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.

Scintillating scotomas are most commonly caused by cortical spreading depression, a pattern of changes in the behavior of nerves in the brain during a migraine. Migraines, in turn, may be caused by genetic influences and hormones. People with migraines often self-report triggers for migraines involving stress and a wide variety of foods. While monosodium glutamate (MSG) is frequently reported as a dietary trigger, some scientific studies do not support this claim.

The Framingham Heart Study, published in 1998, surveyed 5,070 people between ages 30–62 and found that scintillating scotomas without other symptoms occurred in 1.23% of the group. The study did not find a link between late-life onset scintillating scotoma and stroke.

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.

Symptoms typically appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes, leading to the headache in classic migraine with aura, or resolving without consequence in acephalgic migraine. Many migraine sufferers change from scintillating scotoma as a prodrome to migraine to scintillating scotoma without migraine. The scotoma typically spontaneously resolves within the stated time frame, leaving few or no subsequent symptoms, though some report fatigue, nausea, and dizziness as sequelae.

Macular degeneration typically produces micropsia due to the swelling or bulging of the macula, an oval-shaped yellow spot near the center of the retina in the human eye. The main factors leading to this disease are age, smoking, heredity, and obesity. Some studies show that consuming spinach or collard greens five times a week cuts the risk of macular degeneration by 43%.

Retinal migraine (also known as ophthalmic migraine, and ocular migraine) is a retinal disease often accompanied by migraine headache and typically affects only one eye. It is caused by ischaemia or vascular spasm in or behind the affected eye.

The terms "retinal migraine" and "ocular migraine" are often confused with "visual migraine", which is a far-more-common symptom of vision loss, resulting from the aura phase of the common migraine. The aura phase of migraine can occur with or without a headache. Ocular or retinal migraines happen in the eye, so only affect the vision in that eye, while visual migraines occur in the brain, so affect the vision in both eyes together. Visual migraines result from cortical spreading depression and are also commonly termed scintillating scotoma.

Young children with strabismus normally suppress the visual field of one eye (or part of it), whereas adults who develop strabismus normally do not suppress and therefore suffer from double vision (diplopia). This also means that adults (and older children) have a higher risk of post-operative diplopia after undergoing strabismus surgery than young children. Patients who have undergone strabismus surgery at a young age often have monofixation syndrome (with peripheral binocular fusion and a central suppression scotoma).

Optic pits occur equally between men and women. They are seen in roughly 1 in 10,000 eyes, and approximately 85% of optic pits are found to be unilateral (i.e. in only one eye of any affected individual). About 70% are found on the temporal side (or lateral one-half) of the optic disc. Another 20% are found centrally, while the remaining pits are located either superiorly (in the upper one-half), inferiorly (in the lower one-half), or nasally (in the medial one-half towards the nose).

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.

Suppression may treated with vision therapy, though there is a wide range of opinions on long-term effectiveness between eye care professionals, with little scientific evidence of long-term improvement of suppression, if the underlying cause is not addressed (strabismus, amblyopia, etc.).

No particular risk factors have been conclusively identified; however, there have been a few reports that demonstrate an autosomal dominant pattern of inheritance in some families. Therefore, a family history of optic pits may be a possible risk factor.

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).

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.

A scotoma (Greek σκότος/"skótos", "darkness"; plural: "scotomas" or "scotomata") is an area of partial alteration in the field of vision consisting of a partially diminished or entirely degenerated visual acuity that is surrounded by a field of normal – or relatively well-preserved – vision.

Every normal mammal eye has a scotoma in its field of vision, usually termed its blind spot. This is a location with no photoreceptor cells, where the retinal ganglion cell axons that compose the optic nerve exit the retina. This location is called the optic disc. There is no direct conscious awareness of visual scotomas. They are simply regions of reduced information within the visual field. Rather than recognizing an incomplete image, patients with scotomas report that things "disappear" on them.

The presence of the blind spot scotoma can be demonstrated subjectively by covering one eye, carefully holding fixation with the open eye, and placing an object (such as one's thumb) in the lateral and horizontal visual field, about 15 degrees from fixation (see the blind spot article). The size of the monocular scotoma is 5×7 degrees of visual angle.

A scotoma can be a symptom of damage to any part of the visual system, such as retinal damage from exposure to high-powered lasers, macular degeneration and brain damage.

The term "scotoma" is also used metaphorically in several fields. The common theme of all the figurative senses is of a gap not in visual function but in the mind's perception, cognition, or world view.

