Studies in the 1970s reported that the use of cannabis may lower intraocular pressure. In an effort to determine whether marijuana, or drugs derived from it, might be effective as a glaucoma treatment, the US National Eye Institute supported research studies from 1978 to 1984. These studies demonstrated some derivatives of marijuana lowered intraocular pressure when administered orally, intravenously, or by smoking, but not when topically applied to the eye.

In 2003, the American Academy of Ophthalmology released a position statement stating that cannabis was not more effective than prescription medications. Furthermore, no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of cannabis use to treat glaucoma compared with the wide variety of pharmaceutical agents now available.

In 2012 the American Glaucoma Society published a position paper discrediting the use of cannabis as a legitimate treatment for elevated intraocular pressure, for reasons including short duration of action and side effects that limit many activities of daily living.

The modern goals of glaucoma management are to avoid glaucomatous damage and nerve damage, and 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.

Vitamin A supplementation plays an important role, specifically vitamin A deficiency is a top causes of preventable childhood blindness. Though in measles cases, the administration of the vitamin to offset visual impairment has not been proven effective, as of yet.

is a program launched by the International Agency for the Prevention of Blindness (IAPB) and is supported by the WHO in 1999 that has made controlling blindness in children a high priority.

Patients usually do not require treatment due to benign nature of the disease. In case cataract develops patients generally do well with cataract surgery.

In 2005, steroids were investigated for the treatment of macular edema due to retinal blood vessel blockage such as CRVO and BRVO.

Untreated glaucoma leads to total blindness. Surgical treatment is required. Presently-utilized surgical procedures include goniotomy, trabeculotomy, or trabeculectomy.

Macular edema sometimes occurs for a few days or weeks after cataract surgery, but most such cases can be successfully treated with NSAID or cortisone eye drops. Prophylactic use of Nonsteroidal anti-inflammatory drugs has been reported to reduce the risk of macular edema to some extent.

In 2010 the US FDA approved the use of Lucentis intravitreal injections for macular edema.

Iluvien, a sustained release intravitreal implant developed by Alimera Sciences, has been approved in Austria, Portugal and the U.K. for the treatment of vision impairment associated with chronic diabetic macular edema (DME) considered insufficiently responsive to available therapies. Additional EU country approvals are anticipated.

In 2013 Lucentis by intravitreal injection was approved by the National Institute for Health and Care Excellence in the UK for the treatment of macular edema caused by diabetes and/or retinal vein occlusion.

On July 29, 2014, Eylea (aflibercept), an intravitreal injection produced by Regeneron Pharmaceuticals Inc., was approved to treat DME in the United States.

While PEX itself is untreatable as of 2011, it is possible for doctors to minimize the damage to vision and to the optic nerves by the same medical techniques used to prevent glaucoma.

- Eyedrops. This is usually the first treatment method. Eyedrops can help reduce intraocular pressure within the eye. The medications within the eyedrops can include beta blockers (such as levobunolol or timolol) which slow the production of the aqueous humor. And other medications can increase its outflow, such as prostaglandin analogues (e.g. latanoprost). And these medicines can be used in various combinations. In most cases of glaucoma, eyedrops alone will suffice to solve the problem.

- Laser surgery. A further treatment is a type of laser therapy known as trabeculoplasty in which a high-energy laser beam is pointed at the trabecular meshwork to cause it to "remodel and open" and improve the outflows of the aqueous humor. These can be done as an outpatient procedure and take less than twenty minutes. One report suggests this procedure is usually effective.

- Eye surgery. Surgery is the treatment method of last resort if the other methods have not worked. It is usually effective at preventing glaucoma. Eye surgery on PEX patients can be subject to medical complications if the fibers which hold the lens have become weakened because of a buildup from the flakes; if the lens-holding fibers have weakened, then the lens may become loose, and complications from eye surgery may result. In such cases, it is recommended that surgeons act quickly to repair the phacodonesis before the lenses have dropped. A surgeon cuts an opening in the white portion of the eye known as the sclera, and removes a tiny area of the trabecular meshwork which enables the aqueous humor to discharge. This lowers the internal pressure within the eye and lessens the chance of future damage to the optic nerve. Cases with pseudophacodonesis and dislocated IOL have been increasing in number, according to one report. In cataract surgery, complications resulting from PEX include capsular rupture and vitreous loss.

