Prisms or "field expanders" that bend light have been prescribed for decades in patients with hemianopsia. Higher power Fresnel ("stick-on") prisms are commonly employed because they are thin and light weight, and can be cut and placed in different positions on a spectacle lens.

Peripheral prism spectacles expand the visual field of patients with hemifield visual defects and have the potential to improve visual function and mobility. Prism spectacles incorporate higher power prisms, with variable shapes and designs. The Gottlieb button prism, and the Peli superior and inferior horizontal bands are some proprietary examples of prism glasses. These high power prisms "create" artificial peripheral vision into the non-blind field for obstacle avoidance and motion detection.

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.

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.

Binasal hemianopsia (or binasal hemianopia) is the medical description of a type of partial blindness where vision is missing in the inner half of both the right and left visual field. It is associated with certain lesions of the eye and of the central nervous system, such as congenital hydrocephalus.

In bitemporal hemianopsia vision is missing in the outer (temporal or lateral) half of both the right and left visual fields. Information from the temporal visual field falls on the nasal (medial) retina. The nasal retina is responsible for carrying the information along the optic nerve, and crosses to the other side at the optic chiasm. When there is compression at optic chiasm the visual impulse from both nasal retina are affected, leading to inability to view the temporal, or peripheral, vision. This phenomenon is known as bitemporal hemianopsia. Knowing the neurocircuitry of visual signal flow through the optic tract is very important in understanding bitemporal hemianopsia.

Bitemporal hemianopsia most commonly occurs as a result of tumors located at the mid-optic chiasm. Since the adjacent structure is the pituitary gland, some common tumors causing compression are pituitary adenomas and craniopharyngiomas. Also another relatively common neoplastic cause is meningiomas. A cause of vascular origin is an aneurysm of the anterior communicating artery which arise superior to the chiasm, enlarge, and compress it from above.

Bitemporal hemianopsia, also known as bitemporal heteronymous hemianopsia or bitemporal hemianopia, is the medical description of a type of partial blindness where vision is missing in the outer half of both the right and left visual field. It is usually associated with lesions of the optic chiasm, the area where the optic nerves from the right and left eyes cross near the pituitary gland.

Hemianopsia, or hemianopia, is a decreased vision or blindness (anopsia) in half the visual field, usually on one side of the vertical midline. The most common causes of this damage are stroke, brain tumor, and trauma.

This article deals only with permanent hemianopsia, and not with transitory or temporary hemianopsia, as identified by William Wollaston PRS in 1824. Temporary hemianopsia can occur in the aura phase of migraine.

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.

An anopsia or anopia is a defect in the visual field. If the defect is only partial, then the portion of the field with the defect can be used to isolate the underlying cause.

Types of partial anopsia:

- Hemianopsia

- Homonymous hemianopsia

- Heteronymous hemianopsia

- Binasal hemianopsia

- Bitemporal hemianopsia

- Superior hemianopia

- Inferior hemianopia

- Quadrantanopia

The term "anopsia" comes from the Ancient Greek ἀν- ("an-"), "un-" and ὄψις ("opsis") "sight".

When the pathology involves both eyes, it is either homonymous or Heteronymous.

In binasal hemianopsia, vision is missing in the inner (nasal or medial) half of both the right and left visual fields. Information from the nasal visual field falls on the temporal (lateral) retina. Those lateral retinal nerve fibers do not cross in the optic chiasm. Calcification of the internal carotid arteries can impinge the uncrossed, lateral retinal fibers leading to loss of vision in the nasal field.

Note: Clinical testing of visual fields (by confrontation) can produce a false positive result (particularly in inferior nasal quadrants).

Current experimental evidence focuses on the involvement of the occipitotemporal pathway in both the perceptual equivalence of objects across translations of retinal position and also across size modifications. Recent evidence points to this pathway as a mediator for an individual's perception of size. Even further, numerous cases suggest that size perception may be dissociated from other aspects of visual perception such as color and movement. However, more research is called for to correctly relate the condition to defined physiological conditions.

Current research is being done on macular degeneration which could help prevent cases of micropsia. A variety of drugs that block vascular endothelial growth factors (VEGFs) are being evaluated as a treatment option. These treatments for the first time have produced actual improvements in vision, rather than simply delaying or arresting the continued loss of vision characteristic of macular degeneration. A number of surgical treatments are also being investigated for macular degeneration lesions that may not qualify for laser treatment, including macular translocation to a healthier area of the eye, displacement of submacular blood using gas, and removing membranes by surgery.

Treatment varies for micropsia due to the large number of different causes for the condition.

Treatments involving the occlusion of one eye and the use of a prism fitted over an eyeglass lens have both been shown to provide relief from micropsia.

