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.

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

Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting 20% of the population, it can be an entirely harmless condition or a symptom of more serious medical problems.

Relative afferent pupillary defect (RAPD) or Marcus Gunn pupil is a medical sign observed during the swinging-flashlight test whereupon the patient's pupils constrict less (therefore appearing to dilate) when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.

The most common cause of Marcus Gunn pupil is a lesion of the optic nerve (between the retina and the optic chiasm) or severe retinal disease. It is named after Scottish ophthalmologist Robert Marcus Gunn.

A second common cause of Marcus Gunn pupil is a contralateral optic tract lesion, due to the different contributions of the intact nasal and temporal hemifields.

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.

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.

When detected during childhood, without any other symptoms and when other disorders are discarded through clinical tests, it should be considered a developmental or genetic phenomenon.

Asymmetric pupil or dyscoria, potential causes of anisocoria, refer to an abnormal shape of the pupil which can happens due to developmental and intrauterine anomalies.

The main characteristic that distinguishes physiological anisocoria is an increase of pupil size with lower light or reduced illumination, such that the pupils differ in size between the two eyes. At any given eye examination, up to 41% of healthy patients can show an anisocoria of 0.4 mm or more at one time or another. It can also occur as the difference between both pupils varies from day to day. A normal population survey showed that during poor light or near dark conditions, differences of 1 mm on average between pupils was found.

The presence of physiologic anisocoria has been estimated at 20% of the normal population, so some degree of pupil difference may be expected in at least 1 in 5 clinic patients.

Without the focusing power of the lens, the eye becomes very farsighted. This can be corrected by wearing glasses, contact lenses, or by implant of an artificial lens. Artificial lenses are described as "pseudophakic." Also, since the lens is responsible for adjusting the focus of vision to different lengths, patients with aphakia have a total loss of accommodation.

Some individuals have said that they perceive ultraviolet light, invisible to those with a lens, as whitish blue or whitish-violet.

Mydriasis () is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs.

Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A "mydriatic" pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.

An informal term for mydriasis is blown pupil, and is used by medical providers. It is usually used to refer to a fixed, unilateral mydriasis, which could be a symptom of raised intracranial pressure.

The opposite, constriction of the pupil, is referred to as miosis. Both mydriasis and miosis can be physiological. Anisocoria is the condition of one pupil being more dilated than the other.

Aphakia is the absence of the lens of the eye, due to surgical removal, a perforating wound or ulcer, or congenital anomaly. It causes a loss of accommodation, far sightedness (hyperopia), and a deep anterior chamber. Complications include detachment of the vitreous or retina, and glaucoma.

Babies are rarely born with aphakia. Occurrence most often results from surgery to remove congenital cataract (clouding of the eye's lens, which can block light from entering the eye and focusing clearly). Congenital cataracts usually develop as a result of infection of the fetus or genetic reasons. It is often difficult to identify the exact cause of these cataracts, especially if only one eye is affected.

People with aphakia have relatively small pupils and their pupils dilate to a lesser degree.

In mechanical anisocoria, this is the result of damage to the iris dilator muscle, which may be caused by trauma, angle-closure glaucoma, surgery such as cataract removal, or uveitis (inflammation of the eye). Slit lamp examination is often used as a diagnostic aid: damage to the dilator muscle is indicated by anisocoria when light intensity is lowered.Anisocoria refers to a common eye condition in which the two pupils differ in size.

The Marcus Gunn pupil is a relative afferent pupillary defect indicating a decreased pupillary response to light in the affected eye.

In the swinging flashlight test, a light is alternately shone into the left and right eyes. A normal response would be equal constriction of both pupils, regardless of which eye the light is directed at. This indicates an intact direct and consensual pupillary light reflex. When the test is performed in an eye with an afferent pupillary defect, light directed in the affected eye will cause only mild constriction of both pupils (due to decreased response to light from the afferent defect), while light in the unaffected eye will cause a normal constriction of both pupils (due to an intact efferent path, and an intact consensual pupillary reflex). Thus, light shone in the affected eye will produce less pupillary constriction than light shone in the unaffected eye.

A Marcus Gunn pupil is distinguished from a total CN II lesion, in which the affected eye perceives "no" light. In that case, shining the light in the affected eye produces no effect.

Anisocoria is absent. A Marcus Gunn pupil is seen, among other conditions, in optic neuritis. It is also common in retrobulbar optic neuritis due to multiple sclerosis but only for 3–4 weeks, until the visual acuity begins to improve in 1–2 weeks and may return to normal.

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.

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.

Laser treatment of drusen has been studied. While it is possible to eliminate drusen with this treatment strategy, it has been shown that this fails to reduce the risk of developing the choroidal neovascularisation which causes the blindness associated with age-related macular degeneration.

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.

