About the presenters: Joe Kalinowski has completed research and taught at the University of Connecticut, Haskins Laboratories, Dalhousie University, and East Carolina University. His research interests are fluency inducement via exogenous and endogenous mechanisms, the role of the second speech signal in inducing fluency in people who stutter, speech naturalness before, during, and after therapy, stuttering stereotypes, and anything else that peaks his interest or that of his colleagues.

Vikram N Dayalu has Master's degree in Speech Language Pathology and is currently pursuing his Ph.D. studies at East Carolina University. His interests are in the area of stuttering reduction via a second speech signal and resultant neural changes.

Tim Saltuklaroglu is a first year doctoral student at CSDI, East Carolina University. He received his Masters degree from The University of Alberta, Canada. His research interests lie in the neurophysiological aspects of stuttering.

You can post Questions/comments about the following paper to Joseph Kalinowski, Vikram N. Dayalu, and Tim Saltuklaroglu before October 22, 2000.

Children who stutter and the "therapy paradox": If every therapy works, then no therapy works.

by Joseph Kalinowski, Vikram N. Dayalu, and Tim Saltuklaroglu
from (USA)

During the last 70 years one aspect of therapy for children who stutter is apparent; almost every therapy "seems" to work. This phenomenon, which we will call the "therapy paradox" in children who stutter, is both disconcerting and compelling. From the beginning to the middle portion of the last century, Johnsonian philosophy identified the etiological core of stuttering within the "ear of the listener". Therapy was simple. Ignore what does not exist. If we name it, we create it. If we create it, then "we must be fixed", not the child. If we (the parents) are not fixed in time, the child is irrevocably "marked" with our defect. The loci of the pathology lies within us, and not within the child's physiological makeup. The child and his or her nervous system are simply reflections of our failures.

We did not question (at least as fervently as one would expect) the illogical nature of this premise. We did what we were told and successes appeared abundantly before us. Who could question an approximately 80% success rate (Johnson, 1955a), and the reputation of Wendell Johnson? Successful remission of stuttering lent credence to this illogical premise and all questions of logic and empiricism were removed from our thoughts. We were told of the horrors of not "following the path" and the misfired and broken child that would result. We followed the path to fluency that appeared clearly before us, and we were satisfied.

By contrast, most contemporary therapeutic procedures for children who stutter address the problem in a direct fashion and train the parent/caregiver to continue the ameliorative procedures at home. The disrupted speech is brought to the child's attention, given its "proper name" (once thought to cause the disorder), and is directly confronted. Therapy usually involves modifying and implementing motoric strategies (e.g., gentle onsets, slowed speech) used with adults. Success rates resulting from these methods are approximately 80% with some claims of up to 100% success (Craig, Hancock, Chang, McCready, Shepley, et al., 1996; Ryan & Van Kirk, 1995; Onslow, Andrews, & Lincoln, 1994).

How can these diametrically opposed scenarios and sets of logic be true? The Johnsonian procedure attempted to divert the parents and the child's attention away from the "perceived" pathology, whereas the contemporary procedures attempt to directly confront the child's "real" stuttering behaviors. Tremendous amounts of time and effort have been expended in devising the most powerful anti-Johnsoniam "diagnostic" and "therapeutic" protocols to help children who stutter. The aforementioned paradox indicates that we have failed to understand how, and if therapy indeed succeeds for children who stutter.

Spontaneous recovery further convolutes the issue of treatment success. For example, therapy A gives 80% success and so does therapy B. But, by not providing any form of therapeutic intervention and relying solely on spontaneous recovery, 80-85% success or "recovery" is also achieved (Yairi & Ambrose, 1992a; Yairi, Ambrose, & Niermann, 1993). What does this tell us about the efficacies of the two therapies? It should be noted that the prevalence of stuttering continues to be unchanged and children still grow up to be chronic stutterers, some after having received years of therapy. This percentage of "non recovering" children who stutter get overshadowed by the exaggerated claims that stuttering therapy has an 80-100% success rate in children who stutter. If 80% success is inevitable via spontaneous recovery, then, why do we take attribution for it? Spontaneous recovery is attainable for most children who stutter and must be taken into account, in some form or fashion when assessing therapy efficacy. As noted earlier, if all therapies work, a troubling paradox exists.

