For all practical purposes, there is no direct cure. Patients may improve if information is presented in other modalities than the damaged one. Different types of therapies can help to reverse the effects of agnosia. In some cases, occupational therapy or speech therapy can improve agnosia, depending on its cause.

Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.

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.

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.

Some of the causes of integrative agnosia include stroke, traumatic brain injury, Alzheimer's disease, an anoxic episode following myocardial infarction, and progressive multifocal leukoencephalopathy.

Organizational strategies may be extremely helpful for an individual with visual agnosia. For example, organizing clothes according to different hangers provides tactile cues for the individual, making it easier to identify certain forms of clothing as opposed to relying solely on visual cues.

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.

Agnosias are sensory modality specific, usually classified as visual, auditory, or tactile. Associative visual agnosia refers to a subtype of visual agnosia, which was labeled by Lissauer (1890), as an inability to connect the visual percept (mental representation of something being perceived through the senses) with its related semantic information stored in memory, such as, its name, use, and description. This is distinguished from the visual apperceptive form of visual agnosia, "apperceptive visual agnosia", which is an inability to produce a complete percept, and is associated with a failure in higher order perceptual processing where feature integration is impaired, though individual features can be distinguished. In reality, patients often fall between both distinctions, with some degree of perceptual disturbances exhibited in most cases, and in some cases, patients may be labeled as integrative agnostics when they fit the criteria for both forms. Associative visual agnosias are often category-specific, where recognition of particular categories of items are differentially impaired, which can affect selective classes of stimuli, larger generalized groups or multiple intersecting categories. For example, deficits in recognizing stimuli can be as specific as familiar human faces or as diffuse as living things or non-living things.

An agnosia that affects hearing, "auditory sound agnosia", is broken into subdivisions based on level of processing impaired, and a "semantic-associative" form is investigated within the auditory agnosias.

Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.

"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.

Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but a neurological inability of the brain to process sound meaning. It is a disruption of the "what" pathway in the brain. Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it "was" a lion creating the noise. Auditory agnosia is caused by damage to the secondary and tertiary auditory cortex of the temporal lobe of the brain.

Auditory verbal agnosia (AVA), also known as pure word deafness, is the inability to comprehend speech. Individuals with this disorder lose the ability to understand language, repeat words, and write from dictation. Some patients with AVA describe hearing spoken language as meaningless noise, often as though the person speaking was doing so in a foreign language. However, spontaneous speaking, reading, and writing are preserved. The maintenance of the ability to process non-speech auditory information, including music, also remains relatively more intact than spoken language comprehension. Individuals who exhibit pure word deafness are also still able to recognize non-verbal sounds. The ability to interpret language via lip reading, hand gestures, and context clues is preserved as well. Sometimes, this agnosia is preceded by cortical deafness; however, this is not always the case. Researchers have documented that in most patients exhibiting auditory verbal agnosia, the discrimination of consonants is more difficult than that of vowels, but as with most neurological disorders, there is variation among patients.

Auditory verbal agnosia (AVA) is not the same as Auditory agnosia; patients with (nonverbal) auditory agnosia have a relatively more intact speech comprehension system despite their impaired recognition of nonspeech sounds.

Due to the subjective nature of autotopagnosia, there are many hypotheses presented as to the underlying causation. Since the condition by definition is an inability to recognize the human body and its parts, the disorder could stem from a language deficit specific to body parts. On the other hand, the patient could suffer from a disrupted body image or a variation of the inability to separate parts from whole. It is also believed that autotopagnosia has multiple underlying causes that cannot be categorized as either language-specific or body-image-specific. The rarity of autotopagnosia, frequently combined with the manifestation of other psychoneurological disorders, makes the prime cause extremely difficult to study. In many cases, one of these accompanying conditions—often aphasia—could be masking the patient’s autotopagnosia altogether.

There are three primary distinctions of auditory agnosia that fall into two categories.

Auditory verbal agnosia has been shown to form as a result of tumor formation, especially in the posterior third ventricle, trauma, lesions, cerebral infarction, encephalitis as a result of herpes simplex, and Landaui-Kleffner syndrome. The exact location of damage which results in pure word deafness is still under debate, but the planum temporale, posterior STG, and white matter damage to the acoustic radiations (AR) have all been implicated.

Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can both present as the result of acute damage or as chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. MRIs showed cortical atrophy in the left superior temporal lobe region.

In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.

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.

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.

Prosopagnosia can be caused by lesions in various parts of the inferior occipital areas (occipital face area), fusiform gyrus (fusiform face area), and the anterior temporal cortex. Positron emission tomography (PET) and fMRI scans have shown that, in individuals without prosopagnosia, these areas are activated specifically in response to face stimuli. The inferior occipital areas are mainly involved in the early stages of face perception and the anterior temporal structures integrate specific information about the face, voice, and name of a familiar person.

Acquired prosopagnosia can develop as the result of several neurologically damaging causes. Vascular causes of prosopagnosia include posterior cerebral artery infarcts (PCAIs) and hemorrhages in the infero-medial part of the temporo-occipital area. These can be either bilateral or unilateral, but if they are unilateral, they are almost always in the right hemisphere. Recent studies have confirmed that right hemisphere damage to the specific temporo-occipital areas mentioned above is sufficient to induce prosopagnosia. MRI scans of patients with prosopagnosia showed lesions isolated to the right hemisphere, while fMRI scans showed that the left hemisphere was functioning normally. Unilateral left temporo-occipital lesions result in object agnosia, but spare face recognition processes, although a few cases have been documented where left unilateral damage resulted in prosopagnosia. It has been suggested that these face recognition impairments caused by left hemisphere damage are due to a semantic defect blocking retrieval processes that are involved in obtaining person-specific semantic information from the visual modality.

Other less common etiologies include carbon monoxide poisoning, temporal lobectomy, encephalitis, neoplasm, right temporal lobe atrophy, trauma, Parkinson's disease, and Alzheimer's disease.

Social-emotional agnosia is mainly caused by abnormal functioning in a particular brain area called the amygdala. Typically this agnosia is only found in people with bilateral amygdala damage; that is damage to amygdala regions in both hemispheres of the brain. It can be accompanied by right or bilateral temporal lobe damage. The amygdala dysfunction causes the inability to select appropriate behaviors in a specific social context. Symptoms can include reduced aggression, fearfulness, competitiveness, and social dominance. Those with social-emotional agnosia have difficulty discerning the emotional meaning and significance behind objects, which causes a loss of fondness and familiarity. Bilateral amygdala damage has also been associated with social unresponsiveness, leading to an avoidance of social interactions and a preference for isolation from their own species. Evidence suggests that damage to the amygdala and the limbic system (specifically the amygdala-hypothalamus pathway) results in the loss of the core ability to recognize and interpret the mental states of others, a vital ability in social interactions. The amygdala evokes highly personal emotional memories and the loss of this function causes hypo-emotionality, a general lack of emotion when presented with different stimuli. Hypersexuality has also been observed in those with disconnection in the amygdala-hypothalamus pathway. Temporal lobe epilepsy has been shown to cause bilateral amygdala damage which could result in symptoms similar to social-emotional agnosia, but the precise relationship between the two disorders is unknown.

Agraphia is an acquired neurological disorder causing a loss in the ability to communicate through writing, either due to some form of motor dysfunction or an inability to spell. The loss of writing ability may present with other language or neurological disorders; disorders appearing commonly with agraphia are alexia, aphasia, dysarthria, agnosia, and apraxia. The study of individuals with agraphia may provide more information about the pathways involved in writing, both language related and motoric. Agraphia cannot be directly treated, but individuals can learn techniques to help regain and rehabilitate some of their previous writing abilities. These techniques differ depending on the type of agraphia.

Agraphia can be broadly divided into central and peripheral categories. Central agraphias typically involve language areas of the brain, causing difficulty spelling or with spontaneous communication, and are often accompanied by other language disorders. Peripheral agraphias usually target motor and visuospatial skills in addition to language and tend to involve motoric areas of the brain, causing difficulty in the movements associated with writing. Central agraphia may also be called aphasic agraphia as it involves areas of the brain whose major functions are connected to language and writing; peripheral agraphia may also be called nonaphasic agraphia as it involves areas of the brain whose functions are not directly connected to language and writing (typically motor areas).

The history of agraphia dates to the mid-fourteenth century, but it was not until the second half of the nineteenth century that it sparked significant clinical interest. Research in the twentieth century focused primary on aphasiology in patients with lesions from strokes.

