1 Types
The most common type, primary open angle glaucoma (POAG), frequently has no symptoms. Adult-onset POAG combines a slow, progressive loss of visual sensitivity with an abnormal appearing optic disc.[4] It occurs in the presence of open anterior chamber angles.[5] One factor may be a relative obstruction on the outflow of aqueous humour from the eye. Aqueous humour is produced by the epithelium lining the eye's ciliary body which then flows through the pupil and into the anterior chamber. The trabecular meshwork then drains the humour to Schlemm's canal, and ultimately to the venous system. All eyes have some intraocular pressure, which is caused by some resistance to the flow of aqueous through the trabeculum and Schlemm's canal. Pressures of anywhere between 7 and 21 mm Hg are considered normal. If the intraocular pressure (IOP) is too high, (>21.5 mm Hg), the pressure exerted on the walls of the eye results in compression of the ocular structures. However, other factors such as disturbances of blood flow in the optic nerve head may interact with IOP to affect the optic nerve. In addition, it has been proposed that the elevated IOP in POAG can impede retrograde transport of the trophic factor BDNF from the brain to the ganglion cell bodies. The deficit in BDNF results in ganglion cell death.
In one third of cases of POAG there is statistically normal IOP. This is called normal tension glaucoma (NTG). Because optic nerve examination and perimetry testing are not always done in addition to IOP measurement in those at risk, NTG is underdiagnosed and the condition presents late.
There are many other forms of open angle glaucoma that have detectable causes, and are grouped as secondary open angle glaucoma. Some examples are Pigmentary glaucoma, and pseudo-exfoliation glaucoma. Pigmentary glaucoma is caused by pigment dispersion syndrome, which results from rubbing of the iris against the lens capsule and zonules, which releases pigment, which can obstruct the trabecular meshwork. The diagnosis is pigmentary disperson syndrome if the pressure is normal and there is no damage to the optic nerve, and pigmentary glaucoma if the pressure is high or there is optic nerve damage.
Pseudo-exfoliation glaucoma is another type of secondary open angle glaucoma when a dandruff-like material derived from the lens and the zonules gradually obstructs the angle drainage in a similar manner as the pigment particles in pigmentary glaucoma do. It has a familial pattern and can cause a rapid deterioration of visual field. Unlike pigmentary glaucoma, pseudo-exfoliation syndrome is a systemic disease, and deposits on basement membranes can be observed throughout the body.
Another type, acute angle-closure glaucoma (AACG) (H40.2), is characterized by an acute rise in the intraocular pressure. This occurs in susceptible eyes, with narrow angles of the anterior chamber, when the pupil dilates (in the dark, secondary to psychological factors, or drug induced) and leading to the peripheral iris blocking the trabecular meshwork. Acute angle-closure glaucoma can cause pain and reduced visual acuity (blurred vision), and may lead to irreversible visual loss within a short time. This is an ocular emergency requiring immediate treatment. Many people with glaucoma experience halos around bright lights as well as the loss of sight characterized by the disease. Recurrent attacks of acute angle closure glaucoma may lead to chronic narrow angle glaucoma due to the formation of adhesions at the angle of the eye between the iris and the peripheral cornea. These adhesions permanently block the drainage angle. Until permanent damage has been caused to the angle, the treatment of choice is a laser peripheral iridectomy, which can prevent acute angle attacks in most individuals. Ideally, people with suceptiple angles can be diagnosed prior to any attacks and get the laser treatment, which should prevent any attacks.
Primary congenital glaucoma (Q15.0) or buphthalmos is a rare genetic disease affecting infants in which newborns exhibit enlarged globes and clouded corneas. It is thought that reduced trabecular permeability is the cause of increased intraocular pressure. Surgery is the treatment.
