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.

Ophthalmoparesis can involve any or all of the extraocular muscles, which include the superior recti, inferior recti, medial recti, lateral recti, inferior oblique and superior oblique muscles.

It can also be classified by the directions of affected movements, e.g. "vertical ophthalmoparesis".

It can be of three types:

1. accommodative iridoplegia- Noncontraction of pupils during accommodation.

2. complete iridoplegia- Iris fails to respond to any stimulation.

3. reflex iridoplegia- The absence of light reflex, with retention of accommodation reflex. Also called Argyll Robertson pupil.

Iridoplegia is the paralysis of the sphincter of the iris. It can occur in due to direct orbital injury, which may result in short lived blurred vision.

Adie syndrome presents with three hallmark symptoms, namely at least one abnormally dilated pupil (mydriasis) which does not constrict in response to light, loss of deep tendon reflexes, and abnormalities of sweating. Other signs may include hyperopia due to accommodative paresis, photophobia and difficulty reading.

Adie syndrome is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). It is frequently seen in females with absent knee or ankle jerks and impaired sweating. It is named after the British neurologist William John Adie. It is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection which causes inflammation, and affects the pupil of the eye and the autonomic nervous system.

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.

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.

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.

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

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.

Myasthenia gravis is a common neurogenic ptosis which could be also classified as neuromuscular ptosis because the site of pathology is at the neuromuscular junction. Studies have shown that up to 70% of myasthenia gravis patients present with ptosis, and 90% of these patients will eventually develop ptosis. In this case, ptosis can be unilateral or bilateral and its severity tends to be oscillating during the day, because of factors such as fatigue or drug effect. This particular type of ptosis is distinguished from the others with the help of a Tensilon challenge test and blood tests. Also, specific to myasthenia gravis is the fact that coldness inhibits the activity of cholinesterase, which makes possible differentiating this type of ptosis by applying ice onto the eyelids. Patients with myasthenic ptosis are very likely to still experience a variation of the drooping of the eyelid at different hours of the day.

The ptosis caused by the oculomotor palsy can be unilateral or bilateral, as the subnucleus to the levator muscle is a shared, midline structure in the brainstem. In cases in which the palsy is caused by the compression of the nerve by a tumor or aneurysm, it is highly likely to result in an abnormal ipsilateral papillary response and a larger pupil. Surgical third nerve palsy is characterized by a sudden onset of unilateral ptosis and an enlarged or sluggish pupil to the light. In this case, imaging tests such as CTs or MRIs should be considered. Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect the pupil and it tends to slowly improve in several weeks. Surgery to correct ptosis due to medical third nerve palsy is normally considered only if the improvement of ptosis and ocular motility are unsatisfactory after half a year. Patients with third nerve palsy tend to have diminished or absent function of the levator.

When caused by Horner's syndrome, ptosis is usually accompanied by miosis and anhidrosis. In this case, the ptosis is due to the result of interruption innervations to the sympathetic, autonomic Muller's muscle rather than the somatic levator palpebrae superioris muscle. The lid position and pupil size are typically affected by this condition and the ptosis is generally mild, no more than 2 mm. The pupil might be smaller on the affected side. While 4% cocaine instilled to the eyes can confirm the diagnosis of Horner's syndrome, Hydroxyamphetamine eye drops can differentiate the location of the lesion.

Chronic progressive external ophthalmoplegia is a systemic condition that occurs and which usually affects only the lid position and the external eye movement, without involving the movement of the pupil. This condition accounts for nearly 45% of myogenic ptosis cases. Most patients develop ptosis due to this disease in their adulthood. Characteristic to ptosis caused by this condition is the fact that the protective up rolling of the eyeball when the eyelids are closed is very poor.

Pseudomyopia refers to an intermittent and temporary shift in refractive error of the eye towards myopia, in which the focusing of light in front of the retina is due to a transient spasm of the ciliary muscle causing an increase in the refractive power of the eye. It may be either organic, through stimulation of the parasympathetic nervous system, or functional in origin, through eye strain or fatigue of ocular systems. It is common in young adults who have active accommodation, and classically occurs after a change in visual requirements, such as students preparing for an exam, or a change in occupation.

The major symptom is intermittent blurring of distance vision particularly noticeable after prolonged periods of near work, and symptoms of asthenopia. The vision may clear temporarily using concave (minus) lenses. The diagnosis is done by cycloplegic refraction using a strong cycloplegic like atropine or homatropine eye drops. Accommodative amplitude and facility may be reduced as a result of the ciliary muscle spasm.

Treatment is dependent on the underlying aetiology. Organic causes may include systemic or ocular medications, brain stem injury, or active ocular inflammation such as uveitis. Functional pseudomyopia is managed though modification of working conditions, an updated refraction, typically involving a reduction of a myopic prescription to some lower myopic prescription, or through appropriate ocular exercises.

A spasm of accommodation (also known as a ciliary spasm, an accommodation, or accommodative spasm) is a condition in which the ciliary muscle of the eye remains in a constant state of contraction. Normal accommodation allows the eye to "accommodate" for near-vision. However in a state of perpetual contraction, the ciliary muscle cannot relax when viewing distant objects. This causes vision to blur when attempting to view objects from a distance. This may cause pseudomyopia or latent hyperopia.

Although antimuscarinic drops (homoatropine 5%) can be applied topically to relax the muscle, this leaves the individual without any accommodation and, depending on refractive error, unable to see well at near distances. Also, excessive pupil dilation may occur as an unwanted side effect. This dilation may pose a problem since a larger pupil is less efficient at focusing light (see pupil, aperture, and optical aberration for more.)

Patients who have accommodative spasm may benefit from being given glasses or contacts that account for the problem or by using vision therapy techniques to regain control of the accommodative system..

Possible clinical findings include:

Normal Amplitude of accommodation and Near point of convergence

Reduced Negative relative accommodation

Difficulty clearing plus on facility testing

Infantile esotropia is an ocular condition of early onset in which one or either eye turns inward. It is a specific sub-type of esotropia and has been a subject of much debate amongst ophthalmologists with regard to its naming, diagnostic features, and treatment.

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).

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%.

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.

"Cross-fixation congenital esotropia", also called "Cianci's syndrome" is a particular type of large-angle infantile esotropia associated with tight medius rectus muscles. With the tight muscles, which hinder adduction, there is a constant inward eye turn. The patient cross-fixates, that is, to fixate objects on the left, the patient looks across the nose with the right eye, and vice versa. The patient tends to adopt a head turn, turning the head to the right to better see objects in the left visual field and turning the head to the left to see those in the right visual field. Binasal occlusion can be used to discourage cross-fixation. However, the management of cross-fixation congenital esotropia usually involves surgery.

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.

The symptoms and signs associated with convergence insufficiency are related to prolonged, visually demanding, near-centered tasks. They may include, but are not limited to, diplopia (double vision), asthenopia (eye strain), transient blurred vision, difficulty sustaining near-visual function, abnormal fatigue,

headache, and abnormal postural adaptation, among others. In some cases, difficulty with making eye contact have been noted as a complaint amongst sufferers.

Note that some Internet resources confuse convergence and divergence dysfunction, reversing them.

Paresis () is a condition typified by a weakness of voluntary movement, or partial loss of voluntary movement or by impaired movement. When used without qualifiers, it usually refers to the limbs, but it can also be used to describe the muscles of the eyes (ophthalmoparesis), the stomach (gastroparesis), and also the vocal cords (Vocal cord paresis). Neurologists use the term "paresis" to describe weakness, and "plegia" to describe paralysis in which all voluntary movement is lost. The term "paresis" comes from the "letting go" from παρίημι "to let go, to let fall".

Accommodative infacility is the inability to change the accommodation of the eye with enough speed and accuracy to achieve normal function. This can result in visual fatigue, headaches, and difficulty reading. The delay in accurate accommodation also makes vision blurry for a moment when switching between distant and near objects. The duration and extent of this blurriness depends on the extent of the deficit.

Convergence insufficiency or convergence disorder is a sensory and neuromuscular anomaly of the binocular vision system, characterized by a reduced ability of the eyes to turn towards each other, or sustain convergence.