Symptoms of conjugate gaze palsies include the impairment of gaze in various directions and different types of movement, depending on the type of gaze palsy. Signs of a person with a gaze palsy may be frequent movement of the head instead of the eyes. For example, a person with a horizontal saccadic palsy may jerk their head around while watching a movie or high action event instead of keeping their head steady and moving their eyes, which usually goes unnoticed. Someone with a nonselective horizontal gaze palsy may slowly rotate their head back and forth while reading a book instead of slowly scanning their eyes across the page.

Conjugate gaze palsies can be classified into palsies affecting horizontal gaze and vertical gaze.

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.

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.

The nerve dysfunction induces esotropia, a convergent squint on distance fixation. On near fixation the affected individual may have only a latent deviation and be able to maintain binocularity or have an esotropia of a smaller size. Patients sometimes adopt a face turned towards the side of the affected eye, moving the eye away from the field of action of the affected lateral rectus muscle, with the aim of controlling diplopia and maintaining binocular vision.

Diplopia is typically experienced by adults with VI nerve palsies, but children with the condition may not experience diplopia due to suppression. The neuroplasticity present in childhood allows the child to 'switch off' the information coming from one eye, thus relieving any diplopic symptoms. Whilst this is a positive adaptation in the short term, in the long term it can lead to a lack of appropriate development of the visual cortex giving rise to permanent visual loss in the suppressed eye; a condition known as amblyopia.

Pathological nystagmus is characterized by "excessive drifts of stationary retinal images that degrades vision and may produce illusory motion of the seen world: oscillopsia (an exception is congenital nystagmus)".

When nystagmus occurs without fulfilling its normal function, it is pathologic (deviating from the healthy or normal condition). Pathological nystagmus is the result of damage to one or more components of the vestibular system, including the semicircular canals, otolith organs, and the vestibulocerebellum.

Pathological nystagmus generally causes a degree of vision impairment, although the severity of such impairment varies widely. Also, many blind people have nystagmus, which is one reason that some wear dark glasses.

Physiological nystagmus is a form of involuntary eye movement that is part of the vestibulo-ocular reflex (VOR), characterized by alternating smooth pursuit in one direction and saccadic movement in the other direction.

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.

Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI (the abducens nerve), which is responsible for causing contraction of the lateral rectus muscle to abduct (i.e., turn out) the eye. The inability of an eye to turn outward results in a convergent strabismus or esotropia of which the primary symptom is diplopia (commonly known as double vision) in which the two images appear side-by-side. The condition is commonly unilateral but can also occur bilaterally.

The unilateral abducens nerve palsy is the most common of the isolated ocular motor nerve palsies.

Parinaud's Syndrome is a cluster of abnormalities of eye movement and pupil dysfunction, characterized by:

1. Paralysis of upgaze: Downward gaze is usually preserved. This vertical palsy is supranuclear, so doll's head maneuver should elevate the eyes, but eventually all upward gaze mechanisms fail.

2. Pseudo-Argyll Robertson pupils: Accommodative paresis ensues, and pupils become mid-dilated and show light-near dissociation.

3. Convergence-Retraction nystagmus: Attempts at upward gaze often produce this phenomenon. On fast up-gaze, the eyes pull in and the globes retract. The easiest way to bring out this reaction is to ask the patient to follow down-going stripes on an optokinetic drum.

4. Eyelid retraction (Collier's sign)

5. Conjugate down gaze in the primary position: "setting-sun sign". Neurosurgeons see this sign most commonly in patients with failed hydrocephalus shunts.

It is also commonly associated with bilateral papilledema. It has less commonly been associated with spasm of accommodation on attempted upward gaze, pseudoabducens palsy (also known as thalamic esotropia) or slower movements of the abducting eye than the adducting eye during horizontal saccades, see-saw nystagmus and associated ocular motility deficits including skew deviation, oculomotor nerve palsy, trochlear nerve palsy and internuclear ophthalmoplegia.

