Cortical deafness in multiple sclerosis

Tabira, Takeshi; Tsuji, Sadatoshi; Nagashima, Takako; Nakajima, Tsutomu; Kuroiwa, Yoshigoro

doi:10.1136/jnnp.44.5.433

Cited by 24 publications

(4 citation statements)

References 9 publications

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“…Some patients with auditory agnosia have been reported to have a deficit in sound localization (Albert and Bear, 1974;Chocholle et al, 1975;Coslett et al, 1984;Goldstein et al, 1975;Jerger et al, 1969;Kazui et al, 1990;Lechevalier et al, 1984;Lhermitte et al, 1971;Michel et al, 1980;Tabira et al, 1981;Tanaka et al, 1965;Woods et al, 1984;Wortis and Pfeffer, 1948). Other patients have been reported not to have a sound localization deficit (Denes and Semenza, 1975;Fujii et al, 1990;Gazzaniga et al, 1973;Jerger et al, 1972;Kanshepolsky et al, 1973;Okada et al, 1963;Spreen et al, 1965).…”

Section: Sound Localization Taskmentioning

confidence: 99%

Functional Mapping of the Human Auditory Cortex

Poliva

Bestelmeyer

Hall

et al. 2015

Cognitive and Behavioral Neurology

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Auditory agnosia reflects dysfunction of the auditory ventral stream. The ventral and dorsal auditory streams are already segregated as early as the primary auditory cortex, with the ventral stream projecting from hR and the dorsal stream from hA1. M.L.'s leftward localization bias, preserved audiovisual integration, and phoneme perception are explained by preserved processing in her right auditory dorsal stream.

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Section: Sound Localization Taskmentioning

confidence: 99%

Functional Mapping of the Human Auditory Cortex

Poliva

Bestelmeyer

Hall

et al. 2015

Cognitive and Behavioral Neurology

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“…More frequently, obvious but not severe damage to writing and speech is described (e.g., Mott, 1907;Marshall, Rappaport & Garcia-Buñuel, 1985;Praamstra, Hagoort, Massen & Crul, 1991;Miceli et al, 2008). 1 Selective disorders of auditory processing have been reported mostly in adults following a stroke (for a review, see Simons & Lambon-Ralph, 1999) and occasionally in other neurological conditions, such as encephalitis (Arias et al, 1995;Goldstein, 1974), primary progressive aphasia (Otsuki, Soma, Sato, Homma, & Tsuji, 1998), multiple sclerosis (Tabira, Tsuji, Nagashima, Nakajima, & Kuroiwa, 1981), head trauma (Franklin, 1989), mitochondrial encephalomyopathy (Miceli et al, 2008), central pontine myelinolysis (Garde & Cowey, 2000) and Creutzfeldt-Jakob disease (Tobias, Mann, Bone, de Silva, & Ironside, 1994). It has also been documented in children with Landau-Kleffner disease (Baynes, Kegl, Brentari, Kussmaul, & Poizner, 1998) and brain tumor (Pan, Kuo, & Hsieh, 2004).…”

Section: Introductionmentioning

confidence: 99%

Pure word deafness following left temporal damage: Behavioral and neuroanatomical evidence from a new case

Maffei

Capasso

Cazzolli

et al. 2017

Cortex

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Pure Word Deafness (PWD) is a rare disorder, characterized by selective loss of speech input processing. Its most common cause is temporal damage to the primary auditory cortex of both hemispheres, but it has been reported also following unilateral lesions. In unilateral cases, PWD has been attributed to the disconnection of Wernicke's area from both right and left primary auditory cortex. Here we report behavioral and neuroimaging evidence from a new case of left unilateral PWD with both cortical and white matter damage due to a relatively small stroke lesion in the left temporal gyrus. Selective impairment in auditory language processing was accompanied by intact processing of nonspeech sounds and normal speech, reading and writing. Performance on dichotic listening was characterized by a reversal of the right-ear advantage typically observed in healthy subjects. Cortical thickness and gyral volume were severely reduced in the left superior temporal gyrus (STG), although abnormalities were not uniformly distributed and residual intact cortical areas were detected, for example in the medial portion of the Heschl's gyrus. Diffusion tractography documented partial damage to the acoustic radiations (AR), callosal temporal connections and intralobar tracts dedicated to single words comprehension. Behavioral and neuroimaging results in this case are difficult to integrate in a pure cortical or disconnection framework, as damage to primary auditory cortex in the left STG was only partial and Wernicke's area was not completely isolated from left or right-hemisphere input. On the basis of our findings we suggest that in this case of PWD, concurrent partial topological (cortical) and disconnection mechanisms have contributed to a selective impairment of speech sounds. The discrepancy between speech and non-speech sounds suggests selective damage to a language-specific left lateralized network involved in phoneme processing.

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“…Bilateral hearing loss, however, was also observed in bilateral lesions of the auditory pathway in the temporal lobe. 4 Less known is a central phonophobia in MS whereby acoustic stimuli provoke unpleasant and painful paresthesia, which leads to a corresponding avoidance behaviour.…”

Section: Introductionmentioning

confidence: 99%

Central hyperacusis with phonophobia in multiple sclerosis

et al. 2002

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Hearing disorders are a well-described symptom in patients with multiple sclerosis (MS). Unilateral or bilateral hyperacusis or deafness in patients with normal sound audiometry is often attributed to demyelinating lesions in the central auditory pathway. Less known in MS is a central phonophobia, whereby acoustic stimuli provoke unpleasant and painful paresthesia and lead to the corresponding avoidance behaviour. In our comparison collective, patient 1 described acute shooting pain attacks in his right cheek each time set off by the ringing of the telephone. Patient 2 complained of intensified, unbearable noise sensations when hearing nonlanguage acoustic stimuli. Patient 3 noticed hearing unpleasant echoes and disorders of the directional hearing. All patients had a clinical brainstem syndrome. ENT inspection, sound audiometry and stapedius reflex were normal. All three patients had pathologically changed auditory evoked potentials (AEPs) with indications of a brainstem lesion, and in magnetic resonance imaging (MRI) demyelinating lesions in the ipsilateral pons and in the central auditory pathway. The origin we presume in case 1 is an abnormal impulse conduction from the leminiscus lateralis to the central trigeminus pathway and, in the other cases, a disturbance in the central sensory modulation. All patients developed in the further course a clinically definite MS. Having excluded peripheral causes for a hyperacusis, such as, e.g., an idiopathic facial nerve palsy or myasthenia gravis, one should always consider the possibility of MS in a case of central phonophobia. Therapeutic possibilities include the giving of serotonin reuptake inhibitors or acoustic lenses for clearly definable disturbing frequencies.

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Cortical deafness in multiple sclerosis

Cited by 24 publications

References 9 publications

Functional Mapping of the Human Auditory Cortex

Functional Mapping of the Human Auditory Cortex

Pure word deafness following left temporal damage: Behavioral and neuroanatomical evidence from a new case

Central hyperacusis with phonophobia in multiple sclerosis

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