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.

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

Miosis is excessive constriction of the pupil. The term is from Ancient Greek , "mūein", "to close the eyes.

The opposite condition, mydriasis, is the dilation of the pupil. Anisocoria is the condition of one pupil being more dilated than the other.

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.

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.

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

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

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.

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.

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.

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.

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.

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.

A synechia is an eye condition where the iris adheres to either the cornea (i.e. "anterior synechia") or lens (i.e. "posterior synechia"). Synechiae can be caused by ocular trauma, iritis or iridocyclitis and may lead to certain types of glaucoma. It is sometimes visible on careful examination but usually more easily through an ophthalmoscope or slit-lamp.

Anterior synechia causes closed angle glaucoma, which means that the iris closes the drainage way of aqueous humour which in turn raises the intraocular pressure. Posterior synechia also cause glaucoma, but with a different mechanism. In posterior synechia, the iris adheres to the lens, blocking the flow of aqueous humor from the posterior chamber to the anterior chamber. This blocked drainage raises the intraocular pressure.

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.

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.

A person with photic retinopathy may notice an impairment in their vision, for example a spot that does not go away after a reasonable recovery time, or blurring. They may also have eye pain or headaches. Vision impairment is usually in both eyes, but "can" be in just one. Impairment of a person with 20/20 vision usually ends up being about 20/40 or 20/60, but can be better or far worse.

A doctor examining an eye with retinopathy may be able to see no signs at all, or a slight macular edema, which is a sort of blister on or under the macula, an oval colored spot normally visible to an eye doctor on each person's retina.

But while even that edema goes away, within a few days the patient will generally develop a discoloration of the retina at the injured point, often yellow or white, turning red over the next few weeks.

Clinical exam may reveal sectoral paresis of the iris sphincter or vermiform iris movements. The tonic pupil may become smaller (miotic) over time which is referred to as "little old Adie's". Testing with low dose (1/8%) pilocarpine may constrict the tonic pupil due to cholinergic denervation supersensitivity. A normal pupil will not constrict with the dilute dose of pilocarpine. CT scans and MRI scans may be useful in the diagnostic testing of focal hypoactive reflexes.

Cycloplegia is paralysis of the ciliary muscle of the eye, resulting in a loss of accommodation. Because of the paralysis of the ciliary muscle, the curvature of the lens can no longer be adjusted to focus on nearby objects. This results in similar problems as those caused by presbyopia, in which the lens has lost elasticity and can also no longer focus on close-by objects. Cycloplegia with accompanying mydriasis (dilation of pupil) is usually due to topical application of muscarinic antagonists such as atropine and cyclopentolate.

A reduction in visual acuity in a 'red eye' is indicative of serious ocular disease, such as keratitis, iridocyclitis, and glaucoma, and never occurs in simple conjunctivitis without accompanying corneal involvement.

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.

Ciliary flush is usually present in eyes with corneal inflammation, iridocyclitis or acute glaucoma, though not simple conjunctivitis.

A ciliary flush is a ring of red or violet spreading out from around the cornea of the eye.

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

With anterior lens luxation, the lens pushes into the iris or actually enters the anterior chamber of the eye. This can cause glaucoma, uveitis, or damage to the cornea. Uveitis (inflammation of the eye) causes the pupil to constrict (miosis) and trap the lens in the anterior chamber, leading to an obstruction of outflow of aqueous humour and subsequent increase in ocular pressure (glaucoma). Better prognosis is valued in lens replacement surgery (retained vision and normal intraocular pressure) when it is performed before the onset of secondary glaucoma. Glaucoma secondary to anterior lens luxation is less common in cats than dogs due to their naturally deeper anterior chamber and the liquification of the vitreous humour secondary to chronic inflammation. Anterior lens luxation is considered to be an ophthalmological emergency.

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.