Though present from birth, symptoms of congenital fourth cranial nerve palsy may start as subtle and increase with age. Hence, diagnosis by a healthcare practitioner may not be made until later childhood or adulthood. Young children adopt a compensatory head position in order to compensate for the underacting superior oblique muscle. The characteristic head tilt is usually away from the affected side to reduce eye strain and prevent double vision (diplopia). Old photographs may reveal the presence of a consistent head tilt (ocular torticollis) from an early age. Most patients with congenital CN IV palsy have facial asymmetry due to the chronic head tilt. Other compensatory measures for congenital fourth nerve palsy are development of large vertical fusional amplitudes and lack of subjective symptoms of , even in the presence of great ocular rotation.

Congenital fourth nerve palsy may remain undetected until adulthood, when intermittent diplopia may arise, due to decompensated ability to overcome the vertical deviation. Until this occurs, many ophthalmologists and optometrists may miss the other signs and symptoms. Reduced vertical fusional reserves result from fatigue (stress, fever, other illnesses, a lot of near work) or simply the effects of old age. Diplopia from congenital fourth nerve palsy has occasionally been reported to manifest transiently during pregnancy. Congenital fourth nerve palsy may also become evident following cataract surgery once binocular vision is restored after a long period of progressive monocular visual loss and accompanying vergence decompensation. Other adult patients complain of neck pain, after years of chronic head tilting (ocular torticollis).

Congenital fourth nerve palsy can affect reading comprehension (and concentration during other near tasks) due to the increased vertical fusional demands and head tilting required to maintain single vision and prevent vertical diplopia. Some patients find they lose their place easily while reading, and find a marker or using a finger to guide them helpful.

The head posture is right 4th nerve palsy can be easily understood by this thumb rule- The body performs the action which the paralysed muscle had to perform. Keeping this thumb rule in mind, let us decipher the head posture in right 4th nerve palsy. As SO causes intorsion, the head tilts towards the left. As SO causes depression in adduction, the head turns towards left and depressed chin. So the patient has left side deflection, tilt and a downward gaze. The left SO palsy head posture can be understood similarly as well.

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.

Oculomotor nerve palsy or third nerve palsy is an eye condition resulting from damage to the third cranial nerve or a branch thereof. As the name suggests, the oculomotor nerve supplies the majority of the muscles controlling eye movements. Thus, damage to this nerve will result in the affected individual being unable to move his or her eye normally. In addition, the nerve also supplies the upper eyelid muscle (levator palpebrae superioris) and the muscles responsible for pupil constriction (sphincter pupillae) . The limitations of eye movements resulting from the condition are generally so severe that the affected individual is unable to maintain normal alignment of their eyes when looking straight ahead, leading to strabismus and, as a consequence, double vision (diplopia).

It is also known as "oculomotor neuropathy".

- "For acquired fourth nerve palsy, see fourth nerve palsy"

Congenital fourth nerve palsy is a condition present at birth characterized by a vertical misalignment of the eyes due to a weakness or paralysis of the superior oblique muscle.

Other names for fourth nerve palsy include superior oblique palsy and trochlear nerve palsy.

When looking to the right/left the nerve/muscle isn't strong enough or is too long and the eye drifts up.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.

Strabismus may also be classified based on time of onset, either congenital, acquired, or secondary to another pathological process. Many infants are born with their eyes slightly misaligned, and this is typically outgrown by six to 12 months of age. Acquired and secondary strabismus develop later. The onset of accommodative esotropia, an overconvergence of the eyes due to the effort of accommodation, is mostly in early childhood. Acquired non-accommodative strabismus and secondary strabismus are developed after normal binocular vision has developed. In adults with previously normal alignment, the onset of strabismus usually results in double vision.

