As of April 2010, there are no known specific treatments for autotopagnosia.

Semenza (2003) investigated Pick's original work surrounding the discovery of autotopagnosia.

Patients are considered to suffer from "pure" autotopagnosia, however, if their deficiency is specific to body part localization.

However, it as also been noted that patients with generalized brain damage present with similar symptoms of autotopagnosia.

However, contemporary neuropsychological therapy seeks to establish the independence of autotopagnosia from other disorders.

De Renzi's studies gave way to countless others to give insight as to the complicated and varied mechanisms behind autotopagnosia.

Rehabilitation is not a definitive treatment and only shows signs of slight improvement in a small percentage of autotopagnosia patients.

As autotopagnosia is not a life threatening condition it is not on the forefront of medical research.

In many cases, one of these accompanying conditions-often aphasia-could be masking the patient's autotopagnosia altogether.

Many different types of brain lesions can cause autotopagnosia; however, neoplastic lesions seem to be the most common.

As autotopagnosia arises from neurological and irreversible damage, options regarding symptom reversal or control are limited.

He explored, on two patients with autotopagnosia in particular, the difficulties of mentally recognizing the physical division of a whole object into sections.

Some patients demonstrating the symptoms of autotopagnosia have a decreased ability to locate parts of other multipart object.

(2002) described a case (EC) of pure autotopagnosia following a left subcortical vascular accident.

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.

Rather, more research is conducted regarding treatments and therapies to alleviate the lesions and traumas that can cause autotopagnosia.

Overall, the subject was unable to locate the correct parts of her body or that of another, thereby presented the classic signs of autotopagnosia.

Pick's studies introduced autotopagnosia and other category specific agnosias, such as visual and tactile agnosia.

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.

Typically, the cause of autotopagnosia is a lesion found in the parietal lobe of the left hemisphere of the brain.

Until the 1980s, there had been no scientifically accredited cases of autotopagnosia, rather agnosias that have been secondary to other neurological deficits such as dementia.

Although it is still unclear what precise deficits in brain function cause the symptoms of autotopagnosia, the location of brain damage is not as ambiguous.

With such a general definition, a patient that presents with a dysfunction of or failure in accessing one of four mental representation systems suffers from autotopagnosia.

Carlo Semenza (1998) analyzed the deficits associated with patients presenting with autotopagnosia compared with the test results of non-afflicted patients.