The cause is unclear. The underlying mechanism is believed to involve excessive excitability of neurons within the cortex of the brain.

Specifically the right lingual gyrus and left cerebellar anterior lobe of the brain.

Persisting visual snow can feature as a leading addition to a migraine complication called persistent aura without infarction, commonly referred to as persistent migraine aura (PMA). In other clinical sub-forms of migraine headache may be absent and the migraine aura may not take the typical form of the zigzagged fortification spectrum, but manifests with a large variety of focal neurological symptoms.

The role of hallucinogens in of visual snow is not clear. Hallucinogen persisting perception disorder (HPPD), a condition caused by hallucinogenic drug use, is sometimes linked to visual snow, but both the connection of visual snow to HPPD and the cause and prevalence of HPPD is disputed. Most of the evidence for both is generally anecdotal, and subject to spotlight fallacy.

Some neuro-ophthalmologists believe that visual snow is not a medical condition, but a poorly understood symptom. People report seeing "snow", much like the visual noise on a TV screen after transmission ends. These authors hypothesize that what the patients see as "snow" is their own intrinsic visual noise.

Many report more visual snow in low light conditions. This has a natural explanation. "The intrinsic dark noise of primate cones is equivalent to ~4000 absorbed photons per second at mean light levels below this the cone signals are dominated by intrinsic noise".

In addition to visual snow, many of those affected have other types of visual disturbances such as starbursts, increased afterimages, floaters, trails, and many others.

Episodes of micropsia or macropsia occur in 9% of adolescents.

10-35% of migraine sufferers experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras.

Micropsia seems to be slightly more common in boys than in girls among children who experience migraines.

Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Central Serous Chorioretinopathy (CSCR) which can produce micropsia predominantly affects persons between the ages of 20 and 50. Women appear to be affected more than men by a factor of almost 3 to 1.

Micropsia can be caused by swelling of the cornea due to infection by the Epstein-Barr virus (EBV) and can therefore present as an initial symptom of EBV mononucleosis, a disease caused by Epstein-Barr virus infection.

In general, the prognosis for retinal migraine is similar to that of migraine headache with typical aura. As the true incidence of retinal migraine is unknown, it is uncertain whether there is a higher incidence of permanent neuroretinal injury. The visual field data suggests that there is a higher incidence of end arteriolar distribution infarction and a higher incidence of permanent visual field defects in retinal migraine than in clinically manifest cerebral infarctions in migraine with aura. One study suggests that more than half of reported "recurrent" cases of retinal migraine subsequently experienced permanent visual loss in that eye from infarcts, but more recent studies suggest such loss is a relatively rare side effect.

Of the published cases of palinopsia that are idiopathic or attributed to migraines, HPPD, prescription drugs, or head trauma, 94% described illusory palinopsia. Trazodone, nefazodone, mirtazapine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. Clomiphene and oral contraceptives are the only prescription drugs reported to cause permanent symptoms. HPPD is most common after LSD ingestion, but can occur after any hallucinogen use. HPPD is commonly described in psychiatric literature and illusory palinopsia symptoms are sometimes not defined as palinopsia. It is not clear if there is a relationship between HPPD and the quantity and strength of hallucinogen doses taken.

Palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is the persistent recurrence of a visual image after the stimulus has been removed. Palinopsia is not a diagnosis, it is a diverse group of pathological visual symptoms with a wide variety of causes. Visual perseveration is synonymous with palinopsia.

In 2014, Gersztenkorn and Lee comprehensively reviewed all cases of palinopsia in the literature and subdivided it into two clinically relevant groups: illusory palinopsia and hallucinatory palinopsia. Hallucinatory palinopsia, usually due to seizures or posterior cortical lesions, describes afterimages that are formed, long-lasting, and high resolution. Illusory palinopsia, usually due to migraines, head trauma, prescription drugs, or hallucinogen persisting perception disorder (HPPD), describes afterimages that are affected by ambient light and motion and are unformed, indistinct, or low resolution.

