Tuesday, November 30, 2010

An Anxious Mind Affects Stuttering, Part 2

In light of the previous post on the anxious mind, we reiterate and recast some of our earlier discussions regarding drugs, mind, and measurement.

First, If the dopaminergic hypothesis of stuttering is valid, reducing dopaminergic activity using, for example, atypical antipsychotic drugs may directly reduce stuttering by acting on the striatum. In addition, since the great majority of neurons in the basal ganglia utilize GABA as a neurotransmitter with inhibitory effects on their targets (namely dopamine neurons), it is no wonder that GABAergic enhancing drugs (such as BZs) also may improve fluency.

Secondly, both dopaminergic antagonistic (i.e., inhibiting) drugs and GABAergic agonist (i.e., enhancing) drugs may modulate hyperactivity of the amygdala to indirectly influence the level of dopamine in the striatum with the end result of further improving fluency.

These drugs are not localized in their effects; instead they "wash" over the brain and affect the responses of neurons in both the basal ganglia and amygdala. So, if the model of behavior discussed in the previous anxious mind post is correct, the issue concerning whether an antipsychotic or BZ medication merely reduces anxiety thus improving fluency is largely irrelevant.

In an earlier post, we argued that the brain problem leading to stuttering may be ranked on a severity scale ranging from 1 to 10. Similarly, the mind component of stuttering can also be ranked on a 1 to 10 scale.

Based on the discussion in the previous post, we could circumvent the amorphous construct of "the mind" and instead rank the hyperactivity of the amygdala on a 1 to 10 scale. We thus may have a potential method of actually measuring the two dimensions of stuttering, namely the mind and the body, by means of existing brain scan technologies.

This may be an oversimplification, but if the activity of the amygdala were measured to have a rank value of A (ranging between 1 and 10) and the striatum were observed through a brain scan to have an activity ranked with a value of S, then the independent activity of the striatum would be ranked (S-A). We subtract the amygdala's activity from the striatum's activity since the brain scan measurement of the striatum involves both the direct effect of the striatum and the indirect effect of the amygdala. The caveat, of course is whether or not existing brain scan technology can provide some meaningful and quantifiable indication of activity in the two organs and that these effects are additive in the striatum.

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