Congenital nystagmus has traditionally been viewed as non-treatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could effectively stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was found to cause improvement in about half the patients who received it to relieve symptoms of nystagmus. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program), 4-aminopyridine, and acetazolamide. Several therapeutic approaches, such as contact lenses, drugs, surgery, and low vision rehabilitation have also been proposed. For example, it has been proposed that mini-telescopic eyeglasses suppress nystagmus.

Surgical treatment of Congenital Nystagmus is aimed at improving the abnormal head posture, simulating artificial divergence or weakening the horizontal recti muscles. Clinical trials of a surgery to treat nystagmus (known as tenotomy) concluded in 2001. Tenotomy is now being performed regularly at numerous centres around the world. The surgery developed by Louis F. Dell'Osso Ph.D. aims to reduce the eye shaking (oscillations), which in turn tends to improve visual acuity.

Acupuncture has conflicting evidence as to having beneficial effects on the symptoms of nystagmus. Benefits have been seen in treatments where acupuncture points of the neck were used, specifically points on the sternocleidomastoid muscle. Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities which led to an increase in foveation duration periods both during and after treatment. By the standards of evidence-based medicine, the quality of these studies can be considered poor (for example, Ishikawa has a study sample size of just six, is unblinded and without proper control), and given high quality studies showing that acupuncture has no effect beyond placebo, the results of these studies have to be considered clinically irrelevant until higher quality studies are produced.

Physical therapy or Occupational therapy is also used to treat nystagmus. Treatment consist of learning compensatory strategies to take over for the impaired system.

Management of this condition is surgical and typically involves reducing the strength of the superior rectus muscle or anterior transposition of the inferior oblique muscle of the affected eyes.

Several different surgical procedures exist for the correction of DVD including: inferior oblique anteriorization, inferior oblique anteriorization plus resection, superior rectus recession, superior rectus recession plus posterior fixation suture, and inferior oblique myectomy, though there is insufficient evidence to determine which procedure results in the best outcomes for patients.

In general, strabismus can be approached and treated with a variety of procedures. Depending on the individual case, treatment options include:

- Correction of refractive errors by glasses

- Prism therapy (if tolerated, to manage diplopia)

- Patching (mainly to manage amblyopia in children and diplopia in adults)

- Botulinum toxin injection

- Surgical correction

Surgical correction of the hypertropia is desired to achieve binocularity, manage diplopia and/or correct the cosmetic defect. Steps to achieve the same depend on mechanism of the hypertropia and identification of the offending muscles causing the misalignment. Various surgical procedures have been described and should be offered after careful examination of eyes, including a detailed orthoptic examination focussing on the disturbances in ocular motility and visual status. Specialty fellowship trained pediatric ophthalmologists and strabismus surgeons are best equipped to deal with these complex procedures.

It is essential that a child with strabismus is presented to the ophthalmologist as early as possible for diagnosis and treatment in order to allow best possible monocular and binocular vision to develop. Initially, the patient will have a full eye examination to identify any associated pathology, and any glasses required to optimise acuity will be prescribed – although infantile esotropia is not typically associated with refractive error. Studies have found that approximately 15% of infantile esotropia patients have accommodative esotropia. For these patients, antiaccommodative therapy (with spectacles) is indicated before any surgery as antiaccommodative therapy fully corrects their esotropia in many cases and significantly decreases their deviation angle in others.

Amblyopia will be treated via occlusion treatment (using patching or atropine drops) of the non-squinting eye with the aim of achieving full alternation of fixation. Management thereafter will be surgical. As alternative to surgery, also botulinum toxin therapy has been used in children with infantile esotropia. Furthermore, as accompaniment to ophtalmologic treatment, craniosacral therapy may be performed in order to relieve tension ("see also:" Management of strabismus).

According to a Cochrane review of 2012, controversies remain regarding type of surgery, non-surgical intervention and age of intervention.

The aims of treatment are as follows:

The elimination of any amblyopia

A cosmetically acceptable ocular alignment

long term stability of eye position

binocular cooperation.

There is no treatment of conjugate gaze palsy itself, so the disease or condition causing the gaze palsy must be treated, likely by surgery. As stated in the causes section, the gaze palsy may be due to a lesion caused by stroke or a condition. Some of the conditions such as Progressive supra nuclear palsy are not curable, and treatment only includes therapy to regain some tasks, not including gaze control. Other conditions such as Niemann-Pick disease type C have limited drug therapeutic options. Stroke victims with conjugate gaze palsies may be treated with intravenous therapy if the patent presents early enough, or with a surgical procedure for other cases.