Why have the procedures implemented with children who stutter failed in reducing the prevalence of the disorder? As mentioned above, the success rates of the current and previously used techniques are diluted by the percentage of spontaneous recovery. The authors propose that the very definition of stuttering being based on overt symptomatology, may be paramount in explaining the existing paradox. As we believe the core problems of the pathology to be the overt manifestations and the associated secondary and cognitive compensations, our therapeutic procedures have confined their efforts to correcting these symptoms. The Johnsonian approach focuses on distracting our efforts from these overt manifestations, whereas the current techniques are aimed at controlling or eradicating these symptoms. We suggest that the repetitions and prolongations may just be an overt manifestation or compensation for a more central pathology. Simply put, these procedures correct the distal part of the pathology (e.g., overt repetitions and prolongations), and this may be the reason for the resultant similarity in success rates. As stated by Bloodstein (1995) "It would seem that therapy itself, apart from what is done in therapy, has considerable capacity for effecting short term change" [italics added](p.438-439). This implies that the type of therapy administered is irrelevant, as it is acting on the overt symptoms at a distal level and, not truly attacking the central pathology.

An option is to investigate the role of the second speech signal in children who stutter. This has been extensively investigated in adults who stutter, and it has been shown to be efficacious in generating automatic and natural sounding speech. In adults, imaging strategies (PET, fMRI) have used choral speech (a second speech signal) as a fluency enhancer to induce fluent speech and compare it with stuttered speech. These studies have indicated that certain areas that have been associated with speech production are overactive during stuttering and are normalized under choral speech, indicating normal neurophysiological functioning. If this is indeed an indictor of differences, the use of the second speech signals may ultimately help in normalizing neural functioning. This may help in enhancing the "recovery" process, especially considering the greater plasticity of the brain functioning in children as compared to adults.

Our preliminary results on DAF, FAF, and other second speech signals in children who stutter have indicated that the amount of fluency enhancement is robust and stable. The pilot data has been based on short delays (50 ms and 100 ms) and small octave shifts (half an octave). We are in the process of further investigating the topography of differences in fluency enhancement in children via these second speech signals.

The obvious conclusion that can be drawn from the statistics mentioned above is that stuttering therapy provides no more remediation than what would occur spontaneously. Our aim is not to downplay the need for stuttering therapy in children. If the pathology is to be treated, it would logically make more sense to treat it at its onset. We would like to suggest that a more concentrated effort be made at discovering the true, proximal etiology of the disorder. This would help raise and maintain therapeutic success rates and thus, reduce the prevalence of the disorder. By doing so, as clinicians and researchers, we may truly be able to claim some credit for therapeutic success.


Bloodstein, O. (1995). A handbook on stuttering (5th ed.). San Diego, CA: Singular.

Craig, A., Hancock, K., Chang, E., McCready, C., Shepley, A., McCaul, A., Costello, D., Harding, S., Kehren, R., Masel, C., & Reilly, K. (1996). A controlled clinical trial for stuttering in persons aged 9 to 14 years. Journal of Speech and Hearing Research, 39, 808-826.

Johnson, W. (1955a). A study of the onset and development of stuttering. In W. Johnson and R. R. Leutenegger (Eds. ), Stuttering in children and adults. Minneapolis: University of Minnesota Press.

Onslow, M., Andrews, C., & Lincoln, M. (1994). A control/experimental trail of an operant treatment for early stuttering. Journal of Speech and Hearing Research, 37, 1244-1259.

Ryan, B., & Van Kirk Ryan, B. (1995). Programmed stuttering therapy treatment for children: comparison of two establishment programs through transfer, maintenance, and follow-up. Journal of Speech and Hearing Research, 38, 61-75.

Yairi, E., & Ambrose, N. (1992a). A longitudinal study of stuttering in children: A preliminary report. Journal of Speech and Hearing Research, 35, 755-760.

Yairi, E., Ambrose, N., & Niermann, R. (1993). The early months of stuttering: A developmental study. Journal of Speech and Hearing Research, 36, 521-528.

You can post Questions/comments about the above paper to Joseph Kalinowski, Vikram N. Dayalu, and Tim Saltuklaroglu before October 22, 2000.

September 17, 2000