Any disease that causes vision loss may also cause strabismus, but it can also result from any severe and/or traumatic injury to the affected eye. Sensory strabismus is strabismus due to vision loss or impairment, leading to horizontal, vertical or torsional misalignment or to a combination thereof, with the eye with poorer vision drifting slightly over time. Most often, the outcome is horizontal misalignment. Its direction depends on the patient age at which the damage occurs: patients whose vision is lost or impaired at birth are more likely to develop esotropia, whereas patients with acquired vision loss or impairment mostly develop exotropia. In the extreme, complete blindness in one eye generally leads to the blind eye reverting to an anatomical position of rest.

Although many possible causes of strabismus are known, among them severe and/or traumatic injuries to the afflicted eye, in many cases no specific cause can be identified. This last is typically the case when strabismus is present since early childhood.

Results of a U.S. cohort study indicate that the incidence of adult-onset strabismus increases with age, especially after the sixth decade of life, and peaks in the eighth decade of life, and that the lifetime risk of being diagnosed with adult-onset strabismus is approximately 4%.

The syndrome usually results from single unilateral lesion of the paramedian pontine reticular formation and the ipsilateral medial longitudinal fasciculus. An alternative anatomical cause is a lesion of the abducens nucleus (VI) on one side (resulting in a failure of abduction of the ipsilateral eye and adduction of the contralateral eye = conjugate gaze palsy towards affected side), with interruption of the ipsilateral medial longitudinal fasciculus after it has crossed the midline from its site of origin in the contralateral abducens (VI) nucleus (resulting in a failure of adduction of the ipsilateral eye).

A complete oculomotor nerve palsy will result in a characteristic "down and out" position in the affected eye. The eye will be displaced outward and displaced downward; outward because the lateral rectus (innervated by the sixth cranial nerve) maintains muscle tone in comparison to the paralyzed medial rectus. The eye will be displaced downward, because the superior oblique (innervated by the fourth cranial or trochlear nerve), is unantagonized by the paralyzed superior rectus, inferior rectus and inferior oblique. The affected individual will also have a ptosis, or drooping of the eyelid, and mydriasis (pupil dilation).

It should be borne in mind, however, that the branched structure of the oculomotor nerve means that damage sustained at different points along its pathway, or damage caused in different ways (compression versus loss of blood supply, for example), will result in different muscle groups or, indeed, different individual muscles being affected, thus producing different presentation patterns.

Compressive oculomotor nerve damage could result in compression of the parasympathetic fibers before any disruption of the motor fibers occurs, since the parasympathetic fibers run on the outside of the nerve. Therefore, one could have lid ptosis and mydriasis (a "blown" pupil) as a result of parasympathetic fiber compression before the "down and out" position is seen.

When observing a person with strabismus, the misalignment of the eyes may be quite apparent. A patient with a constant eye turn of significant magnitude is very easy to notice. However, a small magnitude or intermittent strabismus can easily be missed upon casual observation. In any case, an eye care professional can conduct various tests, such as cover testing, to determine the full extent of the strabismus.

Symptoms of strabismus include double vision and/or eye strain. To avoid double vision, the brain may adapt by ignoring one eye. In this case, often no noticeable symptoms are seen other than a minor loss of depth perception. This deficit may not be noticeable in someone who has had strabismus since birth or early childhood, as they have likely learned to judge depth and distances using monocular cues. However, a constant unilateral strabismus causing constant suppression is a risk for amblyopia in children. Small-angle and intermittent strabismus are more likely to cause disruptive visual symptoms. In addition to headaches and eye strain, symptoms may include an inability to read comfortably, fatigue when reading, and unstable or "jittery" vision.

Concomitant esotropia – that is, an inward squint that does not vary with the direction of gaze – mostly sets in before 12 months of age (this constitutes 40% of all strabismus cases) or at the age of three or four. Most patients with "early-onset" concomitant esotropia are emmetropic, whereas most of the "later-onset" patients are hyperopic. It is the most frequent type of natural strabismus not only in humans, but also in monkeys.

Concomitant esotropia can itself be subdivided into esotropias that are ether "constant," or "intermittent."

- Constant esotropia

- Intermittent esotropia

A patient can have a constant esotropia for reading, but an intermittent esotropia for distance (but rarely vice versa).

