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.

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.

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.

Agraphia cannot be directly treated, but individuals can be rehabilitated to regain some of their previous writing abilities.

For the management of phonological agraphia, individuals are trained to memorize key words, such as a familiar name or object, that can then help them form the grapheme for that phoneme. Management of allographic agraphia can be as simple as having alphabet cards so the individual can write legibly by copying the correct letter shapes. There are few rehabilitation methods for apraxic agraphia; if the individual has considerably better hand control and movement with typing than they do with handwriting, then they can use technological devices. Texting and typing do not require the same technical movements that handwriting does; for these technological methods, only spatial location of the fingers to type is required. If copying skills are preserved in an individual with apraxic agraphia, repeated copying may help shift from the highly intentional and monitored hand movements indicative of apraxic agraphia to a more automated control.

Micrographia is a condition that can occur with the development of other disorders, such as Parkinson's disease, and is when handwriting becomes illegible because of small writing. For some individuals, a simple command to write bigger eliminates the issue.

- Anagram and Copy Treatment (ACT) uses the arrangement of component letters of target words and then repeated copying of the target word. This is similar to the CART; the main difference is that the target words for ACT are specific to the individual. Target words that are important in the life of the individual are emphasized because people with deep or global agraphias do not typically have the same memory for the words as other people with agraphia may. Writing can be even more important to these people as it can cue spoken language. ACT helps in this by facilitating the relearning of a set of personally relevant written words for use in communication.

- Copy and Recall Treatment (CART) method helps to reestablish the ability to spell specific words that are learned through repeated copying and recall of target words. CART is more likely to be successful in treating lexical agraphia when a few words are trained to mastery than when a large group of unrelated words is trained. Words chosen can be individualized to the patient, which makes treatment more personalized.

- Graphemic buffer uses the training of specific words to improve spelling. Cueing hierarchies and copy and recall method of specific words are used, to work the words into the short-term memory loop, or graphemic buffer. The segmentation of longer words into shorter syllables helps bring words into short-term memory.

- Problem solving approach is used as a self-correcting method for phonological errors. The individual sounds out the word and attempts to spell it, typically using an electronic dictionary-type device that indicates correct spelling. This method takes advantage of the preserved sound-to-letter correspondences when they are intact. This approach may improve access to spelling memory, strengthen orthographic representations, or both.

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.

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.

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.

In incidents where tumors and their pressure effects are the cause of pure word deafness, removal of the tumor has been shown to allow for the return of most auditory verbal comprehension.

There is currently no known curative treatment for SD. The average duration of illness is 8–10 years, and its progression cannot be slowed. Progression of SD can lead to behavioral and social difficulties, thus supportive care is essential for improving quality of life in SD patients as they grow more incomprehensible.

Continuous practice in lexical learning has been shown to improve semantic memory in SD patients.

SD has no known preventative measures.

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.

Treatment for aphasias is generally individualized, focusing on specific language and communication improvements, and regular exercise with communication tasks. Regular therapy for conduction aphasics has been shown to result in steady improvement on the Western Aphasia Battery. However, conduction aphasia is a mild aphasia, and conduction aphasics score highly on the WAB at baseline.

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.

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.

Motor imagery has been explored as a potential therapy for constructional apraxia patients. Motor imagery is a process by which a specific action is mimicked in the working memory without a corresponding motor output. Since constructional apraxia is a visuospatial problem not a motor problem, rehabilitation-treatment based on motor imagery has not proven to be an effective in patients with right hemisphere stroke or hemispatial neglect.

Since the underlying cause of the disorder is damage to the brain, at present ideational apraxia is not reversible. However, Occupational or Physical Therapy may be able to slow the progression and help patients regain some functional control, with the treatment approach being the same as that of ideomotor apraxia. Some recovery may occur in younger patients after stroke, because brain plasticity may allow the functions of these damaged regions to be remapped. As patients develop new behaviors to cope with their apraxia, their brain's functioning neurons may take on some of the functions of the dead or damaged regions.

In the context of dementia, apraxia is a major cause of morbidity, and progresses with the underlying disease sometimes to the extent that patients may be unable to feed themselves or use simple utensils. Patients often become highly dependent or require nursing home placement because of their inability to properly use objects.

Brain imaging techniques such as fMRI, EEG, and PET scans may help in understanding the neuroanatomical and computational basis of ideational apraxia. Understanding these mechanisms is likely to be crucial in developing new modes of therapy to help patients cope with their disorder.

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.

For patients with visuospatial dysgnosia, the information input may be strengthened by adding tactile, motor, and verbal perceptual inputs. This comes from the general occupational therapy practice of teaching clients suffering from intellectual dysfunctions to use the most effective combinations of perceptual input modalities, which may enable them to complete a task.

Indifference to illness may have an adverse impact on a patient's engagement in neurological rehabilitation, cognitive rehabilitation and physical rehabilitation. Patients are not likely to implement rehabilitation for a condition about which they are indifferent. Although anosognosia often resolves in days to weeks after stroke, anosodiaphoria often persists. Therefore, the therapist has to be creative in their rehabilitation approach in order to maintain the interest of the patient.

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.

The onset of Wernicke's encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. Prompt administration of thiamine to patients with Wernicke's encephalopathy can prevent the disorder from developing into Wernicke–Korsakoff syndrome, or reduce its severity. Treatment can also reduce the progression of the deficits caused by WKS, but will not completely reverse existing deficits. WKS will continue to be present, at least partially, in 80% of patients. Patients suffering from WE should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. If no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. Such prompt administration of thiamine may be a life-saving measure. Banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment.

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.

There is no cure for Gerstmann syndrome. Treatment is symptomatic and supportive. Occupational and speech therapies may help diminish the dysgraphia and apraxia. In addition, calculators and word processors may help school children cope with the symptoms of the disorder.

Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids (such as prednisone), and speech therapy, which should be started early. Some patients improve with the use of corticosteroids or adrenocorticotropin hormone (ACTH) which lead researches to believe that inflammation and vasospasm may play a role in some cases of acquired epileptic aphasia.

A controversial treatment option involves a surgical technique called multiple subpial transection in which multiple incisions are made through the cortex of the affected part of the brain beneath the pia mater, severing the axonal tracts in the subjacent white matter. The cortex is sliced in parallel lines to the midtemporal gyrus and perisylvian area to attenuate the spread of the epileptiform activity without causing cortical dysfunction. There is a study by Morrell "et al." in which results were reported for 14 patients with acquired epileptic aphasia who underwent multiple subpial transections. Seven of the fourteen patients recovered age-appropriate speech and no longer required speech therapy. Another 4 of the 14 displayed improvement of speech and understanding instructions given verbally, but they still required speech therapy. Eleven patients had language dysfunction for two or more years. Another study by Sawhney "et al." reported improvement in all three of their patients with acquired epileptic aphasia who underwent the same procedure.

Various hospitals contain programs designed to treat conditions such as LKS like the Children's Hospital Boston and its Augmentative Communication Program. It is known internationally for its work with children or adults who are non-speaking or severely impaired. Typically, a care team for children with LKS consists of a neurologist, a neuropsychologist, and a speech pathologist or audiologist. Some children with behavioral problems may also need to see a child psychologist and a psychopharmacologist. Speech therapy begins immediately at the time of diagnosis along with medical treatment that may include steroids and anti-epileptic or anti-convulsant medications.

Patient education has also proved to be helpful in treating LKS. Teaching them sign language is a helpful means of communication and if the child was able to read and write before the onset of LKS, that is extremely helpful too.

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.

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.