Glyndon Riley, Ph.D.
Professor Emeritus
California State University, Fullerton
Summer 2002

If a medication is developed that is useful for people who stutter, it will not be a "cure" that can work in the absence of other forms of therapy. There is a rationale for including some medical aspects of stuttering in our diagnosis and treatment protocols, but not for excluding established therapies. The history of stuttering theory parallels the history of other complex disorders.

First, environmental factors were thought to be the primary cause and it was labeled "functional" or "emotional" and mothers got most of the blame. Stuttering fell into this category in the 1940s and '50s when it was supposed to start in the ears of the listeners.

Second, genetic evidence began to emerge for stuttering as it had for such disorders as heart disease, autism, and schizophrenia. Environmental causes seem to present an incomplete picture. For stuttering, the genetic influence is even stronger than for other complex disorders. Monozygotic twins have a concordance rate of about 60% or more and dyzygotic twins and brothers have a concordance of 20-26%. In addition, the fact that stuttering, like most childhood speech and learning disorders, occurs in three times as many boys as girls implies that something in addition to environment is part of the etiology.

Third, neurological findings led to proposed new theories that included medical aspects of each of these disorders and treatments were modified to include medical management (especially medications) as part of the overall treatment.

We view stuttering as a multi-dimensional, multiple risks disorder that includes such aspects as social interactions, emotional reactions, auditory processing, language production and speech motor programming. Smith and Kelly describe this perspective in more detail. The results of studies that evaluate the possible relation of dopamine to stuttering need to be considered in a context of these parallel, contributing systems.

A Dopamine Hypothesis

The hypothesis under consideration states that adults who stutter, as a group, have excessive dopamine in the striatal (sub-cortical) regions of the brain.* Recently, Costa & Kroll provided an update for physicians who need to apply medical findings to treating people who stutter. They stated that, "research data and the effectiveness of dopamine receptor antagonists in developmental stuttering seem to support the theory of a hyperdopaminergic origin [of stuttering]."

In an earlier study, dopamine levels in the striatum of three people who stutter (moderate to severe stuttering) were compared with levels in six people who do not stutter. All of the subjects were male. Positron emission tomography used 6-FDOPA as a marker of pre-synaptic dopaminergic activity. Stuttering subjects showed a 100-300 percent increase in dopamine activation in areas related to the hypotheses under consideration. The authors conclude, "Elevated 6-FDOPA uptake in ventral limbic cortical and sub cortical regions is compatible with the hypotheses that stuttering is associated with an overactive pre-synaptic dopamine system in brain regions that modulate verbalization."

More recently, 12 males and 4 females who stutter (mean age 40.8 years) were enrolled in a double blind, placebo controlled study of the effects of low doses of risperadone versus a placebo on stuttering.** There were no significant differences between groups in age or gender. Stuttering severity ranged from mild to very severe in each group at baseline. The percent of syllables stuttered was reduced from 9.6 to 4.7 (50.4%) by the active medication compared with a reduction from 7.0 to 5.1 (27.1%) by the placebo. The mean scores on the Stuttering Severity Instrument-3 (Riley, 1994) were reduced by 7.8 (from 25.3 to 17.5) following the medication and 3.5 (from 24 to 20.5) following the placebo. Both of these measures reached statistical significance at p =

In other findings, 23 people who stutter were included in a double-blind, placebo controlled study to examine the effects of olanzapine (another dopamine blocker) on stuttering: 12 received olanzapine and 11 received a placebo. The group on active medication reduced their SSI-3 scores by an average of 33 percent; the group on placebo by 14 percent. Based on a clinical global impression obtained from the examiners who worked most closely with 14 of the group, 5 of the 7 were clinically improved by the medication compared with 1 of 7 on the placebo. All participants filled out a self-report Subjective Stuttering Scale (J. Riley & G. Riley, 1998). Those on the medication reported 22 percent less stuttering and the ones on placebo reported less than 1 percent. All three of the measures indicated statistically better effects of olanzapine than of the placebo.

These three studies provide some support for the hypothesis that excessive dopamine reduces efficiency in the striatal level of the brain on people who stutter. If this is true, stuttering shares many similarities with Tourette's syndrome in that it is a dopamine based, basal ganglia disorder. Both stuttering and Tourette's begin in childhood, follow a waxing and waning course, are made worse by anxiety, and occur in a 4:1 ratio of male to female. The role of dopamine in stuttering development remains unclear. It may not be present in children who stutter but may develop as a by-product of the stuttering.

Because medication does not provide a comprehensive, complete treatment, research needs to be designed and conducted that includes both traditional (behavioral, cognitive, and attitudinal) stuttering treatment and a selected medication in order to better describe the roles of each approach. Medically induced changes in cortical and sub-cortical activation that are possibly related to stuttering occur in the context of social, cognitive, and emotional conditions and need to be viewed as only one part of a very complex, multi-dimensional process. Even if some medications can be demonstrated to be useful in reducing the frequency and severity of stuttering, they will not provide a total treatment. Rather, each person who stutters needs to work with a speech-language pathologist who specializes in stuttering to work out a comprehensive therapy program in which the use of a given medication may play a part. Perhaps people who have given up on stuttering therapy will find that some medication can make enough difference to help them get back into a treatment program or support group.

For more information contact the Stuttering Foundation at 1-800-992-9392 or


* For a summary of early, related findings, see Riley, Wu, and Maguire (1997) and Wu, Riley, Maguire, and Najafi and Tang (1997).

** Maguire, Gottschalk, Riley, & Franklin, 2000.



  1. Costa, D. & Kroll, R. (2000). Stuttering: An update for physicians. Canadian Medical Association Journal, 1621, 1849-1855.
  2. Felsenfeld, S. (1997). Epidemiology and genetics of stuttering. In R. F. Curlee & G. M. Siegel (Eds.), Nature and treatment of stuttering: New directions, (2nd Edition), pp. 1-23.
  3. Maguire, G.A., Gottschalk, L.A., & Riley, G.D. & Franklin, D.L. (2000). Risperidone in the treatment of stuttering. Journal of Clinical Psychopharmacology, 20, 479-482.
  4. Riley, G.D. (1994). Stuttering Severity Instrument for Children and Adults (3rd ed.). Austin, TX: PRO-ED.
  5. Riley, G., Maguire, G., Franklin, D., Ortiz, T., & Riley, J. (2001, November). Effects of olanzapine on stuttering in adults. Paper presented at the meeting of the American Speech-Language-Hearing, New Orleans.
  6. Riley, G., Wu, J. & Maguire, G. (1997). PET scan evidence of parallel cerebral systems related to treatment effects. In W. Hulstijn, H.F.M. Peters, P. van Lieshout (Eds.), Speech production: Motor control, brain research, and fluency disorders, pp. 321-327.
  7. Riley, J. & Riley, G. (1998, April). The measurement of cognitive factors. A paper presented at a meeting of the American Speech-Language-Hearing Association, Special Interest Division in Fluency, Florida.
  8. Smith, A. & Kelly, E. (1997). Stuttering: A dynamic, multifactorial model. In R.F. Curlee & G.M. Siegel (Eds.), Nature and treatment of stuttering (pp 97-127). Boston: Allyn & Bacon.
  9. Wolf, S.S., Jones, D.W., Knable, M.B., Gorey, J.G., Lee, K.S., Hyde, T.M., Coppola, R., & Weinberger, D.R. (1996). Tourette syndrome: Prediction of phenotypic variation in monozygotic twins by caudate nucleus D2 receptor binding. Science, 273, 1225-1227.
  10. Wu, J.C., Maguire, G.A., Riley, G.D., Fallon, J., LaCasse, L., Chin, S., Klein, E., Tang, C., Cadwell, S., & Lottenberg, S. (1995). A positron emission tomography [18F] deoxyglucose study of developmental stuttering. Neuroreport 6: 501-505.
  11. Wu, J.C., Maguire, G.A., Riley, G.D., Lee, A., Keator, D., Tang, C., Fallon, J., & Najafi, A. (1997). Increased dopamine activity associated with stuttering. Neuroreport, 8: 767-770.
  12. Wu, J.C., Riley, G.D., Maguire, G., Najafi, A. & Tang, C. (1997). PET scan evidence of parallel cerebral systems related to treatment effects: FDG and FDOPA PET scan findings. In W. Hulstijn, H.F.M. Peters, P. van Lieshout (Eds.), Speech production: Motor control, brain research, and fluency disorders, pp. 329-339.