community sample." Risk factors for glaucoma and other eye disease were determined.
Classification of glaucomaEdit
Glaucoma has been classified into specific types:
Primary glaucoma and its variants (H40.1-H40.2) Edit
- Primary glaucoma
- Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
- Low-tension glaucoma
- Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, pupil-block glaucoma, acute congestive glaucoma
- Acute angle-closure glaucoma
- Chronic angle-closure glaucoma
- Intermittent angle-closure glaucoma
- Superimposed on chronic open-angle closure glaucoma ("combined mechanism" - uncommon)
- Variants of primary glaucoma
- Pigmentary glaucoma
- Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare
Primary open-angle glaucoma - This is caused by trabecular blockage which is where the aqueous humor in the eye drains out. Because the microscopic passage ways are blocked, the pressure builds up in the eye and causes imperceptible very gradual vision loss. Peripheral vision is affected first but eventually the entire vision will be lost if not treated. Diagnosis is made by looking for cupping of the optic nerve. The treatment's goal is to release the fluid by opening uveoscleral passageways, which are acted upon by prostoglandin agonists. Beta blockers such as timolol, work by decreasing aqueous formation. Carbonic anhydrase inhibitors decrease bicarbonate formation from ciliary processes in the eye, thus decreasing formation of Aqueous humor. Parasympathetic analogs are drugs that work on the trabecular outflow by opening up the passageway and constricting the pupil. Alpha 2 agonists (brimonidine, apraclonidine) both decrease fluid production (via. inhibition of AC) and increase drainage.
Primary angle-closure glaucoma - This is caused by contact between the iris and trabecular meshwork, which in turn obstructs outflow of the aqueous humor from the eye. This contact between iris and trabecular meshwork (TM) may gradually damage the function of the meshwork until it fails to keep pace with aqueous production, and the pressure rises. In over half of all cases, prolonged contact between iris and TM causes the formation of synechiae (effectively "scars"). These cause permanent obstruction of aqueous outflow. In some cases, pressure may rapidly build up in the eye causing pain and redness (symptomatic, or so called "acute" angle-closure). In this situation the vision may become blurred, and halos may be seen around bright lights. Accompanying symptoms may include headache and vomiting. Diagnosis is made from physical signs and symptoms: pupils mid-dilated and unresponsive to light, cornea edematous (cloudy), reduced vision, redness, pain. However, the majority of cases are asymptomatic. Prior to very severe loss of vision, these cases can only be identified by examination, generally by an eye care professional. Once any symptoms have been controlled, the first line (and often definitive) treatment is laser iridotomy. This may be performed using either Nd:YAG or argon lasers, or in some cases by conventional incisional surgery. The goal of treatment is to reverse, and prevent, contact between iris and trabecular meshwork. In early to moderately advanced cases, iridotomy is successful in opening the angle in around 75% of cases. In the other 25% laser iridoplasty, medication (pilocarpine) or incisional surgery may be required.
Developmental glaucoma (Q15.0)Edit
- Developmental glaucoma
- Primary congenital glaucoma
- Infantile glaucoma
- Glaucoma associated with hereditary of familial diseases
Secondary glaucoma (H40.3-H40.6) Edit
- Secondary glaucoma
- Inflammatory glaucoma
- Uveitis of all types
- Fuchs heterochromic iridocyclitis
- Phacogenic glaucoma
- Angle-closure glaucoma with mature cataract
- Phacoanaphylactic glaucoma secondary to rupture of lens capsule
- Phacolytic glaucoma due to phacotoxic meshwork blockage
- Subluxation of lens
- Glaucoma secondary to intraocular hemorrhage
- Hemolytic glaucoma, also known as erythroclastic glaucoma
- Traumatic glaucoma
- Angle recession glaucoma: Traumatic recession on anterior chamber angle
- Postsurgical glaucoma
- Aphakic pupillary block
- Ciliary block glaucoma
- Neovascular glaucoma (see below for more details)
- Drug-induced glaucoma
- Corticosteroid induced glaucoma
- Alpha-chymotrypsin glaucoma. Postoperative ocular hypertension from use of alpha chymotrypsin.
