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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. It occurs in the presence of open anterior chamber angles. 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 galucoma 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) (), 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 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 () 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 (-). 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. 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 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. Risk factors and diagnosis
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. 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. 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. The possible neuroprotective effects of various topical and systemic medications are also being investigated. 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. Generally, these surgeries are a temporary solution, as there is not yet a cure for glaucoma. A newer form of laser surgery called Selective Laser Trabeculoplasty shows promise as a long term treatment. In SLT a laser is used to selectively target the melanocytes in the trabecular meshwork. Though the mechanism by which SLT functions is not well understood, it has been shown in trials to be as effective as the older Argon Laser Trabeculoplasty. However, because SLT is performed using a much lower power laser, it does not appear to effect the physical integrity of the trabecular meshwork, so retreatment is possible if the effects from the original treatment should begin wear off. Major studies Classification of glaucoma Glaucoma has been classfied into specific types:
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