- Drug therapy. There are speculations that if genetics plays a role in PEX, and if the specific genes involved can be identified, that possibly drugs can be developed to counteract these mutations or their effects. But such drugs have not been developed as of 2011.

Patients should continue to have regular eye examinations so that physicians can monitor pressure levels and check whether medicines are working.

Ocular hypertension is treated with either medications or laser. Medications that lower intraocular pressure work by decreasing aqueous humor production and/or increasing aqueous humor outflow. Laser trabeculoplasty works by increasing outflow. The cannabinoids found in cannabis sativa and indica (marijuana) have been shown to reduce intraocular pressure, by up to 50% for approximately four to five hours. But due to the duration of effect, significant side-effect profile, and lack of research proving efficacy, the American Glaucoma Society issued a position statement in 2009 regarding the use of marijuana as a treatment for glaucoma.

The preferred treatment of congenital glaucoma is surgical not medical. The initial procedures of choice are goniotomy or trabeculotomy if the cornea is clear, and trabeculectomy ab externo if the cornea is hazy. The success rates are similar for both procedures in patients with clear corneas. Trabeculectomy and shunt procedures should be reserved for those cases in which goniotomy or trabeculotomy has failed. Cyclophotocoagulation is necessary in some intractable cases but should be avoided whenever possible because of its potential adverse

effects on the lens and the retina.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

If caught early, the neovascularization can be reversed with prompt pan retinal photocoagulation (PRP), or injection of anti-VEGF medications with subsequent PRP. The injection blocks the direct effect of VEGF and acts more quickly but will wear off in about 6 weeks. PRP has a slower onset of action but can last permanently. Once the neovascularization has been longstanding, the new vessels recruit fibrous tissue, and as this forms and contracts, the angle can be permanently damaged, and will not respond to treatment. If this occurs, then surgical intervention is required to reduce the pressure (such as a glaucoma drainage implant)

Scientists are studying different populations and relationships to try to learn more about the disease. They have found associations with different groups but it is not yet clear what the underlying factors are and how they affect different peoples around the world.

- Glaucoma patients. While PEX and glaucoma are believed to be related, there are cases of persons with PEX without glaucoma, and persons with glaucoma without PEX. Generally, a person with PEX is considered as having a risk of developing glaucoma, and vice versa. One study suggested that the PEX was present in 12% of glaucoma patients. Another found that PEX was present in 6% of an "open-angle glaucoma" group. Pseudoexfoliation syndrome is considered to be the most common of identifiable causes of glaucoma. If PEX is diagnosed without glaucoma, there is a high risk of a patient subsequently developing glaucoma.

- Country and region. Prevalence of PEX varies by geography. In Europe, differing levels of PEX were found; 5% in England, 6% in Norway, 4% in Germany, 1% in Greece, and 6% in France. One contrary report suggested that levels of PEX were higher among Greek people. One study of a county in Minnesota found that the prevalence of PEX was 25.9 cases per 100,000 people. It is reportedly high in northern European countries such as Norway, Sweden and Finland, as well as among the Sami people of northern Europe, and high among Arabic populations, but relatively rare among African Americans and Eskimos. In southern Africa, prevalence was found to be 19% of patients in a glaucoma clinic attending to persons of the Bantu tribes.

- Race. It varies considerably according to race.

- Gender. It affects women more than men. One report was that women were three times more likely than men to develop PEX.

- Age. Older persons are more likely to develop PEX. And persons younger than 50 are highly unlikely to have PEX. A study in Norway found that the prevalence of PEX of persons aged 50–59 was 0.4% while it was 7.9% for persons aged 80–89 years. If a person is going to develop PEX, the average age in which this will happen is between 69 and 75 years, according to the Norwegian study. A second corroborating report suggested that it happens primarily to people 70 and older. While older people are more likely to develop PEX, it is not seen as a "normal" part of aging.

