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Cortical and subcortical mechanisms in persistent stuttering ...

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Chapter 1 Introduction<br />

accord<strong>in</strong>g to the German version of the stutter<strong>in</strong>g severity <strong>in</strong>dex (S<strong>and</strong>rieser <strong>and</strong> Schneider,<br />

2008) as described <strong>in</strong> the methods sections of the <strong>in</strong>cluded studies.<br />

1.3 Subtypes of stutter<strong>in</strong>g<br />

Scientific approaches to expla<strong>in</strong> stutter<strong>in</strong>g are diverse <strong>and</strong> consequently many different<br />

attempts to classify the disorder exist. These attempts are clearly <strong>in</strong>fluenced by the Zeitgeist <strong>in</strong><br />

which they emerged. Ehud Yairi wrote an excellent review on these attempts of subtyp<strong>in</strong>g<br />

stutter<strong>in</strong>g (Yairi, 2007). A reliable <strong>and</strong> st<strong>and</strong>ardized categorization would obviously be of<br />

great advantage for scientific studies. A current PubMed search clearly <strong>in</strong>dicates that a<br />

separation between acquired [neurogenic] stutter<strong>in</strong>g, psychogenic stutter<strong>in</strong>g, <strong>and</strong> <strong>persistent</strong><br />

[developmental, idiopathic] stutter<strong>in</strong>g is commonly used these days (Lundgren et al., 2010).<br />

Therefore this etiology-based classification is briefly <strong>in</strong>troduced here.<br />

1.3.1 Acquired stutter<strong>in</strong>g<br />

Acquired stutter<strong>in</strong>g occurs <strong>in</strong> adulthood <strong>and</strong> is related to aberrant neurogenic conditions<br />

<strong>in</strong>clud<strong>in</strong>g for example cerebrovascular lesions, traumatic bra<strong>in</strong> <strong>in</strong>juries, seizure disorders <strong>and</strong><br />

Park<strong>in</strong>son’s disease (Lundgren et al., 2010). Various cortical <strong>and</strong> <strong>subcortical</strong> lesion sites are<br />

related to acquired stutter<strong>in</strong>g (see Appendix B, Table B-1). There is a lot to ga<strong>in</strong> from studies<br />

of acquired stutter<strong>in</strong>g, where the causal disruption is more easily identified <strong>and</strong> the short<br />

period between onset <strong>and</strong> exam<strong>in</strong>ation helps to assure that observed abnormalities are not<br />

secondary but <strong>in</strong>deed causal. Therefore, a detailed overview on locations of bra<strong>in</strong> <strong>in</strong>juries that<br />

<strong>in</strong>duce speech dysfluencies, criteria for the differential diagnosis, cases of chased stutter<strong>in</strong>g<br />

due to bra<strong>in</strong> lesions <strong>and</strong> current knowledge from deep bra<strong>in</strong> simulation <strong>and</strong> stutter<strong>in</strong>g is given<br />

<strong>in</strong> Appendix B.<br />

1.3.2 Psychogenic stutter<strong>in</strong>g<br />

Psychogenic stutter<strong>in</strong>g occurs <strong>in</strong> adulthood as a result of psychological trauma (Baumgartner<br />

<strong>and</strong> Duffy, 1997). A reliable differential diagnosis of acquired from psychogenic stutter<strong>in</strong>g,<br />

based on perceptual features of speech characteristics, is problematic. It appears that the rapid,<br />

favorable response to the treatment serves best to differentiate the psychogenic cases from the<br />

neurologic cases (Lundgren et al., 2010).<br />

1.3.3 Persistent stutter<strong>in</strong>g<br />

All studies <strong>in</strong>troduced <strong>in</strong> this dissertation aim at elucidat<strong>in</strong>g patho<strong>mechanisms</strong> <strong>in</strong> <strong>persistent</strong><br />

stutter<strong>in</strong>g because it is a frequent disorder with unclear etiology. For that reason I give more<br />

details on this disorder. Persistent stutter<strong>in</strong>g occurs <strong>in</strong> childhood without obvious reason. The<br />

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