Cerebral achromatopsia is a type of color-blindness caused by damage to the cerebral cortex of the brain, rather than abnormalities in the cells of the eye's retina. It is often confused with congenital achromatopsia but underlying physiological deficits of the disorders are completely distinct.

Patients with cerebral achromatopsia deny having any experience of color when asked and fail standard clinical assessments like the Farnsworth-Munsell 100-hue test (a test of color ordering with no naming requirements). Patients may often not notice their loss of color vision and merely describe the world they see as being "drab". Most describe seeing the world in "shades of gray". This observation notes a key difference between cerebral and congenital achromatopsia, as those born with achromatopsia have never had an experience of color or gray.

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.

Many applications for iPhone and iPad have been developed to help colorblind people to view the colors in a better way. Many applications launch a sort of simulation of colorblind vision to make normal-view people understand how the color-blinds see the world. Others allow a correction of the image grabbed from the camera with a special "daltonizer" algorithm.

The GNOME desktop environment provides colorblind accessibility using the gnome-mag and the libcolorblind software. Using a gnome applet, the user may switch a color filter on and off, choosing from a set of possible color transformations that will displace the colors in order to disambiguate them. The software enables, for instance, a colorblind person to see the numbers in the Ishihara test.

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.

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.

Achromatopsia (ACHM), also known as total color blindness, is a medical syndrome that exhibits symptoms relating to at least five conditions. The term may refer to acquired conditions such as cerebral achromatopsia, also known as color agnosia, but it typically refers to an autosomal recessive congenital color vision condition, the inability to perceive color and to achieve satisfactory visual acuity at high light levels (typically exterior daylight). The syndrome is also present in an incomplete form which is more properly defined as dyschromatopsia. It is estimated to affect 1 in 40,000 live births worldwide.

There is some discussion as to whether achromats can see color or not. As illustrated in "The Island of the Colorblind" by Oliver Sacks, some achromats cannot see color, only black, white, and shades of grey. With five different genes currently known to cause similar symptoms, it may be that some do see marginal levels of color differentiation due to different gene characteristics. With such small sample sizes and low response rates, it is difficult to accurately diagnose the 'typical achromatic conditions'. If the light level during testing is optimized for them, they may achieve corrected visual acuity of 20/100 to 20/150 at lower light levels, regardless of the absence of color. One common trait is hemeralopia or blindness in full sun. In patients with achromatopsia, the cone system and fibres carrying color information remain intact. This indicates that the mechanism used to construct colors is defective.

As autotopagnosia arises from neurological and irreversible damage, options regarding symptom reversal or control are limited. As of April 2010, there are no known specific treatments for autotopagnosia.

No medications or pharmaceutical remedies have been approved by the U.S. Food and Drug Administration to treat or cure autotopagnosia. There have been cases in which extensive rehabilitation has been beneficial following restitution, repetitive training to correct the impaired function, and compensation of other skills to make up for the deficit. Rehabilitation is not a definitive treatment and only shows signs of slight improvement in a small percentage of autotopagnosia patients. The condition of the disease can be monitored with continued neurological examination and using a CT scan to note the progression of the parietal lesion.

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.

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.

Treatment for topographical disorientation has been achieved through a case by case basis. Prognosis is largely dependent on the organic cause. Neuropsychological assessment followed by an assessment of unaffected cognitive abilities can be employed in therapy. Treatment for recovering navigational skills require strengthening unaffected navigational strategies to bypass defective ones.

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.

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.

"Developmental prosopagnosia" (DP), also called "Congenital prosopagnosia" (CP), is a face-recognition deficit that is lifelong, manifesting in early childhood, and that cannot be attributed to acquired brain damage. A number of studies have found functional deficits in DP both on the basis of EEG measures and fMRI. It has been suggested that a genetic factor is responsible for the condition. The term "hereditary prosopagnosia" was introduced if DP affected more than one family member, essentially accenting the possible genetic contribution of this condition. To examine this possible genetic factor, 689 randomly selected students were administered a survey in which seventeen developmental prosopagnosics were quantifiably identified. Family members of fourteen of the DP individuals were interviewed to determine prosopagnosia-like characteristics, and in all fourteen families, at least one other affected family member was found.

In 2005, a study led by Ingo Kennerknecht showed support for the proposed congenital disorder form of prosopagnosia. This study provides epidemiological evidence that congenital prosopagnosia is a frequently occurring cognitive disorder that often runs in families. The analysis of pedigree trees formed within the study also indicates that the segregation pattern of hereditary prosopagnosia (HPA) is fully compatible with autosomal dominant inheritance. This mode of inheritance explains why HPA is so common among certain families (Kennerknecht et al. 2006).