The prognosis for each patient with esotropia will depend upon the origin and classification of their condition. However, in general, management will take the following course:

1. Identify and treat any underlying systemic condition.

2. Prescribe any glasses required and allow the patient time to 'settle into' them.

3. Use occlusion to treat any amblyopia present and encourage alternation.

4. Where appropriate, orthoptic exercises can be used to attempt to restore binocularity.

5. Where appropriate, prismatic correction can be used, either temporarily or permanently, to relieve symptoms of double vision.

6. In specific cases, and primarily in adult patients, botulinum toxin can be used either as a permanent therapeutic approach, or as a temporary measure to prevent contracture of muscles prior to surgery

7. Where necessary, extra-ocular muscle surgery can be undertaken to improve cosmesis and, on occasion, restore binocularity.

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 prognosis of a lesion in the visual neural pathways that causes a conjugate gaze palsy varies greatly. Depending on the nature of the lesion, recovery may happen rapidly or recovery may never progress. For example, optic neuritis, which is caused by inflammation, may heal in just weeks, while patients with an ischemic optic neuropathy may never recover.

DVD is often mistaken for over-action of the inferior oblique extra-ocular muscles. DVD can be revealed on ocular movement testing when one eye is occluded by the nose on lateral gaze. This eye will then elevate, simulating an inferior oblique over action. However, in a unilateral case, overaction of the superior rectus muscle in the unaffected dominant eye, can also be a causing factor as well as causing a V pattern exophoria.

The cause for pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder. It also may be induced temporarily by disorientation (such as on roller coaster rides) or by certain drugs (alcohol and other central nervous system depressants, inhalant drugs, stimulants, psychedelic drugs, and dissociative drugs).

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.

There is generally no treatment to cure achromatopsia. However, dark red or plum colored filters are very helpful in controlling light sensitivity.

Since 2003, there is a cybernetic device called eyeborg that allows people to perceive color through sound waves. Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004, the eyeborg allowed him to start painting in color by memorizing the sound of each color.

Moreover, there is some research on gene therapy for animals with achromatopsia, with positive results on mice and young dogs, but less effectiveness on older dogs. However, no experiments have been made on humans. There are many challenges to conducting gene therapy on humans. See Gene therapy for color blindness for more details about it.

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

If an optokinetic drum is available, rotate the drum in front of the patient. Ask the patient to look at the drum as you rotate it slowly. If an optokinetic drum is not available, move a strip of paper with alternating 2-inch black and white strips across the patient's visual field. Pass it in front of the patient's eye at reading distance while instructing the patient to look at it as it rapidly moves by. With normal vision, a nystagmus develops in both adults and infants. The nystagmus consists of initial slow phases in the direction of the stimulus (smooth pursuits), followed by fast, corrective phases (saccade). Presence of nystagmus indicates an intact visual pathway.

Another effective method is to hold a mirror in front of the patient and slowly rotate the mirror to either side of the patient. The patient with an intact visual pathway will maintain eye contact with herself or himself. This compelling optokinetic stimulus forces reflex slow eye movements.

OKN can be used as a crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for optokinetic nystagmus to determine whether there is an intact visual pathway.

The optokinetic response is a combination of a slow-phase and fast-phase eye movements. It is seen when an individual follows a moving object with their eyes, which then moves out of the field of vision at which point their eye moves back to the position it was in when it first saw the object. The reflex develops at about 6 months of age.

Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is present normally. The optokinetic response allows the eye to follow objects in motion when the head remains stationary (e.g., observing individual telephone poles on the side of the road as one travels by them in a car, or observing stationary objects while walking past them).

Accommodative esotropia (also called "refractive esotropia") is an inward turning of the eyes due to efforts of accommodation. It is often seen in patients with moderate amounts of hyperopia. The person with hyperopia, in an attempt to "accommodate" or focus the eyes, converges the eyes as well, as convergence is associated with activation of the accommodation reflex. The over-convergence associated with the extra accommodation required to overcome a hyperopic refractive error can precipitate a loss of binocular control and lead to the development of esotropia.

The chances of an esotropia developing in a hyperopic child will depend to some degree on the amount of hyperopia present. Where the degree of error is small, the child will typically be able to maintain control because the amount of over-accommodation required to produce clear vision is also small. Where the degree of hyperopia is large, the child may not be able to produce clear vision no matter how much extra-accommodation is exerted and thus no incentive exists for the over-accommodation and convergence that can give rise to the onset of esotropia. However, where the degree of error is small enough to allow the child to generate clear vision by over-accommodation, but large enough to disrupt their binocular control, esotropia will result.

Only about 20% of children with hyperopia greater than +3.5 diopters develop strabismus.

