There is no cure for ONH; however, many therapeutic interventions exist for the care of its symptoms. These may include hormone replacement therapy for hypopituitarism, occupational, physical, and/or speech therapy for other issues, and services of a teacher of students with blindness/visually impairment. Special attention should be paid to early development of oral motor skills and acclimation to textured foods for children with texture aversion, or who are otherwise resistant to eating.

Sleep dysfunction can be ameliorated using melatonin in the evening in order to adjust a child's circadian clock.

Treatment for strabismus may include patching of the better eye, which may result in improved vision in the worse eye; however, this should be reserved for cases in which the potential for vision improvement in both eyes is felt to be good. Surgery to align the eyes can be performed once children with strabismus develop equal visual acuity in both eyes, most often after the age of three. Generally surgery results in improved appearance only and not in improved visual function.

Colobomas of the iris may be treated in a number of ways. A simple cosmetic solution is a specialized cosmetic contact lens with an artificial pupil aperture. Surgical repair of the iris defect is also possible. Surgeons can close the defect by stitching in some cases. More recently artificial iris prosthetic devices such as the Human Optics artificial iris have been used successfully by specialist surgeons. This device cannot be used if the natural lens is in place and is not suitable for children. Suture repair is a better option where the lens is still present.

Vision can be improved with glasses, contact lenses or even laser eye surgery but may be limited if the retina is affected or there is amblyopia.

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.

Currently there is no effective therapy for dominant optic atrophy, and consequently, these patients are simply monitored for changes in vision by their eye-care professional. Children of patients should be screened regularly for visual changes related to dominant optic atrophy. Research is underway to further characterize the disease so that therapies may be developed.

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.

Most ophthalmologists will not advocate any treatment unless visual loss is present and ongoing. Reports of patients with ONSM having no change in their vision for multiple years are not uncommon. If loss of vision occurs, radiation therapy will improve vision in about ⅓ of cases, and preserve vision in about ⅓ of cases. Surgery has traditionally been associated with rapid deteroriation of vision. However, newer surgical techniques may prove better for the treatment of ONSM.

Treatment is dependent upon diagnosis and the stage at which the diagnosis is secured. For toxic and nutritional optic neuropathies, the most important course is to remove the offending agent if possible and to replace the missing nutritional elements, orally, intramuscularly, or intravenously. If treatment is delayed, the injury may be irreversible. The course of treatment varies with the congenital forms of these neuropathies. There are some drug treatments that have shown modest success, such as Idebenone used to treat LOHN. Often treatment is relegated to lifestyle alterations and accommodations and supportive measures.

ONSM does not improve without treatment. In many cases, there is gradual progression until vision is lost in the affected eye. However, this takes at least several months to occur, and a minority of patients remain stable for a number of years.

Optic pits themselves do not need to be treated. However, patients should follow up with their eye care professional annually or even sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit.

Though there is no treatment for Cone dystrophy, certain supplements may help in delaying the progression of the disease.

The beta-carotenoids, lutein and zeaxanthin, have been evidenced to reduce the risk of developing age related macular degeneration (AMD), and may therefore provide similar benefits to Cone dystrophy sufferers.

Consuming omega-3 fatty acids (docosahexaenoic acid and eicosapentaenoic acid) has been correlated with a reduced progression of early AMD, and in conjunction with low glycemic index foods, with reduced progression of advanced AMD, and may therefore delay the progression of cone dystrophy.

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.

Treatment requires careful consideration of angiographic findings when a choroidal neovascular membrane is suspected which is a condition that responds to treatment. A vitreo-retinal specialist (an ophthalmologist specialized in treatment of retinal diseases) should be consulted for proper management of the case.

Presumed ocular histoplasmosis syndrome and age-related macular degeneration (AMD) have been successfully treated with laser, anti-vascular endothelial growth factors and photodynamic therapy. Ophthalmologists are using anti-vascular endothelial growth factors to treat AMD and similar conditions since research indicates that vascular endothelial growth factor (VEGF) is one of the causes for the growth of the abnormal vessels that cause these conditions.

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.

Laser treatment of drusen has been studied. While it is possible to eliminate drusen with this treatment strategy, it has been shown that this fails to reduce the risk of developing the choroidal neovascularisation which causes the blindness associated with age-related macular degeneration.

Initial treatment in lumbar disc disease is one or two days of bedrest (although growing number of studies shows that it makes little difference) and pain relieving medications. In cases with ongoing pain despite conservative treatments, a surgical operation that will remove the compressing disc material, a microdiscectomy or discectomy may be recommended to treat a lumbar disc herniation.

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.

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.

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.

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.

In the majority of cases, spinal disc herniation doesn't require surgery, and a study on sciatica, which can be caused by spinal disc herniation, found that "after 12 weeks, 73% of people showed reasonable to major improvement without surgery." The study, however, did not determine the number of individuals in the group that had sciatica caused by disc herniation.

- Initial treatment usually consists of non-steroidal anti-inflammatory pain medication (NSAIDs), but the long-term use of NSAIDs for people with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity.

- Epidural corticosteroid injections provide a slight and questionable short-term improvement in those with sciatica but are of no long term benefit. Complications occur in 0 to 17% of cases when performed on the neck and most are minor. In 2014, the US Food and Drug Administration (FDA) suggested that the "injection of corticosteroids into the epidural space of the spine may result in rare but serious adverse events, including loss of vision, stroke, paralysis, and death." and that "The effectiveness and safety of epidural administration of corticosteroids have not been established, and FDA has not approved corticosteroids for this use.".

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.

Non-surgical methods of treatment are usually attempted first, leaving surgery as a last resort. Pain medications are often prescribed as the first attempt to alleviate the acute pain and allow the patient to begin exercising and stretching. There are a variety of other non-surgical methods used in attempts to relieve the condition after it has occurred, often in combination with pain killers. They are either considered indicated, contraindicated, relatively contraindicated, or inconclusive based on the safety profile of their risk-benefit ratio and on whether they may or may not help:

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.

Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder.

- Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis is variable.

- Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables, vitamin supplementation (thiamine, vitamin B, folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment. Again, prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis.

In both toxic and nutritional neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.

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.