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

Differential diagnosis is rarely difficult in adults. Onset is typically sudden with symptoms of horizontal diplopia. Limitations of eye movements are confined to abduction of the affected eye (or abduction of both eyes if bilateral) and the size of the resulting convergent squint or esotropia is always larger on distance fixation - where the lateral rectii are more active - than on near fixation - where the medial rectii are dominant. Abduction limitations which mimic VIth nerve palsy may result secondary to surgery, to trauma or as a result of other conditions such as myasthenia gravis or thyroid eye disease.

In children, differential diagnosis is more difficult because of the problems inherent in getting infants to cooperate with a full eye movement investigation. Possible alternative diagnosis for an abduction deficit would include:

1. Mobius syndrome - a rare congenital disorder in which both VIth and VIIth nerves are bilaterally affected giving rise to a typically 'expressionless' face.

2. Duane's syndrome - A condition in which both abduction and adduction are affected arising as a result of partial innervation of the lateral rectus by branches from the IIIrd oculomotor cranial nerve.

3. Cross fixation which develops in the presence of infantile esotropia or nystagmus blockage syndrome and results in habitual weakness of lateral rectii.

4. Iatrogenic injury. Abducens nerve palsy is also known to occur with halo orthosis placement.The resultant palsy is identified through loss of lateral gaze after application of the orthosis and is the most common cranial nerve injury associated with this device.

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.

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.

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 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.

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.

Aponeurotic and congenital ptosis may require surgical correction if severe enough to interfere with vision or if cosmetics is a concern.

Treatment depends on the type of ptosis and is usually performed by an ophthalmic plastic and reconstructive surgeon, specializing in diseases and problems of the eyelid.

Surgical procedures include:

- Levator resection

- Müller muscle resection

- Frontalis sling operation (preferred option for oculopharyngeal muscular dystrophy)

Non-surgical modalities like the use of "crutch" glasses or Ptosis crutches or special scleral contact lenses to support the eyelid may also be used.

Ptosis that is caused by a disease may improve if the disease is treated successfully, although some related diseases, such as oculopharyngeal muscular dystrophy currently have no treatments or cures.

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

Causes of anisocoria range from benign (normal) to life-threatening conditions.

Clinically, it is important to establish whether anisocoria is more apparent in dim or bright light to clarify whether the larger pupil or smaller pupil is the abnormal one.

- Anisocoria which is worsened (greater asymmetry between the pupils) in the dark suggests the small pupil (which should dilate in dark conditions) is the abnormal pupil and suggests Horner's syndrome or mechanical anisocoria. In Horner's syndrome sympathetic nerve fibers have a defect, therefore the pupil of the involved eye will not dilate in darkness. If the smaller pupil dilates in response to instillation of apraclonidine eye drops, this suggests Horner's syndrome is present.

- Anisocoria which is greater in bright light suggests the larger pupil (which should constrict in bright conditions) is the abnormal pupil. This may suggest Adie tonic pupil, pharmacologic dilation, oculomotor nerve palsy, or damaged iris.

A relative afferent pupillary defect (RAPD) also known as a Marcus Gunn pupil does not cause anisocoria.

Some of the causes of anisocoria are life-threatening, including Horner's syndrome (which may be due to carotid artery dissection) and oculomotor nerve palsy (due to a brain aneurysm, uncal herniation, or head trauma).

If the examiner is unsure whether the abnormal pupil is the constricted or dilated one, and if a one-sided drooping of the eyelid is present then the abnormally sized pupil can be presumed to be the one on the side of the ptosis. This is because Horner's syndrome and oculomotor nerve lesions both cause ptosis.

Anisocoria is usually a benign finding, unaccompanied by other symptoms (physiological anisocoria). Old face photographs of patients often help to diagnose and establish the type of anisocoria.

It should be considered an emergency if a patient develops acute onset anisocoria. These cases may be due to brain mass lesions which cause oculomotor nerve palsy. Anisocoria in the presence of confusion, decreased mental status, severe headache, or other neurological symptoms can forewarn a neurosurgical emergency. This is because a hemorrhage, tumor or another intracranial mass can enlarge to a size where the third cranial nerve (CN III) is compressed, which results in uninhibited dilatation of the pupil on the same side as the lesion.

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.

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.

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.

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".

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

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.

A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.