Illusory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistence or recurrence of a visual image after the stimulus has been removed. Palinopsia is a broad term describing a heterogeneous group of symptoms, which is divided into hallucinatory palinopsia and illusory palinopsia. Illusory palinopsia is likely due to sustained awareness of a stimulus and is similar to a visual illusion: the distorted perception of a real external stimulus.

Illusory palinopsia is caused by migraines, hallucinogen persisting perception disorder (HPPD), prescription drugs, and head trauma, but is also sometimes idiopathic. Illusory palinopsia consists of afterimages that are short-lived or unformed, occur at the same location in the visual field as the original stimulus, and are often exposed or exacerbated based on environmental parameters such as stimulus intensity, background contrast, fixation, and movement. Illusory palinopsia symptoms occur continuously or predictably, based on environmental conditions.

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

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

Posterior visual pathway cortical lesions (tumor, abscess, hemorrhage, infarction, arteriovenous malformation, cortical dysplasia, aneurysm) and various seizure causes (hyperglycemia, ion channel mutations, Creutzfeldt–Jakob disease, idiopathic seizures, etc.) cause focal cortical hyperactivity or hyperexcitability, resulting in inappropriate, persistent activation of a visual memory circuit.

Illusory palinopsia is a dysfunction of visual perception, resulting from diffuse, persistent alterations in neuronal excitability that affect physiological mechanisms of light or motion perception. Illusory palinopsia is caused by migraines, HPPD, prescription drugs, head trauma, or may be idiopathic. Trazodone, nefazodone, mirtazepine, topiramate, clomiphene, oral contraceptives, and risperidone have been reported to cause illusory palinopsia. A patient frequently has multiple types of illusory palinopsia, which represent dysfunctions in both light and motion perception. Light and motion are processed via different pathways, suggesting diffuse or global excitability alterations.

Quadrantanopia, quadrantanopsia, or quadrant anopia refers to an anopia affecting a quarter of the field of vision.

It can be associated with a lesion of an optic radiation. While quadrantanopia can be caused by lesions in the temporal and parietal lobes, it is most commonly associated with lesions in the occipital lobe.

Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy. Blindness in combination with hearing loss is known as deafblindness.

It has been estimated that over half of completely blind people have non-24-hour sleep–wake disorder, a condition in which a person's circadian rhythm, normally slightly longer than 24 hours, is not entrained (synchronized) to the light/dark cycle.

Closed-eye hallucinations and closed-eye visualizations (CEV) are a distinct class of hallucination. These types of hallucinations generally only occur when one's eyes are closed or when one is in a darkened room. They can be a form of phosphene. Some people report closed-eye hallucinations under the influence of psychedelics. These are reportedly of a different nature than the "open-eye" hallucinations of the same compounds.

The cause(s) of HPPD are not yet known. It has been theorized that HPPD is an anomaly in executive function brought on by the dis-inhibition of the COMT enzyme in the breakdown of catecholamines in the brain following hallucinogen use, resulting in sensory gating disruption.

In some cases, HPPD appears to have a sudden onset after a single drug experience, strongly suggesting the drug played a direct role in triggering symptoms. But in other cases, people report gradual worsening of symptoms with ongoing drug use. Drugs that have been associated with HPPD include CBD, LSD, 5-MeO-DiPT MDA, MDMA, psilocybin, diphenhydramine, PCP, synthetic cannabinoids, zolpidem, eszopiclone, and high doses of dextromethorphan, a high dose of the wakefulness enhancing agent modafinil combined with a CNS stimulant, namely, caffeine can also be a trigger. Additionally there are anecdotal reports of the atypical psychedelic "Salvia divinorum" causing persisting symptoms consistent with HPPD.

There are five known levels of CEV perception which can be achieved either through chemical stimuli or through meditative relaxation techniques. Level 1 and 2 are very common and often happen every day. It is still normal to experience level 3, and even level 4, but only a small percentage of the population does this without psychedelic drugs, meditation or extensive visualization training.

Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.

