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:

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).

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 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.

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.

While preventive measures, such as taking breaks from activities that cause eye strain are suggested, there are certain treatments which a person suffering from the condition can take to ease the pain or discomfort that the affliction causes. Perhaps the most effective of these is to remove all light sources from a room and allow the eyes to relax in darkness. Free of needing to focus, the eyes will naturally relax over time, and relieve the discomfort that comes with the strain. Cool compresses also help to some degree, though care should be taken to not use anything cold enough to damage the eyes themselves (such as ice). A number of companies have released "computer glasses" which, through the use of specially tinted lenses, help alleviate many of the factors which cause eye strain, though they do not completely prevent it. Rather, they just make it harder to strain the eye.

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.

Although treatment may be unnecessary, there may be social implications, especially in young children when venturing from a supportive home environment to a public environment (e.g., starting school). Continued support, including monitoring behavior and educating the child about his or her appearance as seen by others, is encouraged. Gradual or sudden withdrawal from interaction with others is a sign that may or may not be related to such behavior. Studies are being conducted to elucidate these implications.

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.

Inverse Marcus Gunn phenomenon is a rare condition that causes the eyelid to fall upon opening of the mouth. In this case, trigeminal innervation to the pterygoid muscles of the jaw is associated with an inhibition of the branch of the oculomotor nerve to the levator palpebrae superioris, as opposed to stimulation in Marcus Gunn jaw-winking.

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.

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 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.

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug. Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination. Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

The majority of patients remain symptom free and able to maintain binocularity with only a slight face turn. Amblyopia is uncommon and, where present, rarely dense. This can be treated with occlusion, and any refractive error can also be corrected.

Duane syndrome cannot be cured, as the "missing" cranial nerve cannot be replaced, and traditionally there has been no expectation that surgery will result in any increase in the range of eye movement. Surgical intervention, therefore, has only been recommended where the patient is unable to maintain binocularity, where they are experiencing symptoms, or where they are forced to adopt a cosmetically unsightly or uncomfortable head posture in order to maintain binocularity. The aims of surgery are to place the eye in a more central position and, thus, place the field of binocularity more centrally also, and to overcome or reduce the need for the adoption of an abnormal head posture. Occasionally, surgery is not needed during childhood, but becomes appropriate later in life, as head position changes (presumably due to progressive muscle contracture).

Surgical approaches include:

- Medial rectus recession in the involved eye or both eyes. By weakening the medial rectus muscles this procedure improves the crossed-eye appearance but does not improve outward eye movements (abductions).

- Morad et al. showed improved abduction after modest unilateral medial rectus recession and lateral rectus resection in a subgroup of patients with mild eye retraction and good adduction before surgery.

- Lateral transposition of the vertical muscles described by Rosenbaum has been shown to improve range of movement of the eye. The surgical procedure produces 40-65 degrees of binocular field. Orbital wall fixation of the lateral rectus muscle (muscle is disinserted and reattached to lateral orbital wall) is recommended an effective method to inactivate a lateral rectus muscle in cases of marked anomalous innervation and severe cocontraction.

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

A gaze palsy is the paresis of conjugate eye movements.

Horizontal gaze palsy may be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion, or from brain stem lesions, which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion. These will result in horizontal gaze deviations from unopposed action of the unaffected extraocular muscles. Another way to remember this is that patients with hemisphere lesions look towards their lesion, while patients with pontine gaze palsies look away from their lesions. Note that patients with gaze palsy still have conjugate eye movements and therefore do not complain of diplopia.

The human Robo gene acts as a receptor for a midline repulsive cue. When Robo is mutated, the longitudinal tract formation is disrupted and therefore normal neuronal connections cannot form. This leads to the reduced hindbrain volume and scoliosis, which are common symptoms of horizontal gaze palsy.

Sometimes asthenopia can be due to specific visual problems—for example, uncorrected refraction errors or binocular vision problems such as accommodative insufficiency or heterophoria. It is often caused by the viewing of monitors such as those of computers or phones for prolonged periods of time.

Most patients are diagnosed by the age of 10 years and Duane's is more common in girls (60 percent of the cases) than boys (40 percent of the cases). A French study reports that this syndrome accounts for 1.9% of the population of strabismic patients, 53.5% of patients are female, is unilateral in 78% of cases, and the left eye (71.9%) is affected more frequently than the right. Around 10–20% of cases are familial; these are more likely to be bilateral than non-familial Duane syndrome. Duane syndrome has no particular race predilection.

Oculomotor apraxia (OMA), also known as Cogan ocular motor apraxia or saccadic initiation failure (SIF) is the absence or defect of controlled, voluntary, and purposeful eye movement. It was first described in 1952 by the American ophthalmologist David Glendenning Cogan. People with this condition have difficulty moving their eyes horizontally and moving them quickly. The main difficulty is in saccade initiation, but there is also impaired cancellation of the vestibulo-ocular reflex. Patients have to turn their head in order to compensate for the lack of eye movement initiation in order to follow an object or see objects in their peripheral vision, but they often exceed their target. There is controversy regarding whether OMA should be considered an apraxia, since apraxia is the inability to perform a learned or skilled motor action to command, and saccade initiation is neither a learned nor a skilled action.

Ophthalmoparesis or ophthalmoplegia refers to weakness (-paresis) or paralysis (-plegia) of one or more extraocular muscles which are responsible for eye movements. It is a physical finding in certain neurologic, ophthalmologic, and endocrine disease.

Internal ophthalmoplegia means involvement limited to the pupillary sphincter and ciliary muscle. External ophthalmoplegia refers to involvement of only the extraocular muscles. Complete ophthalmoplegia indicates involvement of both.

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).

It may be mistaken for choreoathetosis, however, these abnormal movements are relatively constant irrespective of whether the eyes are open or closed and occur in the absence of proprioceptive loss.