There are few neuropsychological assessments that can definitively diagnose prosopagnosia. One commonly used test is the famous faces tests, where individuals are asked to recognize the faces of famous persons. However, this test is difficult to standardize. The Benton Facial Recognition Test (BFRT) is another test used by neuropsychologists to assess face recognition skills. Individuals are presented with a target face above six test faces and are asked to identify which test face matches the target face. The images are cropped to eliminate hair and clothes, as many people with prosopagnosia use hair and clothing cues to recognize faces. Both male and female faces are used during the test. For the first six items only one test face matches the target face; during the next seven items, three of the test faces match the target faces and the poses are different. The reliability of the BFRT was questioned when a study conducted by Duchaine and Nakayama showed that the average score for 11 self-reported prosopagnosics was within the normal range.

The test may be useful for identifying patients with apperceptive prosopagnosia, since this is mainly a matching test and they are unable to recognize both familiar and unfamiliar faces. They would be unable to pass the test. It would not be useful in diagnosing patients with associative prosopagnosia since they are able to match faces.

The Cambridge Face Memory Test (CFMT) was developed by Duchaine and Nakayama to better diagnose people with prosopagnosia. This test initially presents individuals with three images each of six different target faces. They are then presented with many three-image series, which contain one image of a target face and two distracters. Duchaine and Nakayama showed that the CFMT is more accurate and efficient than previous tests in diagnosing patients with prosopagnosia. Their study compared the two tests and 75% of patients were diagnosed by the CFMT, while only 25% of patients were diagnosed by the BFRT. However, similar to the BFRT, patients are being asked to essentially match unfamiliar faces, as they are seen only briefly at the start of the test. The test is not currently widely used and will need further testing before it can be considered reliable.

The 20-item Prosopagnosia Index (PI20) is a freely available and validated self-report questionnaire that is able to identify individuals with prosopagnosia. It has been validated against the famous faces test and Cambridge Face Memory Test, with evidence that PI20 scores are correlated with performance on these objective measures of face recognition. It can be downloaded from the Royal Society's Open Science website and on . Alternatively, the questionnaire can be completed online on the official website.

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.

Alternate cues may be particularly useful to an individual with environmental agnosia or prosopagnosia. Alternate cues for an individual with environmental agnosia may include color cues or tactile markers to symbolize a new room or to remember an area by. Prosopagnosics may use alternate cues such as a scar on an individual's face or crooked teeth in order to recognize the individual. Hair color and length can be helpful cues as well.

Using verbal descriptions may be helpful for individuals with certain types of agnosia. Individuals such as prosopagnosics may find it useful to listen to a description of their friend or family member and recognize them based on this description more easily than through visual cues.

Specialists, like ophthalmologists or audiologists, can test for perceptual abilities. Detailed testing is conducted, using specially formulated assessment materials, and referrals to neurological specialists is recommended to support a diagnosis via brain imaging or recording techniques. The separate stages of information processing in the object recognition model are often used to localize the processing level of the deficit.

Testing usually consists of object identification and perception tasks including:

- object-naming tasks

- object categorization or figure matching

- drawing or copying real objects or images or illustrations

- unusual views tests

- overlapping line drawings

- partially degraded or fragmented image identification

- face or feature analysis

- fine line judgment

- figure contour tracking

- visual object description

- object-function miming

- tactile ability tests (naming by touch)

- auditory presentation identification

Sensory modality testing allows practitioners to assess for generalized versus specific deficits, distinguishing visual agnosias from optic aphasia, which is a more generalized deficit in semantic knowledge for objects that spans multiple sensory modalities, indicating an impairment in the semantic representations themselves.

Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or low intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.

Recognition of visual objects occurs at two primary levels. At an apperceptive level, the features of the visual information from the retina are put together to form a perceptual representation of an object. At an associative level, the meaning of an object is attached to the perceptual representation and the object is identified. If a person is unable to recognize objects because they cannot perceive correct forms of the objects, although their knowledge of the objects is intact (i.e. they do not have anomia), they have apperceptive agnosia. If a person correctly perceives the forms and has knowledge of the objects, but cannot identify the objects, they have associative agnosia.

