Regular ArticleCategorical Speech Perception in Cerebellar Disorders☆,☆☆,★
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Cited by (91)
The cerebellum as a movement sensor
2019, Neuroscience LettersCitation Excerpt :In the domain of speech perception, altered movement at the vocal chords produces temporal difference in energy at the fundamental frequency between words. Patients with cerebellar degeneration are unable to discriminate between speech stimuli with differing temporal cues [42]. Importantly though, cerebellar damage does not disrupt the ability to judge other, non-temporal, properties of sensory stimuli, such as intensity [40,41].
Patients with focal cerebellar lesions show reduced auditory cortex activation during silent reading
2016, Brain and LanguageCitation Excerpt :In contrast, the evidence of cerebellar involvement in language from the clinical literature is more equivocal (Mariën et al., 2014). Subtle language deficits have been reported in cerebellar patients, including dysarthric speech (Urban, 2013), problems discriminating between phonemes based on temporal cues (Ackermann, Gräber, Hertrich, & Daum, 1997), reduced verbal working memory capacity (Kirschen et al., 2008), mild agrammatism (Mariën et al., 2014) and problems with aspects of higher-level language function (Murdoch, 2010). However, profound persistent language deficits are uncommon following cerebellar pathology (Alexander, Gillingham, Schweizer, & Stuss, 2012).
The Role of the Cerebellum in Speech Perception and Language Comprehension
2016, The Linguistic CerebellumCerebellar Contributions to Speech and Language
2015, Neurobiology of LanguageTime perception networks and cognition in schizophrenia: A review and a proposal
2014, Psychiatry ResearchCitation Excerpt :Evidence about the participation of each particular region of timing networks comes from brain lesion reports and from transcraneal magnetic stimulation (TMS) studies. Patients with cerebellar damage are impaired at perceptual timing tasks such as judging the duration of brief tones (Ivry and Keele, 1989; Mangels et al., 1998; Ackermann et al., 1997). Similar findings have been observed in other reports of damage (Meck, 2005) in basal ganglia (Harrington et al., 1998a; Rao et al., 2001; Coull and Nobre, 2008), supplementary motor area (Coull et al., 2004; Macar et al., 2006) and the prefrontal cortex, especially in the right hemisphere (Harrington et al., 1998b; Lewis and Miall, 2006) inferior parietal areas (Buhussi and Meck, 2005), right parietal supramarginal gyrus (Wiener and Coslett, 2008), cerebellum (Harrington et al., 2004), and right prefrontal cortex (Harrington et al., 1998a; Nichelli et al., 1995; Wiener and Coslett, 2008).
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This study was supported by grants from the DFG (SFB 307) and the BMFT (01 KL9001 O). The authors thank Prof. Dr. Johannes Dichgans and Dr. M. M. Schugens for critical discussion and helpful comments.
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Address correspondence and reprint requests to Hermann Ackermann, Department of Neurology, University of Tübingen, Hoppe-Seyler-Strasse 3, D-72076 Tübingen, Germany.
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D. E. MeyerS. Kornblum