Charles Van Riper, one of the early pioneers of stuttering research and treatment, once paraphrased Winston Churchill by stating that stuttering is a riddle wrapped in a mystery inside an enigma." Today, the cause of developmental stuttering still eludes us, although many of the layers of the riddle are slowly starting to come unwrapped. A very influential theory of stuttering, which had its origins in the 1950s and was promoted by Wendell Johnson at Iowa University, proposed that stuttering was the result of negative reactions by parents or other people in the child's immediate environment to normal developmental disfluencies. As a result, parents were often advised to ignore early signs of stuttering and told that if left alone, a child would spontaneously outgrow his or her speech difficulties. Even today, many parents still receive this message when they express concern about their childs early signs of stuttering.
We now know that factors such as traumatic life events, illness or other environmental factors may act as triggers for the onset of stuttering in some individuals. Other variables, such as anticipatory anxiety or listener reactions may influence the development and maintenance of stuttering. It is widely accepted today, however, that children who develop stuttering must have a predisposition to the disorder that is biological in nature and, in many instances, genetic. The nature of this predisposition is most likely to be found in brain processes involved in the planning and execution of speech movements. Several observations point directly or indirectly to such a neurobiological etiology:
- The reported incidence of stuttering is around 5 percent worldwide, regardless of language, culture or particular child-rearing practices within a culture.
- The sex ratio for stuttering is about four males to every female. This male predominance for the speech disorder is similar to many other biologically-based disorders such as Tourette's syndrome, congenital deafness, learning disabilities, and Down syndrome, to name a few.
- Acquired stuttering, which can develop in patients with brain trauma, strokes or neurodegenerative diseases who previously were fluent speakers, provides clear evidence for the role of neural systems in the control of speech fluency.
- A number of medical drugs are known to affect speech fluency in people who stutter. Trials are underway to investigate the therapeutic potential of some of these drugs.
- There is clear evidence for the role of genetic influences in the onset and development of stuttering. Research on twins has shown clearly that the concordance for stuttering in twins is far higher than for non-twin siblings who grow up in the same family. Family studies also have demonstrated a clear genetic inheritance pattern spanning various generations. Up to 75 percent of persons who stutter have family members who stutter or who have stuttered in the past.
- Atypical motor patterns in person who stutter can be observed not only during moments of disfluencies, but also during perceptually fluent speech, suggesting the presence of a pervasive underlying speech motor control deficiency. A number of investigations also have provided evidence that the motor control problems are not limited to oral articulatory movements but may extent to sequential movements executed by the fingers, hands and limbs as well.
Recently a number of research groups, including the one in our lab, have started to use modern functional neuroimaging technology such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) to investigate differences in neural activation between people who stutter and those who do not. The results from these investigations have revealed some interesting differences in how the brain is active in people with stuttering difficulties. Stuttering individuals typically show a general overactivation of the neural systems involved in motor control, including the cerebellum. Many of these neural systems are known to cause difficulties with speech motor control and disruptions of speech fluency in patients who suffer damage to these areas. Conditions that enhance fluency, such as speaking in unison with someone else or behavioural fluency treatment, seem to result in a partial normalization of the activation in these cortical and subcortical regions.
Research is currently underway to analyze these observed activation differences in more detail. Undoubtedly, this work will yield a better understanding of how brain processes are involved in the control of speech fluency. More importantly, it could clarify what deficiencies in these processes, either at the system or cellular level, or both, result in stuttering. We already know that intervention early in the development of stuttering can be very effective, whereas treatment at an older age is often much more difficult and prone to relapse. A better understanding of the brain processes underlying fluency disorders should allow us to develop more effective intervention tools for the treatment of this often devastating speech disorder.