Stuttering and the Medial Premotor System

In previous posts we have discussed the possible role of dopamine imbalances in the basal ganglia as a cause of stuttering. We now elaborate in greater detail as to how these imbalances may lead to disfluency by means of a model for speech production initially proposed by Van Riper and further elaborated by Per Alm.

Figure 1 is a schematic representation of the medial premotor system, the components of which are responsible for the production of speech. The medial premotor cortex (a part of the brain in the cerebral cortex responsible for the planning, selection and execution of actions) sends signals to the basal ganglia. These signals pass via neuronal pathways and are mediated by neurotransmitters.

In turn, the basal ganglia provides signals to the supplementary motor area (SMA). The SMA is an area in the cerebral cortex involved in actions under internal control, like the performance of a sequence of movements from memory. Speaking the syllables making up a word constitutes such a sequence.

The basal ganglia play a role in the initiation and regulation of motor commands. In particular, the basal ganglia system may very well contain the timer that influences the production of speech. Speech is a sequential motor task requiring exact timing and in order to execute each syllable, a "go" signal is required. The signal that is provided by the basal ganglia as a feed into the SMA cues the SMA to release the next segment (i.e., syllable) in the word sequence. Stuttering is viewed as a disruption of this sequencing of the syllables making up a word as a result of disturbed timing. If the signal is weak, then the next segment may not be released resulting in repetitions, haltings, and prolongations of the previous segment.

The neurotransmitter dopamine is the principal mediator of basal ganglia functions such as timing. The timing resulting from "normal" levels of dopamine is shown in Figure 2. A weak timing signal from the basal ganglia can occur in two ways. First, insufficient dopaminergic activity in the basal ganglia may lead to a weak signal feeding into the SMA, as shown in Figure 3.

Secondly, excessive levels of dopamine in the basal ganglia may result in an effectively weakened signal to the SMA due to noise drowning out much of the signal. This situation is shown in Figure 4. The "useful" part of the signal is that portion jutting above the noise and its amplitude is obviously diminished. Medications that reduce the level of dopaminergic activity and reduce the noise would be appropriate for this group of stutterers.

In both of these cases, the problem may originate either directly in the basal ganglia or, alternatively, through impaired inputs from the premotor area leading to an out of control basal ganglia with either a too weak signal or one attenuated by too much noise.

The medial premotor system, connecting the cerebral cortex to the basal ganglia, involves the nigrostriatal pathway. This pathway has close associations with the mesolimbic pathway (governing emotions), and because of this association, emotional states engendered by a particular context may influence motor activities such as those involving speech (see the previous "Anxious Brain" posts).

In a subsequent post, we will discuss the role of the lateral premotor system in the production of speech.