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.

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.

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.

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.

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.

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.

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).

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.

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.

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.

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.

Anosognosia (, ; from Ancient Greek ἀ- "a-", "without", νόσος "nosos", "disease" and γνῶσις "gnōsis", "knowledge") is a deficit of self-awareness, a condition in which a person with some disability seems unaware of its existence. It was first named by the neurologist Joseph Babinski in 1914. Anosognosia results from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neurological disorder. While this distinguishes the condition from denial, which is a psychological defense mechanism, attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of their limbs.

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.

Visual fields associated with chiasmal syndrome usually leads to an MRI. Contrast can delineate arterial aneurysms and will enhance most intrinsic chiasmal lesions. If a mass is confirmed on MRI, an endocrine panel can help determine if a pituitary adenoma is involved.

In patients with functional adenomas diagnosed by other means, visual field tests are a good screen to test for chiasmal involvement. Visual fields tests will delinate chiasmal syndromes because the missing fields will not cross the midline. Junctional scotomas classically show ipsilateral optic disc neuropathy with contralateral superotemporal defects. Bitemporal hemianopia with or without central scotoma is present if the lesions have affected the body of the chiasm. A posterior chiasm lesion should only produce defects on the temporal sides of the central visual field.

A Posterior Circulation Infarct (POCI) is a type of cerebral infarction affecting the posterior circulation supplying one side of the brain.

Posterior Circulation Stroke Syndrome (POCS) refers to the symptoms of a patient who clinically appears to have had a posterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It can cause the following symptoms:

- Cranial nerve palsy AND contralateral motor/sensory defect

- motor or sensory defect

- Eye movement problems (e.g.nystagmus)

- Cerebellar dysfunction

- Isolated homonymous hemianopia

It has also been associated with deafness.

Many studies have shown that disconnection syndromes such as aphasia, agnosia, apraxia, pure alexia and many others are not caused by direct damage to functional neocortical regions. They can also be present on only one side of the body which is why these are categorized as hemispheric disconnections. The cause for hemispheric disconnection is if the interhemispheric fibers, as mentioned earlier, are cut or reduced.

An example is commissural disconnect in adults which usually results from surgical intervention, tumor, or interruption of the blood supply to the corpus callosum or the immediately adjacent structures. Callosal disconnection syndrome is characterized by left ideomotor apraxia and left-hand agraphia and/or tactile anomia, and is relatively rare.

Other examples include commissurotomy, the surgical cutting of cerebral commissures to treat epilepsy and callosal agenesis which is when individuals are born without a corpus callosum. Those with callosal agenesis can still perform interhemispheric comparisons of visual and tactile information but with deficits in processing complex information when performing the respective tasks.

Intracerebral hemorrhages is a severe condition requiring prompt medical attention. Treatment goals include lifesaving interventions, supportive measures, and control of symptoms. Treatment depends on the location, extent, and cause of the bleeding. Often, treatment can reverse the damage that has been done.

A craniotomy is sometimes done to remove blood, abnormal blood vessels, or a tumor. Medications may be used to reduce swelling, prevent seizures, lower blood pressure, and control pain.

A Total Anterior Circulation Infarct (TACI) is a type of cerebral infarction affecting the entire anterior circulation supplying one side of the brain.

Total Anterior Circulation Stroke Syndrome (TACS) refers to the symptoms of a patient who clinically appears to have suffered from a total anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed when it causes all 3 of the following symptoms:

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Decreased level of consciousness

- Homonymous hemianopia

- Motor and Sensory Defects (≥2/3 of face, arm, leg)

For more information, see stroke.

Partial Anterior Circulation Infarct (PACI) is a type of cerebral infarction affecting part of the anterior circulation supplying one side of the brain.

Partial Anterior Circulation Stroke Syndrome (PACS) refers to the symptoms of a patient who clinically appears to have suffered from a partial anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed by any one of the following

- 2 out of 3 features of

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Homonymous hemianopia

- Motor and Sensory Defects (>2/3 of face, arm, leg)

- Higher dysfunction alone

- Partial Motor or Sensory Defect

If all of the above symptoms are present, a Total Anterior Circulation Infarct is more likely.

For more information, see stroke.

It is named for the neurosurgeon Theodore Rasmussen (1910–2002), who succeeded Wilder Penfield as head of the Montreal Neurological Institute, and served as Neurosurgeon-in-Chief at the Royal Victoria Hospital.

Bonnet–Dechaume–Blanc syndrome, also known as Wyburn-Mason syndrome, is a rare congential arteriovenous malformation of the brain, retina or facial nevi. The syndrome has a number of possible symptoms and can affect the skin, bones, kidneys, muscles, and gastrointestinal tract. When the syndrome affects the brain, people can experience severe headaches, seizures, acute stroke, meningism and progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting.

As for the retina, the syndrome causes retinocephalic vascular malformations that tend to be present with intracranial hemorrhage and lead to decreased visual acuity, proptosis, pupillary defects, optic atrophy, congestion of bulbar conjunctiva, and visual field defects. Retinal lesions can be unilateral and tortuous, and symptoms begin to appear in the second and third decades of life.

The syndrome can present cutaneous lesions, or skin with different texture, thickness, and color, usually on the face. The facial features caused by the syndrome vary from slight discoloration to extensive nevi and angiomas of the skin. In some cases, the frontal and maxillary sinus can present problems in the subject due to the syndrome.

There have only been 52 reported cases of patients with Bonnet–Dechaume–Blanc syndrome as of 2012. Symptoms are rarely noticed in children and the syndrome is often diagnosed in late childhood or early adulthood when visual impairment is noticed. Fluorescein angiography is commonly used to diagnose the syndrome.

There have been several methods in treating patients who display Bonnet–Dechaume–Blanc syndrome. However, which method seems to work the most is within argument. Patients with intracranial lesions have been treated with surgical intervention and in some cases, this procedure has been successful. Other treatments include embolization, radiation therapy, and continued observation.

With limited research on Bonnet–Dechaume–Blanc syndrome, researchers have focused on the clinical and radiological findings rather than how to manage this rare and non-heritable syndrome.