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 main treatment is symptomatic, since the underlying genetic defect cannot be corrected as of 2015. Symptomatic treatment is surgical.

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.

A surgeon trained to do eyelid surgery, such as a plastic surgeon or ophthalmologist, is required to decide and perform the appropriate surgical procedure. The following procedures have been described for blepharochalasis:

- External levator aponeurosis tuck

- Blepharoplasty

- Lateral canthoplasty

- Dermis fat grafts

These are used to correct atrophic blepharochalasis after the syndrome has run its course.

Treatment and prognosis depend on the underlying condition. For example, in thiamine deficiency, treatment would be the immediate administration of vitamin B1.

There is currently no defined treatment to ameliorate the muscle weakness of CPEO. Treatments used to treat other pathologies causing ophthalmoplegia has not been shown to be effective.

Experimental treatment with tetracycline has been used to improve ocular motility in one patient. Coenzyme Q has also been used to treat this condition. However, most neuro-ophthalmologists do not ascribe to any treatment.

Ptosis associated with CPEO may be corrected with surgery to raise the lids, however due to weakness of the orbicularis oculi muscles, care must be taken not to raise the lids in excess causing an inability to close the lids. This results in an exposure keratopathy. Therefore, rarely should lid surgery be performed and only by a neuro-ophthalmologist familiar with the disease.

The most common strabismus finding is large angle exotropia which can be treated by maximal bilateral eye surgery, but due to the progressive nature of the disease, strabismus may recur. Those that have diplopia as a result of asymmetric ophthalmoplegia may be corrected with prisms or with surgery to create a better alignment of the eyes.

There have been cases of improvement in extra-ocular movement with botulinum toxin injection.

Medical management may involve immunosuppressive drugs such as methotrexate, corticosteroids, cyclophosphamide, and azathioprine. No randomized controlled trials have yet been conducted to evaluate such treatments, so the benefits have not been clearly established.

Affected individuals may benefit from autologous fat transfer or fat grafts to restore a more normal contour to the face. However, greater volume defects may require microsurgical reconstructive surgery which may involve the transfer of an island parascapular fasciocutaneous flap or a free flap from the groin, rectus abdominis muscle (Transverse Rectus Abdominis Myocutaneous or "TRAM" flap) or latissimus dorsi muscle to the face. Severe deformities may require additional procedures, such as pedicled temporal fascia flaps, cartilage grafts, bone grafts, orthognathic surgery, and bone distraction. The timing of surgical intervention is controversial; some surgeons prefer to wait until the disease has run its course while others recommend early intervention.

Treatment of THS includes immunosuppressives such as corticosteroids (often prednisolone) or steroid-sparing agents (such as methotrexate or azathioprine).

Radiotherapy has also been proposed.

The prognosis tends to be good for patients with MG. It is often best not to treat mild cases of MG. Management necessitates avoidance of medications that can worsen neuromuscular transmission, such as aminoglycoside antibiotics, quinolone antibiotics, beta-blockers, chloroquine, anti-arrhythmics, calcium channel blockers, some anticonvulsants and intravenous iodinated contrast should be avoided.

MG is characteristically variable in course, with the frequency of diplopia and ptosis affected by environmental, emotional and physical factors such as bright sunlight, stress, viral illness, menstruation, pregnancy, etc. Spontaneous remission can occur in any patient and remain for years. In a study of the natural history of generalized MG among 168 patients (with an average follow-up of 12 years), 14% experienced complete remission.

Patients with mild-to-moderate ocular myasthenia are usually treated initially with oral anticholinesterase agents, Mestinon (pyridostigmine) being the most commonly employed. There have not been any randomized clinical trials conducted with these agents, and this treatment is often unsuccessful, particularly in resolving diplopia. Immunosuppressive therapy is then started and the agent of choice is usually prednisone. In a small controlled study this drug demonstrated greater efficacy than pyridostigmine. Steroid therapy is controversial, but in another study the results suggested that prednisone does decrease progression to generalized MG. There is no single recommended dosing regimen in light of the side effects commonly associated with chronic corticosteroid therapy, and the difficulty in weaning patients from steroids without exacerbation of symptoms. Response to prednisone therapy is variable.

Additionally, MG patients should be examined for thymomas, and if found, should undergo surgery to address this condition. A prophylactic thymectomy is controversial, but has been shown to be helpful in young MG patients with acute disease within 3 years of disease onset, in patients with enlarged thymus glands and for whom surgery is low-risk, and patients with generalized MG who are unresponsive to medical treatment.

The symptoms of ocular MG can also be addressed by non-medicinal means. Ptosis can be corrected with placement of crutches on eyeglasses and with ptosis tape to elevate eyelid droop. Diplopia can be addressed by occlusion with eye patching, frosted lens, occluding contact lens, or by simply placing opaque tape over a portion of eyeglasses. Also, plastic prisms (Fresnel prisms) can be attached to eyeglasses of a diplopic patient, allowing for alignment of vision from both eyes in the affected direction, but are often problematic if the degree of muscle weakness, and therefore ocular misalignment, fluctuates frequently.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

The prognosis of THS is usually considered good. Patients usually respond to corticosteroids, and spontaneous remission can occur, although movement of ocular muscles may remain damaged. Roughly 30–40% of patients who are treated for THS experience a relapse.

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.

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.

Use of high doses of opioid drugs such as morphine, oxycodone, heroin, or hydrocodone can cause ptosis. Pregabalin (Lyrica), an anticonvulsant drug, has also been known to cause mild ptosis.

