The Auditory Agnosias: a Short Review of Neurofunctional Evidence.

PURPOSE OF REVIEW: To investigate the neurofunctional correlates of pure auditory agnosia and its varieties (global, verbal, and nonverbal), based on 116 anatomoclinical reports published between 1893 and 2022, with emphasis on hemispheric lateralization, intrahemispheric lesion site, underlying cognitive impairments. RECENT FINDINGS: Pure auditory agnosia is rare, and observations accumulate slowly. Recent patient reports and neuroimaging studies on neurotypical subjects offer insights into the putative mechanisms underlying auditory agnosia, while challenging traditional accounts. Global auditory agnosia frequently results from bilateral temporal damage. Verbal auditory agnosia strictly correlates with language-dominant hemisphere lesions. Damage involves the auditory pathways, but the critical lesion site is unclear. Both the auditory cortex and associative areas are reasonable candidates, but cases resulting from brainstem damage are on record. The hemispheric correlates of nonverbal auditory input disorders are less clear. They correlate with unilateral damage to either hemisphere, but evidence is scarce. Based on published cases, pure auditory agnosias are neurologically and functionally heterogeneous. Phenotypes are influenced by co-occurring cognitive impairments. Future studies should start from these facts and integrate patient data and studies in neurotypical individuals.

Cortical disorders of speech processing: Pure word deafness and auditory agnosia.

Selective disorders of auditory speech processing due to brain lesions are reviewed. Over 120 years after the first anatomic report (Dejerine and Sérieux, 1898), fewer than 80 cumulative cases of generalized auditory agnosia and pure word deafness with documented brain lesions are on record. Most patients (approximately 70%) had vascular lesions. Damage is very frequently bilateral in generalized auditory agnosia, and more frequently unilateral in pure word deafness. In unilateral cases, anatomical disconnection is not a prerequisite, and disorders may be due to functional disconnection. Regardless of whether lesions are unilateral or bilateral, speech processing difficulties emerge in the presence of damage to the superior temporal regions of the language-dominant hemisphere, suggesting that speech input is processed asymmetrically at early stages already. Extant evidence does not allow establishing whether processing asymmetry originates in the primary auditory cortex or in higher associative cortices, nor whether auditory processing in the brainstem is entirely symmetric. Results are consistent with the view that the difficulty in processing auditory input characterized by quick spectral and/or temporal changes is one of the critical dimensions of the disorder. Forthcoming studies should focus on detailed audiologic, neurolinguistic, and neuroanatomic descriptions of each case.