- Other diseases. Sometimes PEX is associated with the development of medical problems other than merely glaucoma. There are conflicting reports about whether PEX is associated with problems of the heart or brain; one study suggested no correlations while other studies found statistical links with Alzheimer's disease, senile dementia, cerebral atrophy, chronic cerebral ischemia, stroke, transient ischemic attacks, heart disease, and hearing loss.

Fuchs heterochromic iridocyclitis (FHI) is a chronic unilateral uveitis appearing with the triad of heterochromia, predisposition to cataract and glaucoma, and keratitic precipitates on the posterior corneal surface. Patients are often asymptomatic and the disease is often discovered through investigation of the cause of the heterochromia or cataract. Neovascularisation (growth of new abnormal vessels) is possible and any eye surgery, such as cataract surgery, can cause bleeding from the fragile vessels in the atrophic iris causing accumulation of blood in anterior chamber of the eye, also known as hyphema.

Pigment dispersion syndrome (PDS) is an affliction of the eye that can lead to a form of glaucoma known as pigmentary glaucoma. It takes place when pigment cells slough off from the back of the iris and float around in the aqueous humor. Over time, these pigment cells can accumulate in the anterior chamber in such a way that it can begin to clog the trabecular meshwork (the major site of aqueous humour drainage), which can in turn prevent the aqueous humour from draining and therefore increases the pressure inside the eye. With PDS, the intraocular pressure tends to spike at times and then can return to normal. Exercise has been shown to contribute to spikes in pressure as well. When the pressure is great enough to cause damage to the optic nerve, this is called pigmentary glaucoma. As with all types of glaucoma, when damage happens to the optic nerve fibers, the vision loss that occurs is irreversible and painless.

This condition is rare, but occurs most often in Caucasians, particularly men, and the age of onset is relatively low: mid 20s to 40s. As the crystalline lens hardens with age, the lens zonules pull away from the iris and the syndrome lessens and stops. Most sufferers are nearsighted.

There is no cure yet, but pigmentary glaucoma can be managed with eye drops or treated with simple surgeries. One of the surgeries is the YAG laser procedure in which a laser is used to break up the pigment clogs, and reduce pressure. If caught early and treated, chances of glaucoma are greatly reduced. Sufferers are often advised not to engage in high-impact sports such as long-distance running or martial arts, as strong impacts can cause more pigment cells to slough off.

A 2016 Cochrane Review sought to determine the effectiveness of YAG laser iridotomy versus no laser iridotomy for pigment dispersion syndrome and pigmentary glaucoma, in 195 participants, across five studies. No clear benefits in preventing loss of visual field were found for eyes treated with peripheral laser iridotomy. There was weak evidence suggesting that laser iridotomy could be more effective in lowering intraocular pressure in eyes versus no treatment.

The pressure within the eye is maintained by the balance between the fluid that enters the eye through the ciliary body and the fluid that exits the eye through the trabecular meshwork.

Treatments for corneal neovascularization are predominately off-lab with a multitude of complications as a result. The desired results from medical therapy may not always occur, ergo an invasive procedure may be needed to prevent further decrease in corneal avascularity.

For contact lenses related hypoxia, ceasing the use of contact lenses is the first step until corneal neovascularization is addressed by a physician. Modern rigid gas permeable and silicon hydrogel contact lenses have a much higher level of oxygen transmissibility, making them effective alternatives to help prevent corneal neovascularization.

Topical administration of steroids and non-steroid anti-inflammatory drugs are first-line treatment for individuals with CNV. The administration of steroids can increase the risk of infection, glaucoma, cataracts, herpes simplex recurrence. The anti-inflammatory drugs, however, increase the risk of corneal ulceration and melting.

Since VEGF plays an important role in vasculogenesis and pathologic neovascularization associated with eye diseases, a potential treatment for CNV is to inhibit VEGF activity by competing the binding of VEGF with specific neutralizing anti-VEGF antibody. VEGF inhibitors include pegatanib sodium, ranibizumab, and off-label bevacizumab are currently used for treatment of various retinal disease. Anti-VEGF antibodies such as the application of ranibizumab or bevacizumab have has been shown to reduce corneal neovascularization. Both ranibizumab and bevacizumab uses the same mechanism and inhibits all iso-forms of VEGF. The significant reduction in invasion of in-growth blood vessels in terms of neovascular area and vessel caliber suggests that treatment with ranibizumab induces thinning of the blood vessels, however, there's no significant change of the blood vessel's length. Using anti-VEGF antibodies to treat CNV has some limitations such as it is not a cure and may require repeated treatments to maintain positive effects over time. Topical and/or subconjunctival administration of bevaicizumab or ranibizumab have demonstrated short-term safety and efficacy, however long term effects have not been documented. Anti-VEGF therapy is currently an experimental treatment.

If the cornea is inflamed via corneal neovascularization, the suppression of enzymes can block CNV by compromising with corneal structural integrity. Corneal neovascularization can be suppressed with a combination of orally administration of doxycycline and with topical corticosteroid.

Surgical Options

Invasive solutions for corneal neovascularization are reserved when the medical therapies do not provide the desired results.

Invading blood tissues and ablating tissues in the cornea can be obstructed by the use of laser treatments such as Argon and s. Irradiation and/or damages to adjacent tissues caused by the procedure can result in corneal hemorrhage and corneal thinning. Obstruction of the blood vessels can be unsuccessful due to the depth, size, and, high blood flow rate of the vessels. In conjunction, thermal damage from the lasers can trigger inflammatory response which can exaggerate the neovascularization.

An effective treatment is photodynamic therapy, however, this treatment has limited clinical acceptance due to high costs and many potential complications involved that are also related to laser ablation. Complications can include irradiation from previously injected photosensitive dye inducing apoptosis and necrosis of the endothelium and basement membrane.

Diathermy and cautery is a treatment where an electrolysis needle is inserted into the feeder vessels in the limbus. The vessels are obstructed by a coagulating current through the use of unipolar diathermy unit or by thermal cautery.

If the diagnostic workup reveals a systemic disease process, directed therapies to treat that underlying cause should be initiated. If the amaurosis fugax is caused by an atherosclerotic lesion, aspirin is indicated, and a carotid endarterectomy considered based on the location and grade of the stenosis. Generally, if the carotid artery is still patent, the greater the stenosis, the greater the indication for endarterectomy. "Amaurosis fugax appears to be a particularly favorable indication for carotid endarterectomy. Left untreated, this event carries a high risk of stroke; after carotid endarterectomy, which has a low operative risk, there is a very low postoperative stroke rate." However, the rate of subsequent stroke after amaurosis is significantly less than after a hemispheric TIA, therefore there remains debate as to the precise indications for which a carotid endarterectomy should be performed. If the full diagnostic workup is completely normal, patient observation is recommended.

Without treatment, NTG leads to progressive visual field loss and in the last consequence to blindness. The mainstay of conventional glaucoma therapy, reducing IOP by pressure-lowering eye drops or by surgery, is applied in cases of NTG as well. The rationale: the lower the IOP, the less the risk of ganglion cell loss and thus in the long run of visual function. The appearance of disc hemorrhages is always a warning sign that therapeutic approaches are not successful - the small bleedings, usually described as flame-shaped, almost always indicate a progression of the disease.

Besides this classical glaucoma therapy, the vascular component that exists in the majority of NTG patients has to be managed as well. Dips in blood pressure or a generally low blood pressure have to be prevented - which is a rather uncommon approach in modern medicine where high blood pressure is always seen as an immense clinical challenge, affecting large segments of the population. In patients with systemic hypertension under therapy, the blood pressure should not be lowered too rigorously. NTG might be the only severe (= sight-threatening) disease caused in numerous cases by a too low blood pressure. Both magnesium and low dose calcium channel blockers have been employed in the treatment of some NTG patients. There are therapeutic approaches to underlying conditions like Flammer syndrome. A change in nutrition like the intake of sodium-rich foods has been tried as has the oral administration of low-dosed steroids. Lifestyle interventions are recommended in patients with Flammer syndrome like avoidance of fasting and certain stimuli like a cold environment and stress.