Broadly, visual agnosia is divided into apperceptive and associative visual agnosia.

Apperceptive agnosia is failure of object recognition even when the basic visual functions (acuity, color, motion) and other mental processing, such as language and intelligence, are normal. The brain must correctly integrate features such as edges, light intensity, and color from sensory information to form a complete percept of an object. If a failure occurs during this process, a percept of an object is not fully formed and thus it cannot be recognized. Tasks requiring copying, matching, or drawing simple figures can distinguish the individuals with apperceptive agnosia because they cannot perform such tasks.

Associative agnosia is an inability to identify objects even with apparent perception and knowledge of them. It involves a higher level of processing than apperceptive agnosia. Individuals with associative agnosia can copy or match simple figures, indicating that they can perceive objects correctly. They also display the knowledge of objects when tested with tactile or verbal information. However, when tested visually, they cannot name or describe common objects. This means that there is an impairment in associating the perception of objects with the stored knowledge of them.

Although visual agnosia can be general, there exist many variants that impair recognition of specific types. These variants of visual agnosia include prosopagnosia (inability to recognize faces), pure word blindness (inability to recognize words, often called "agnosic alexia" or "pure alexia"), agnosias for colors (inability to differentiate colors), agnosias for the environment (inability to recognize landmarks or difficult with spatial layout of an environment, i.e. topographagnosia) and simultanagosia (inability to sort out multiple objects in a visual scene).

A patient with cortical blindness has no vision but the response of his/her pupil to light is intact (as the reflex does not involve the cortex). Therefore, one diagnostic test for cortical blindness is to first objectively verify the optic nerves and the non-cortical functions of the eyes are functioning normally. This involves confirming that patient can distinguish light/dark, and that his/her pupils dilate and contract with light exposure. Then, the patient is asked to describe something he/she would be able to recognize with normal vision. For example, the patient would be asked the following:

- "How many fingers am I holding up?"

- "What does that sign (on a custodian's closet, a restroom door, an exit sign) say?"

- "What kind of vending machine (with a vivid picture of a well-known brand name on it) is that?"

Patients with cortical blindness will not be able to identify the item being questioned about at all or will not be able to provide any details other than color or perhaps general shape. This indicates that the lack of vision is neurological rather than ocular. It specifically indicates that the occipital cortex is unable to correctly process and interpret the intact input coming from the retinas.

Fundoscopy should be normal in cases of cortical blindness. Cortical blindness can be associated with visual hallucinations, denial of visual loss (Anton–Babinski syndrome), and the ability to perceive moving but not static objects. (Riddoch syndrome).

The prognosis of a patient with acquired cortical blindness depends largely on the original cause of the blindness. For instance, patients with bilateral occipital lesions have a much lower chance of recovering vision than patients who suffered a transient ischemic attack or women who experienced complications associated with eclampsia. In patients with acquired cortical blindness, a permanent complete loss of vision is rare. The development of cortical blindness into the milder cortical visual impairment is a more likely outcome. Furthermore, some patients regain vision completely, as is the case with transient cortical blindness associated with eclampsia and the side effects of certain anti-epilepsy drugs.

Recent research by Krystel R. Huxlin and others on the relearning of complex visual motion following V1 damage has offered potentially promising treatments for individuals with acquired cortical blindness. These treatments focus on retraining and retuning certain intact pathways of the visual cortex which are more or less preserved in individuals who sustained damage to V1. Huxlin and others found that specific training focused on utilizing the "blind field" of individuals who had sustained V1 damage improved the patients' ability to perceive simple and complex visual motion. This sort of 'relearning' therapy may provide a good workaround for patients with acquired cortical blindness in order to better make sense of the visual environment.

Homonymous hemianopsia secondary to posterior cerebral artery occlusion – may result in syndromes of memory impairment, opposite visual field loss (homonymous hemianopsia), and sometimes hemisensory deficits.

