There is no definite treatment.

Because syphilis may be an underlying cause, it should be treated.

Treatment includes penicillin g benzathine 2.4mU IM as a single dose

Or Doxycycline (100 mg PO aid)for those being allergic to penicillin.

Aponeurotic and congenital ptosis may require surgical correction if severe enough to interfere with vision or if cosmetics is a concern.

Treatment depends on the type of ptosis and is usually performed by an ophthalmic plastic and reconstructive surgeon, specializing in diseases and problems of the eyelid.

Surgical procedures include:

- Levator resection

- Müller muscle resection

- Frontalis sling operation (preferred option for oculopharyngeal muscular dystrophy)

Non-surgical modalities like the use of "crutch" glasses or Ptosis crutches or special scleral contact lenses to support the eyelid may also be used.

Ptosis that is caused by a disease may improve if the disease is treated successfully, although some related diseases, such as oculopharyngeal muscular dystrophy currently have no treatments or cures.

The usual treatment of a standardised Adie syndrome is to prescribe reading glasses to correct for impairment of the eye(s). Pilocarpine drops may be administered as a treatment as well as a diagnostic measure. Thoracic sympathectomy is the definitive treatment of diaphoresis, if the condition is not treatable by drug therapy.

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.

Cycloplegic drugs are generally muscarinic receptor blockers. These include atropine, cyclopentolate, homatropine, scopolamine and tropicamide. They are indicated for use in cycloplegic refraction (to paralyze the ciliary muscle in order to determine the true refractive error of the eye) and the treatment of uveitis. All cycloplegics are also mydriatic (pupil dilating) agents and are used as such during eye examination to better visualize the retina.

When cycloplegic drugs are used as a mydriatic to dilate the pupil, the pupil in the normal eye regains its function when the drugs are metabolized or carried away. Some cycloplegic drugs can cause dilation of the pupil for several days. Usually the ones used by ophthalmologists or optometrists wear off in hours, but when the patient leaves the office strong sunglasses are provided for comfort.

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 treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).

The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by Laser treatment or cryotherapy, and detached retinas are reattached surgically.

Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina,long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.

Photic retinopathy generally goes away on its own over time, but there is no specific treatment known to be reliable for speeding recovery. One path sometimes attempted, which has unclear results, is to treat the initial macular edema with corticosteroids.

Argon laser trabeculoplasty (ALT) may be used to treat open-angle glaucoma, but this is a temporary solution, not a cure. A 50-μm argon laser spot is aimed at the trabecular meshwork to stimulate the opening of the mesh to allow more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty uses a thermal argon laser in an argon laser trabeculoplasty procedure.

A newer type of laser trabeculoplasty uses a "cold" (nonthermal) laser to stimulate drainage in the trabecular meshwork. This newer procedure, selective laser trabeculoplasty (SLT), uses a 532-nm, frequency-doubled, Q-switched , which selectively targets melanin pigment in the trabecular meshwork cells. Studies show SLT is as effective as ALT at lowering eye pressure. In addition, SLT may be repeated three to four times, whereas ALT can usually be repeated only once.

Nd:YAG laser peripheral iridotomy (LPI) may be used in patients susceptible to or affected by angle closure glaucoma or pigment dispersion syndrome. During laser iridotomy, laser energy is used to make a small, full-thickness opening in the iris to equalize the pressure between the front and back of the iris, thus correcting any abnormal bulging of the iris. In people with narrow angles, this can uncover the trabecular meshwork. In some cases of intermittent or short-term angle closure, this may lower the eye pressure. Laser iridotomy reduces the risk of developing an attack of acute angle closure. In most cases, it also reduces the risk of developing chronic angle closure or of adhesions of the iris to the trabecular meshwork.

Diode laser cycloablation lowers IOP by reducing aqueous secretion by destroying secretory ciliary epithelium.

The best treatment for light sensitivity is to address the underlying cause. Once the triggering factor is treated, photophobia disappears in many but not all cases.

People with photophobia will avert their eyes from direct light, such as sunlight and room lights. They may seek the shelter of a dark room. They may wear sunglasses designed to filter peripheral light and wide-brimmed sun hats.

Wearing sunglasses indoors can make symptoms worse over time as it will dark-adapt the retina which aggravates sensitivity to light. Indoor photophobia symptoms may be relieved with the use of precision tinted lenses which block the green-to-blue end of the light spectrum without blurring or impeding vision.

A paper by Stringham and Hammond, published in the "Journal of Food Science", reviews studies of effects of consuming Lutein and Zeaxanthin on visual performance, and notes a decrease in sensitivity to glare.

Low order aberrations (hyperopia, Myopia and regular astigmatism), are correctable by eyeglasses, soft contact lenses and refractive surgery. Neither spectacles nor soft contact lenses nor routine keratorefractive surgery adequately corrects high order aberrations. Significant high order aberration usually requires a rigid gas-permeable contact lens for optimal visual rehabilitation.

