There are clinical trials being done to further research for treatments. At the National Institute of Neurological Disorders and Stroke (NINDS) they support research for rare diseases like agnosia. Some organizations that are recruiting for trials are using clincaltrials.gov and give status updates on the trials.

These strategies elicit the use of an unaffected modality. For example, visual agnosics can use tactile information in replacement of visual information. Alternatively, an individual with prosopagnosia can use auditory information in order to replace visual information. For example, an individual with prosopagnosia can wait for someone to speak, and will usually recognize the individual from their speech.

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.

The affected individual may not realize that they have a visual problem and may complain of becoming "clumsy" or "muddled" when performing familiar tasks such as setting the table or simple DIY.

Anosognosia, a lack of awareness of the deficit, is common and can cause therapeutic resistance. In some agnosias, such as prosopagnosia, awareness of the deficit is often present; however shame and embarrassment regarding the symptoms can be a barrier in admission of a deficiency. Because agnosias result from brain lesions, no direct treatment for them currently exists, and intervention is aimed at utilization of coping strategies by patients and those around them. Sensory compensation can also develop after one modality is impaired in agnostics

General principles of treatment:

- restitution

- repetitive training of impaired ability

- development of compensatory strategies utilizing retained cognitive functions

Partial remediation is more likely in cases with traumatic/vascular lesions, where more focal damage occurs, than in cases where the deficit arises out of anoxic brain damage, which typically results in more diffuse damage and multiple cognitive impairments. However, even with forms of compensation, some afflicted individuals may no longer be able to fulfill the requirements of their occupation or perform common tasks, such as, eating or navigating. Agnostics are likely to become more dependent on others and to experience significant changes to their lifestyle, which can lead to depression or adjustment disorders.

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.

Associative visual agnosia is a form of visual agnosia. It is an impairment in recognition or assigning meaning to a stimulus that is accurately perceived and not associated with a generalized deficit in intelligence, memory, language or attention. The disorder appears to be very uncommon in a "pure" or uncomplicated form and is usually accompanied by other complex neuropsychological problems due to the nature of the etiology. Afflicted individuals can accurately distinguish the object, as demonstrated by the ability to draw a picture of it or categorize accurately, yet they are unable to identify the object, its features or its functions.

Prosopagnosia, also called face blindness, is a cognitive disorder of face perception in which the ability to recognize familiar faces, including one's own face (self-recognition), is impaired, while other aspects of visual processing (e.g., object discrimination) and intellectual functioning (e.g., decision making) remain intact. The term originally referred to a condition following acute brain damage (acquired prosopagnosia), but a congenital or developmental form of the disorder also exists, which may affect up to 2.5% of the United States population. The specific brain area usually associated with prosopagnosia is the fusiform gyrus, which activates specifically in response to faces. The functionality of the fusiform gyrus allows most people to recognize faces in more detail than they do similarly complex inanimate objects. For those with prosopagnosia, the new method for recognizing faces depends on the less-sensitive object recognition system. The right hemisphere fusiform gyrus is more often involved in familiar face recognition than the left. It remains unclear whether the fusiform gyrus is only specific for the recognition of human faces or if it is also involved in highly trained visual stimuli.

There are two types of prosopagnosia: acquired and congenital (developmental). Acquired prosopagnosia results from occipito-temporal lobe damage and is most often found in adults. This is further subdivided into apperceptive and associative prosopagnosia. In congenital prosopagnosia, the individual never adequately develops the ability to recognize faces.

Though there have been several attempts at remediation, no therapies have demonstrated lasting real-world improvements across a group of prosopagnosics. Prosopagnosics often learn to use "piecemeal" or "feature-by-feature" recognition strategies. This may involve secondary clues such as clothing, gait, hair color, skin color, body shape, and voice. Because the face seems to function as an important identifying feature in memory, it can also be difficult for people with this condition to keep track of information about people, and socialize normally with others. Prosopagnosia has also been associated with other disorders that are associated with nearby brain areas: left hemianopsia (loss of vision from left side of space, associated with damage to the right occipital lobe), achromatopsia (a deficit in color perception often associated with unilateral or bilateral lesions in the temporo-occipital junction) and topographical disorientation (a loss of environmental familiarity and difficulties in using landmarks, associated with lesions in the posterior part of the parahippocampal gyrus and anterior part of the lingual gyrus of the right hemisphere). It is from the Greek: "prosopon" = "face" and "agnosia" = "not knowing".