With posterior lens luxation, the lens falls back into the vitreous humour and lies on the floor of the eye. This type causes fewer problems than anterior lens luxation, although glaucoma or ocular inflammation may occur. Surgery is used to treat dogs with significant symptoms. Removal of the lens before it moves to the anterior chamber may prevent secondary glaucoma.

The physical abnormalities resulting from SCS are typically mild and only require a minor surgical procedure or no procedure at all. One of the common symptoms of SCS is the development of short (brachydactyly), webbed fingers and broad toes (syndactyly). These characteristics do not cause any problems to the function of the hands or feet, and thus, no medical procedure is required to fix the abnormalities, unless the patient requests it. Webbing of the fingers may affect the base of the fingers, resulting in delayed hand growth during childhood, but this contributes no functional impairments. Sometimes, individuals with SCS develop broad toes because the bones at the ends of the toes are duplicating themselves. This is especially seen in the big toe, but requires no surgical intervention because it doesn't negatively affect the overall function of the foot. Individuals with these toe abnormalities walk normally and can wear normal footwear.

In more severe cases, frequent surgeries and clinical monitoring are required throughout development. A child born with asymmetrical unilateral coronal synostosis should undergo cranioplasty within its first year of life in order to prevent increased intracranial pressure and to prevent progressive facial asymmetry. Cranioplasty is a surgical procedure to correct prematurely fused cranial bones. The surgery acts to reconstruct and reposition the bones and sutures in order to promote the most normal growth. Cranioplasty is necessary in order to continue to grow and is important for two main reasons. First of all, the skull needs to be able to accommodate the growing brain following childbirth, which it can't because the skull doesn't grow as fast as the brain as long as the sutures remain fused. This results in an increase in pressure surrounding the brain and inhibits the brain from growing, causing the individual to experience significant problems, and if left untreated can eventually lead to death. Secondly, cranioplasty may be required for appearance purposes. This is especially the case in individuals with asymmetrical unilateral coronal synostosis, which requires reconstructive surgery of the face and skull. If cranioplasty is not performed, especially in individuals with unilateral coronal synostosis, then facial asymmetry will get worse and worse over time, which is why cranioplasty should be performed as soon as possible.

Surgery may also be required in individuals with vision problems. Vision problems usually arise due to a lack of space in the eye orbit and skull because of the abnormal bone structure of the face. Decreased space may also lead to abnormal or missing tear ducts and nerve damage. Reconstructive surgery is usually required in order to increase cranial space, correct tear duct stenosis, and/or correct ptosis of the eyelids in order to prevent amblyopia (lazy eye).

Midfacial surgery may also be required during early childhood to correct respiratory problems, dental malocclusion, and swallowing difficulties. A cleft palate is also corrected with surgery, and may involve the use of tympanostomy tubes. If needed, an individual will undergo orthognathic treatment and/or orthodontic treatment after facial development is complete. Since hearing loss is frequently associated with SCS, it is recommended that audiology screening persist throughout childhood.

After cranial reconstructive surgery, a child may be required to wear a molding helmet or some other form of head protection until the cranial bones set into place. This typically takes about three months and depends on the child's age and the severity of the condition. Following recovery, individuals with SCS look and act completely normal, so no one would even be able to tell that they have SCS.

Horses that suffer from this disease can never be considered cured, although they can be managed by careful use of the therapy described above, and fast detection of new flare-ups. If the disease is not properly treated, it will eventually lead to blindness.

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.

Causes of the one and a half syndrome include pontine hemorrhage, ischemia, tumors, infective mass lesions such as tuberculomas, and demyelinating conditions like multiple sclerosis.

Anisocoria is a common condition, defined by a difference of 0.4 mm or more between the sizes of the pupils of the eyes.

Anisocoria has various causes:

- Physiological anisocoria: About 20% of normal people have a slight difference in pupil size which is known as physiological anisocoria. In this condition, the difference between pupils is usually less than 1 mm.

- Horner's syndrome

- Mechanical anisocoria: Occasionally previous trauma, eye surgery, or inflammation (uveitis, angle closure glaucoma) can lead to adhesions between the iris and the lens.

- Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.

- Oculomotor nerve palsy: Ischemia, intracranial aneurysm, demyelinating diseases (e.g., multiple sclerosis), head trauma, and brain tumors are the most common causes of oculomotor nerve palsy in adults. In ischemic lesions of the oculomotor nerve, pupillary function is usually spared whereas in compressive lesions the pupil is involved.

- Pharmacological agents with anticholinergic or sympathomimetic properties will cause anisocoria, particularly if instilled in one eye. Some examples of pharmacological agents which may affect the pupils include pilocarpine, cocaine, tropicamide, MDMA, dextromethorphan, and ergolines. Alkaloids present in plants of the genera "Brugmansia" and "Datura", such as scopolamine, may also induce anisocoria.

- Migraines

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

Von Graefe's sign is the lagging of the upper eyelid on downward rotation of the eye, indicating exophthalmic goiter (Graves' Disease). It is a dynamic sign, whereas lid lag is a static sign which may also be present in cicatricial eyelid retraction or congenital ptosis.

A pseudo Graefe's sign (pseudo lid lag) shows a similar lag, but is due to aberrant regeneration of fibres of the oculomotor nerve (III) into the elevator of the upper lid. It occurs in paramyotonia congenita.

A pseudo Graefe's sign is most commonly manifested in just one eye but can occasionally be observed in both. The reason only one eye is affected is not yet clear.

Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting 20% of the population, it can be an entirely harmless condition or a symptom of more serious medical problems.