Cortical Deafness and Auditory Agnosias: Case reports
Cortical deafness and Auditory agnosias are impairments that, even though they were uncovered since long time ago, we don’t know a lot of them. In the literature there are some case reports about these pathologies which sometimes they are not very exactly, especially regards the brain lesion due to their large size. The details about the assessments of the possible alterations on the auditory processing of every patient are not very common find them on the case reports, so the article is focused on the most striking alterations in the patient.
Nevertheless, if we read several of those articles we can see, among other things, the damaged area (with more or less precision) and the features of the deficits (or at least the most striking it), as well as the evaluations on the peripheral audition. But if we are focalizing on the brain damage variable on each type of pathology, we see that there are some areas which are repeating with more frequency than other, giving the possibility of they are the responsible areas of each sort of deficit. Here, we are going to show you some appreciations about the lesion and clinic manifestations from those articles.
We are going to start with the cortical deafness because it was uncovered by Wernicke and Friedlander (1883) in a patient who had a lesion on both temporal lobes. Since then it seems that those areas could be provoking this pathology, although thanks to the technology from the last years we know that the specific areas are primary cortexes on both temporal lobes. However, it was also reported a case who patient had cortical deafness by an injury on the left Sylvian fissure.
The patients with pure word deafness (PWD) cannot process the hearing word sounds and sometimes they have affected the recognizing of complex sounds, too. In the articles about the PWD there is an area called superior temporal gyrus (STG) which is the most frequent affected area on the case reports with this pathology. However, another case of PWD was reported which showed bilateral damage on the putamina, head of caudate nucleus and partial splenium of the corpus callosum, while the temporal lobes were preserved.
About the auditory agnosias, the damaged STG was more relevance than the rest of areas, too. The feature of this pathology is the absence of the ability to sound processing while the word processing is intact. In this case, we also found a patient with both temporal lobes preserved, but he had a bilateral lesion on the auditory radiations.
Taking this into account, it seems that it is not possible set up an association between damaged area and the clinic manifestations. Perhaps, the auditory processing deficits on the cortical deafness and auditory agnosia could not be associated to a specific damaged brain area, although it could be something more cognitive-neural what is affecting to the auditory processing on these pathologies.
Nonetheless, it is important carry on the research to find the cause and make an effective rehabilitation.