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.

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.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development.

Thereafter, a period of observation of around 9 to 12 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

This is most commonly achieved through the use of fresnel prisms. These slim flexible plastic prisms can be attached to the patient's glasses, or to plano glasses if the patient has no refractive error, and serve to compensate for the inward misalignment of the affected eye. Unfortunately, the prism only correct for a fixed degree of misalignment and, because the affected individual's degree of misalignment will vary depending upon their direction of gaze, they may still experience diplopia when looking to the affected side. The prisms are available in different strengths and the most appropriate one can be selected for each patient. However, in patients with large deviations, the thickness of the prism required may reduce vision so much that binocularity is not achievable. In such cases it may be more appropriate simply to occlude one eye temporarily. Occlusion would never be used in infants though both because of the risk of inducing stimulus deprivation amblyopia and because they do not experience diplopia.

Other management options at this initial stage include the use of botulinum toxin, which is injected into the ipsilateral medial rectus (botulinum toxin therapy of strabismus). The use of BT serves a number of purposes. Firstly, it helps to prevent the contracture of the medial rectus which might result from its acting unopposed for a long period. Secondly, by reducing the size of the deviation temporarily it might allow prismatic correction to be used where this was not previously possible, and, thirdly, by removing the pull of the medial rectus it may serve to reveal whether the palsy is partial or complete by allowing any residual movement capability of the lateral rectus to operate. Thus, the toxin works both therapeutically, by helping to reduce symptoms and enhancing the prospects for fuller ocular movements post-operatively, and diagnostically, by helping to determine the type of operation most appropriate for each patient.

Medication is used for strabismus in certain circumstances. In 1989, the US FDA approved Botulinum toxin therapy for strabismus in patients over 12 years old. Most commonly used in adults, the technique is also used for treating children, in particular children affected by infantile esotropia. The toxin is injected in the stronger muscle, causing temporary and partial paralysis. The treatment may need to be repeated three to four months later once the paralysis wears off. Common side effects are double vision, droopy eyelid, overcorrection, and no effect. The side effects typically resolve also within three to four months. Botulinum toxin therapy has been reported to be similarly successful as strabismus surgery for people with binocular vision and less successful than surgery for those who have no binocular vision.

Congenital fourth cranial nerve palsy can be treated with strabismus surgery, where muscle attachment sites on the globe are modified to realign the eyes. Some eye doctors prefer conservative or no management of congenital fourth nerve palsy.

Other eye doctors recommend surgery early in a patient's life to prevent the compensatory torticollis and facial asymmetry that develop with age.

Prism lenses set to make minor optical changes in the vertical alignment may be prescribed instead of or after surgery to fine-tune the correction. Prism lenses do not address torsional misalignment and this may limit their use in certain cases. An additional consideration of prism lenses is that they must be worn at all times. Prism lenses reduce vertical fusional demands by allowing the eyes to rest in their vertically misaligned state. When they are removed the patient may experience vertical diplopia they find hard to resolve due to the rested state of their eyes.

Cases of congenital fourth nerve palsy vary in magnitude and way they affect the motion of the superior oblique muscle. Therefore different surgeries are available dependent upon the type of misalignment. Sometimes surgery on more than one eye muscle is required. In some simpler, unilateral cases a single surgery may suffice. In these cases the main problem is that the inferior oblique muscle of the same eye acts unopposed by the weakened superior oblique muscle, pulling the eye up. An example of a safe and effective procedure is a disinsertion of the inferior oblique muscle to allow it to reattach itself further down the globe of the eye. This acts to 'weaken' its action and allow the eye to move back into a more neutral alignment.

In all cases of congenital fourth nerve palsy, it is important to see an experienced strabismologist about management/treatment options. A strabismologist is an ophthalmologist (eye doctor) specialising in eye movement disorders.

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.

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.

In cases of accommodative esotropia, the eyes turn inward due to the effort of focusing far-sighted eyes, and the treatment of this type of strabismus necessarily involves refractive correction, which is usually done via corrective glasses or contact lenses, and in these cases surgical alignment is considered only if such correction does not resolve the eye turn.

In case of strong anisometropia, contact lenses may be preferable to spectacles because they avoid the problem of visual disparities due to size differences (aniseikonia) which is otherwise caused by spectacles in which the refractive power is very different for the two eyes. In a few cases of strabismic children with anisometropic amblyopia, a balancing of the refractive error eyes via refractive surgery has been performed before strabismus surgery was undertaken.

