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

Many people of East Asian descent are prone to developing angle closure glaucoma due to shallower anterior chamber depths, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Higher rates of glaucoma have also been reported for Inuit populations, compared to white populations, in Canada and Greenland.

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.

No clear evidence indicates vitamin deficiencies cause glaucoma in humans. It follows, then, that oral vitamin supplementation is not a recommended treatment for glaucoma. Caffeine increases intraocular pressure in those with glaucoma, but does not appear to affect normal individuals.

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.

Leukocoria (also leukokoria or white pupillary reflex) is an abnormal white reflection from the retina of the eye. Leukocoria resembles eyeshine, but leukocoria can occur in humans and other animals that lack eyeshine because their retina lacks a "tapetum lucidum".

Leukocoria is a medical sign for a number of conditions, including Coats disease, congenital cataract, corneal scarring, melanoma of the ciliary body, Norrie disease, ocular toxocariasis, persistence of the tunica vasculosa lentis (PFV/PHPV), retinoblastoma, and retrolental fibroplasia.

Because of the potentially life-threatening nature of retinoblastoma, a cancer, that condition is usually considered in the evaluation of leukocoria. In some rare cases (1%) the leukocoria is caused by Coats' disease (leaking retinal vessels).

The eye is made up of the sclera, the iris, and the pupil, a black hole located at the center of the eye with the main function of allowing light to pass to the retina. Due to certain muscle spasms in the eye, the pupil can resemble a tadpole, which consists of a circular body, no arms or legs, and a tail.

When the pupil takes on the shape of a tadpole, the condition is called tadpole pupil. Tadpole pupil, also known as episodic segmental iris mydriasis, is an ocular condition where the muscles of the iris begin to spasm causing the elongation, or lengthening, of parts of the iris. These spasms can affect any segment, or portion, of the iris and involve the iris dilator muscle. Contractions of the iris dilator muscle, a smooth muscle of the eye running radially in the iris, can cause irregular distortion of the pupil, thus making the pupil look tadpole shaped and giving this condition its name. Episodic segmental iris mydriasis was first described and termed “tadpole pupil” in 1912 by HS Thompson

Causes of photophobia relating directly to the eye itself include:

- Achromatopsia

- Aniridia

- Anticholinergic drugs may cause photophobia by paralyzing the iris sphincter muscle.

- Aphakia (absence of the lens of the eye)

- Blepharitis

- Buphthalmos (abnormally narrow angle between the cornea and iris)

- Cataracts

- Coloboma

- Cone dystrophy

- Congenital abnormalities of the eye

- Viral conjunctivitis ("pink eye")

- Corneal abrasion

- Corneal dystrophy

- Corneal ulcer

- Disruption of the corneal epithelium, such as that caused by a corneal foreign body or keratitis

- Ectopia lentis

- Endophthalmitis

- Eye trauma caused by disease, injury, or infection such as chalazion, episcleritis, glaucoma, keratoconus, or optic nerve hypoplasia

- Hydrophthalmos, or congenital glaucoma

- Iritis

- The drug isotretinoin (Accutane/Roaccutane) has been associated with photophobia

- Optic neuritis

- Pigment dispersion syndrome

- Pupillary dilation (naturally or chemically induced)

- Retinal detachment

- Scarring of the cornea or sclera

- Uveitis

Exophthalmos is commonly found in dogs. It is seen in brachycephalic (short-nosed) dog breeds because of the shallow orbit. However, it can lead to keratitis secondary to exposure of the cornea. Exophthalmos is commonly seen in the Pug, Boston Terrier, Pekingese, and Shih Tzu.

It is a common result of head trauma and pressure exerted on the front of the neck too hard in dogs. In cats, eye proptosis is uncommon and is often accompanied by facial fractures.

About 40% of proptosed eyes retain vision after being replaced in the orbit, but in cats very few retain vision. Replacement of the eye requires general anesthesia. The eyelids are pulled outward, and the eye is gently pushed back into place. The eyelids are sewn together in a procedure known as tarsorrhaphy for about five days to keep the eye in place. Replaced eyes have a higher rate of keratoconjunctivitis sicca and keratitis and often require lifelong treatment. If the damage is severe, the eye is removed in a relatively simple surgery known as enucleation of the eye.

The prognosis for a replaced eye is determined by the extent of damage to the cornea and sclera, the presence or absence of a pupillary light reflex, and the presence of ruptured rectus muscles. The rectus muscles normally help hold the eye in place and direct eye movement. Rupture of more than two rectus muscles usually requires the eye to be removed, because significant blood vessel and nerve damage also usually occurs. Compared to brachycephalic breeds, dochilocephalic (long-nosed) breeds usually have more trauma to the eye and its surrounding structures, so the prognosis is worse .

The primary symptom is pupillary distortion (changing of the size or shape of the pupil). Distortion can occur in any segment of the iris. One part of the iris is pulled to a peak, and then returns to normal after the episode. Other symptoms may include blurred vision, abnormal periocular sensations (unusual feelings around the eyes), migraines, and feelings of a chilled face. Some patients who demonstrate tadpole pupil symptoms also experienced Horner’s syndrome or Adie’s tonic pupil

Tadpole pupil symptoms occur in episodes. Episodes are generally brief and less than 5 minutes, however, some episodes have been reported to last anywhere from 3 to 15 minutes. The episodes can occur multiple times a day for days, weeks, or months.

Studies show that a majority of those experiencing tadpole pupil are younger women from an age range of 24 to 48 years old, with no apparent health problems. Although women generally have the tadpole pupil, men are not unaffected by this disease and some have been reported to experience the symptoms.

