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.

Since this condition is usually coupled with other neurological disorders or deficits, there is no known cure for cerebral polyopia. However, measures can be taken to reduce the effects of associated disorders, which have proven to reduce the effects of polyopia. In a case of occipital lobe epilepsy, the patient experienced polyopia. Following administration of valproate sodium to reduce headaches, the patient’s polyopia was reduced to palinopsia. Further, after administering the anticonvulsant drug Gabapentin in addition to valproate sodium, the effects of palinopsia were decreased, as visual perseveration is suppressed by this anticonvulsant drug. Thus, in cases of epilepsy, anticonvulsant drugs may prove to reduce the effects of polyopia and palinopsia, a topic of which should be further studied.

In other cases of polyopia, it is necessary to determine all other present visual disturbances before attempting treatment. Neurological imaging can be performed to determine if there are present occipital or temporal lobe infarctions that may be causing the polyopia. CT scans are relatively insensitive to the presence of cerebral lesions, so other neurological imaging such as PET and MRI may be performed. The presence of seizures and epilepsy may also be assessed through EEG. In addition, motor visual function should be assessed through examination of pupillary reactions, ocular motility, optokinetic nystagmus, slit-lamp examination, visual field examination, visual acuity, stereo vision, bimicroscopic examination, and funduscopic examination. Once the performance of such functions have been assessed, a plan for treatment can follow accordingly. Further research should be conducted to determine if the treatment of associated neurological disturbances can reduce the effects of polyopia.

Palinopsia from cerebrovascular accidents generally resolves spontaneously, and treatment should be focused on the vasculopathic risk factors. Palinopsia from neoplasms, AVMs, or abscesses require treatment of the underlying condition, which usually also resolves the palinopsia. Palinopsia due to seizures generally resolves after correcting the primary disturbance and/or treating the seizures. In persistent hallucinatory palinopsia, a trial of an anti-epileptic drug can be attempted. Anti-epileptics reduce cortical excitability and could potentially treat palinopsia caused by cortical deafferentation or cortical irritation. Patients with idiopathic hallucinatory palinopsia should have close follow-up.

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.

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

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.

Speech and language therapy is typically the primary treatment for individuals with aphasia. The goal of speech and language therapy is to increase the person’s communication abilities to a level functional for daily life. Goals are chosen based on collaboration between speech language pathologists, patients, and their family/caregivers. Goals should be individualized based on the person’s aphasia symptoms and communicative needs. In 2016, Wallace et al. found the following outcomes were commonly prioritized in therapy: communication, life participation, physical and emotional well-being, normalcy, and health and support services. However, available research is inconclusive about which specific approach to speech and language therapy is most effective in treating global aphasia.

Therapy can be either group or individual. Group therapies that integrate the use of visual aids allow for enhanced social and communication-skill development. Group therapy sessions typically revolve around simple, preplanned activities or games, and aim to facilitate social communication.

One particular therapy designed specifically for treatment of aphasia is Visual Action Therapy (VAT). VAT is a non-verbal gestural output program with 3 phases and 30 total steps. The program teaches unilateral gestures as symbolic representations of real life objects. Research on the effectiveness of VAT is limited and inconclusive.

One important therapy technique includes teaching family members and caregivers strategies for more effectively communicating with their loved ones. Research offers such strategies including, simplifying sentences and using common words, gaining the person's attention before speaking, using pointing and visual cues, allowing for adequate response time, and creating a quiet environment free of distractions.

Another approach to speech and language treatment is constraint-induced language therapy (CILT). CILT involves teaching the patient to use speech in small segments but avoid using gestures and familiar words . The speech language pathologist provides positive feedback throughout and ignores any mistakes made by the patient. The intensity with which this treatment is provided has been debated in the literature. One study, performed in 2015, compared the outcomes of patients with aphasia who received CILT for either 30 hours total over 2 weeks or 30 hours distributed over 10 weeks. Results showed that both groups made significant speech and language improvements. Overall, CILT is an effective treatment at a variety of intensities.

Research supporting the efficacy of pharmacological treatments for aphasia is limited. To date, no large scale clinical trials have proven benefits of pharmacological treatment.

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.

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.

In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not "aware" of their disability). Another commonly used method is the use of feedback – comparing clients' self-predicted performance with their actual performance on a task in an attempt to improve insight.

Neurorehabilitation is difficult because, as anosognosia impairs the patient's desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.

In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalization. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognize their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.

Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.

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.

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).

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".

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).

Hallucinatory palinopsia (Greek: "palin" for "again" and "opsia" for "seeing") is a subtype of palinopsia, a visual disturbance defined as the persistent 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. Hallucinatory palinopsia refers to the projection of an already-encoded visual memory and is similar to a complex visual hallucination: the creation of a formed visual image where none exists.

Hallucinatory palinopsia usually arises from posterior cortical lesions or seizures and can be the presenting symptom of a serious neurological disease. Hallucinatory palinopsia describes afterimages or scenes that are formed, long-lasting, high resolution, and isochromatic. The palinoptic images are not typically reliant on environmental parameters and often present with homonymous visual field deficits. Hallucinatory palinopsia occurs unpredictably and the persistent images can appear anywhere in the visual field, regardless of the location of the original stimulus. A patient will often have only a few episodes of hallucinatory palinopsia. Visual perseveration is synonymous with palinopsia.

