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.

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)

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.

Intraocular pressure can be lowered with medication, usually eye drops. Several classes of medications are used to treat glaucoma, with several 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 them 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. Wiping the eye with an absorbent pad after the administration of eye drops may result in fewer adverse effects, like the growth of eyelashes and hyperpigmentation in the eyelid.

Poor compliance with medications and follow-up visits is a major reason for vision loss in glaucoma patients. A 2003 study of patients in an HMO found half failed to fill their prescriptions the first time, and one-fourth failed to refill their prescriptions a second time. Patient education and communication must be ongoing to sustain successful treatment plans for this lifelong disease with no early symptoms.

The possible neuroprotective effects of various topical and systemic medications are also being investigated.

- Prostaglandin analogs, such as latanoprost, bimatoprost and travoprost, increase uveoscleral outflow of aqueous humor. Bimatoprost also increases trabecular outflow.

- Topical beta-adrenergic receptor antagonists, such as timolol, levobunolol, and betaxolol, decrease aqueous humor production by the epithelium of the ciliary body.

- Alpha2-adrenergic agonists, such as brimonidine and apraclonidine, work by a dual mechanism, decreasing aqueous humor production and increasing uveoscleral outflow.

- Less-selective alpha agonists, such as epinephrine, decrease aqueous humor production through vasoconstriction of ciliary body blood vessels, useful only in open-angle glaucoma. Epinephrine's mydriatic effect, however, renders it unsuitable for closed-angle glaucoma due to further narrowing of the uveoscleral outflow (i.e. further closure of trabecular meshwork, which is responsible for absorption of aqueous humor).

- Miotic agents (parasympathomimetics), such as pilocarpine, work by contraction of the ciliary muscle, opening the trabecular meshwork and allowing increased outflow of the aqueous humour. Echothiophate, an acetylcholinesterase inhibitor, is used in chronic glaucoma.

- Carbonic anhydrase inhibitors, such as dorzolamide, brinzolamide, and acetazolamide, lower secretion of aqueous humor by inhibiting carbonic anhydrase in the ciliary body.

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.

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.

If a diagnosis of GCA is suspected, treatment with steroids should begin immediately. A sample (biopsy) of the temporal artery should be obtained to confirm the diagnosis and guide future management, but should not delay initiation of treatment. Treatment does not recover lost vision, but prevents further progression and second eye involvement. High dose corticosteroids may be tapered down to low doses over approximately one year.

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.

Rapid blood transfusions, to correct anemia and raise blood pressure, may improve PION outcomes. In one report of a related disease, hypotension-induced AION, 3 out of 3 patients who received rapid transfusions reported partial recovery of vision. While rapid transfusions offer some hope, the prognosis for perioperative PION remains poor. Prevention remains the best way to reduce PION.

One retrospective report proposes that incidence of PION could be reduced in high-risk cases by altering surgical management. For example, for patients undergoing spine surgery, measures could be taken to minimize intraoperative hypotension, to accelerate the process of blood replacement, and to aggressively treat facial swelling.

Because SO is so rarely encountered following eye injury, even when the injured eye is retained, the first choice of treatment may not be enucleation or evisceration, especially if there is a chance that the injured eye may regain some function. Additionally, with current advanced surgical techniques, many eyes once considered nonviable now have a fair prognosis.

However, only if the injured eye has completely lost its vision and has no potential for any visual recovery, prevention of SO is done by enucleation of the injured eye preferably within the first 2 weeks of injury. Evisceration—the removal of the contents of the globe while leaving the sclera and extraocular muscles intact—is easier to perform, offers long-term orbital stability, and is more aesthetically pleasing, i.e., a greater measure of movement of the prosthesis and thus a more natural appearance. There is concern, however, that evisceration may lead to a higher incidence of SO compared to enucleation. Several retrospective studies involving over 3000 eviscerations, however, have failed to identify a single case of SO.

Once SO is developed, Immunosuppressive therapy is the mainstay of treatment. When initiated promptly following injury, it is effective in controlling the inflammation and improving the prognosis. Mild cases may be treated with local application of corticosteroids and pupillary dilators. More severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc.), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin.

Quick determination of the cause may lead to urgent measures to save the eye and life of the patient. High clinical suspicion should be kept for painless vision loss in patients with atherosclerosis, deep venous thrombosis, atrial fibrillation, pulmonary thromboembolism or other previous embolic episodes. Those caused by a carotid artery embolism or occlusion have the potential for further stroke by detachment of embolus and migration to an end-artery of the brain. Hence, proper steps to prevent such an eventuality need to be taken.

Retinal arterial occlusion is an ophthalmic emergency, and prompt treatment is essential. Completely anoxic retina in animal models causes irreversible damage in about 90 minutes. Nonspecific methods to increase blood flow and dislodge emboli include digital massage, 500 mg IV acetazolamide and 100 mg IV methylprednisolone (for possible arteritis). Additional measures include paracentesis of aqueous humor to decrease IOP acutely. An ESR should be drawn to detect possible giant cell arteritis. Improvement can be determined by visual acuity, visual field testing, and by ophthalmoscopic examination.

At a later stage, pan-retinal photocoagulation (PRP) with an argon laser appears effective in reducing the neovascular components and their sequelae.

The visual prognosis for ocular ischemic syndrome varies from usually poor to fair, depending on speed and effectiveness of the intervention. However, prompt diagnosis is crucial as the condition may be a presenting sign of serious cerebrovascular and ischemic heart diseases.

In 2009, the Undersea and Hyperbaric Medical Society added "central retinal artery occlusion" to their list of approved indications for hyperbaric oxygen (HBO). When used as an adjunctive therapy, the edema reducing properties of HBO, along with down regulation of inflammatory cytokines may contribute to the improvement in vision. Prevention of vision loss requires that certain conditions be met: the treatment be started before irreversible damage has occurred (over 24 hours), the occlusion must not also occur at the ophthalmic artery, and treatment must continue until the inner layers of the retina are again oxygenated by the retinal arteries.

Topical ciclosporin (topical ciclosporin A, tCSA) 0.05% ophthalmic emulsion is an immunosuppressant. The drug decreases surface inflammation. In a trial involving 1200 people, Restasis increased tear production in 15% of people, compared to 5% with placebo.

It should not be used while wearing contact lenses, during eye infections or in people with a history of herpes virus infections. Side effects include burning sensation (common), redness, discharge, watery eyes, eye pain, foreign body sensation, itching, stinging, and blurred vision. Long term use of ciclosporin at high doses is associated with an increased risk of cancer.

Cheaper generic alternatives are available in some countries.

Inflammation occurring in response to tears film hypertonicity can be suppressed by mild topical steroids or with topical immunosuppressants such as ciclosporin (Restasis). Elevated levels of tear NGF can be decreased with 0.1% prednisolone.

Diquafosol, an agonist of the P2Y2 purinogenic receptor, is approved in Japan for managing dry eye disease by promoting tear secretion.

Lifitegrast is a new drug that was approved by the FDA for the treatment of the condition in 2016.

Historically, papilledema was a potential contraindication to lumbar puncture, as it indicates a risk for tentorial herniation and subsequent death via cerebral herniation, however newer imaging techniques have been more useful at determining when and when not to conduct a lumbar puncture. Imaging by CT or MRI is usually performed to elicit whether there is a structural cause i.e., tumor. An MRA and MRV may also be ordered to rule out the possibility of stenosis or thrombosis of the arterial or venous systems.

The treatment depends largely on the underlying cause. However, the root cause of papilledema is the increased intracranial pressure (ICP). This is a dangerous sign, indicative of a brain tumor, CNS inflammation or idiopathic intracranial hypertension (IIH) that may become manifest in the near future.

Thus, a biopsy is routinely performed prior to the treatment in the initial stages of papilledema to detect whether a brain tumor is present. If detected, laser treatment, radiation and surgeries can be used to treat the tumor.

To decrease ICP, medications can be administered by increasing the absorption of Cerebrospinal fluid (CSF), or decreasing its production. Such medicines include diuretics like acetazolamide and furosemide. These diuretics, along with surgical interventions, can also treat IIH. In IIH, weight loss (even a loss of 10-15%) can lead to normalization of ICP.

Meanwhile, steroids can reduce inflammation (if this is a contributing factor to increased ICP), and may help to prevent vision loss. However, steroids have also been known to cause increased ICP, especially with a change in dosage. However, if a severe inflammatory condition exists, such as multiple sclerosis, steroids with anti-inflammatory effects such as Methylprednisolone and prednisone can help.

Other treatments include repeated lumbar punctures to remove excess spinal fluid in the cranium. The removal of potentially causative medicines including tetracyclines and vitamin A analogues may help decrease ICP; however, this is only necessary if the medication is truly felt to contribute to the ICP increase.

Patients with optic disc drusen should be monitored periodically for ophthalmoscopy, Snellen acuity, contrast sensitivity, color vision, intraocular pressure and threshold visual fields. For those with visual field defects optical coherence tomography has been recommended for follow up of nerve fiber layer thickness. Associated conditions such as angioid streaks and retinitis pigmentosa should be screened for. Both the severity of optic disc drusen and the degree of intraocular pressure elevation have been associated with visual field loss. There is no widely accepted treatment for ODD, although some clinicians will prescribe eye drops designed to decrease the intra-ocular pressure and theoretically relieve mechanical stress on fibers of the optic disc. Rarely choroidal neovascular membranes may develop adjacent to the optic disc threatening bleeding and retinal scarring. Laser treatment or photodynamic therapy or other evolving therapies may prevent this complication.

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.

The development of accurate and reliable non-invasive ICP measurement methods for VIIP has the potential to benefit many patients on earth who need screening and/or diagnostic ICP measurements, including those with hydrocephalus, intracranial hypertension, intracranial hypotension, and patients with cerebrospinal fluid shunts. Current ICP measurement techniques are invasive and require either a lumbar puncture, insertion of a temporary spinal catheter, insertion of a cranial ICP monitor, or insertion of a needle into a shunt reservoir.

Mydriatic/cycloplegic agents, such as topical homatropine, which is similar in action to atropine, are useful in breaking and preventing the formation of posterior synechia by keeping the iris dilated and away from the crystalline lens. Dilation of the pupil in an eye with the synechia can cause the pupil to take an irregular, non-circular shape (Dyscoria) as shown in the photograph. If the pupil can be fully dilated during the treatment of iritis, the prognosis for recovery from synechia is good. This is a treatable status.

To subdue the inflammation, use topical corticosteroids. If the intra-ocular pressure is elevated then use a PGA such as Travatan Z.

The best-studied medical treatment for intracranial hypertension is acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57 percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte levels of newborn babies. The diuretic furosemide is sometimes used for a treatment if acetazolamide is not tolerated, but this drug sometimes has little effect on the ICP.

Various analgesics (painkillers) may be used in controlling the headaches of intracranial hypertension. In addition to conventional agents such as paracetamol, a low dose of the antidepressant amitriptyline or the anticonvulsant topiramate have shown some additional benefit for pain relief.

The use of steroids in the attempt to reduce the ICP is controversial. These may be used in severe papilledema, but otherwise their use is discouraged.

The first step in symptom control is drainage of cerebrospinal fluid by lumbar puncture. If necessary, this may be performed at the same time as a diagnostic LP (such as done in search of a CSF infection). In some cases, this is sufficient to control the symptoms, and no further treatment is needed.

The procedure can be repeated if necessary, but this is generally taken as a clue that additional treatments may be required to control the symptoms and preserve vision. Repeated lumbar punctures are regarded as unpleasant by patients, and they present a danger of introducing spinal infections if done too often. Repeated lumbar punctures are sometimes needed to control the ICP urgently if the patient's vision deteriorates rapidly.

The first line of management for chemical injuries is usually copious irrigation of the eye with an isotonic saline or sterile water. In the cases of chemical burns, one should not try to buffer the solution, but instead it with copious flushing.

Depending on the type of ocular injury, either a "pressure patch" or "shield patch" should be applied. Up until circa 1987, pressure patches were the preferred method of treatment for corneal abrasions in non-contact lens wearers; Multiple controlled studies conducted by accredited organizations such as the American Academy of Ophthalmology have shown that pressure patching is of little or no value in healing corneal abrasions and is actually detrimental to healing in some cases. A Cochrane Review found that patching simple corneal abrasions may not improve healing or reduce pain. Pressure patching should never be used on an individual presenting with a corneal abrasion who has a history of contact lens wear. In this circumstance, a virulent infection caused by the bacterium Pseudomonas aeruginosa is at a clearly delineated increased risk for occurrence. These infections can cause blindness within 24 – 48 hours and there is a possibility that the infection can move into the peri-orbital socket, resulting in the need for evisceration of the eyeball. In rare cases, the infection can enter the brain and cause death to the patient.

In cases of globe penetration, pressure patches should never be applied, and instead a shield patch should be applied that protects the eye without applying any pressure. If a shield patch is applied to one eye, the other eye should also be patched due to eye movement. If the uninjured eye moves, the injured eye will also move involuntarily possibly causing more damage.

Even though some patients undergo spontaneous remission of symptoms within a year, many need treatment. The first step is the regulation of thyroid hormone levels by a physician.

There is some published evidence that a total or sub-total thyroidectomy may assist in reducing levels of TSH receptor antibodies (TRAbs) and as a consequence reduce the eye symptoms, perhaps after a 12-month lag. However, a 2015 meta review found no such benefits, and there is some evidence that suggests that surgery is no better than medication; and there are risks associated with a Thyroidectomy, as there are with long-term use of anti-thyroid medication.

Topical lubrication of the ocular surface is used to avoid corneal damage caused by exposure. Tarsorrhaphy is an alternative option when the complications of ocular exposure can't be avoided solely with the drops.

Corticosteroids are efficient in reducing orbital inflammation, but the benefits cease after discontinuation. Corticosteroids treatment is also limited because of their many side effects. Radiotherapy is an alternative option to reduce acute orbital inflammation. However, there is still controversy surrounding its efficacy. A simple way of reducing inflammation is to stop smoking, as pro-inflammatory substances are found in cigarettes.

Surgery may be done to decompress the orbit, to improve the proptosis, and to address the strabismus causing diplopia. Surgery is performed once the patient's disease has been stable for at least six months. In severe cases, however, the surgery becomes urgent to prevent blindness from optic nerve compression. Because the eye socket is bone, there is nowhere for eye muscle swelling to be accommodated, and, as a result, the eye is pushed forward into a protruded position. In some patients, this is very pronounced. Orbital decompression involves removing some bone from the eye socket to open up one or more sinuses and so make space for the swollen tissue and allowing the eye to move back into normal position and also relieving compression of the optic nerve that can threaten sight.

Eyelid surgery is the most common surgery performed on Graves ophthalmopathy patients. Lid-lengthening surgeries can be done on upper and lower eyelid to correct the patient's appearance and the ocular surface exposure symptoms. Marginal myotomy of levator palpebrae muscle can reduce the palpebral fissure height by 2–3 mm. When there is a more severe upper lid retraction or exposure keratitis, marginal myotomy of levator palpebrae associated with lateral tarsal canthoplasty is recommended. This procedure can lower the upper eyelid by as much as 8 mm. Other approaches include müllerectomy (resection of the Müller muscle), eyelid spacer grafts, and recession of the lower eyelid retractors. Blepharoplasty can also be done to debulk the excess fat in the lower eyelid.

An article in the New England Journal of Medicine reports that treatment with selenium is effective in mild cases.

A large European study performed by the European Group On Graves' Orbitopathy (EUGOGO) has recently shown that the trace element selenium had a significant effect in patients with mild, active thyroid eye disease. Six months of selenium supplements had a beneficial effect on thyroid eye disease and were associated with improvement in the quality of life of participants. These positive effects persisted at 12 months. There were no side effects.

A summary of treatment recommendations was published in 2015 by an Italian taskforce, which largely supports the other studies.

Small extramacular lesions (lesions not threatening vision) may be observed without treatment. Sight-threatening lesions are treated for 4–6 weeks with triple therapy consisting of pyrimethamine, sulfadiazine, and folinic acid. During treatment with pyrimethamine, leukocyte and platelet counts should be monitored weekly. Folinic acid protects against the decrease in platelets and white blood cells induced by pyrimethamine.

Prednisone may be used for 3–6 weeks to reduce macular or optic nerve inflammation and can be started on day 3 of antibiotic therapy. Corticosteroids should not be used without concurrent antibiotic treatment or in immunocompromised patients due to the risk of exacerbation of the disease. Currently, there is no published evidence from randomized controlled trials demonstrating that corticosteroids would be an effective adjunct for treating ocular toxoplasmosis.

Trimethoprim-Sulfamethoxazole has been shown to be equivalent to triple therapy in the treatment of ocular toxoplasmosis and may be better tolerated. Clindamycin and azithromycin can also be considered as alternative therapies. Spiramycin may be used safely without undue risk of teratogenicity and may reduce the rate of transmission to the fetus.

AIDS patients require chronic maintenance treatment.

Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.