The main goals of treatment are to decrease the risk of rebleeding within the eye, corneal blood staining, and atrophy of the optic nerve. Small hyphemas can usually be treated on an outpatient basis. Most treatment plans consist of elevating the head at night, wearing a patch and shield, and controlling any increase in intraocular pressure. Surgery may be necessary for non-resolving hyphemas, or hyphaemas that are associated with high pressure that does not respond to medication. Surgery can be effective for cleaning out the anterior chamber and preventing corneal blood staining.

Elevation of the head of the bed by approximately 45 degrees (so that the hyphema can settle out inferiorly and avoid obstruction of vision, as well as to facilitate resolution). Bedrest may be considered, although evidence suggests that it does not improve outcomes. Wearing of an eye shield at night time (to prevent accidental rubbing of the eyes during sleep, which can precipitate a rebleed). An eye patch should be worn throughout the day to protect the injured eye.

If pain management is necessary, acetaminophen can be used. Aspirin and ibuprofen should be avoided, because they interfere with platelets' ability to form a clot and consequently increase the risk of additional bleeding. Sedation is not usually necessary for patients with hyphema. It is controversial amongst ophthalmologists whether a steroid medication or a dilating eye drop (mydriatic) should be used in treatment of hyphema. Steroids aim to reduce the amount of inflammation, but also cause side effects. Dilating drops aim to increase comfort from the traumatized iris as well as reduce bleeding, but can also cause the pupil to be fixed in a dilated state via posterior synechiae (adhesions).

Aminocaproic or tranexamic acids are often prescribed for hyphema. Although these medications actually cause hyphemas to take longer to clear, they reduce the risk of rebleeding and its associated complications. Tranexamic and aminocaproic acids inhibit the conversion of plasminogen to plasmin, plasmin being the agent of fibrin breakdown in blood clots. Keeping the clots intact allows time for the vessels to heal properly and avert a secondary bleed.

In the early stages, there are a few treatment options. Laser surgery or cryotherapy (freezing) can be used to destroy the abnormal blood vessels, thus halting progression of the disease. However, if the leaking blood vessels are clustered around the optic nerve, this treatment is not recommended as accidental damage to the nerve itself can result in permanent blindness. Although Coats' disease tends to progress to visual loss, it may stop progressing on its own, either temporarily or permanently. Cases have been documented in which the condition even reverses itself. However, once total retinal detachment occurs, sight loss is permanent in most cases. Removal of the eye (enucleation) is an option if pain or further complications arise.

While the vast majority of hyphemas resolve on their own without issue, sometimes complications occur. Traumatic hyphema may lead to increased intraocular pressure, peripheral anterior synechiae, atrophy of the optic nerve, staining of the cornea with blood, re-bleeding, and impaired accommodation.

Secondary hemorrhage, or rebleeding of the hyphema, is thought to worsen outcomes in terms of visual function. Rebleeding occurs in 4-35% of hyphema cases and is a risk factor for glaucoma.

Although intermediate uveitis can develop at any age, it primarily afflicts children and young adults. There is a bimodal distribution with one peak in the second decade and another peak in the third or fourth decade.

In the United States the proportion of patients with intermediate uveitis is estimated to be 4-8% of uveitis cases in referral centers. The National Institutes of Health reports a higher percentage (15%), which may indicate improved awareness or the nature of the uveitis referral clinic. In the pediatric population, intermediate uveitis can account for up to 25% of uveitis cases.

In the United States, the incidence of primary congenital glaucoma is about one in 10,000 live births. Worldwide, the incidence ranges from a low of 1:22,000 in Northern Ireland to a high of 1:2,500 in Saudi Arabia and 1:1,250 in Romania. In about two-thirds of cases, it is bilateral. The distribution between males and females varies with geography. In North America and Europe it is more common in boys, whereas in Japan it is more common in girls.

- Congenital glaucoma

- Incidence: one in every 10000-15000 live births.

- Bilateral in up to 80% of cases.

- Most cases are sporadic (90%). However, in the remaining 10% there appears to be a strong familial component.