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Acute auditory agnosia as the presenting hearing disorder in MELAS.

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Title: Acute auditory agnosia as the presenting hearing disorder in MELAS.
Authors: Miceli, Gabriele, Conti, Guido, Cianfoni, Alessandro, Di Giacopo, Raffaella, Zampetti, Patrizia, Servidei, Serenella
Source: Neurological Sciences. Dec2008, Vol. 29 Issue 6, p459-462. 4p. 1 Chart, 1 Graph.
Subjects: Cortical deafness, Hearing disorders, DNA, Magnetic resonance imaging, Aphasia, Precancerous conditions
Abstract: MELAS is commonly associated with peripheral hearing loss. Auditory agnosia is a rare cortical auditory impairment, usually due to bilateral temporal damage. We document, for the first time, auditory agnosia as the presenting hearing disorder in MELAS. A young woman with MELAS (A3243G mtDNA mutation) suffered from acute cortical hearing damage following a single stroke-like episode, in the absence of previous hearing deficits. Audiometric testing showed marked central hearing impairment and very mild sensorineural hearing loss. MRI documented bilateral, acute lesions to superior temporal regions. Neuropsychological tests demonstrated auditory agnosia without aphasia. Our data and a review of published reports show that cortical auditory disorders are relatively frequent in MELAS, probably due to the strikingly high incidence of bilateral and symmetric damage following stroke-like episodes. Acute auditory agnosia can be the presenting hearing deficit in MELAS and, conversely, MELAS should be suspected in young adults with sudden hearing loss. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Acute auditory agnosia as the presenting hearing disorder in MELAS.
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  Data: <searchLink fieldCode="JN" term="%22Neurological+Sciences%22">Neurological Sciences</searchLink>. Dec2008, Vol. 29 Issue 6, p459-462. 4p. 1 Chart, 1 Graph.
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  Data: <searchLink fieldCode="DE" term="%22Cortical+deafness%22">Cortical deafness</searchLink><br /><searchLink fieldCode="DE" term="%22Hearing+disorders%22">Hearing disorders</searchLink><br /><searchLink fieldCode="DE" term="%22DNA%22">DNA</searchLink><br /><searchLink fieldCode="DE" term="%22Magnetic+resonance+imaging%22">Magnetic resonance imaging</searchLink><br /><searchLink fieldCode="DE" term="%22Aphasia%22">Aphasia</searchLink><br /><searchLink fieldCode="DE" term="%22Precancerous+conditions%22">Precancerous conditions</searchLink>
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  Data: MELAS is commonly associated with peripheral hearing loss. Auditory agnosia is a rare cortical auditory impairment, usually due to bilateral temporal damage. We document, for the first time, auditory agnosia as the presenting hearing disorder in MELAS. A young woman with MELAS (A3243G mtDNA mutation) suffered from acute cortical hearing damage following a single stroke-like episode, in the absence of previous hearing deficits. Audiometric testing showed marked central hearing impairment and very mild sensorineural hearing loss. MRI documented bilateral, acute lesions to superior temporal regions. Neuropsychological tests demonstrated auditory agnosia without aphasia. Our data and a review of published reports show that cortical auditory disorders are relatively frequent in MELAS, probably due to the strikingly high incidence of bilateral and symmetric damage following stroke-like episodes. Acute auditory agnosia can be the presenting hearing deficit in MELAS and, conversely, MELAS should be suspected in young adults with sudden hearing loss. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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