Treatment is usually unnecessary. In severe cases, surgery with a bilateral levator excision and frontalis brow suspension may be used.

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.

Three tests are useful in confirming the presence and severity of Horner syndrome:

- Cocaine drop test: Cocaine eyedrops block the reuptake of post-ganglionic norepinephrine resulting in the dilation of a normal pupil from retention of norepinephrine in the synapse. However, in Horner's syndrome the lack of norepinephrine in the synaptic cleft causes mydriatic failure. A more recently introduced approach that is more dependable and obviates the difficulties in obtaining cocaine is to apply the alpha-agonist apraclonidine to both eyes and observe the increased mydriatic effect (due to hypersensitivity) on the affected side of Horner syndrome (the opposite effect to what the cocaine test would produce in the presence of Horner's).

- Paredrine test: This test helps to localize the cause of the miosis. If the third order neuron (the last of three neurons in the pathway which ultimately discharges norepinephrine into the synaptic cleft) is intact, then the amphetamine causes neurotransmitter vesicle release, thus releasing norepinephrine into the synaptic cleft and resulting in robust mydriasis of the affected pupil. If the lesion itself is of the third order neuron, then the amphetamine will have no effect and the pupil remains constricted. There is no pharmacological test to differentiate between a first and second order neuron lesion.

- Dilation lag test

It is important to distinguish the ptosis caused by Horner's syndrome from the ptosis caused by a lesion to the oculomotor nerve. In the former, the ptosis occurs with a constricted pupil (due to a loss of sympathetics to the eye), whereas in the latter, the ptosis occurs with a dilated pupil (due to a loss of innervation to the sphincter pupillae). In a clinical setting, these two ptoses are fairly easy to distinguish. In addition to the blown pupil in a CNIII (oculomotor nerve) lesion, this ptosis is much more severe, occasionally occluding the whole eye. The ptosis of Horner syndrome can be quite mild or barely noticeable (partial ptosis).

When anisocoria occurs and the examiner is unsure whether the abnormal pupil is the constricted or dilated one, if a one-sided ptosis is present then the abnormally sized pupil can be presumed to be on the side of the ptosis.

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.

The origins of the vast majority of congenital oculomotor palsies are unknown, or idiopathic to use the medical term. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma.

Anisocoria is a common condition, defined by a difference of 0.4 mm or more between the sizes of the pupils of the eyes.

Anisocoria has various causes:

- Physiological anisocoria: About 20% of normal people have a slight difference in pupil size which is known as physiological anisocoria. In this condition, the difference between pupils is usually less than 1 mm.

- Horner's syndrome

- Mechanical anisocoria: Occasionally previous trauma, eye surgery, or inflammation (uveitis, angle closure glaucoma) can lead to adhesions between the iris and the lens.

- Adie tonic pupil: Tonic pupil is usually an isolated benign entity, presenting in young women. It may be associated with loss of deep tendon reflex (Adie's syndrome). Tonic pupil is characterized by delayed dilation of iris especially after near stimulus, segmental iris constriction, and sensitivity of pupil to a weak solution of pilocarpine.

- Oculomotor nerve palsy: Ischemia, intracranial aneurysm, demyelinating diseases (e.g., multiple sclerosis), head trauma, and brain tumors are the most common causes of oculomotor nerve palsy in adults. In ischemic lesions of the oculomotor nerve, pupillary function is usually spared whereas in compressive lesions the pupil is involved.

- Pharmacological agents with anticholinergic or sympathomimetic properties will cause anisocoria, particularly if instilled in one eye. Some examples of pharmacological agents which may affect the pupils include pilocarpine, cocaine, tropicamide, MDMA, dextromethorphan, and ergolines. Alkaloids present in plants of the genera "Brugmansia" and "Datura", such as scopolamine, may also induce anisocoria.

- Migraines

Clinical diagnosis is conducted on individuals with age onset between late teens and late forties who show the initial characteristics for the recessive autosomal cerebellar ataxia.

The following tests are performed:

- MRI brain screening for cerebellum atrophy.

- Molecular genetic testing for SYNE-1 sequence analysis.

- Electrophysiologic studies for polyneurotherapy

- Neurological examination

Prenatal diagnosis and preimplantation genetic diagnosis (PGD) can be performed to identify the mothers carrying the recessive genes for cerebellar ataxia.

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.