Common causes of scotomata include demyelinating disease such as multiple sclerosis (retrobulbar neuritis), damage to nerve fiber layer in the retina (seen as cotton wool spots) due to hypertension, toxic substances such as methyl alcohol, ethambutol and quinine, nutritional deficiencies, vascular blockages either in the retina or in the optic nerve, stroke or other brain injury, and macular degeneration, often associated with aging. Scintillating scotoma is a common visual aura in migraine. Less common, but important because they are sometimes reversible or curable by surgery, are scotomata due to tumors such as those arising from the pituitary gland, which may compress the optic nerve or interfere with its blood supply.

Rarely, scotomata are . One important variety of bilateral scotoma may occur when a pituitary tumour begins to compress the optic chiasm (as distinct from a single optic nerve) and produces a bitemporal paracentral scotoma, and later, when the tumor enlarges, the scotomas extend out to the periphery to cause the characteristic bitemporal hemianopsia. This type of visual-field defect tends to be obvious to the person experiencing it but often evades early objective diagnosis, as it is more difficult to detect by cursory clinical examination than the classical or textbook bitemporal peripheral hemianopia and may even elude sophisticated electronic modes of visual-field assessment.

In a pregnant woman, scotomata can present as a symptom of severe preeclampsia, a form of pregnancy-induced hypertension. Similarly, scotomata may develop as a result of the increased intracranial pressure that occurs in malignant hypertension.

The scotoma is also caused by the aminoglycoside antibiotics mainly by Streptomycin.

Visual looming syndrome is a problem with visual perception that causes people to inaccurately think that a stationary object is moving towards them, and might poke their eyes.

It is a neurological and muscular state, where faulty eye coordination causes the brain to interpret incoming information as a visual looming event (i.e. feeling that an object is approaching and might hit the eye). Because this condition is muscular in nature, anything that causes eye cooperation to fail, such as being tired, under the of narcotics or alcohol, or even minor differences in eye pressure or eyesight (e.g. nearsightedness), may be the cause of an episode. The is usually a narrow or pointy object which is near enough to cause confusion in the eyes, or which is in front of an undetermined or busy background. Some peer to peer studies have indicated that certain conditions, such as nyctalopia or night blindness, may worsen the syndrome.

The probability of developing HPPD after consuming a hallucinogen is unknown. In their review article, John Halpern and Harrison Pope write that "the data does not permit us to estimate, even crudely, the prevalence of ‘strict’ HPPD." These authors noted that they had not encountered it in their evaluation of 500 Native American Church members who had taken the hallucinogenic cactus peyote on at least 100 occasions. In a presentation of preliminary results from ongoing research, Matthew Baggott and colleagues from University of California Berkeley found that HPPD-like symptoms occurred in 4.1% of participants (107 of 2,679) in a web-based survey of hallucinogen users. These people reported visual problems after drug use that were serious enough that they considered seeking professional help. This number may overestimate the prevalence of HPPD, since people with visual problems may have been more interested in completing the researchers' questionnaire. The authors reported that 16,192 people viewed the study information but did not complete the questionnaire. If all these people had used hallucinogens without developing visual problems, then the prevalence of serious visual problems in this larger group would be 0.66%. Since these people were not formally diagnosed in person (and may have had visual problems caused by other disorders), this number may provide a reasonable upper limit on the prevalence of HPPD, or they might be statistically meaningless.

It is possible the prevalence of HPPD has been underestimated by authorities because many people with visual problems relating to drug use either do not seek treatment or, when they do seek treatment, do not admit to having used illicit drugs. In the sample of Baggott, only 16 of the 107 people with possible HPPD had sought help and two of these people had been diagnosed with HPPD. Thus, it may be that HPPD occurs more often than is detected by the health care system.

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.

Streff syndrome is a vision condition primarily exhibited by children under periods of visual or emotional stress.