The PCA supplies the occipital lobe and the medial portion of the temporal lobe.

Infarction of occipital cortex typically causes macular sparing hemianopias due to dual blood supply.

Occlusion of the calcarine artery that results in infarction of the superior part of the occipital lobe causes a lower peripheral visual field defect.

Posterior cerebral artery penetrating branch occlusion may result in infarction of the posterior capsule, causing hemisensory loss, and (if low enough) a transient hemianopia may also occur.

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 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.

Deafblind people communicate in many different ways as determined by the nature of their condition, the age of onset, and what resources are available to them. For example, someone who grew up deaf and experienced vision loss later in life is likely to use a sign language (in a visually modified or tactile form). Others who grew up blind and later became deaf are more likely to use a tactile mode of their spoken/written language. Methods of communication include:

- Use of residual hearing (speaking clearly, hearing aids) or sight (signing within a restricted visual field, writing with large print).

- Tactile signing, sign language, or a manual alphabet such as the American Manual Alphabet or Deaf-blind Alphabet (also known as "two-hand manual") with tactile or visual modifications.

- Interpreting services (such as sign language interpreters or communication aides).

- Communication devices such as Tellatouch or its computerized versions known as the TeleBraille and Screen Braille Communicator.

Multisensory methods have been used to help deafblind people enhance their communication skills. These can be taught to very young children with developmental delays (to help with pre-intentional communication), young people with learning difficulties, and older people, including those with dementia. One such process is Tacpac.

Deafblind amateur radio operators generally communicate on 2-way radios using Morse code.

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

Braille equipment includes a variety of multipurpose devices, which enhance access to distance communication. Some can be used as stand-alone devices connected via Wi-Fi, while others are paired with a mobile device to provide tactile access to e-mail, text messaging, and other modern communication resources. To receive Braille equipment, an eligible consumer must be proficient in Braille and must have access to the Internet or cellular service.

The Telebraille does not have a computer communications modem but does have a TTY (TDD) modem. It was designed as a TTY for deaf-blind people and is also useful for face-to-face conversation. It has two components. The sighted component is a modified SuperCom TTY device. It has a qwerty keyboard and a single-line LED display. The display is regular size and is not particularly suited to people with low vision. The SuperCom TTY can be connected directly to the telephone line using a conventional telephone jack or the telephone receiver can be coupled to the SuperCom on a cradle on top of the device. Text flows past the display in a continuous stream, like tickertape. The SuperCom is connected to the Braille portion of the device by a cable that is about two feet long. The Braille display is about 15 characters in width, although there is a knockout to allow additional characters to be installed, at considerable additional cost. The Telebraille is able to communicate in ASCII mode but is not compatible with conventional computer modems. There is what looks like a RS-232 socket on the back of the Braille component, but the instructions for the Telebraille state that this jack is for "future use" and that no computer devices should be attached to it.

A graphic Braille display can be used in sensing graphic data such as maps, images, and text data that require multiline display capabilities such spreadsheets and equations. Graphic Braille displays available in the market are DV-2 (from KGS ), Hyperbraille, and TACTISPLAY Table/Walk (from Tactisplay Corp.). For example, TACTISPLAY Table can show 120*100 resolution refreshable Braille graphics on one page. This video shows operation of the device.

Anton–Babinski syndrome, also known as visual anosognosia, is a rare symptom of brain damage occurring in the occipital lobe. Those who suffer from it are "cortically blind", but affirm, often quite adamantly and in the face of clear evidence of their blindness, that they are capable of seeing. Failing to accept being blind, the sufferer dismisses evidence of their condition and employs confabulation to fill in the missing sensory input. It is named after Gabriel Anton and Joseph Babinski.