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.

CPEO is a slowly progressing disease. It may begin at any age and progresses over a period of 5–15 years. The first presenting symptom of ptosis is often unnoticed by the patient until the lids droop to the point of producing a visual field defect. Often, patients will tilt the head backwards to adjust for the slowly progressing ptosis of the lids. In addition, as the ptosis becomes complete, the patients will use the frontalis (forehead) muscle to help elevate the lids. The ptosis is typically bilateral, but may be unilateral for a period of months to years before the fellow lid becomes involved.

Ophthalmoplegia or the inability or difficulty to move the eye is usually symmetrical. As such, double vision is sometimes a complaint of these patients. The progressive ophthalmoplegia is often unnoticed till decreased ocular motility limits peripheral vision. Often someone else will point out the ocular disturbance to the patient. Patients will move their heads to adjust for the loss of peripheral vision caused by inability to abduct or adduct the eye. All directions of gaze are affected; however, downward gaze appears to be best spared. This is in contrast to progressive supranuclear palsy (PSP), which typically affects vertical gaze and spares horizontal gaze.

Argyll Robertson pupils (AR pupils or, colloquially, "prostitute's pupils") are bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do "not" constrict when exposed to bright light (i.e., they do not react to light). They are a highly specific sign of neurosyphilis; however, Argyll Robertson pupils may also be a sign of diabetic neuropathy. In general, pupils that accommodate but do not react are said to show light-near dissociation (i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation/convergence).

AR pupils are extremely uncommon in the developed world. There is continued interest in the underlying pathophysiology, but the scarcity of cases makes ongoing research difficult.

Weakness of extraocular muscle groups including, the orbicularis oculi muscle as well as facial and limb muscles may be present in up to 25% of patients with CPEO. As a result of the orbicularis oculi weakness, patients may suffer from exposure keratopathy (damage to cornea) from the inability to close the eyes tightly. Frontalis muscle weakness may exacerbate the ptotic lids with the inability to compensate for the ptosis. Facial muscles may be involved which lead to atrophy of facial muscle groups producing a thin, expressionless face with some having difficulty with chewing. Neck, shoulder and extremity weakness with atrophy may affect some patients and can be mild or severe.

Mild visual impairment was seen in 95% of patients that were evaluated using the Visual Function Index (VF-14).

The ciliary muscles that control the lens shape and the iris muscles are often unaffected by CPEO.

Additional symptoms are variable, and may include exercise intolerance, cataracts, hearing loss, sensory axonal neuropathy, ataxia, clinical depression, hypogonadism, and parkinsonism.

Kearns–Sayre syndrome is characterized by onset before 15 years of age of CPEO, heart block and pigmentary retinopathy.

Depending upon the cause it can be classified into:

- "Neurogenic ptosis" which includes oculomotor nerve palsy, Horner's syndrome, Marcus Gunn jaw winking syndrome, third cranial nerve misdirection.

- "Myogenic ptosis" which includes oculopharyngeal muscular dystrophy, myasthenia gravis, myotonic dystrophy, ocular myopathy, simple congenital ptosis, blepharophimosis syndrome

- "Aponeurotic ptosis" which may be involutional or post-operative

- "Mechanical ptosis" which occurs due to edema or tumors of the upper lid

- "Neurotoxic ptosis" which is a classic symptom of envenomation by elapid snakes such as cobras, kraits, mambas and taipans. Bilateral ptosis is usually accompanied by diplopia, dysphagia and/or progressive muscular paralysis. Regardless, neurotoxic ptosis is a precursor to respiratory failure and eventual suffocation caused by complete paralysis of the thoracic diaphragm. It is therefore a medical emergency and immediate treatment is required. Similarly, ptosis may occur in victims of Botulism (caused by Botulinum toxin) and this is also regarded as a life-threatening symptom

- "Pseudo ptosis" due to:

1. Lack of lid support: empty socket or atrophic globe.

2. Higher lid position on the other side: as in lid retraction