An Anxious Mind Affects Stuttering, Part 3

In this post, we continue to recast earlier posts in terms of the anxious mind perspective of the last two posts. In particular, we revisit the diagram presented in the post entitled "Parkinson's Disease, Dopamine, and Stuttering." This diagram can now be presented from a more (structurally) neurological perspective.

The node previously characterized as "Excessive dopamine activity" is replaced by "Striatum" and the node characterized as "Mind" is replaced by "Amygdala."  Anxiety is regarded as a manifestation of a hyperactive amygdala and, as such, is not regarded from this perspective as a causative factor. The striatum affects fluency by virtue of its excessive dopaminergic activity the source of which is the substantia nigra (not shown in the diagram). Similarly, the amygdala by way of the ventral segmental area (not shown in the diagram) feeds additional dopamine to the striatum further affecting fluency.

Finally, in keeping with the previous post on "Stuttering, Placebos, and Nocebos," the "Context" node is replaced by "Conditioned Stimulus." The idea here is that a previous (otherwise neutral) event/situation becomes associated with (consciously or subconsciously) an episode of disfluency; so essentially that event/situation (e.g., speaking before an audience) is a conditioned stimulus that triggers greater activity (i.e., a conditioned response) in the amygdala.

What has not been taken into account in this diagram is that secondary stuttering is qualitatively different from primary stuttering. An amygdala that becomes excited does not only change the frequency of disfluency but also leads to modifications in the nature of the disfluency (i.e., blocks vs. easy rhythmical repetitions).

From a mechanical point of view, we can understand what is happening: A child experiencing primary stuttering develops awareness of his problem and, attempting to consciously intervene, then develops secondary symptoms like blocking. The motor neuron system simply will not allow him to bypass and override the rhythmical repetitions. But from a neurological perspective, the mechanism of action is, at this point in time, not clear. So we have to limit the applicability of the diagram above to individuals already in the secondary stuttering phase.