Customized Wavefront-guided refractive corneal laser treatments are designed to reduce existing aberrations and to help prevent the creation of new aberrations. The wavefront map of the eye may be transferred to a Lasik system and enable the surgeon to treat the aberration. Perfect alignment of the treatment and the pupil on which the Wavefront is measured is required, which is usually achieved through iris feature detection. An efficient eye tracking system and small spot size laser is necessary for treatment . Wavefront customization of ablation increases the depth of ablation because additional corneal tissue must be ablated to compensate for the high order aberrations. Actual results with Wavefront guided LASIK showed that not only it cannot remove HOA but also the optical aberrations are increased. However, the amount of increase in aberrations are less than conventional Lasik. Corneal optical aberrations after photorefractive keratectomy with a larger ablation zone and a transition zone are less pronounced and more physiologic than those associated with first-generation (5 mm) ablations with no transition zone. An upcoming systematic review will seek to compare the safety and effectiveness of wavefront excimer laser refractive surgery with conventional excimer laser refractive surgery, and will measure differences in residual higher order aberrations between the two procedures.

Aspherical intraocular lenses (IOLs) have been used clinically to compensate for positive corneal spherical aberrations. Although Aspherical IOLs may give better contrast sensitivity, it is doubtful, whether they have a beneficial effect on distance visual acuity. Conventional (not Aspherical) IOLs give better depth of focus and better near vision. The reason for improved depth of focus in conventional lenses is linked to residual spherical aberration. The small improvement in depth of focus with the conventional IOLs enhances uncorrected near vision and contribute to reading ability.

Wavefront customized lenses can be used in eyeglasses. Based on Wavefront map of the eye and with the use of laser a lens is shaped to compensate for the aberrations of the eye and then put in the eyeglasses. Ultraviolet Laser can alter the refractive index of curtain lens materials such as epoxy polymer on a point by point basis in order to generate the desired refractive profile.

Wavefront customized contact lenses can theoretically correct HOA. The rotation and decentration reduces the predictability of this method.

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 eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

People with hemeralopia may benefit from sunglasses. Wherever possible, environmental illumination should be adjusted to comfortable level. Light-filtering lenses appear to help in people reporting photophobia.

Otherwise, treatment relies on identifying and treating any underlying disorder.

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.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

Adie's syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.

In general, the younger the child, the greater the urgency in removing the cataract, because of the risk of amblyopia. For optimal visual development in newborns and young infants, a visually significant unilateral congenital cataract should be detected and removed before age 6 weeks, and visually significant bilateral congenital cataracts should be removed before age 10 weeks.

Some congenital cataracts are too small to affect vision, therefore no surgery or treatment will be done. If they are superficial and small, an ophthalmologist will continue to monitor them throughout a patient's life. Commonly, a patient with small congenital cataracts that do not affect vision will eventually be affected later in life; generally this will take decades to occur.

Since the condition appears to slowly subside or diminish on its own, there are no specific treatments for this condition available.

Some precautions include regular visits to an ophthalmologist or optometrist and general testing of the pupil and internal eye through fundamental examinations (listed below). The examinations can determine if any of the muscles of the eye or retina, which is linked to the pupil, have any problems that could relate to the tadpole pupil condition.

Photophobia may also affect patients' socioeconomic status by limiting their career choices, since many workplaces require bright lights for safety or to accommodate the work being done. Sufferers may be shut out of a wide range of both skilled and unskilled jobs, such as in warehouses, offices, workshops, classrooms, supermarkets and storage spaces. Some photophobes are only able to work night shifts, which reduces their prospects for finding work.

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.

Practical surgical procedures used for treating synkinesis are neurolysis and selective myectomy. Neurolysis has been shown to be effective in relieving synkinesis but only temporarily and unfortunately symptoms return much worse than originally. Selective myectomy, in which a synkinetic muscle is selectively resected, is a much more effective technique that can provide permanent relief and results in a low recurrence rate; unfortunately, it also has many post-operative complications that can accompany including edema, hematoma, and ecchymosis. Therefore, surgical procedures are very minimally used by doctors and are used only as last-resort options for patients who do not respond well to non-invasive treatments.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

Botox (botulinum toxin) is a new and versatile tool for the treatment of synkinesis. Initially used for reducing hyperkinesis after facial palsy, Botox was later attempted on patients with post-facial palsy synkinesis to reduce unwanted movements. The effects of Botox have shown to be remarkable, with synkinetic symptoms disappearing within 2 or 3 days. The most common treatment targets are the orbicularis oculi, depressor anguli oris (DAO), mentalis, platysma and the contralateral depressor labii inferioris muscles. Due to the short span of Botox effects though, patients must come back to the doctor for re-injection approximately every 3 months. More notable is that in a majority of patients, various synkinetic movements completely disappeared after 2-3 sessions of trimonthly Botox injections.

A more specific synkinesis, crocodile tears syndrome (hyperlacrimation upon eating), has been shown to respond exceedingly well to Botox injection. Botox is injected directly into the lacrimal gland and has shown to reduce hyperlacrimation within 24–48 hours. The procedure was shown to be simple and safe with very little chance of side-effects (although on rare occasions ptosis can occur due to botulinum toxin diffusion). Furthermore, reduction in hyper-lacrimation was shown to last longer than the expected 3 months (about 12 months).

Since Botox can mimic facial paralysis, an optimized dose has been determined that reduces involuntary synkinesis of the muscle while not affecting muscle tone.

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.