Micropsia that is induced by macular degeneration can be treated in several ways. A study called AREDS (age-related eye disease study) determined that taking dietary supplements containing high-dose antioxidants and zinc produced significant benefits with regard to disease progression. This study was the first ever to prove that dietary supplements can alter the natural progression and complications of a disease state. Laser treatments also look promising but are still in clinical stages.

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.

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.

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.

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.

It is essential that a child with strabismus is presented to the ophthalmologist as early as possible for diagnosis and treatment in order to allow best possible monocular and binocular vision to develop. Initially, the patient will have a full eye examination to identify any associated pathology, and any glasses required to optimise acuity will be prescribed – although infantile esotropia is not typically associated with refractive error. Studies have found that approximately 15% of infantile esotropia patients have accommodative esotropia. For these patients, antiaccommodative therapy (with spectacles) is indicated before any surgery as antiaccommodative therapy fully corrects their esotropia in many cases and significantly decreases their deviation angle in others.

Amblyopia will be treated via occlusion treatment (using patching or atropine drops) of the non-squinting eye with the aim of achieving full alternation of fixation. Management thereafter will be surgical. As alternative to surgery, also botulinum toxin therapy has been used in children with infantile esotropia. Furthermore, as accompaniment to ophtalmologic treatment, craniosacral therapy may be performed in order to relieve tension ("see also:" Management of strabismus).

According to a Cochrane review of 2012, controversies remain regarding type of surgery, non-surgical intervention and age of intervention.

The aims of treatment are as follows:

The elimination of any amblyopia

A cosmetically acceptable ocular alignment

long term stability of eye position

binocular cooperation.

Treatment consists of finding ways to bring the patient's attention toward the left, usually done incrementally, by going just a few degrees past midline, and progressing from there. Rehabilitation of neglect is often carried out by neuropsychologists, occupational therapist,

speech-language pathologists, neurologic music therapists, physical therapists, optometrists and orthoptists.

Forms of treatment that have been tested with variable reports of success include prismatic adaptation, where a prism lens is worn to pull the vision of the patient towards the left, constrained movement therapy where the "good" limb is constrained in a sling to encourage use of the contralesional limb. Eye-patching has similarly been used, placing a patch over the "good" eye. Pharmaceutical treatments have mostly focused on dopaminergic therapies such as bromocriptine, levodopa, and amphetamines, though these tests have had mixed results, helping in some cases and accentuating hemispatial neglect in others. Caloric vestibular stimulation (CVS) has been shown to bring about a brief remission in some cases. however this technique has been known to elicit unpleasant side-effects such as nystagmus, vertigo and vomiting.

A study done by Schindler and colleagues examined the use of neck muscle vibration on the contralesional posterior neck muscles to induce diversion of gaze from the subjective straight ahead. Subjects received 15 consecutive treatment sessions and were evaluated on different aspects of the neglect disorder including perception of midline, and scanning deficits. The study found that there is evidence that neck muscle stimulation may work, especially if combined with visual scanning techniques. The improvement was evident 2 months after the completion of treatment.

Other areas of emerging treatment options include the use of prisms, visual scanning training, mental imagery training, video feedback training, trunk rotation, galvanic vestibular stimulation (GVS), transcranial magnetic stimulation (TMS) and transcranial direct-current stimulation (tDCS). Of these emerging treatment options, the most studied intervention is prism adaptation and there is evidence of relatively long-term functional gains from comparatively short-term usage. However, all of these treatment interventions (particularly the stimulation techniques) are relatively new and randomised, controlled trial evidence is still limited. Further research is mandatory in this field of research in order to provide more support in evidence-based practice.

In a review article by Pierce & Buxbaum (2002), they concluded that the evidence for Hemispheric Activation Approaches, which focuses on moving the limb on the side of the neglect, has conflicting evidence in the literature. The authors note that a possible limitation in this approach is the requirement for the patients to actively move the neglected limb, which may not be possible for many patients. Constraint-Induced Therapy (CIT), appears to be an effective, long-term treatment for improving neglect in various studies. However, the use of CIT is limited to patients who have active control of wrist and hand extension. Prism Glasses, Hemispatial Glasses, and Eye-Patching have all appear to be effective in improving performance on neglect tests. Caloric Stimulation treatment appears to be effective in improving neglect; however, the effects are generally short-term. The review also suggests that Optokinetic Stimulation is effective in improving position sense, motor skills, body orientation, and perceptual neglect on a short-term basis. As with Caloric Stimulation treatment, long-term studies will be necessary to show its effectiveness. A few Trunk Rotation Therapy studies suggest its effectiveness in improving performance on neglect tests as well as the Functional Independence Measure (FIM). Some less studied treatment possibilities include treatments that target Dorsal Stream of visual processing, Mental Imagery Training, and Neck Vibration Therapy. Trunk rotation therapies aimed at improving postural disorders and balance deficits in patients with unilateral neglect, have demonstrated optimistic results in regaining voluntary trunk control when using specific postural rehabilitative devices. One such device is the Bon Saint Côme apparatus, which uses spatial exploratory tasks in combination with auditory and visual feedback mechanisms to develop trunk control. The Bon Saint Côme device has been shown to be effective with hemiplegic subjects due to the combination of trunk stability exercises, along with the cognitive requirements needed to perform the postural tasks.