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.

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.

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.

While most cases of visual agnosia are seen in older adults who have experienced extensive brain damage, there are also cases of young children with less brain damage during developmental years acquiring the symptoms. Commonly, visual agnosia presents as an inability to recognize an object in the absence of other explanations, such as blindness or partial blindness, anomia, memory loss, etc.. Other common manifestations of visual agnosia that are generally tested for include difficulty identifying objects that look similar in shape, difficulty with identifying line drawings of objects, and recognizing objects that are shown from less common views, such as a horse from a top-down view.

Within any given patient, a variety of symptoms can occur, and the impairment of ability is not only binary but can range in severity. For example, Patient SM is a prosopagnosic with a unilateral lesion to left extrastriate cortex due to an accident in his twenties who displays behavior similar to congenital prosopagnosia. Although he can recognize facial features and emotions – indeed he sometimes uses a standout feature to recognize a face – face recognition is almost impossible purely from visual stimuli, even for faces of friends, family, and himself. The disorder also affects his memory of faces, both in storing new memories of faces and recalling stored memories.

Nevertheless, it is important to note the reach of symptoms to other domains. SM’s object recognition is similarly impaired though not entirely; when given line drawings to identify, he was able to give names of objects with properties similar to the drawing, implying that he is able to see the features of the drawing. Similarly, copying a line drawing of a beach scene led to a simplified version of the drawing, though the main features were accounted for. For recognition of places, he is still impaired but familiar places are remembered and new places can be stored into memory.

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.

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.

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.

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

Blind people may use talking equipment such as thermometers, watches, clocks, scales, calculators, and compasses. They may also enlarge or mark dials on devices such as ovens and thermostats to make them usable. Other techniques used by blind people to assist them in daily activities include:

- Adaptations of coins and banknotes so that the value can be determined by touch. For example:

- In some currencies, such as the euro, the pound sterling and the Indian rupee, the size of a note increases with its value.

- On US coins, pennies and dimes, and nickels and quarters are similar in size. The larger denominations (dimes and quarters) have ridges along the sides (historically used to prevent the "shaving" of precious metals from the coins), which can now be used for identification.

- Some currencies' banknotes have a tactile feature to indicate denomination. For example, the Canadian currency tactile feature is a system of raised dots in one corner, based on Braille cells but not standard Braille.

- It is also possible to fold notes in different ways to assist recognition.

- Labeling and tagging clothing and other personal items

- Placing different types of food at different positions on a dinner plate

- Marking controls of household appliances

Most people, once they have been visually impaired for long enough, devise their own adaptive strategies in all areas of personal and professional management.

For the blind, there are books in braille, audio-books, and text-to-speech computer programs, machines and e-book readers. Low vision people can make use of these tools as well as large-print reading materials and e-book readers that provide large font sizes.

Computers are important tools of integration for the visually impaired person. They allow, using standard or specific programs, screen magnification and conversion of text into sound or touch (Braille line), and are useful for all levels of visual handicap. OCR scanners can, in conjunction with text-to-speech software, read the contents of books and documents aloud via computer. Vendors also build closed-circuit televisions that electronically magnify paper, and even change its contrast and color, for visually impaired users. For more information, consult Assistive technology.

In adults with low vision there is no conclusive evidence supporting one form of reading aid over another. In several studies stand-based closed-circuit television and hand-held closed-circuit television allowed faster reading than optical aids. While electronic aids may allow faster reading for individuals with low vision, portability, ease of use, and affordability must be considered for people.