- Glaucoma of miscellaneous origin
- Associated with intraocular tumors
- Associated with retinal detachments
- Secondary to severe chemical burns of the eye
- Associated with essential iris atrophy
- Toxic Glaucoma
Neovascular glaucoma is an uncommon type of glaucoma that is difficult or nearly impossible to treat. This condition is often caused by proliferative diabetic retinopathy (PDR) or central retinal vein occlusion (CRVO). It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood flow to the eye are highly at risk for this condition.
Neovascular glaucoma results when new, abnormal vessels begin developing in the angle of the eye that begin blocking the drainage. Patients with such condition begin to rapidly lose their eyesight. Sometimes, the disease appears very rapidly, specially after cataract surgery procedure. A new treatment for this disease, as first reported by Kahook and colleagues, involves use of a novel group of medications known as Anti-VEGF agents. These injectable medications can lead to a dramatic decrease in new vessel formation and, if injected early enough in the disease process, may lead to normalization of intraocular pressure.
Toxic glaucoma is open angle glaucoma with an unexplained significant rise of intraocular pressure following unknown pathogenesis. Intraocular pressure can sometimes reach Template:Convert/mmHgTemplate:Convert/test/Aon. It characteristically manifests as ciliary body inflammation and massive trabecular oedema that sometimes extends to Schlemm's Canal. This condition is differentiated from malignant glaucoma by the presence of a deep and clear anterior chamber and a lack of aqueous misdirection. Also, the corneal appearance is not as hazy. A reduction in visual acuity can occur followed neuroretinal breakdown. Associated factors include inflammation, drugs, trauma and intraocular surgery, including cataract surgery and vitrectomy procedures. Gede Pardianto (2005) reports on four patients who had toxic glaucoma. One of them underwent phaecoemulsification with small particle nucleus drops. Some cases can be resolved with some medication, vitrectomy procedures or trabeculectomy. Valving procedures can give some relief but further research is required.
Absolute glaucoma (H44.5)Edit
- Absolute glaucoma
- List of eye diseases and disorders
- Ocular hypertension
- Glaucoma valves
- Mansour F. Armaly
- Laszlo Z. Bito
- Charles D. Phelps
- American Glaucoma Society
- ↑ "Global data on visual impairment in the year 2002" Bulletin of the World Health Organization Volume 82, Number 11, November 2004, 811-890
- ↑ Alguire P (1990). "The Eye Chapter 118 Tonometry>Basic Science" Walker HK, Hall WD, Hurst JW Clinical methods: the history, physical, and laboratory examinations, 3rd, London: Butterworths.
- ↑ Mozaffarieh M, Grieshaber MC, Flammer J (2008). Oxygen and blood flow: players in the pathogenesis of glaucoma. Mol Vis. 14: 224–33.
- ↑ Osborne NN, Wood JP, Chidlow G, Bae JH, Melena J, Nash MS (August 1999). Ganglion cell death in glaucoma: what do we really know?. Br J Ophthalmol 83 (8): 980–6.
- ↑ Levin LA, Peeples P (February 2008). History of neuroprotection and rationale as a therapy for glaucoma. Am J Manag Care 14 (1 Suppl): S11–4.
- ↑ Varma R, Peeples P, Walt JG, Bramley TJ (February 2008). Disease progression and the need for neuroprotection in glaucoma management. Am J Manag Care 14 (1 Suppl): S15–9.
- ↑ Hernández M, Urcola JH, Vecino E (May 2008). Retinal ganglion cell neuroprotection in a rat model of glaucoma following brimonidine, latanoprost or combined treatments. Exp Eye Res. 86 (5): 798–806.
- ↑ Cantor LB (December 2006). Brimonidine in the treatment of glaucoma and ocular hypertension. Ther Clin Risk Manag 2 (4): 337–46.
- ↑ Schwartz M (June 2007). Modulating the immune system: a vaccine for glaucoma?. Can J Ophthalmol. 42 (3): 439–41.
- ↑ Morrison JC (2006). Integrins in the optic nerve head: potential roles in glaucomatous optic neuropathy (an American Ophthalmological Society thesis). Trans Am Ophthalmol Soc 104: 453–77.
- ↑ Knox DL, Eagle RC, Green WR (March 2007). Optic nerve hydropic axonal degeneration and blocked retrograde axoplasmic transport: histopathologic features in human high-pressure secondary glaucoma. Arch Ophthalmol. 125 (3): 347–53.
- ↑ Tezel G, Luo C, Yang X (March 2007). Accelerated aging in glaucoma: immunohistochemical assessment of advanced glycation end products in the human retina and optic nerve head. Invest. Ophthalmol. Vis. Sci. 48 (3): 1201–11.
- ↑ Berry FB, Mirzayans F, Walter MA (April 2006). Regulation of FOXC1 stability and transcriptional activity by an epidermal growth factor-activated mitogen-activated protein kinase signaling cascade. J Biol Chem. 281 (15): 10098–104.
- ↑ (June 2007). Issue on neuroprotection. Can J Ophthalmol. 42 (3).
- ↑ Sommer A, Tielsch JM, Katz J, et al. (August 1991). Relationship between intraocular pressure and primary open angle glaucoma among white and black Americans. The Baltimore Eye Survey. Arch Ophthalmol. 109 (8): 1090–5.
- ↑ Wang N, Wu H, Fan Z (November 2002). Primary angle closure glaucoma in Chinese and Western populations. Chin Med J. 115 (11): 1706–15.
- ↑ OMIM 137760
- ↑ OMIM 606657
- ↑ 19.0 19.1 Rhee DJ, Katz LJ, Spaeth GL, Myers JS (2001). Complementary and alternative medicine for glaucoma. Surv Ophthalmol 46 (1): 43–55.
- ↑ Pardianto G et al. (2005). Aqueous Flow and the Glaucoma. Mimbar Ilmiah Oftalmologi Indonesia 2: 12–5.
- ↑ Chaum E et al.. A 5 year old girl who failed her school vision screening. Case presentation of Persistent fetal vasculature (PFV), also called persistent hyperplastic primary vitreous (PHPV). Digital Journal of Ophthalmology.
- ↑ Hunt A, Rowe N, Lam A, Martin F (July 2005). Outcomes in persistent hyperplastic primary vitreous. Br J Ophthalmol 89 (7): 859–63.
- ↑ Chang B, Smith RS, Peters M, et al. (2001). Haploinsufficient Bmp4 ocular phenotypes include anterior segment dysgenesis with elevated intraocular pressure. BMC Genet. 2: 18.
- ↑ National Institutes of Health
- ↑ 25.0 25.1 25.2 25.3 Pardianto G et al. Some difficulties on Glaucoma. Mimbar Ilmiah Oftalmologi Indonesia.2006;3: 49-52.
- ↑ Thomas R, Parikh RS (September 2006). How to assess a patient for glaucoma. Community Eye Health 19 (59): 36–7.
- ↑ Johnson, Chris A. The use of a visual illusion to detect glaucoma. In Visual Perception: The Influence of H. W. Leibowitz, eds. Andre, J., Owens, D. A., and Harvey, Jr., L. O. (2003); 45-56. Washington, D.C.: The American Psychological Association.
- ↑ Noecker RJ (June 2006). The management of glaucoma and intraocular hypertension: current approaches and recent advances. Ther Clin Risk Manag 2 (2): 193–206.
- ↑ Parikh RS, Parikh SR, Navin S, Arun E, Thomas R (May 2008). Practical approach to medical management of glaucoma. Indian J Ophthalmol 56 (3): 223–30.
- ↑ Leffler CT, Amini L (2007). Interpretation of uniocular and binocular trials of glaucoma medications: an observational case series. BMC Ophthalmol 7: 17.
- ↑ 31.0 31.1 Ritch R (June 2007). Natural compounds: evidence for a protective role in eye disease. Can J Ophthalmol. 42 (3): 425–38.
