Neurology -- Correspondence for Vitte et al., 58 (6) 970-973

Correspondence published:

Midbrain deafness with normal brainstem auditory evoked potentials: Ken Johkura (24 June 2002)

Midbrain deafness with normal brainstem auditory evoked potentials 24 June 2002

Ken Johkura
Hiratsuka Kyosai Hospital Kanagawa Japan
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Re: Midbrain deafness with normal brainstem auditory evoked potentials

johkura-k{at}kkr.hiratsuka.kanagawa.jp Ken Johkura

We read with interest the paper by Vitte et al. [1] The authors describe two patients with midbrain lesions who had total clinical deafness but normal elicited brainstem auditory evoked potentials (BAEP). Because the midbrain lesions were shown on MRI to involve the inferior colliculi, the authors concluded that bilateral inferior colliculus lesions induce deafness but do not affect BAEP. We think, however, Vitte’s two cases have a more important neurological implication.
We recently reported a patient with, like Vitte’s patients, total clinical deafness that occurred after a small traumatic hemorrhage partially involving the inferior colliculi. [2] In our patient, although thresholds for pure tone were audiometrically normal, comprehension of spoken words, environmental sounds, and melody were impaired. Not only BAEP but also middle latency auditory evoked potentials (MLAEP, whose main component is thought to be generated primarily by the bilateral temporal lobes) were elicited in our patient. The preserved BAEP and MLAEP suggest that auditory input was relayed by the brainstem auditory pathway and reached the temporal lobes. The processing of sounds is considered to start in the brainstem, [3, 4] and the recognition of sounds is impaired if the brainstem auditory pathway can relay but not adequately process auditory input. [2] The brainstem auditory processing disorder at the inferior colliculi level manifested in our case as a defective auditory recognition ability, like that found in auditory agnosia resulting from bitemporal lobe disorders. [2] However, little attention has been paid to such auditory dysfunction.
Vitte et al. [1] reported that their two patients showed total clinical deafness, although tests for recognition of environmental sounds and music were not mentioned. However, the patients’ thresholds for pure tone were relatively preserved. [1] Thus, Vitte’s paper seems to show that the midbrain lesion at the level of the inferior colliculi induces total clinical deafness despite relatively preserved hearing ability. This is consistent with our findings [2] In Vitte’s paper, [1] lesion localization is rather vague because of the lack of pathologic analysis, and thus, the discussion of generators of wave V on BAEP seems inadequate. Preserved wave V on BAEP, together with preserved hearing ability for pure tone, indicated rather that the brainstem auditory pathway without discontinuation relayed the auditory input. Therefore, Vitte’s paper implied the presence of auditory agnosia resulting from a brainstem auditory processing disorder due to partial impairment of the brainstem auditory pathway at the level of the inferior colliculi. Such partial impairment may not affect BAEP.
References:
1. Vitte E, Tankéré F, Bernat I, Zouaoui A, Lamas G, Soudant J. Midbrain deafness with normal brainstem auditory evoked potentials. Neurology 2002;58:970-973.
2. Johkura K, Matsumoto S, Hasegawa O, Kuroiwa Y. Defective auditory recognition after small hemorrhage in the inferior colliculi. J Neurol Sci 1998;161:91-96.
3. Rupert AL, Caspary DM, Moushegian G. Response characteristics of cochlear nucleus neurons to vowel sounds. Ann Otol Rhinol Laryngol 1977;86:37-48.
4. Leroy SA, Wenstrup JJ. Spectral integration in the inferior colliculus of the mustached bat. J Neurosci 2000;20:8533-8541.