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| title | chunk | source | category | tags | date_saved | instance |
|---|---|---|---|---|---|---|
| Auditory agnosia | 2/5 | https://en.wikipedia.org/wiki/Auditory_agnosia | reference | science, encyclopedia | 2026-05-05T07:26:21.081452+00:00 | kb-cron |
== History == A relationship between hearing and the brain was first documented by Ambroise Paré, a 16th century battlefield doctor, who associated parietal lobe damage with acquired deafness (reported in Henschen, 1918). Systematic research into the manner in which the brain processes sounds, however, only began toward the end of the 19th century. In 1874, Wernicke was the first to ascribe to a brain region a role in auditory perception. Wernicke proposed that the impaired perception of language in his patients was due to losing the ability to register sound frequencies that are specific to spoken words (he also suggested that other aphasic symptoms, such as speaking, reading and writing errors occur because these speech specific frequencies are required for feedback). Wernicke localized the perception of spoken words to the posterior half of the left STG (superior temporal gyrus). Wernicke also distinguished between patients with auditory agnosia (which he labels as receptive aphasia) with patients who cannot detect sound at any frequency (which he labels as cortical deafness). In 1877, Kussmaul was the first to report auditory agnosia in a patient with intact hearing, speaking, and reading-writing abilities. This case-study led Kussmaul to propose of distinction between the word perception deficit and Wernicke's sensory aphasia. He coined the former disorder as "word deafness". Kussmaul also localized this disorder to the left STG. Wernicke interpreted Kussmaul's case as an incomplete variant of his sensory aphasia. In 1885, Lichtheim also reported of an auditory agnosia patient. This patient, in addition to word deafness, was impaired at recognizing environmental sounds and melodies. Based on this case study, as well as other aphasic patients, Lichtheim proposed that the language reception center receives afferents from upstream auditory and visual word recognition centers, and that damage to these regions results in word deafness or word blindness (i.e., alexia), respectively. Because the lesion of Lichtheim's auditory agnosia patient was sub-cortical deep to the posterior STG (superior temporal gyrus), Lichtheim renamed auditory agnosia as "sub-cortical speech deafness". The language model proposed by Wernicke and Lichtheim wasn't accepted at first. For example, in 1897 Bastian argued that, because aphasic patients can repeat single words, their deficit is in the extraction of meaning from words. He attributed both aphasia and auditory agnosia to damage in Lichtheim's auditory word center. He hypothesized that aphasia is the outcome of partial damage to the left auditory word center, whereas auditory agnosia is the result of complete damage to the same area. Bastian localized the auditory word center to the posterior MTG (middle temporal gyrus). Other opponents to the Wernicke-Lichtheim model were Sigmund Freud and Carl Freund. Freud (1891) suspected that the auditory deficits in aphasic patients was due to a secondary lesion to cochlea. This assertion was confirmed by Freund (1895), who reported two auditory agnosia patients with cochlear damage (although in a later autopsy, Freund reported also the presence of a tumor in the left STG in one of these patients). This argument, however, was refuted by Bonvicini (1905), who measured the hearing of an auditory agnosia patient with tuning forks, and confirmed intact pure tone perception. Similarly, Barrett's aphasic patient, who was incapable of comprehending speech, had intact hearing thresholds when examined with tuning forks and with a Galton whistle. The most adverse opponent to the model of Wernicke and Lichtheim was Marie (1906), who argued that all aphasic symptoms manifest because of a single lesion to the language reception center, and that other symptoms such as auditory disturbances or paraphasia are expressed because the lesion encompasses also sub-cortical motor or sensory regions. In the following years, increasing number of clinical reports validated the view that the right and left auditory cortices project to a language reception center located in the posterior half of the left STG, and thus established the Wernicke-Lichtheim model. This view was also consolidated by Geschwind (1965) who reported that, in humans, the left planum temporale is larger in the left hemisphere than on the right. Geschwind interpreted this asymmetry as anatomical verification for the role of left posterior STG in the perception of language. The Wernicke-Lichtheim-Geschwind model persisted throughout the 20th century. However, with the advent of MRI and its usage for lesion mapping, it was shown that this model is based on incorrect correlation between symptoms and lesions. Although this model is considered outdated, it is still widely mentioned in Psychology and medical textbooks, and consequently in medical reports of auditory agnosia patients. As will be mentioned below, based on cumulative evidence the process of sound recognition was recently shifted to the left and right anterior auditory cortices, instead of the left posterior auditory cortex.
== Related disorders == After auditory agnosia was first discovered, subsequent patients were diagnosed with different types of hearing impairments. In some reports, the deficit was restricted to spoken words, environmental sounds or music. In one case study, each of the three sound types (music, environmental sounds, speech) was also shown to recover independently (Mendez and Geehan, 1988-case 2). It is yet unclear whether general auditory agnosia is a combination of milder auditory disorders, or whether the source of this disorder is at an earlier auditory processing stage.