Between 12 and 60% of people report foods as triggers. Evidence for such triggers, however, mostly relies on self-reports and is not rigorous enough to prove or disprove any particular triggers. A clear explanation for why food might trigger migraines is also lacking.

There does not appear to be evidence for an effect of tyramine on migraine. Likewise, while monosodium glutamate (MSG) is frequently reported, evidence does not consistently support that it is a dietary trigger.

Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches). Psychological stress has been reported as a factor by 50 to 80% of people. Migraines have also been associated with post-traumatic stress disorder and abuse. Migraines are more likely to occur around menstruation. Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role. These hormonal influences seem to play a greater role in migraine without aura. Migraines typically do not occur during the second and third trimesters or following menopause.

Although a definitive cause (or set of causes) for the symptoms outlined in the Existing Long-Duration Flight Occurrences section is unknown, it is thought that venous congestion in the brain brought about by cephalad-fluid shifts may be a unifying pathologic mechanism. Additionally, a recent study reports changes in CSF hydrodynamics and increased diffusivity around the optic nerve under simulated microgravity conditions which may contribute to ocular changes in spaceflight. As part of the effort to elucidate the cause(s), NASA has initiated an enhanced occupational monitoring program for all mission astronauts with special attention to signs and symptoms related to ICP.

Similar findings have been reported among Russian Cosmonauts who flew long-duration missions on MIR. The findings were published by Mayasnikov and Stepanova in 2008.

Animal research from the Russian Bion-M1 mission indicates duress of the cerebral arteries may induce reduced blood flow, thereby contributing to impaired vision.

On 2 November 2017, scientists reported that significant changes in the position and structure of the brain have been found in astronauts who have taken trips in space, based on MRI studies. Astronauts who took longer space trips were associated with greater brain changes.

Hemianopsia or hemianopia is a visual field loss on the left or right side of the vertical midline. It can affect one eye but usually affects both eyes. Homonymous hemianopsia, or homonymous hemianopia, is hemianopic visual field loss on the same side of both eyes. Homonymous hemianopsia occurs because the right half of the brain has visual pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the right hemifield of both eyes. When one of these pathways is damaged, the corresponding visual field is lost.

A blind spot, scotoma, is an obscuration of the visual field. A particular blind spot known as the "physiological blind spot", "blind point", or "punctum caecum" in medical literature, is the place in the visual field that corresponds to the lack of light-detecting photoreceptor cells on the optic disc of the retina where the optic nerve passes through the optic disc. Because there are no cells to detect light on the optic disc, the corresponding part of the field of vision is invisible. Some process in our brains interpolates the blind spot based on surrounding detail and information from the other eye, so we do not normally perceive the blind spot.

Although all vertebrates have this blind spot, cephalopod eyes, which are only superficially similar, do not. In them, the optic nerve approaches the receptors from behind, so it does not create a break in the retina.

The first documented observation of the phenomenon was in the 1660s by Edme Mariotte in France. At the time it was generally thought that the point at which the optic nerve entered the eye should actually be the most sensitive portion of the retina; however, Mariotte's discovery disproved this theory.

The blind spot is located about 12–15° temporally and 1.5° below the horizontal and is roughly 7.5° high and 5.5° wide.

Mobility can be difficult for people with homonymous hemianopsia. “Patients frequently complain of bumping into obstacles on the side of the field loss, thereby bruising their arms and legs.”

People with homonymous hemianopsia often experience discomfort in crowds. “A patient with this condition may be unaware of what he or she cannot see and frequently bumps into walls, trips over objects or walks into people on the side where the visual field is missing.”

A related phenomenon is Hemispatial neglect, the possible neglect of the right or left. The patient is not conscious of its existence. The right side of the face is not shaven, make up is applied to one side of the face only and only half of a plate of food is eaten. This, however, is not necessarily due to a sensory abnormality, and is therefore distinct from hemianopsia.

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine, but the symptoms are usually less severe than those of classic migraine, so treatment is less likely to be required.

Spaceflight induced visual impairment is hypothesized to be a result of increased intracranial pressure. The study of visual changes and intracranial pressure (ICP) in astronauts on long-duration flights is a relatively recent topic of interest to Space Medicine professionals. Although reported signs and symptoms have not appeared to be severe enough to cause blindness in the near term, long term consequences of chronically elevated intracranial pressure is unknown.

