Foundas (2004) is of the opinion that people who stutter have an auditory perception defect. She has postulated that the manipulation of the hearing signal with DAF/FAF can influence the degree of fluency amongst some patients that stutter: 'The auditory system, at least at the level of auditory input, is involved in both of these fluency inducing conditions. Thus there may be a defect at the level of auditory processing that is at least partially reversed with these procedures.' (Foundas et al, 2004, s.1640)
Van Riper described stuttering as a consequence of a dis-synchronization of sequential motor speech movements (Guitar 2006). Can this be a consequence of an auditory perception defect or a dysfunction of the basal ganglia?
In 1991, G. Goldberg proposed a hypothesis which crudely simplified states there exist two routes which can be used for initiating motor activity. The dual system is composed of a medial tract, which includes the basal ganglia , and a lateral tract, which includes the cerebellum. The lateral tract encompasses the premotor cerebal cortex, cerebellum, and the connections between them. According to the hypothesis, the lateral tract is activated during conscious coordinated movement. Activation of this lateral tract can be helpful in reducing symptoms which are caused by a dysfunction in the medial tract, basal ganglia for example with Parkinson's disease. (Goldberg,1991) Alm (2004) has further hypothesized about the etiology of stuttering: ' The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues for the initiation of the next motor segment in speech.' (Alm, 2004, s.325)
According to Foundas (2004) and Alm (2004) one can induce the brain to shift tracts by changing the auditory feedback. A large portion of the relationship between the different structures and their role in the pathogenesis of stuttering is still unknown. Nevertheless, it seems reasonable to use Goldberg's hypothesis (1991) on lateral versus medial tracts as a working model for stuttering. (Alm 2004) If that the error does indeed occur in the medial tract / basal ganglia, by activating the lateral coordinated tract, one can bypass the "faulty circuit." In such a system, it would seem reasonable to observe more fluent speech, thus establishing the basis for understanding the therapeutic effects of choral reading and auditory feedback (DAF/FAF). By fluent speech we mean speech production that is even, rhythmic and not strained (Lind 2004).
Foundas (2004) is of the opinion that people who stutter have an auditory perception defect. She has postulated that the manipulation of the hearing signal with DAF/FAF can influence the degree of fluency amongst some patients that stutter: 'The auditory system, at least at the level of auditory input, is involved in both of these fluency inducing conditions. Thus there may be a defect at the level of auditory processing that is at least partially reversed with these procedures.' (Foundas et al, 2004, s.1640)Van Riper described stuttering as a consequence of a dis-synchronization of sequential motor speech movements (Guitar 2006). Can this be a consequence of an auditory perception defect or a dysfunction of the basal ganglia?In 1991, G. Goldberg proposed a hypothesis which crudely simplified states there exist two routes which can be used for initiating motor activity. The dual system is composed of a medial tract, which includes the basal ganglia , and a lateral tract, which includes the cerebellum. The lateral tract encompasses the premotor cerebal cortex, cerebellum, and the connections between them. According to the hypothesis, the lateral tract is activated during conscious coordinated movement. Activation of this lateral tract can be helpful in reducing symptoms which are caused by a dysfunction in the medial tract, basal ganglia for example with Parkinson's disease. (Goldberg,1991) Alm (2004) has further hypothesized about the etiology of stuttering: ' The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues for the initiation of the next motor segment in speech.' (Alm, 2004, s.325)According to Foundas (2004) and Alm (2004) one can induce the brain to shift tracts by changing the auditory feedback. A large portion of the relationship between the different structures and their role in the pathogenesis of stuttering is still unknown. Nevertheless, it seems reasonable to use Goldberg's hypothesis (1991) on lateral versus medial tracts as a working model for stuttering. (Alm 2004) If that the error does indeed occur in the medial tract / basal ganglia, by activating the lateral coordinated tract, one can bypass the "faulty circuit." In such a system, it would seem reasonable to observe more fluent speech, thus establishing the basis for understanding the therapeutic effects of choral reading and auditory feedback (DAF/FAF). By fluent speech we mean speech production that is even, rhythmic and not strained (Lind 2004).
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