There are many developmental disorders associated with an increased likelihood that the person will have difficulties in face perception, of which the person may or may not be aware. The mechanism by which these perceptual deficits take place is largely unknown. A partial list of some disorders that often have prosopagnosiac components would include nonverbal learning disorder, Alzheimer's disease, and autism in general. However, these types of disorders are very complicated, so arbitrary assumptions should be avoided.

In 2012, it was shown that developmental prosopagnosia cases show poor integration of low and high spatial frequency information.

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.

Topographical disorientation, also known as topographical agnosia and topographagnosia, is the inability to orient oneself in one's surroundings as a result of focal brain damage. This disability may result from the inability to make use of selective spatial information (e.g., environmental landmarks) or to orient by means of specific cognitive strategies such as the ability to form a mental representation of the environment, also known as a cognitive map. It may be part of a syndrome known as visuospatial dysgnosia.

Dichromacy ("di" meaning "two" and "chroma" meaning "color") is the state of having two types of functioning color receptors, called cone cells, in the eyes. Organisms with dichromacy are called dichromats. Dichromats can match any color they see with a mixture of no more than two pure spectral lights. By comparison, trichromats require three pure spectral lights to match all colors that they can perceive, and tetrachromats require four.

Dichromacy in humans is a color vision defect in which one of the three basic color mechanisms is absent or not functioning. It is hereditary and sex-linked, predominantly affecting males. Dichromacy occurs when one of the cone pigments is missing and color is reduced to two dimensions.

One treatment thought to be effective is the repeated exposure to a particular face or object, where impaired perception may be reorganized in memory, leading to improvement on tests of imagery relative to tests of perception. The key factor for this type of treatment to be successful is a regular and consistent exposure, which will lead to improvements in the long run. Results may not be seen right away, but are eventually possible.

Visuospatial dysgnosia is a loss of the sense of "whereness" in the relation of oneself to one's environment and in the relation of objects to each other. Visuospatial dysgnosia is often linked with topographical disorientation.

As in many other agnosias, those with the disorder have difficulty recognizing their errors and often do not correct themselves.

There is no known treatment for finger agnosia. Typically, finger agnosia does not present difficulties in daily life. In most cases, visual guidance can help with any difficulty in distinguishing or moving the appropriate finger.

In adults, many of the symptoms diminish over time. Although it has been suggested that a similar diminishing of symptoms occurs in children as well, it appears more likely that most do not overcome their deficits, but instead simply learn to adjust.

As autotopagnosia is not a life-threatening condition it is not on the forefront of medical research. Rather, more research is conducted regarding treatments and therapies to alleviate the lesions and traumas that can cause autotopagnosia. Of all the agnosias, visual agnosia is the most common subject of investigation because it is easiest to assess and has the most promise for potential treatments. Most autotopagnosia studies are centered on a few test subjects as part of a group of unaffected or “controlled” participants, or a simple case study. Case studies surrounding a single patient are most common due to the vague nature of the disease.

There are various kinds of color blindness:

- Protanopia is a severe form of red-green color blindness, in which there is impairment in perception of very long wavelengths, such as reds. To these individuals, reds are perceived as beige or grey and greens tend to look beige or grey like reds. It is also the most common type of dichromacy today. This problem occurs because patients do not have the red cone cells in the retina. Protanomaly is a less severe version.

- Deuteranopia consists of an impairment in perceiving medium wavelengths, such as greens. Deuteranomaly is a less severe form of deuteranopia. Those with deuteranomaly cannot see reds and greens like those without this condition; however, they can still distinguish them in most cases. It is very similar to protanopia. In this form, patients do not have green cone cells in the retina, which makes it hard to see the green color.

- A rarer form of color blindness is tritanopia, where there exists an inability to perceive short wavelengths, such as blues. Sufferers have trouble distinguishing between yellow and blue. They tend to confuse greens and blues, and yellow can appear pink. This is the rarest of all dichromacy, and occurs in around 1 in 100,000 people. Patients do not have the blue cone cells in the retina.

Treating auditory verbal agnosia with intravenous immunoglobulin (IVIG) is controversial because of its inconsistency as a treatment method. Although IVIG is normally used to treat immune diseases, some individuals with auditory verbal agnosia have responded positively to the use of IVIG. Additionally, patients are more likely to relapse when treated with IVIG than other pharmacological treatments. IVIG is, thus, a controversial treatment as its efficacy in treating auditory verbal agnosia is dependent upon each individual and varies from case to case.

Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within

knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which

determines the specificity of the disease being Integrative.

This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to

integrate parts such as spatial distances or producing visual images from short or long-term memory.