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.

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.

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.

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.

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.

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.

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.

Psychopharmacological treatments include anti-psychotic medications. Psychology research shows that first step in treatment is for the patient to realize that the voices they hear are creation of their own mind. This realization is argued to allow patients to reclaim a measure of control over their lives. Some additional psychological interventions might allow for the process of controlling these phenomena of auditory hallucinations but more research is needed.

The primary means of treating auditory hallucinations is antipsychotic medications which affect dopamine metabolism. If the primary diagnosis is a mood disorder (with psychotic features), adjunctive medications are often used (e.g., antidepressants or mood stabilizers). These medical approaches may allow the person to function normally but are not a cure as they do not eradicate the underlying thought disorder.

Treatment of APD typically focuses on three primary areas: changing learning environment, developing higher-order skills to compensate for the disorder, and remediation of the auditory deficit itself. However, there is a lack of well-conducted evaluations of intervention using randomized controlled trial methodology. Most evidence for effectiveness adopts weaker standards of evidence, such as showing that performance improves after training. This does not control for possible influences of practice, maturation, or placebo effects. Recent research has shown that practice with basic auditory processing tasks (i.e. auditory training) may improve performance on auditory processing measures and phonemic awareness measures. Changes after auditory training have also been recorded at the physiological level. Many of these tasks are incorporated into computer-based auditory training programs such as Earobics and Fast ForWord, an adaptive software available at home and in clinics worldwide, but overall, evidence for effectiveness of these computerised interventions in improving language and literacy is not impressive. One small-scale uncontrolled study reported successful outcomes for children with APD using auditory training software.

Treating additional issues related to APD can result in success. For example, treatment for phonological disorders (difficulty in speech) can result in success in terms of both the phonological disorder as well as APD. In one study, speech therapy improved auditory evoked potentials (a measure of brain activity in the auditory portions of the brain).

While there is evidence that language training is effective for improving APD, there is no current research supporting the following APD treatments:

- Auditory Integration Training typically involves a child attending two 30-minute sessions per day for ten days.

- Lindamood-Bell Learning Processes (particularly, the Visualizing and Verbalizing program)

- Physical activities that require frequent crossing of the midline (e.g., occupational therapy)

- Sound Field Amplification

- Neuro-Sensory Educational Therapy

- Neurofeedback

However, use of a FM transmitter has been shown to produce significant improvements over time with children.

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.

To date, there is no successful method of treatment that "cures" musical hallucinations. There have been successful therapies in single cases that have ameliorated the hallucinations. Some of these successes include drugs such as neuroleptics, antidepressants, and certain anticonvulsive drugs. A musical hallucination was alleviated, for example, by antidepressant medications given to patients with depression. Sanchez reported that some authors have suggested that the use of hearing aids may improve musical hallucination symptoms. They believed that the external environment influences the auditory hallucinations, showing worsening of symptoms in quieter environments than in noisier ones. Oliver Sacks' patient, Mrs. O'C, reported being in an "ocean of sound" despite being in a quiet room due to a small thrombosis or infarction in her right temporal lobe. After treatment, Mrs. O'C was relinquished of her musical experience but said that, "I do miss the old songs. Now, with lots of them, I can't even recall them. It was like being given back a forgotten bit of my childhood again." Sacks also reported another elderly woman, Mrs. O'M, who had a mild case of deafness and reported hearing musical pieces. When she was treated with anticonvulsive medications, her musical hallucinations ceased but when asked if she missed them, she said "Not on your life."

Given the unknown nature of MES, treatments have been largely dependent on an individual basis. Treatments can vary from being as little as self-reassurance to pharmaceutical medications.

Medications can be helpful, such as antipsychotics, benzodiazepines or antiepileptics, but there is very limited evidence for this. Some case studies have found that switching to a prednisolone steroid after a betamethasone steroid which caused MES helped alleviate hallucinations or the use of the acetylcholinesterase inhibitor, Donepezil, have also found that it successfully treated an individual's MES. However, because of the heterogeneous etiology, these methods cannot be applied as general treatment.

Other than treatment by medicinal means, individuals have also successfully alleviated musical hallucinations by cochlear implants, listening to different songs via an external source, or by attempting to block them through mental effort, depending on how severe their condition is.

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.

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.

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.

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.

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

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.

Auditory perception can improve with time.There seems to be a level of neuroplasticity that allows patients to recover the ability to perceive environmental and certain musical sounds. Patients presenting with cortical hearing loss and no other associated symptoms recover to a variable degree, depending on the size and type of the cerebral lesion. Patients whose symptoms include both motor deficits and aphasias often have larger lesions with an associated poorer prognosis in regard to functional status and recovery.

Cochlear or auditory brainstem implantation could also be treatment options. Electrical stimulation of the peripheral auditory system may result in improved sound perception or cortical remapping in patients with cortical deafness. However, hearing aids are an inappropriate answer for cases like these. Any auditory signal, regardless if has been amplified to normal or high intensities, is useless to a system unable to complete its processing. Ideally, patients should be directed toward resources to aid them in lip-reading, learning American Sign Language, as well as speech and occupational therapy. Patients should follow-up regularly to evaluate for any long-term recovery.

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.

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.

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.

Conduction aphasia, also called associative aphasia, is a relatively rare form of aphasia. An acquired language disorder, it is characterized by intact auditory comprehension, fluent (yet paraphasic) speech production, but poor speech repetition. They are fully capable of understanding what they are hearing, but fail to encode phonological information for production. This deficit is load-sensitive as patients show significant difficulty repeating phrases, particularly as the phrases increase in length and complexity and as they stumble over words they are attempting to pronounce. Patients will display frequent errors during spontaneous speech, such as substituting or transposing sounds. They will also be aware of their errors, and will show significant difficulty correcting them. For example: "Clinician: Now, I want you to say some words after me. Say ‘boy’. Patient: Boy. Clinician: Home. Patient: Home. Clinician: Seventy-nine. Patient: Ninety-seven. No … sevinty-sine … siventy-nice…. Clinician: Let’s try another one. Say ‘refrigerator’. Patient: Frigilator … no? how about … frerigilator … no frigaliterlater … aahh! It’s all mixed up!"

Shallice and Warrington (1970) were able to differentiate two variants of

this constellation: the reproduction and the repetition type. These authors suggested an exclusive deficit of auditory-verbal short-term memory in repetition conduction aphasia whereas the other variant was assumed to reflect disrupted phonological encoding mechanism, afflicting confrontation tasks such as repetition, reading and naming in a similar manner.

Left-hemisphere damage involving auditory regions often result in speech deficits. Lesions in this area that damage the sensorimotor dorsal stream suggest that the sensory system aid in motor speech. Studies have suggested that conduction aphasia is a result of damage specifically to the left superior temporal gyrus and/or the left supra marginal gyrus. The classical explanation for conduction aphasia is that of a disconnection between the brain areas responsible for speech comprehension (Wernicke's area) and speech production (Broca's area), due specifically to damage to the arcuate fasciculus, a deep white matter tract. Patients are still able to comprehend speech because the lesion does not disrupt the ventral stream pathway.