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.

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.

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.

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

When evaluating the prognosis of a patient, the main contributing participant factors that influence the extent of neuroplasticity, or the brain's ability to change are: age, lesion location, pre-existing cognitive status, motivation, age, overall health, and interaction amongst these. After brain damage, initial signs of global aphasia may appear within the first two days due to brain swelling (cerebral edema). With some time and natural recovery, impairment presentation may progress into expressive aphasia (most commonly) or receptive aphasia. Due to the size and location of the lesion associated with global aphasia, the prognosis for language abilities is poor. Research has shown that the prognosis of long-term language abilities is determined by the initial severity level of aphasia within the first four weeks after a stroke. As a result, there is a poor prognosis for persons who retain a diagnosis of aphasia after one month due to limited initial language abilities. Nonetheless, in the first year post-stroke, patients with global aphasia showed improvement in their Western Aphasia Battery (WAB) scores from baseline. When compared to individuals with Broca’s, Wernicke’s, anomic, and conduction types of aphasia, those with Broca’s aphasia showed the best rate and extent of improvement followed by global aphasia. The rate of improvement in language function was highest in the first four weeks after stroke.

Although the prognosis for persons diagnosed with global aphasia is poor, improvement in varying aspects of language is possible. For example, in 1992, Ferro performed research in which he studied the recovery of individuals with acute global aphasia, resulting from the five different lesion sites. The first lesion site was in the fronto-tempo-parietal region of the brain; patients with lesions in this location saw the least amount of gains out of all of the participants in the study, and they often never recovered from global aphasia. However, the second lesion site was the anterior, suprasylvian, frontal part of the brain; the third lesion site was the subcortical infarcts; and the fourth lesion site was the posterior, suprasylvian, parietal infarcts. Participants with lesions two, three, and four often recovered to a less severe form of aphasia, such as Broca's or transcortical. The fifth lesion site was a double lesion in both the frontal and temporal infarcts; patients with lesions at this site showed slight improvement. However, studies show that spontaneous improvement, if it happens, occurs within six months, but complete recovery is rare.

Studies have shown that persons with global aphasia have improved their verbal and nonverbal speech and language skills through speech and language therapy. One study examined the recovery of a group of individuals who were classified as having global aphasia at 3 months poststroke. The individuals received intensive speech and language intervention. The results of the study illustrated that all of the patients showed improvement. The greatest area of improvement was in auditory comprehension, and the least in the use of propositional speech. After 6 months poststroke, the individuals showed an increased use of gestures to communicate, as their communication skills remained severely impaired.

During therapy, most progress is seen within the first 3 years, but it is possible for language abilities to continuously improve at a steady rate due to long-term intensive language intervention. While improvement in language abilities is possible with intervention, only 20 percent of persons diagnosed with global aphasia achieve functional use of language. Communication of basic needs and the comprehension of simple conversations on highly familiar topics, are examples of common functional language use for this population.

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.

During the acute stage, treatment is aimed at reducing the inflammation. As in other inflammatory diseases, steroids may be used first of all, either as a short course of high-dose treatment, or in a lower dose for long-term treatment. Intravenous immunoglobulin is also effective both in the short term and in the long term, particularly in adults where it has been proposed as first-line treatment. Other similar treatments include plasmapheresis and tacrolimus, though there is less evidence for these. None of these treatments can prevent permanent disability from developing.

During the residual stage of the illness when there is no longer active inflammation, treatment is aimed at improving the remaining symptoms. Standard anti-epileptic drugs are usually ineffective in controlling seizures, and it may be necessary to surgically remove or disconnect the affected cerebral hemisphere, in an operation called hemispherectomy. This usually results in further weakness, hemianopsia and cognitive problems, but the other side of the brain may be able to take over some of the function, particularly in young children. The operation may not be advisable if the left hemisphere is affected, since this hemisphere contains most of the parts of the brain that control language. However, hemispherectomy is often very effective in reducing seizures.

The treatment for Bonnet–Dechaume–Blanc syndrome is controversial due to a lack of consensus on the different therapeutic procedures for treating arteriovenous malformations. The first successful treatment was performed by Morgan et al. They combined intracranial resection, ligation of ophthalmic artery, and selective arterial ligature of the external carotid artery, but the patient did not have retinal vascular malformations.

If lesions are present, they are watched closely for changes in size. Prognosis is best when lesions are less than 3 cm in length. Most complications occur when the lesions are greater than 6 cm in size. Surgical intervention for intracranial lesions has been done successfully. Nonsurgical treatments include embolization, radiation therapy, and continued observation. Arterial vascular malformations may be treated with the cyberknife treatment. Possible treatment for cerebral arterial vascular malformations include stereotactic radiosurgery, endovascular embolization, and microsurgical resection.

When pursuing treatment, it is important to consider the size of the malformations, their locations, and the neurological involvement. Because it is a congenital disorder, there are not preventative steps to take aside from regular follow ups with a doctor to keep an eye on the symptoms so that future complications are avoided.