A homonymous hemianopsia is the loss of half of the visual field on the same side in both eyes. The visual images that we see to the right side travel from both eyes to the left side of the brain, while the visual images we see to the left side in each eye travel to the right side of the brain. Therefore, damage to the right side of the posterior portion of the brain or right optic tract can cause a loss of the left field of view in both eyes. Likewise, damage to the left posterior brain or left optic radiation can cause a loss of the right field of vision.

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

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.

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.

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.

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.

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".

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 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.

Symptom-producing, or pathological, scotomata may be due to a wide range of disease processes, affecting any part of the visual system, including the retina (in particular its most sensitive portion, the macula), the optic nerve and even the visual cortex. A pathological scotoma may involve any part of the visual field and may be of any shape or size. A scotoma may include and enlarge the normal blind spot. Even a small scotoma that happens to affect central or macular vision will produce a severe visual disability, whereas a large scotoma in the more peripheral part of a visual field may go unnoticed by the bearer because of the normal reduced optical resolution in the peripheral visual field.

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.

Relatively little has been discovered about the cause of the condition since its initial identification. Recent studies from the empirical data are prone to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis, (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia, or the paralysis of one side of the body, may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the maneuver of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Those diagnosed with Alzheimer's disease often display this lack of awareness and insist that nothing is wrong with them.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows "anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him". This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.

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.

Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognize that they have a mental illness. There is evidence that 'anosognosia' related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

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.

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.

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.

Typically not diagnosed until late childhood or later, Bonnet–Dechaume–Blanc syndrome usually presents itself with a combination of central nervous system features (midbrain), ophthalmic features (retina), and facial features. The degree of expression of the syndrome's components varies both clinically and structurally. Common symptoms that lead to diagnosis are headaches, retro-orbital pain and hemianopia.

The ophthalmic features of the Bonnet–Dechaume–Blanc syndrome occur as retinal arteriovenous malformation (AVMs). There are three categories of AVMs that are categorized depending on the severity of the malformation. The first category consists of the patient having small lesions that usually are asymptomatic. The second category, more severe than the first, is when the patient’s malformation is missing a connecting capillary. The missing capillary is meant to serve as a link between an artery and a vein; without it, edemas, hemorrhages, and visual impairments can result. Category three, the most severe, occurs when the patient’s malformations are so severe that the dilated vessels cause no distinction between artery and vein. When the symptoms are this severe, the patient has a significantly increased risk of developing vision loss. Since the retinal lesions categorized vary from large vascular malformations that affect a majority of the retina to malformations that are barely visible, the lesions cause a wide range of symptoms including decrease in visual sharpness, proptosis, pupillary defects, optic degeneration and visual field defects. The most common type of visual field impairment due to AVMs is homonymous hemianopia. Homonymous hemianopia typically presents unilaterally, but bilateral cases have been reported as well.

The extent of the central nervous system (CNS) features/symptoms of Bonnet–Dechaume–Blanc syndrome is highly dependent of the location of the cerebral AVMs and the extent of the malformation. The most common symptom affecting the CNS is an intracranial hemangioma in the midbrain. Along with hemangiomas, the malformations result in severe headaches, cerebral hemorrhages, vomiting, meningism, seizures, acute strokes or progressive neurological deficits due to acute or chronic ischaemia caused by arteriovenous shunting.

The distinguishable facial features that result from Bonnet–Dechaume–Blanc syndrome vary from case to case. A person showing signs of the syndrome may display faint skin discoloration, nevi and angiomas of the skin. Some patients with this disorder also present with high flow arteriovenous malformations of the maxillofacial or mandibular (jaw) regions. Another facial indicator of this disease is malformations affecting the frontal and/or maxillary sinuses.

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.

The condition mostly affects children, with an average age of 6 years. However, one in ten people with the condition develops it in adulthood.

There are two main stages, sometimes preceded by a 'prodromal stage' of a few months. In the "acute stage", lasting four to eight months, the inflammation is active and the symptoms become progressively worse. These include weakness of one side of the body (hemiparesis), loss of vision for one side of the visual field (hemianopia), and cognitive difficulties (affecting learning, memory or language, for example). Epileptic seizures are also a major part of the illness, although these are often partial. Focal motor seizures or epilepsia partialis continua are particularly common, and may be very difficult to control with drugs.

In the chronic or "residual stage", the inflammation is no longer active, but the sufferer is left with some or all of the symptoms because of the damage that the inflammation has caused. In the long term, most patients are left with some epilepsy, paralysis and cognitive problems, but the severity varies considerably.

Rasmussen's encephalitis, also known as chronic focal encephalitis (CFE), is a rare inflammatory neurological disease, characterized by frequent and severe seizures, loss of motor skills and speech, hemiparesis (weakness on one side of the body), encephalitis (inflammation of the brain), and dementia. The illness affects a single cerebral hemisphere and generally occurs in children under the age of 15.

Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness