Saturday, August 14, 2010

Stuttering and Dopamine

The current hypothesis regarding the physiological cause of stuttering is that there is excessive dopaminergic activity in the motor neuron portion of the brain. We emphasize that this is a hypothesis which does not yet have the status of a highly tested theory. Although brain imaging studies have shown that people who stutter exhibit above average motor neuron dopaminergic activity, this observation is a correlation rather than a cause/effect chain. The administration of certain atypical antipsychotic drugs which are known to reduce dopaminergic activity also reduce the level of disfluency and this provides some support for a cause/effect relationship. But additional evidence is needed to further support the hypothesis.

Stuttering begins to manifest itself in preschool children and some children outgrow this fluency problem. Is excessive dopaminergic activity present in the brains of these children? Is there any difference in the dopaminergic activity of children who outgrow their stuttering compared to those who do not? Are there any environmental influences that govern the different paths that children take toward fluency that may influence dopaminergic activity?

In addition, we may inquire as to whether or not any of the psychologically based speech therapies affect dopamine levels. If the effects of these therapies are temporary, can changes in dopamine activity be observed? Also, to what extent does the administration of placebos affect dopamine levels? Do illegal drugs, most of which accentuate dopamine activity, have a negative effect on all or most stutterers?

We also want to get at the question as to what causes the physiological structure of the brain that results in excessive dopaminergic activity. Is it nature or nurture? Are there specific genes that can unambiguously be associated with stuttering? Or does nurture in the way of the environment play a major role in the development of disfluency? If the problem is principally with genes, is some sort of gene therapy possible for the treatment of this problem?

These are some of the questions that need to be answered before the dopamine hypothesis can be accepted as a theory.

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