Yonago acta medica · 2018
Decreased Wave V Amplitude in Auditory Brainstem Responses of Children with Cerebellar Lesions.
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Matsuura Yuka, Oguri Masayoshi, Saito Yoshiaki, Aoe Yasutaka, Ogawa Ayame, Akiyama Shota, Yasuda Nanako, Sato Kengo, Maegaki Yoshihiro, Hirooka Yasuaki
Аннотация
BACKGROUND: This study aims to elucidate the effect of isolated cerebellar lesions sparing the brainstem on the auditory brainstem responses in children.
METHODS: We enrolled 10 children (aged 1-16 years) with cerebellar lesions on neuroimaging but lacking clinical brainstem involvement signs and with normal brainstem volumes on magnetic resonance imaging.
RESULTS: The interpeak latency of waves I and V was normal in 9 patients and was marginally prolonged in 1 patient. While amplitudes of waves I and III were normal, we noted a decreased amplitude of wave V and/or an increased I/V amplitude ratio in 6 patients; these included 5 of 8 patients with cerebellar hypoplasia/atrophy and 1 patient with acute cerebellar ataxia.
CONCLUSION: Our results support the hypothesis of an inhibitory input from the cerebellar fastigial nucleus on the inferior colliculus, which might be disinhibited because of Purkinje cells dysfunction due to cerebellar cortex lesions, especially within the cerebellar vermis.
METHODS: We enrolled 10 children (aged 1-16 years) with cerebellar lesions on neuroimaging but lacking clinical brainstem involvement signs and with normal brainstem volumes on magnetic resonance imaging.
RESULTS: The interpeak latency of waves I and V was normal in 9 patients and was marginally prolonged in 1 patient. While amplitudes of waves I and III were normal, we noted a decreased amplitude of wave V and/or an increased I/V amplitude ratio in 6 patients; these included 5 of 8 patients with cerebellar hypoplasia/atrophy and 1 patient with acute cerebellar ataxia.
CONCLUSION: Our results support the hypothesis of an inhibitory input from the cerebellar fastigial nucleus on the inferior colliculus, which might be disinhibited because of Purkinje cells dysfunction due to cerebellar cortex lesions, especially within the cerebellar vermis.