Frequently patients will have reduced stereopsis, large accommodative lag on dynamic retinoscopy, and a reduced visual field (tubular or spiral field). Streff Syndrome was first described in 1962 by an optometrist, Dr. John Streff as Non-malingering syndrome. In 1962, Dr. Streff and Dr. Richard Apell expanded the concept to add early adaptive syndrome as a precursor to Streff syndrome. Dr. Streff believed the visual changes were induced by stress from reading. There is dispute on the taxonomy of functional vision defects. Some research indicates that Streff syndrome may be caused by a dysfunction in the magnocellular pathway of the retinal ganglion cells. These cells are only 10% of the retinal nerve cells and register motion detection.

Early Adaptive Syndrome

Individuals with quadrantanopia often modify their behavior to compensate for the disorder, such as tilting of the head to bring the affected visual field into view. Drivers with quadrantanopia, who were rated as safe to drive, drive slower, utilize more shoulder movements and, generally, corner and accelerate less drastically than typical individuals or individuals with quadrantanopia who were rated as unsafe to drive. The amount of compensatory movements and the frequency with which they are employed is believed to be dependent on the cognitive demands of the task; when the task is so difficult that the subject's spatial memory is no longer sufficient to keep track of everything, patients are more likely to employ compensatory behavior of biasing their gaze to the afflicted side. Teaching individuals with quadrantanopia compensatory behaviors could potentially be used to help train patients to re-learn to drive safely.

The most common causes of visual impairment globally in 2010 were:

1. Refractive error (42%)

2. cataract (33%)

3. glaucoma (2%)

4. age related macular degeneration (1%)

5. corneal opacification (1%)

6. diabetic retinopathy (1%)

7. childhood blindness

8. trachoma (1%)

9. undetermined (18%)

The most common causes of blindness in 2010 were:

1. cataracts (51%)

2. glaucoma (8%)

3. age related macular degeneration (5%)

4. corneal opacification (4%)

5. childhood blindness (4%)

6. refractive errors (3%)

7. trachoma (3%)

8. diabetic retinopathy (1%)

9. undetermined (21%)

About 90% of people who are visually impaired live in the developing world. Age-related macular degeneration, glaucoma, and diabetic retinopathy are the leading causes of blindness in the developed world.

Among working age adults who are newly blind in England and Wales the most common causes in 2010 were:

1. Hereditary retinal disorders (20.2%)

2. Diabetic retinopathy (14.4%)

3. Optic atrophy (14.1%)

4. Glaucoma (5.9%)

5. Congenital abnormalities (5.1%)

6. Disorders of the visual cortex (4.1%)

7. Cerebrovascular disease (3.2%)

8. Degeneration of the macula and posterior pole (3.0%)

9. Myopia (2.8%)

10. Corneal disorders (2.6%)

11. Malignant neoplasms of the brain and nervous system (1.5%)

12. Retinal detachment (1.4%)

Cerebral diplopia or polyopia describes seeing two or more images arranged in ordered rows, columns, or diagonals after fixation on a stimulus. The polyopic images occur monocular bilaterally (one eye open on both sides) and binocularly (both eyes open), differentiating it from ocular diplopia or polyopia. The number of duplicated images can range from one to hundreds. Some patients report difficulty in distinguishing the replicated images from the real images, while others report that the false images differ in size, intensity, or color. Cerebral polyopia is sometimes confused with palinopsia (visual trailing), in which multiple images appear while watching an object. However, in cerebral polyopia, the duplicated images are of a stationary object which are perceived even after the object is removed from the visual field. Movement of the original object causes all of the duplicated images to move, or the polyopic images disappear during motion. In palinoptic polyopia, movement causes each polyopic image to leave an image in its wake, creating hundreds of persistent images (entomopia).

Infarctions, tumors, multiple sclerosis, trauma, encephalitis, migraines, and seizures have been reported to cause cerebral polyopia. Cerebral polyopia has been reported in extrastriate visual cortex lesions, which is important for detecting motion, orientation, and direction. Cerebral polyopia often occurs in homonymous field deficits, suggesting deafferentation hyperexcitability could be a possible mechanism, similar to visual release hallucinations (Charles Bonnet syndrome).