Management strategies for acquired prosopagnosia, such as a person who has difficulty recognizing people's faces after a stroke, generally have a low rate of success. Acquired prosopagnosia sometimes spontaneously resolves on its own.

Hemispatial neglect, also called hemiagnosia, hemineglect, unilateral neglect, spatial neglect, contralateral neglect, unilateral visual inattention, hemi-inattention, neglect syndrome or contralateral hemispatialagnosia, is a neuropsychological condition in which, after damage to one hemisphere of the brain is sustained, a deficit in attention to and awareness of one side of the field of vision is observed. It is defined by the inability of a person to process and perceive stimuli on one side of the body or environment, where that inability is not due to a lack of sensation. Hemispatial neglect is very commonly contralateral to the damaged hemisphere, but instances of ipsilesional neglect (on the same side as the lesion) have been reported.

"Developmental prosopagnosia" (DP), also called "Congenital prosopagnosia" (CP), is a face-recognition deficit that is lifelong, manifesting in early childhood, and that cannot be attributed to acquired brain damage. A number of studies have found functional deficits in DP both on the basis of EEG measures and fMRI. It has been suggested that a genetic factor is responsible for the condition. The term "hereditary prosopagnosia" was introduced if DP affected more than one family member, essentially accenting the possible genetic contribution of this condition. To examine this possible genetic factor, 689 randomly selected students were administered a survey in which seventeen developmental prosopagnosics were quantifiably identified. Family members of fourteen of the DP individuals were interviewed to determine prosopagnosia-like characteristics, and in all fourteen families, at least one other affected family member was found.

In 2005, a study led by Ingo Kennerknecht showed support for the proposed congenital disorder form of prosopagnosia. This study provides epidemiological evidence that congenital prosopagnosia is a frequently occurring cognitive disorder that often runs in families. The analysis of pedigree trees formed within the study also indicates that the segregation pattern of hereditary prosopagnosia (HPA) is fully compatible with autosomal dominant inheritance. This mode of inheritance explains why HPA is so common among certain families (Kennerknecht et al. 2006).

There are many developmental disorders associated with an increased likelihood that the person will have difficulties in face perception, of which the person may or may not be aware. The mechanism by which these perceptual deficits take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Alzheimer's disease, and autism in general. However, these types of disorders are very complicated, so arbitrary assumptions should be avoided.

In 2012, it was shown that developmental prosopagnosia cases show poor integration of low and high spatial frequency information.

Dyslexic children require special instruction for word analysis and spelling from an early age. While there are fonts that may help people with dyslexia better understand writing, this might simply be due to the added spacing between words. The prognosis, generally speaking, is positive for individuals who are identified in childhood and receive support from friends and family.

Through the use of compensation strategies, therapy and educational support, dyslexic individuals can learn to read and write. There are techniques and technical aids which help to manage or conceal symptoms of the disorder. Removing stress and anxiety alone can sometimes improve written comprehension. For dyslexia intervention with alphabet-writing systems, the fundamental aim is to increase a child's awareness of correspondences between graphemes (letters) and phonemes (sounds), and to relate these to reading and spelling by teaching how sounds blend into words. It has been found that reinforced collateral training focused on reading and spelling yields longer-lasting gains than oral phonological training alone. Early intervention that is done for children at a young age can be successful in reducing reading failure.

There is some evidence that the use of specially-tailored fonts may help with dyslexia. These fonts, which include Dyslexie, OpenDyslexic, and Lexia Readable, were created based on the idea that many of the letters of the Latin alphabet are visually similar and may, therefore, confuse people with dyslexia. Dyslexie and OpenDyslexic both put emphasis on making each letter more distinctive in order to be more easily identified. The benefits, however, might simply be due to the added spacing between words.

There have been many studies conducted regarding intervention in dyslexia. Among these studies one meta-analysis found that there was functional activation as a result.

There is no evidence demonstrating that the use of music education is effective in improving dyslexic adolescents' reading skills.