Children with low vision sometimes have reading delays, but do benefit from phonics-based beginning reading instruction methods. Engaging phonics instruction is multisensory, highly motivating, and hands-on. Typically students are first taught the most frequent sounds of the alphabet letters, especially the so-called short vowel sounds, then taught to blend sounds together with three-letter consonant-vowel-consonant words such as cat, red, sit, hot, sun. Hands-on (or kinesthetically appealing) VERY enlarged print materials such as those found in "The Big Collection of Phonics Flipbooks" by Lynn Gordon (Scholastic, 2010) are helpful for teaching word families and blending skills to beginning readers with low vision. Beginning reading instructional materials should focus primarily on the lower-case letters, not the capital letters (even though they are larger) because reading text requires familiarity (mostly) with lower-case letters. Phonics-based beginning reading should also be supplemented with phonemic awareness lessons, writing opportunities, and lots of read-alouds (literature read to children daily) to stimulate motivation, vocabulary development, concept development, and comprehension skill development. Many children with low vision can be successfully included in regular education environments. Parents may need to be vigilant to ensure that the school provides the teacher and students with appropriate low vision resources, for example technology in the classroom, classroom aide time, modified educational materials, and consultation assistance with low vision experts.

Aside from medical help, various sources provide information, rehabilitation, education, and work and social integration.

Whether blindness is treatable depends upon the cause. Surgical intervention can be performed in PCG which is childhood glaucoma, usually starting early in childhood. Primary congenital glaucoma is caused by an abnormal drainage of the eye. However, surgical intervention is yet to prove effective.

There is generally no treatment to cure color deficiencies. ″The American Optometric Association reports a contact lens on one eye can increase the ability to differentiate between colors, though nothing can make you truly see the deficient color.″

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.

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).

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.

Optometrists can supply colored spectacle lenses or a single red-tint contact lens to wear on the non-dominant eye, but although this may improve discrimination of some colors, it can make other colors more difficult to distinguish. A 1981 review of various studies to evaluate the effect of the X-chrom contact lens concluded that, while the lens may allow the wearer to achieve a better score on certain color vision tests, it did not correct color vision in the natural environment. A case history using the X-Chrom lens for a rod monochromat is reported and an X-Chrom manual is online.

Lenses that filter certain wavelengths of light can allow people with a cone anomaly, but not dichromacy, to see better separation of colors, especially those with classic "red/green" color blindness. They work by notching out wavelengths that strongly stimulate both red and green cones in a deuter- or protanomalous person, improving the distinction between the two cones' signals. As of 2013, sunglasses that notch out color wavelengths are available commercially.

People with hemeralopia may benefit from sunglasses. Wherever possible, environmental illumination should be adjusted to comfortable level. Light-filtering lenses appear to help in people reporting photophobia.

Otherwise, treatment relies on identifying and treating any underlying disorder.

Why patients with Anton–Babinski syndrome deny their blindness is unknown, although there are many theories. One hypothesis is that damage to the visual cortex results in the inability to communicate with the speech-language areas of the brain. Visual imagery is received but cannot be interpreted; the speech centers of the brain confabulate a response.

This is often seen in immunosuppressed patients with JC virus. Specifically, patients being treated with natalizumab—a monoclonal antibody currently used as a staple in treatment for multiple sclerosis—are quickly becoming classical examples of Anton–Babinski syndrome.

Patients have also reported visual anosognosia after suffering from ischemic vascular cerebral disease. A 96-year-old man, who was admitted to an emergency room complaining of a severe headache and sudden loss of vision, was discovered to have suffered from a posterior cerebral artery thrombosis and consequently lost his vision. He adamantly claimed he was able to see despite an ophthalmologic exam proving otherwise. An MRI of his brain proved that his right occipital lobe was ischemic. Similarly, a 56-year-old woman was admitted to the emergency room in a confused state and with severely handicapped psychomotor skills. Ocular movements and pupil reflexes were still intact, but the patient could not name objects and was not aware of light changes in the room, and seemed unaware of her visual deficit.