Hutchinson's pupil is a clinical sign in which the pupil on the side of an intracranial mass lesion is dilated and unreactive to light, due to compression of the oculomotor nerve on that side. The sign is named after Sir Jonathan Hutchinson.

These can be due to concussion injury to the brain and is associated with subdural haemorrhage and unconsciousness.

The parasympathetic fibers to the pupil are responsible for pupillary constriction. The fibers pass through the periphery of the oculomotor nerve, and hence are the first to be affected in case of compression of the nerve. In Stage 1, the parasympathetic fibers on the side of injury are irritated, leading to constriction of pupil on that side. In stage 2, the parasympathetic fibers on the side of injury are paralysed, leading to dilatation of pupil. The fibers on the opposite oculomotor nerve are irritated, leading to constriction on opposite side. In stage 3, the parasympathetic fibers on both sides are paralysed - leading to bilateral pupillary dilatation. Pupils become fixed. This could typically indicates a very serious underlying condition.

As with almost every kind of surgery, the main complications in both treatments of hypertelorism include excessive bleeding, risk of infection and CSF leaks and dural fistulas. Infections and leaks can be prevented by giving perioperative antibiotics and identifying and closing of any dural tears. The risk of significant bleeding can be prevented by meticulous technique and blood loss is compensated by transfusions. Blood loss can also be reduced by giving hypotensive anesthesia. Rarely major eye injuries, including blindness, are seen. Visual disturbances can occur due to the eye muscle imbalance after orbital mobilization. Ptosis and diplopia can also occur postoperatively, but this usually self-corrects. A quite difficult problem to correct postoperatively is canthal drift, which can be managed best by carefully preserving the canthal tendon attachments as much as possible. Despite the extensiveness in these procedures, mortality is rarely seen in operative correction of hypertelorism.

Usually being asymptomatic, drusen are typically found during routine eye exams where the pupils have been dilated.

To create an acceptable aesthetic result in the correction of orbital hypertelorism, it is also important to take soft-tissue reconstruction in consideration. In this context, correction of the nasal deformities is one of the more difficult procedures. Bone and cartilage grafts may be necessary to create a nasal frame and local rotation with for example forehead flaps, or advancement flaps can be used to cover the nose.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

The prognosis of a patient with acquired cortical blindness depends largely on the original cause of the blindness. For instance, patients with bilateral occipital lesions have a much lower chance of recovering vision than patients who suffered a transient ischemic attack or women who experienced complications associated with eclampsia. In patients with acquired cortical blindness, a permanent complete loss of vision is rare. The development of cortical blindness into the milder cortical visual impairment is a more likely outcome. Furthermore, some patients regain vision completely, as is the case with transient cortical blindness associated with eclampsia and the side effects of certain anti-epilepsy drugs.

Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients' ability to perceive simple and complex visual motion. This sort of 'relearning' therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment.

Cortical blindness is the total or partial loss of vision in a normal-appearing eye caused by damage to the brain's occipital cortex. Cortical blindness can be acquired or congenital, and may also be transient in certain instances. Acquired cortical blindness is most often caused by loss of blood flow to the occipital cortex from either unilateral or bilateral posterior cerebral artery blockage (ischemic stroke) and by cardiac surgery. In most cases, the complete loss of vision is not permanent and the patient may recover some of their vision (Cortical visual impairment). Congenital cortical blindness is most often caused by perinatal ischemic stroke, encephalitis, and meningitis.

Rarely, a patient with acquired cortical blindness may have little or no insight that they have lost vision, a phenomenon known as Anton–Babinski syndrome.

Cortical blindness and cortical visual impairment (CVI), which refers to the partial loss of vision caused by cortical damage, are both classified as subsets of neurological visual impairment (NVI). NVI and its three subtypes—cortical blindness, cortical visual impairment, and delayed visual maturation—must be distinguished from ocular visual impairment in terms of their different causes and structural foci, the brain and the eye respectively. One diagnostic marker of this distinction is that the pupils of individuals with cortical blindness will respond to light whereas those of individuals with ocular visual impairment will not.

Microcoria is a congenital disease in which the pupils of the subject are narrower than 2 mm in diameter. Microcoria is associated with juvenile-onset glaucoma. It is also associated with Pierson syndrome chararacterized by microcoria and congenital nephrotic syndrome. The defect is in the Laminin beta 2 gene on chromosome 3p21 which encodes a protein essential to the glomerular basement membrane.

It is also part of the known manifestations of a born infant to a mother suffering from uncontrolled hyperglycemia. Other symptoms include transposition of great vessels, respiratory distress secondary to surfactant defect, sacral agensis, jitteriness, irritability, and lethargy due to rebound fetal hypoglycemia. Congenital microcoria is an autosomal dominant trait. However, it can also occur sporadically.