Neurological causes for photophobia include:

- Autism spectrum disorders

- Chiari malformation

- Occipital Neuralgia

- Dyslexia

- Encephalitis including Myalgic encephalomyelitis aka Chronic fatigue syndrome

- Meningitis

- Trigeminal disturbance causes central sensitization (hence, multiple other associated hypersensitivities. Causes can be bad bite, infected tooth, etc.

- Subarachnoid haemorrhage

- Tumor of the posterior cranial fossa

Sympathetic ophthalmia is rare, affecting 0.2% to 0.5% of non-surgical eye wounds, and less than 0.01% of surgical penetrating eye wounds. There are no gender or racial differences in incidence of SO.

The disease is chronic and often progresses slowly. Prognosis is generally poor when associated with glaucoma [1,2].

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.

This condition is linked to the X chromosome.

- Siberian Husky - Night blindness by two to four years old.

- Samoyed - More severe disease than the Husky.

Persistent pupillary membrane (PPM) is a condition of the eye involving remnants of a fetal membrane that persist as strands of tissue crossing the pupil. The pupillary membrane in mammals exists in the fetus as a source of blood supply for the lens. It normally atrophies from the time of birth to the age of four to eight weeks. PPM occurs when this atrophy is incomplete. It generally does not cause any symptoms. The strands can connect to the cornea or lens, but most commonly to other parts of the iris. Attachment to the cornea can cause small corneal opacities, while attachment to the lens can cause small cataracts. Using topical atropine to dilate the pupil may help break down PPMs.

In dogs, PPM is inherited in the Basenji but can occur in other breeds such as the Pembroke Welsh Corgi, Chow Chow, Mastiff, and English Cocker Spaniel. It is also rarely seen in cats, horses, and cattle.

Coloboma of optic nerve, is a rare defect of the optic nerve that causes moderate to severe visual field defects.

Coloboma of the optic nerve is a congenital anomaly of the optic disc in which there is a defect of the inferior aspect of the optic nerve. The issue stems from incomplete closure of the embryonic fissure while in utero. A varying amount of glial tissue typically fills the defect, manifests as a white mass.

There is another retinal disease in Briards known as hereditary retinal dysplasia. These dogs are night blind from birth, and day vision varies. Puppies affected often have nystagmus. It is also known as lipid retinopathy.

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.

Congenital heterochromia is usually inherited as an autosomal dominant trait.

Penetrating karatoplasty and endothelial keratoplasty can be used as treatments for severe cases of ICE [2,8]. Because glaucoma and elevated intraocular pressure are often present in ICE patients, long term follow up may be needed to ensure adequate intraocular pressures are maintained [2,7]

A third cause of light-near dissociation is Parinaud syndrome, also called dorsal midbrain syndrome. This uncommon syndrome involves vertical gaze palsy associated with pupils that “accommodate but do not react." The causes of Parinaud syndrome include brain tumors (pinealomas), multiple sclerosis and brainstem infarction.

Due to the lack of detail in the older literature and the scarcity of AR pupils at the present time, it is not known whether syphilis can cause Parinaud syndrome. It is not known whether AR pupils are any different from the pupils seen in other dorsal midbrain lesions.

The condition is diagnosed clinically but physician

In segmental heterochromia, sometimes referred to as sectoral heterochromia, areas of the same iris contains two completely different colors.

Segmental heterochromia is rare in humans; it is estimated that only about 1% of the population have it.

Inflammatory/Infection:

- Graves' ophthalmopathy due to Graves' disease, usually causes bilateral proptosis.

- Orbital cellulitis – often with unilateral proptosis, severe redness, and moderate to severe pain, sinusitis and an elevated white blood cell count.

- Dacryoadenitis

- Erdheim-Chester Disease

- Mucormycosis

- Orbital pseudotumor – presents with acute, usually unilateral proptosis with severe pain.

- High altitude cerebral edema

- Granulomatosis with polyangiitis

Neoplastic:

- Leukemias

- Meningioma, (of sphenoid wing)

- Nasopharyngeal angiofibroma

- Hand–Schüller–Christian disease

- Hemangioma, cavernous

Cystic:

- Dermoid cyst

Vascular:

- Carotid-cavernous fistula

- Aortic insufficiency: manifests as a pulsatile pseudoproptosis, described by British cardiothoracic surgeon, Hutan Ashrafian in 2006

Others:

- Orbital fracture: apex, floor, medial wall, zygomatic

- Retrobulbar hemorrhage: trauma to the orbit can lead to bleeding behind the eye. The hemorrhage has nowhere to escape and the increased pressure pushes the eye out of the socket, leading to proptosis and can also cause blindness if not treated promptly.

- Cushing's syndrome (due to fat in the orbital cave)

- Pfeiffer syndrome

Though there is no clear cause of cerebral polyopia, many cases show associations with occipital or temporal lobe lesions. Most cases of polyopia occur when there are bilateral lesions to occipital or temporal cortex, however some cases are present with unilateral lesions. Thus, polyopia can result from any kind of infarction to the occipital or temporal lobes, though the exact mechanism remains unclear. Some cases have shown that polyopia is experienced when the infarctions were seen to be at the tips and outer surfaces of the occipital lobes. By contrast, some patients experience cerebral polyopia associated with headaches and migraines in the frontotemporal lobe.

The mechanism of infarction differs by patient, but polyopia is experienced most commonly in patients that suffer from epilepsy in the occipital cortex, or in patients who suffer from cerebral strokes. In cases of epilepsy, polyopia is often experienced alongside palinopsia as these two conditions share an epileptic mechanism.