NASA has reported that fifteen long-duration male astronauts (45–55 years of age) have experienced confirmed visual and anatomical changes during or after long-duration flights. Optic disc edema, globe flattening, choroidal folds, hyperopic shifts and an increased intracranial pressure have been documented in these astronauts. Some individuals experienced transient changes post-flight while others have reported persistent changes with varying degrees of severity.

Although the exact cause is not known at this time, it is suspected that microgravity-induced cephalad fluid shift and comparable physiological changes play a significant role in these changes. Other contributing factors may include pockets of increased CO and an increase in sodium intake. It seems unlikely that resistive or aerobic exercise are contributing factors, but they may be potential countermeasures to reduce intraocular pressure (IOP) or intracranial pressure (ICP) in-flight.

Monofixation syndrome (MFS) (also: microtropia or microstrabismus) is an eye condition defined by less-than-perfect binocular vision. It is defined by a small angle deviation with suppression of the deviated eye and the presence of binocular peripheral fusion. That is, MFS implies peripheral fusion without central fusion.

Aside the manifest small-angle deviation ("tropia"), subjects with MFS often also have a large-angle latent deviation ("phoria"). Their stereoacuity is often in the range of 3000 to 70 arcsecond, and a small central suppression scotoma of 2 to 5 deg.

A rare condition, MFS is estimated to affect only 1% of the general population. There are three distinguishable forms of this condition: primary constant, primary decompensating, and consecutive MFS. It is believed that primary MFS is a result of a primary sensorial defect, predisposing to anomalous retinal correspondence.

Secondary MFS is a frequent outcome of surgical treatment of congenital esotropia. A study of 1981 showed MFS to result in the vast majority of cases if surgical alignment is reached before the age of 24 months and only in a minority of cases if it is reached later.

MFS was first described by Marshall Parks.

Foroozen divides the causes of chiasmal syndromes into intrinsic and extrinsic causes. Intrinsic implies thickening of the chiasm itself and extrinsic implies compression by another structure. Other less common causes of chiasmal syndrome are metabolic, toxic, traumatic or infectious in nature.

Intrinsic etiologies include gliomas and multiple sclerosis. Gliomas of the optic chiasm are usually derived from astrocytes. These tumors are slow growing and more often found children. However, they have a worse prognosis, especially if they have extended into the hypothalamus. They are frequently associated with neurofibromatosis type 1 (NF-1). Their treatment involves the resection of the optic nerve. The supposed artifactual nature of Wilbrand's knee has implications for the degree of resection that can be obtained, namely by cutting the optic nerve immediately at the junction with the chiasm without fear of potentially resulting visual field deficits.

The vast majority of chiasmal syndromes are compressive. Ruben et al. describe several compressive etiologies, which are important to understand if they are to be successfully managed. The usual suspects are pituitary adenomas, craniopharyngiomas, and meningiomas.

Pituitary tumors are the most common cause of chiasmal syndromes. Visual field defects may be one of the first signs of non-functional pituitary tumor. These are much less frequent than functional adenomas. Systemic hormonal aberrations such as Cushing’s syndrome, galactorrhea and acromegaly usually predate the compressive signs. Pituitary tumors often encroach upon the middle chiasm from below. Pituitary apoplexy is one of the few acute chiasmal syndromes. It can lead to sudden visual loss as the hemorrhagic adenoma rapidly enlarges.

The embryonic remnants of Rathke’s pouch may undergo neoplastic change called a craniopharyngioma. These tumors may develop at any time but two age groups are most at risk. One peak occurs during the first twenty years of life and the other occurs between fifty and seventy years of age. Craniopharyngiomas generally approach the optic chiasm from behind and above. Extension of craniopharyngiomas into the third ventricle may cause hydrocephalus.

Meningiomas can develop from the arachnoid layer. Tuberculum sellae and sphenoid planum meningiomas usually compress the optic chiasm from below. If the meningioma arises from the diaphragma sellae the posterior chiasm is damaged. Medial sphenoid ridge types can push on the chiasm from the side. Olfactory groove subfrontal types can reach the chiasm from above. Meningiomas are also associated with neurofibromatosis type 1. Women are more prone to develop meningiomas.

Chiasmal syndrome is the set of signs and symptoms that are associated with lesions of the optic chiasm, manifesting as various impairments of the sufferer's visual field according to the location of the lesion along the optic nerve. Pituitary adenomas are the most common cause; however, chiasmal syndrome may be caused by cancer, or associated with other medical conditions such as multiple sclerosis and neurofibromatosis.