Despite its prevalence, stuttering has not received as much attention as other psychiatric disorders from patients or psychiatrists—with good reason. Until recently, little was known about the neurophysiology of stuttering, and treatment was generally ineffective especially in adults (Box 1). Despite their own personal struggles with the disorder, patients have questioned the need for psychiatric treatment.
That has now changed. We know now that stuttering is likely a disorder of brain chemistry. Studies suggests that olanzapine, a novel dopamine antagonist, is a useful, well-tolerated medication for the treatment of stuttering. As a result, psychiatrists are now equipped to play an important role in its management.
Furthermore, we can give patients the therapeutic opportunity to discuss what often has been a lifetime of frustration with stuttering. We can enable them to understand the course and treatment of this disorder and encourage them to take advantage of the opportunities to lessen the symptoms of stuttering and, ultimately, improve their quality of life.
How stuttering develops
Stuttering is a speech disorder characterized by frequent prolongations, repetitions, or blocks of spoken sounds and/or syllables. A common disorder affecting 1% of adults and 4% of children, stuttering is classified in DSM-IV as an Axis I disorder (Box 2).1
Neither tongue cutting nor psychoanalysis has worked
By definition, stuttering can interfere with social, academic, or occupational functioning. Persons who stutter often develop secondary behaviors such as avoidances of words, phrases, or even social situations, which in turn leads to a high level of social anxiety.2Stuttering has occurred throughout history, with descriptions from the ancient Egyptians and Greeks. For centuries, theories on its etiology involved abnormalities in the tongue or larynx, and the treatments addressed such ideology. Even today, some stuttering treatments involve such archaic methods as cauterizing or cutting the tongue. Treatments focused on the tongue or larynx have not demonstrated consistent efficacy.
The pioneering work of Orton21 and Travis22 signaled a significant change in the understanding of stuttering. They postulated that stuttering may arise from abnormal cerebral activity, signaling a significant change in the theories of the etiology of stuttering. Unfortunately, stuttering treatments did not reflect this new understanding until fairly recently.
Psychoanalytic theorists believed that stuttering arose from the individual’s attempt to fulfill some type of unconscious neurotic need, usually resulting from disturbed early parent-child interaction.23 Psychoanalytic therapy was largely ineffective, however.
Most stuttering treatment practiced today involves speech therapy utilizing cognitive and behavioral methods. Such methods are often limited in their efficacy, especially in adults.24 Some forms of therapy involving speech motor training have been shown effective in young children while the brain is still in development.25 The pharmacologic treatment of stuttering is not widespread today, but new and recent research identifying certain cerebral abnormalities is providing clues for pharmacologic interventions.
Stuttering usually begins in childhood and is likely a developmental disorder. Rare cases of acquired stuttering begin in adulthood but are related to secondary causes such as medications, brain trauma, or stroke.3 Some 80% to 90% of developmental stuttering begins by age 6; onset after age 9 is likely to have some psychogenic or neurogenic basis.4 In approximately 60% of the children who stutter, the symptoms will remit by age 16. Children who stutter require early intervention, given the importance of communication in a child’s development.5
Stuttering shares many similarities with Tourette syndrome. Both begin in childhood, follow a waxing or waning course, have a 4:1 male-to-female ratio, are made worse by anxiety, involve abnormalities in the basal ganglia, and respond to dopamine antagonist therapy.6 Persons who stutter often exhibit tic motions, similar to those seen in Tourette syndrome, which are associated with the struggles to produce speech. Genetic studies have shown possible high additive genetic effects; pair-wise concordance for stuttering was significantly higher in identical twins (63%) than it was in fraternal same-sex twins (19%).7,8 Researchers are investigating potential molecular genetic markers for stuttering.
Functional brain imaging studies suggest that stuttering is associated with abnormal cerebral activation primarily involving abnormally low metabolism of the cortical speech areas and the striatum. The defects in stuttering occur primarily in the timing and initiation of spontaneous speech, with such tasks as singing and reading in chorus being spared. A clue to understanding stuttering lies with these “induced fluency” tasks.
Functional positron emission tomography studies utilizing18 F-deoxyglucose showed that stuttering is associated with abnormally low metabolism of speech cortical areas (Wernicke’s and Broca’s) and low metabolism of the basal ganglia, notably the striatum. During the induced fluency, Wernicke’s and Broca’s areas normalize but the striatum remains abnormally low.