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.

It may be acquired from:

- Diseases. Some of the diseases that present nystagmus as a pathological sign:

- Aniridia

- Toxic or metabolic reasons could be the result of the following:

- Central nervous system (CNS) disorders, such as with a cerebellar problem, the nystagmus can be in any direction "including" horizontal. Purely vertical nystagmus is usually central in origin, but it is also a frequent adverse effect of high phenytoin toxicity. Causes include:

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.

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).

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.

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.

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

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.

The disorder is caused by injury or dysfunction in the medial longitudinal fasciculus (MLF), a heavily myelinated tract that allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF)-abducens nucleus complex of the contralateral side to the oculomotor nucleus of the ipsilateral side.

In young patients with bilateral INO, multiple sclerosis is often the cause. In older patients with one-sided lesions a stroke is a distinct possibility. Other causes are possible.

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.

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).

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.

Amaurotic nystagmus is defined as the nystagmus associated with blindness or the central vision defects. It is characterized by the pendular or jerky movements of the eyes in the patients who have visual impairement for a long period of time.

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.

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 one and a half syndrome is a rare weakness in eye movement affecting both eyes, in which one cannot move laterally at all, and the other can move in only one lateral direction (inward or outward). More formally, it is characterized by ""a conjugate horizontal gaze palsy in one direction and an internuclear ophthalmoplegia in the other"". The most common manifestation of this unusual syndrome is limitation of horizontal eye movement to abduction (moving away from the midline) of one eye (e.g. right eye in the diagram on the right) with no horizontal movement of the other eye (e.g. left eye in the diagram on the right). Nystagmus is also present when the eye on the opposite side of the lesion is abducted. Convergence is classically spared as cranial nerve III (oculomotor nerve) and its nucleus is spared bilaterally.

The number of cases is around 0.5 to 0.7 per 10,000 births, making it a relatively rare condition.

Bruns nystagmus is an unusual type of bilateral nystagmus most commonly occurring in patients with cerebellopontine angle tumours. It is caused by the combination of slow, large amplitude nystagmus (gaze paretic nystagmus) when looking towards the side of the lesion, and rapid, small amplitude nystagmus (vestibular nystagmus) when looking away from the side of the lesion. It occurs in 11% of patients with vestibular schwannoma, and occurs mainly in patients with larger tumours (67% of patients with tumours over 3.5 cm diameter). Bruns nystagmus is also associated with an increased incidence of balance disturbance in patients with vestibular schwannoma. It may be caused by the compression of both flocculi, the vestibular part of the cerebellum, and improvement in both the nystagmus and balance problems occur commonly after removal of the tumour.

Bruns nystagmus is named for Ludwig Bruns (1858 – 1915).

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.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

Zonular cataract and nystagmus, also referred as Nystagmus with congenital zonular cataract is a rare congenital disease associated with Nystagmus and zonular cataract of the eye.

Diagnosing CVI is difficult. A diagnosis is usually made when visual performance is poor but it is not possible to explain this from an eye examination. Before CVI was widely known among professionals, some would conclude that the patient was faking their problems or had for some reason engaged in self-deception. However, there are now testing techniques that do not depend on the patient's words and actions, such as fMRI scanning, or the use of electrodes to detect responses to stimuli in both the retina and the brain. These can be used to verify that the problem is indeed due to a malfunction of the visual cortex and/or the posterior visual pathway.

It has been suggested that the disease follows a x-linked pattern of inheritance though studies done on this particular disease are few.

Persistent hyperplastic primary vitreous (PHPV), also known as Persistent Fetal Vasculature (PFV), is a rare congenital developmental anomaly of the eye that results

following failure of the embryological, primary vitreous and hyaloid vasculature to regress. It can be present in three forms: purely anterior (persistent tunica vasculosa lentis and persistent posterior fetal fibrovascular sheath of the lens), purely posterior (falciform retinal septum and ablatio falcicormis congenita) and a combination of both. Most examples of PHPV are unilateral and non-hereditary. When bilateral, PHPV may follow an autosomal recessive or autosomal dominant inheritance pattern.

Alexanders law refers to spontaneous nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

Alexander's law states that in individuals with nystagmus, the amplitude of the nystagmus increases when the eye moves in the direction of the fast phase (saccade).

It is manifested during spontaneous nystagmus in a patient with a vestibular lesion. The nystagmus becomes more intense when the patient looks in the quick-phase than in the slow-phase direction.

The law was named after Gustav Alexander who described it in 1912.