Early treatment of strabismus when the person is a baby may reduce the chance of developing amblyopia and depth perception problems. However, a review of randomized controlled trials concluded that the use of corrective glasses to prevent strabismus is not supported by existing research. Most children eventually recover from amblyopia if they have had the benefit of patches and corrective glasses. Amblyopia has long been considered to remain permanent if not treated within a critical period, namely before the age of about seven years; however, recent discoveries give reason to challenge this view and to adapt the earlier notion of a critical period to account for stereopsis recovery in adults.

Eyes that remain misaligned can still develop visual problems. Although not a cure for strabismus, prism lenses can also be used to provide some temporary comfort and to prevent double vision from occurring.

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.

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.

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.

Although no cure exists, there are many different treatments which are currently being used to help control symptoms. These include short term treatment with some drugs (such as Botox) which relax the muscles, use of temperature changes to control muscle tremors, and a balanced approach of coordinated care and support involving physical therapists, orthopedic surgeons, and psychiatrists.

Because there is no cure for ataxic cerebral palsy, current methods of treatment are diverse, often consisting of multiple focuses designed to limit the severity of symptoms. Many children suffering from ataxic cerebral palsy are treated by teams consisting of individuals from numerous disciplines, including physical therapists, occupational therapist, orthopedic surgeons, and psychiatrists. Treatment by such teams involves multiple approaches. Providing a primary care medical home to support children suffering from common symptoms of nutritional deficiencies, pain, dental care, bowel and bladder continence, and orthopedic complications is an essential aspect of treatment. In addition, utilizing diagnostic techniques to identify the nature and severity of brain abnormalities has become increasingly beneficial for treatment in recent years.

Different medications have been used to temporarily treat ataxic cerebral palsy. Medications like primidone and benzodiazepine, while not recommended for long term use, can alleviate some of the tremor symptoms. Botox which relaxes tightened muscles has been effective in treating voice, hand and head tremors. A few recently published papers outlined a potential method for treating intention tremor which consisted of cooling the forearm by wrapping it in a cryomanchet using a circulating fluid. After the treatment most patients experienced reduced tremor for up to half an hour. This practical, however short-term treatment can facilitate performing normal daily activities like applying make up, eating, or signing documents. This potential treatment method is also significant in that it reduces one’s reliance on caregivers.

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.

Medications that impede the release of excitatory neurotransmitters have been used to control or prevent spasms. Treatment with intrathecal baclofen, a gamma-aminobutyric acid (GABA) agonist, decreases muscle tone and has been shown to decrease the frequency of muscle spasms in ADCP patients. Tetrabenazine, a drug commonly used in the treatment of Huntington's disease, has been shown to be effective treating chorea.

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.

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.

Corticosteroids such as prednisone improve recovery at 6 months and are thus recommended. Early treatment (within 3 days after the onset) is necessary for benefit with a 14% greater probability of recovery.

Physical therapy and Occupational Therapy are staple treatments of ADCP. Physical therapy is initiated soon after diagnosis and typically focuses on trunk strength and maintaining posture. Physical therapy helps to improve mobility, range of motion, functional ability, and quality of life. Specific exercises and activities prescribed by a therapist help to prevent muscles from deteriorating or becoming locked in position and help to improve coordination. Occupational therapy interventions for children with CP can include feeding, dressing, bathing, toileting, grooming, pencil grasp and handwriting skills, play, and use of adaptive equipment.

Physiotherapy can be beneficial to some individuals with Bell’s palsy as it helps to maintain muscle tone of the affected facial muscles and stimulate the facial nerve. It is important that muscle re-education exercises and soft tissue techniques be implemented prior to recovery in order to help prevent permanent contractures of the paralyzed facial muscles. To reduce pain, heat can be applied to the affected side of the face. There is no high quality evidence to support the role of electrical stimulation for Bell's palsy.

Current forms of prevention are focused during pregnancy, while others are focused immediately after birth. Some methods that have been used include prolonging the pregnancy using interventions such as 17-alpha progesterone, limiting the number of gestations during pregnancy (for pregnancies induced by assistive reproductive technology), antenatal steroid for mothers likely to deliver prematurely, high caffeine for premature births with extremely low birth weights.

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

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.

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.

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.