Autotopagnosia from the Greek "a" and "gnosis," meaning "without knowledge", "topos" meaning "place", and "auto" meaning "oneself", autotopagnosia virtually translates to the "lack of knowledge about one's own space," and is clinically described as such.

Autotopagnosia is a form of agnosia, characterized by an inability to localize and orient different parts of the body. The psychoneurological disorder has also been referred to as "body-image agnosia" or "somatotopagnosia." "Somatotopagnosia" has been argued to be a better suited term to describe the condition. While autotopagnosia emphasizes the deficiencies in localizing only one's own body parts and orientation, "somatotopagnosia" also considers the inability to orient and recognize the body parts of others or representations of the body (e.g., manikins, diagrams).

Typically, the cause of autotopagnosia is a lesion found in the parietal lobe of the left hemisphere of the brain. However, it as also been noted that patients with generalized brain damage present with similar symptoms of autotopagnosia.

As a concept, autotopagnosia has been criticized as nonspecific; some claim that this is a manifestation of a greater symptomatic complex of anomia, marked by an inability to name things in general—not just parts of the human body.

Agraphia has a multitude of causes ranging from strokes, lesions, traumatic brain injury, and dementia. Twelve regions of the brain are associated with handwriting. The four distinct functional areas are the left superior frontal area composed of the middle frontal gyrus and the superior frontal sulcus, the left superior parietal area composed of the inferior parietal lobule, the superior parietal lobule and the intraparietal sulcus and lastly the primary motor cortex and the somatosensory cortex. The eight other areas are considered associative areas and are the right anterior cerebellum, the left posterior nucleus of the thalamus, the left inferior frontal gyrus, the right posterior cerebellum, the right superior frontal cortex, the right inferior parietal lobule, the left fusiform gyrus and the left putamen. The specific type of agraphia resulting from brain damage will depend on which area of the brain was damaged.

Phonological agraphia is linked to damage in areas of the brain involved in phonological processing skills (sounding out words), specifically the language areas around the sylvian fissure, such as Broca's area, Wernicke's area, and the supramarginal gyrus.

Lexical agraphia is associated with damage to the left angular gyrus and/or posterior temporal cortex. The damage is typically posterior and inferior to the perisylvian language areas.

Deep agraphia involves damage to the same areas of the brain as lexical agraphia plus some damage to the perisylvian language areas as well. More extensive left hemisphere damage can lead to global agraphia.

Gerstmann's syndrome is caused by a lesion of the dominant (usually the left) parietal lobe, usually an angular gyrus lesion.

Apraxic agraphia with ideomotor apraxia is typically caused by damage to the superior parietal lobe (where graphomotor plans are stored) or the premotor cortex (where the plans are converted into motor commands). Additionally, some individuals with cerebellar lesions (more typically associated with non-apraxic motor dysfunction) develop apraxic agraphia. Apraxic agraphia without ideomotor apraxia may be caused by damage to either of the parietal lobes, the dominant frontal lobe, or to the dominant thalamus.

Visuospatial agraphia typically has a right hemisphere pathology. Damage to the right frontal area of the brain may cause more motor defects, whereas damage to the posterior part of the right hemisphere leads predominantly to spatial defects in writing.

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.

Topographical disorientation is the inability to orient in the surrounding as a result of focal brain damage.

Topographical Disorientation has been studied for decades using case studies of patients who have selectively lost their ability to find their way within large-scale, locomotor environments. Several dozen case reports of topographical disorientation have been presented over the last century. Studying these people will aid in the understanding of the complex, multi-component behavior of navigation. Topographical disorientation may result from a stroke or part of a progressive illness, hemispatial neglect, dementia, Alzheimer's disease.

Constructional apraxia is characterized by an inability or difficulty to build, assemble, or draw objects. Apraxia is a neurological disorder in which people are unable to perform tasks or movements even though they understand the task, are willing to complete it, and have the physical ability to perform the movements. Constructional apraxia may be caused by lesions in the parietal lobe following stroke or it may serve as an indicator for Alzheimer's disease.

A key deficit in constructional apraxia patients is the inability to correctly copy or draw an image. There are qualitative differences between patients with left hemisphere damage, right hemisphere damage, and Alzheimer's Disease.