Anton–Babinski syndrome is mostly seen following a stroke, but may also be seen after head injury. Neurologist Macdonald Critchley describes it thus:

The sudden development of bilateral occipital dysfunction is likely to produce transient physical and psychical effects in which mental confusion may be prominent. It may be some days before the relatives, or the nursing staff, stumble onto the fact that the patient has actually become sightless. This is not only because the patient ordinarily does not volunteer the information that they have become blind, but he furthermore misleads his entourage by behaving and talking as though they were sighted. Attention is aroused however when the patient is found to collide with pieces of furniture, to fall over objects, and to experience difficulty in finding his way around. They may try to walk through a wall or through a closed door on his way from one room to another. Suspicion is still further alerted when they begin to describe people and objects around them which, as a matter of fact, are not there at all.

Thus we have the twin symptoms of anosognosia (or lack of awareness of defect) and confabulation, the latter affecting both speech and behaviour.

Anton–Babinski syndrome may be thought of ideally as the opposite of blindsight, blindsight occurring when part of the visual field is not consciously experienced, but some reliable perception does in fact occur.

Visual impairment has the ability to create consequences for health and well being. Visual impairment is increasing especially among older people. It is recognized that those individuals with visual impairment are likely to have limited access to information and healthcare facilities, and may not receive the best care possible because not all health care professionals are aware of specific needs related to vision.

- A prerequisite of effective health care could very well be having staff that are aware that people may have problems with vision.

- Communication and different ways of being able to communicate with visually impaired clients must be tailored to individual needs and available at all times.

It is important that people be examined by someone specializing in low vision care prior to other rehabilitation training to rule out potential medical or surgical correction for the problem and to establish a careful baseline refraction and prescription of both normal and low vision glasses and optical aids. Only a doctor is qualified to evaluate visual functioning of a compromised visual system effectively. The American Medical Association provides an approach to evaluating visual loss as it affects an individual's ability to perform activities of daily living.

Screening adults who have no symptoms is of uncertain benefit.

The Ishihara color test, which consists of a series of pictures of colored spots, is the test most often used to diagnose red–green color deficiencies. A figure (usually one or more Arabic digits) is embedded in the picture as a number of spots in a slightly different color, and can be seen with normal color vision, but not with a particular color defect. The full set of tests has a variety of figure/background color combinations, and enable diagnosis of which particular visual defect is present. The anomaloscope, described above, is also used in diagnosing anomalous trichromacy.

Because the Ishihara color test contains only numerals, it may not be useful in diagnosing young children, who have not yet learned to use numerals. In the interest of identifying these problems early on in life, alternative color vision tests were developed using only symbols (square, circle, car).

Besides the Ishihara color test, the US Navy and US Army also allow testing with the Farnsworth Lantern Test. This test allows 30% of color deficient individuals, whose deficiency is not too severe, to pass.

Another test used by clinicians to measure chromatic discrimination is the Farnsworth-Munsell 100 hue test. The patient is asked to arrange a set of colored caps or chips to form a gradual transition of color between two anchor caps.

The HRR color test (developed by Hardy, Rand, and Rittler) is a red–green color test that, unlike the Ishihara, also has plates for the detection of the tritan defects.

Most clinical tests are designed to be fast, simple, and effective at identifying broad categories of color blindness. In academic studies of color blindness, on the other hand, there is more interest in developing flexible tests to collect thorough datasets, identify copunctal points, and measure just noticeable differences.

Aphantasia is similar to invisible disabilities such as face blindness, word blindness, and tone deafness, though aphantasia itself has not been associated with any functional deficits.

There is generally no treatment to cure achromatopsia. However, dark red or plum colored filters are very helpful in controlling light sensitivity.

Since 2003, there is a cybernetic device called eyeborg that allows people to perceive color through sound waves. Achromatopsic artist Neil Harbisson was the first to use such a device in early 2004, the eyeborg allowed him to start painting in color by memorizing the sound of each color.

Moreover, there is some research on gene therapy for animals with achromatopsia, with positive results on mice and young dogs, but less effectiveness on older dogs. However, no experiments have been made on humans. There are many challenges to conducting gene therapy on humans. See Gene therapy for color blindness for more details about it.

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.