As noted above, there are many forms of Secondary glaucoma (H40.3-H40.6). Glaucoma is also always a possible complication of various medical conditions such as eye surgery, advanced cataracts(lens-induced or phacomorphic glaucoma), eye injuries, some eye tumors, uveitis, diabetes or use of corticosteroid drugs. Anyone who has had eye problems in the past, or anyone over age 40 should be examined routinely by an optometrist or ophthalmologist for routine and preventative care.
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2- Symptoms
While glaucoma may or may not have distinct symptoms, an almost inevitable complication of glaucoma is vision loss. Visual loss from glaucoma usually first affects peripheral vision, but can also affect central vision. Early vision loss is subtle, and is not noticed by the patient. Moderate to severe vision loss may be noticed by the patient by careful examination of the full visual field. This can be done by an optometrist or ophthalmologist using a visual field analyser by closing one eye and examining the level of vision at various places in the visual field, then repeating with the other eye closed. All too often, the patient does not notice the loss of vision until he or she experiences "tunnel vision". If the disease is not treated, the visual field will become more and more narrow, obscuring central vision, and finally progressing to blindness in the affected eye(s).
Waiting for symptoms of visual loss to occur is not optimal care. Visual loss related to glaucoma is irreversible, but can be prevented or slowed by treatment. Those at risk for glaucoma are typically advised to consult with an ophthalmologist or optometrist on a regular basis. With advances in testing, treatment and surgery, most people diagnosed with early glaucoma are able to maintain their vision and function well, which was not always the case in the past.
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3- Risk factors and diagnosis
A normal range of vision. Courtesy NIH National Eye Institute
The same view with advanced vision loss from glaucoma.
People with a family history of glaucoma have about a six percent chance of developing glaucoma. Diabetics and African people are three times more likely to develop primary open angle glaucoma. Asians are prone to develop angle-closure glaucoma, and Inuit have a 20 to 40 times higher risk than white people to develop primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallower anterior chambers. Use of steroids can also cause glaucoma.
There is increasing evidence of ocular blood flow to be involved in the pathogenesis of glaucoma. Current data indicate that fluctuations in blood flow are more harmful to GON 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 that there is a correlative, not necessarily causal, relationship between glaucoma and systemic hypertension (i.e. high blood pressure).
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, and an examination of the optic nerve to look for any damage to it. If there is any suspicion of damage to the optic nerve, a formal visual field test should be performed. Scanning laser ophthalmoscopy may also be performed.
Those at risk for glaucoma are advised to have dilated eye examination at least every two years.[6]
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3.1- Who’s at Risk?
Everyone is at risk for glaucoma. But some groups have a higher susceptibility than other groups. Only a complete eye exam with dilation can screen for this disease.
Some of the groups at higher risk for developing glaucoma are:
- African-Americans (It is six to eight times more common than in Caucasians)
- People Over 60 (you are six times more likely to get glaucoma than you were)
- You are six times more likely to get glaucoma if you are over 60 years old.
- Family Members with Glaucoma (glaucoma is hereditary),
- Hispanics in Older Age Groups
- Asians
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4- Treatment
Although intraocular pressure is only one of the risk factors (albeit a major one) of glaucoma, lowering it via pharmaceuticals or surgery is currently the mainstay of glaucoma treatment. In Europe, Japan, and Canada laser treatment is often the first line of therapy. In the U.S., adoption of early laser has lagged, even though prospective, multi-centered, peer-reviewed studies, since the early '90's, have shown laser to be at least as effective as topical medications in controlling intraocular pressure and preserving visual field.
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4.1- Drugs
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. Prostaglandin analogs like latanoprost (Xalatan), bimatoprost (Lumigan) and travoprost (Travatan) increase uveoscleral outflow of aqueous. 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 uveo-scleral 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 aqueous through traditional pathways. Carbonic anhydrase inhibitors like dorzolamide (Trusopt), brinzolamide (Azopt), acetazolamide (Diamox) lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body. Each of these medicines may have local and systemic side effects. Adherence to the 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.
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.