Where the esotropia is solely a consequence of uncorrected hyperopic refractive error, providing the child with the correct glasses and ensuring that these are worn all the time, is often enough to control the deviation. In such cases, known as 'fully accommodative esotropias,' the esotropia will only be seen when the child removes their glasses. Many adults with childhood esotropias of this type make use of contact lenses to control their 'squint.' Some undergo refractive surgery for this purpose.

A second type of accommodative esotropia also exists, known as 'convergence excess esotropia.' In this condition the child exerts excessive accommodative convergence relative to their accommodation. Thus, in such cases, even when all underlying hyperopic refractive errors have been corrected, the child will continue to squint when looking at very small objects or reading small print. Even though they are exerting a normal amount of accommodative or 'focusing' effort, the amount of convergence associated with this effort is excessive, thus giving rise to esotropia. In such cases an additional hyperopic correction is often prescribed in the form of bifocal lenses, to reduce the degree of accommodation, and hence convergence, being exerted. Many children will gradually learn to control their esotropias, sometimes with the help of orthoptic exercises. However, others will eventually require extra-ocular muscle surgery to resolve their problems.

One form of LCA, patients with LCA2 bearing a mutation in the RPE65 gene, has been successfully treated in clinical trials using gene therapy. The results of three early clinical trials were published in 2008 demonstrating the safety and efficacy of using adeno-associated virus to deliver gene therapy to restore vision in LCA patients. In all three clinical trials, patients recovered functional vision without apparent side-effects. These studies, which used adeno-associated virus, have spawned a number of new studies investigating gene therapy for human retinal disease.

The results of a phase 1 trial conducted by the University of Pennsylvania and Children’s Hospital of Philadelphia and published in 2009 showed sustained improvement in 12 subjects (ages 8 to 44) with RPE65-associated LCA after treatment with AAV2-hRPE65v2, a gene replacement therapy. Early intervention was associated with better results. In that study, patients were excluded based on the presence of particular antibodies to the vector AAV2 and treatment was only administered to one eye as a precaution. A 2010 study testing the effect of administration of AAV2-hRPE65v2 in both eyes in animals with antibodies present suggested that immune responses may not complicate use of the treatment in both eyes.

Eye Surgeon Dr. Al Maguire and gene therapy expert Dr. Jean Bennett developed the technique used by the Children's Hospital.

Dr. Sue Semple-Rowland at the University of Florida has recently restored sight in an avian model using gene therapy.

A number of maneuvers have been found to be effective including: the Epley maneuver, the Semont maneuver, and to a lesser degree Brandt–Daroff exercises. Both the Epley and the Semont maneuver are equally effective.

A rostral lesion within the midbrain may affect the convergence center thus causing bilateral divergence of the eyes which is known as the WEBINO syndrome (Wall Eyed Bilateral INO) as each eye looks at the opposite "wall".

If the lesion affects the PPRF (or the abducens nucleus) and the MLF on the same side (the MLF having crossed from the opposite side), then the "one and a half syndrome" occurs which, simply put, involves paralysis of all conjugate horizontal eye movements other than abduction of the eye on the opposite side to the lesion.

Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus. Additionally, the divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side. Convergence is generally preserved.

Unfortunately, there is no real way to prevent against vertiginous episodes out of the means of managing the disease. As head trauma is a major cause for vertiginous epilepsy, protecting the head from injury is an easy way to avoid possible onset of these seizures. With recent advances in science it is also possible for an individual to receive genetic screening, but this only tells if the subject is predisposed to developing the condition and will not aid in preventing the disease.

There is a range of ways to manage vertiginous epilepsy depending on the severity of the seizures. For simple partial seizures medical treatment is not always necessary. To the comfort of the patient, someone ailed with this disease may be able to lead a relatively normal life with vertiginous seizures. If, however, the seizures become too much to handle, antiepileptic medication can be administered as the first line of treatment. There are several different types of medication on the market to deter epileptic episodes but there is no support to show that one medication is more effective than another. In fact, research has shown that simple partial seizures do not usually respond well to medication, leaving the patient to self-manage their symptoms. A third option for treatment, used only in extreme cases when seizure symptoms disrupt daily life, is surgery wherein the surgeon will remove the epileptic region.

Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and hyoscine butylbromide (scopolamine) respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications) have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor- or ion channel-specific. Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménière's disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the patient's symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition.

No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

Pendular nystagmus is a sinusoidal oscillation, which refers to the waveform of involuntary eye movements that may occur in any direction. It is characterized by the multidimensional slow eye movements of the eyes (1 Hz frequency) with an equal velocity in each direction that resembles the trajectory of a pendulum. These pattern of these movements may differ between the two eyes. Depending upon the pattern of movements, pendular nystagmus has been divided into different subtypes such as congenital nystagmus, acquired pendular nystagmus, and amaurotic nystagmus.