Individuals who stutter might be perplexed by their sudden fluency in certain contexts. For example, when speaking in unison as part of a chorus, they tend to be quite fluent. Similarly, fluency is enhanced when singing, speaking to the beat of a metronome, or consciously engaging in rhythmic monotonic speech. And the use of altered audio feedback devices improves fluency, at least temporarily.
Speech that is consciously controlled by role playing, imitating a foreign accent, or reducing the speech rate may also enhance fluency. Some individuals also observe that hyper-preparation for a public speaking engagement results in greater fluency by virtue of allowing for greater attention to the speech process; similarly, repeatedly reading a sentence in a clinical setting has been shown to improve fluency.
What all of these instances of enhanced fluency have in common is that the neural circuitry used in these situations circumvents the upstream medial premotor system (see the post on "Stuttering and the Medial Premotor System") which involves the basal ganglia as a timing mechanism. Instead of the medial premotor system, speech production is initiated further downstream by the lateral premotor system. This system involves only the cerebellum as the timing mechanism and, consequently, the faulty timing signals of the basal ganglia/SMA complex does not come into play.
A diagrammatic representation of the lateral premotor system is shown in Figure 1. Note that neural signals are passed from the lateral premotor cortex to the cerebellum, and from there to the arcuate premotor area (APA) in the cortex instead of the supplementary motor area (SMA) as was the case with the medial premotor system. Presumably, the dopamine receptor imbalance that may be present in the basal ganglia/SMA complex is absent from the neural circuitry of the lateral premotor system.
In the speaking contexts cited above, either the speech process relies on external timing cues or the cerebral cortex is relieved of certain planning and initiation actions. In either case, the circumvention of the neurally dysfunctional medial premotor system is facilitated and, instead, the lateral premotor system, operating in relation to sensory input, is directly activated.
On the other hand, the medial premotor system is brought into play for self-initiated, internally cued speaking situations. These situations reflect thoughts and emotions and involve the execution of automatized sequences of learned movements (i.e., speaking syllables of words) without attention. Consequently, such situations may lead to greater disfluency. Also, since there are limbic system inputs (i.e. the system relating to emotions) to the medial premotor system both at the cortical and basal ganglia levels, emotional responses may have an additional impact on fluency.
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