Marijuana has been shown to lower the intraocular pressure in a few studies but this is generally not used clinically. Studies in the 1970s showed that marijuana, when smoked, lowers intraocular pressure.[7]. In an effort to determine whether marijuana, or drugs derived from marijuana, might be effective as a glaucoma treatment, the 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. However, none of these studies demonstrated that marijuana -- or any of its components -- could safely and effectively lower intraocular pressure any more than a variety of drugs then on the market. In 2003, the American Academy of Ophthalmology released a position statement asserting 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." [7]
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.[8]
The possible neuroprotective effects of various topical and systemic medications are also being investigated.
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4.2- Surgery
Main article: Glaucoma surgery
Both laser and conventional surgeries are performed to treat glaucoma. Laser trabeculoplasty may be used to treat open angle glaucoma. An argon or Nd:YAG laser spot is aimed at the trabecular meshwork to stimulate opening of the mesh to allow more outflow of aqueous fluid. Laser peripheral iridectomy may be used in patients susceptible to angle closure glaucoma. In it, the laser is aimed at the iris to make an opening in it. This allows a new channel for fluid to flow when the usual channel through the dilated pupil is blocked.
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. 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 type.
There are also several different glaucoma drainage implants, which may be the old design non-valved tubes, like Molteno implant or the Baerveldt tube shunt, or or the newer valved implant, like the Ahmed glaucoma valve implant. 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. Molteno and other non-valved implants require ligating the tube till the surgical wound is mildly fibrosed and water-tight. This induced potentially dangerous spikes in the intraocular pressure (IOP). Ahmed glaucoma valve on the other hand does not have such a limitation and avoids spikes in IOP. 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 creating a necessity for additional surgery.
Surgery is the primary therapy for those with congenital glaucoma. [9]
Generally, these surgeries are a temporary solution, as there is not yet a cure for glaucoma.
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5- Major studies
- 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.
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6- Classification of glaucoma
Glaucoma has been classfied into specific types:[10]
- Primary glaucoma
- Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
- Low-tension glaucoma
- Primary closed-angle glaucoma, also known as primary angle-closure glaucoma, narrow-angle glaucoma, iris-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)
- Variants of primary glaucoma
- Pigmentary glaucoma
- Exfoliation glaucoma, also known as pseudoexfoliative glaucoma or glaucoma capsulare
- Developmental glaucoma
- Primary congenital glaucoma
- Infantile glaucoma
- Glaucoma associated with hereditary of familial diseases
- 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
- Hyphema
- 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
- 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 deatchments
- Secondary to severe chemical burns of the eye
- Associated with essential iris atrophy
- Absolute glaucoma
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7-References
- ^ "Glaucoma." Centre for Vision Research. Accessed October 17, 2006.
- ^ "Glaucoma, Normal Tension, Susceptibility To." OMIM - Online Mendelian Inheritance in Man. Accessed October 17, 2006.
- ^ "Who is at Risk for Glaucoma?" Prevent Blindness America: The Glaucoma Learning Center. Accessed October 18, 2006.
- ^ "Glaucoma, Primary Open Angle, Adult-Onset; POAG." OMIM - Online Mendelian Inheritance in Man. Accessed October 17, 2006.
- ^ Bell JA. "Glaucoma, Primary Open Angle." eMedicine.com. August 16, 2005. Accessed October 17, 2006.
- ^ National Institutes of Health
- ^ a b American Academy of Ophthalmology. Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma. Retrieved August 2, 2006.
- ^ http://blogs.salon.com/0002762/stories/2005/02/18/irvRosenbergAndTheCompassi.html
- ^ "Glaucoma, Congenital: GLC3 Buphthalmos." OMIM - Online Mendelian Inheritance in Man. Accessed October 17, 2006.
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^ Paton D, Craig JA. "Glaucomas. Diagnosis and management." Clin Symp. 1976;28(2):1-47. PMID 1053095. |