- ↑ 32.0 32.1 Tsai JC, Song BJ, Wu L, Forbes M (September 2007). Erythropoietin: a candidate neuroprotective agent in the treatment of glaucoma. J Glaucoma 16 (6): 567–71.
- ↑ 33.0 33.1 Mozaffarieh M, Flammer J (November 2007). Is there more to glaucoma treatment than lowering IOP?. Surv Ophthalmol 52 (Suppl 2): S174–9.
- ↑ 34.0 34.1 American Academy of Ophthalmology. Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma. Retrieved September 30, 2008.
- ↑ Complementary Therapy Assessments : American Academy of Ophthalmology
- ↑ Irvin Rosenfeld and the Compassionate IND - Medical Marijuana Proof and Government Lies
- ↑ Sharif NA, Kelly CR, Crider JY, Davis TL (December 2006). Serotonin-2 (5-HT2) receptor-mediated signal transduction in human ciliary muscle cells: role in ocular hypotension. J Ocul Pharmacol Ther 22 (6): 389–401.
- ↑ Sharif NA, McLaughlin MA, Kelly CR (February 2007). AL-34662: a potent, selective, and efficacious ocular hypotensive serotonin-2 receptor agonist. J Ocul Pharmacol Ther 23 (1): 1–13.
- ↑ OMIM 231300
- ↑ Shingleton B, Tetz M, Korber N (March 2008). Circumferential viscodilation and tensioning of Schlemm canal (canaloplasty) with temporal clear corneal phacoemulsification cataract surgery for open-angle glaucoma and visually significant cataract: one-year results. J Cataract Refract Surg 34 (3): 433–40.
- ↑ Lewis RA, von Wolff K, Tetz M, et al. (July 2007). Canaloplasty: circumferential viscodilation and tensioning of Schlemm's canal using a flexible microcatheter for the treatment of open-angle glaucoma in adults: interim clinical study analysis. J Cataract Refract Surg 33 (7): 1217–26.
- ↑ Molteno AC, Polkinghorne PJ, Bowbyes JA (November 1986). The vicryl tie technique for inserting a draining implant in the treatment of secondary glaucoma. Aust N Z J Ophthalmol 14 (4): 343–54.
- ↑ Roberts S, Woods C. Effects of a novel porous implant in refractory glaucomatous dogs. ACVO abstract 2008, Boston, MA.
- ↑ Paton D, Craig JA (1976). Glaucomas. Diagnosis and management. Clin Symp 28 (2): 1–47.
- ↑ Difficulties on glaucoma by Pardianto G et al., in Mimbar Ilmiah Oftalmologi Indonesia.2006;3: 48-9.
- Glaucoma Resource Guide from the National Eye Institute (NEI).
- National Glaucoma Research
- Global Association of International Glaucoma Societies - featuring a hymn about the successful treatment of glaucoma
- EUROPEAN GLAUCOMA SOCIETY
- Glaucoma Research Foundation
- Glaucoma - What is Glaucoma?. NLM. URL accessed on 2007-04-21. video
- Nonprofit Foundation for Glaucoma
- Asia Ophthalmology Center
- DJO | Digital Journal of Ophthalmology
- Lions Eye Institute, Perth, Australia
- Mar 2008 BBC article on diagnosis advances
- Glaucoma Associates Of New York
- Pediatric Glaucoma and Cataract Family Association
- World Glaucoma Day, March 12, 2009
- Morrison JC, Pollack IP (2003) Glaucoma: Science and Practice. Thieme ISBN 0865779155 Google Books
- Kahook MY, Schuman JS, Noecker RJ (2006). Intravitreal bevacizumab in a patient with neovascular glaucoma. Ophthalmic Surg Lasers Imaging 37 (2): 144–6.
- Clinical Pearls
- Canadian Glaucoma Guidelines Podcast
Photographs of glaucomatous eyes:http://webeye.ophth.uiowa.edu/eyeforum/atlassearch1.htm ] This URL will download the search form of the University of Iowa Eye Atlas. Type glaucoma into the Diagnosis space and then click on Run Query to download the annotated photographs.
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