Can stuttering be cured through the induction of plastic change in the brain?

 

Kathleen Henriksen, M.D.
Emergency Room, Ullevål University Hospital, 0407 Oslo, Norway

Eirik Solheim M.D.
Sørlandet Hospital, 4809 Arendal, Norway

Hilda Sønsterud
Speech and Language Pathologist, Oslo, Norway

Greg Jablonski, M.D., Ph.D.
Senior Ear Surgeon 
Department of Ear Nose and Throat , ØPO-klinikken,
Rikshospitalet University Hospital and University of Oslo
N-0027 Oslo, Norway 

Espen Dietrichs, M.D., Ph.D.
Professor of Neurology, Head of Department
Department of Neurology
Center for Clinical Neuroscience
Rikshospitalet University Hospital and University of Oslo
N-0027 Oslo, Norway

This is the English translation of an article published October 2007 issue of Norsk Tidskrift for Logopedi.

It is well established that some stutters can experience spontaneous improvement in fluency when speaking in chorus or with song, a so called choral effect. We are of the belief that if technical intervention against stuttering or moderated speech is initiated while the brain is still plastic, before the age of 7 years, it may be possible to induce persistent fluency as the brain re-modulates to circumvent dysfunctional nerve tracts. This hypothesis is based on the brains significant potential for plastic change and logical deduction from the empirical treatment of astigmatism.

Background

The estimated prevalence for stuttering in the adult population is between 0.7 to 1%. Stuttering can be a significant social handicap. Traditionally it has been diagnosed and treated by speech pathologists and psychologists. Stuttering is a complex neuro-motor speech disorder often with a genetic predisposition. Essential stuttering is often characterized by blocks with full stops of air and sound, repetition of sounds or prolongation of syllables. The consensus has defined stuttering as a percentage of dysfluency per one hundred words, 5% representing a mild stutter while 12% or more is considered a sever condition. (Guitar 2006) By essential stuttering we mean that stuttering is the fundamental dysfunction and not that it is a symptom of another illness.

It has been known since ancient times that physical manipulation while stuttering can affect stuttering frequency. It is written that as a boy Demosthenes (384-322) cured himself of stuttering by speaking with pebbles in his mouth. In the 1960's it was discovered that a portion of the stuttering population experienced remission when they were exposed to Delayed Auditory Feedback (DAF). Subsequently, there have been many devices developed that deliver DAF therapy. We will refer to this as technical intervention. Technical intervention encompasses fitting the patient with a device that provides an echo of the patient's own voice with a delay between 50 to 200 ms. In an effort to avoid resistance development over time the frequency of the patient's own voice is also adjusted up or down, from +/- 1000Hz to 500Hz. This is referred to as Frequency Altered Feedback (FAF). What percent of patients respond to the effect of DAF/FAF is not yet properly documented. However, DAF/FAF has been used and is being used for stuttering therapy.

Existing Hypotheses

Foundas (2004) is of the opinion that people who stutter have an auditory perception defect. She has postulated that the manipulation of the hearing signal with DAF/FAF can influence the degree of fluency amongst some patients that stutter: 'The auditory system, at least at the level of auditory input, is involved in both of these fluency inducing conditions. Thus there may be a defect at the level of auditory processing that is at least partially reversed with these procedures.' (Foundas et al, 2004, s.1640)

Van Riper described stuttering as a consequence of a dis-synchronization of sequential motor speech movements (Guitar 2006). Can this be a consequence of an auditory perception defect or a dysfunction of the basal ganglia?

In 1991, G. Goldberg proposed a hypothesis which crudely simplified states there exist two routes which can be used for initiating motor activity. The dual system is composed of a medial tract, which includes the basal ganglia , and a lateral tract, which includes the cerebellum. The lateral tract encompasses the premotor cerebal cortex, cerebellum, and the connections between them. According to the hypothesis, the lateral tract is activated during conscious coordinated movement. Activation of this lateral tract can be helpful in reducing symptoms which are caused by a dysfunction in the medial tract, basal ganglia for example with Parkinson's disease. (Goldberg,1991) Alm (2004) has further hypothesized about the etiology of stuttering: ' The core dysfunction in stuttering is suggested to be impaired ability of the basal ganglia to produce timing cues for the initiation of the next motor segment in speech.' (Alm, 2004, s.325)

According to Foundas (2004) and Alm (2004) one can induce the brain to shift tracts by changing the auditory feedback. A large portion of the relationship between the different structures and their role in the pathogenesis of stuttering is still unknown. Nevertheless, it seems reasonable to use Goldberg's hypothesis (1991) on lateral versus medial tracts as a working model for stuttering. (Alm 2004) If that the error does indeed occur in the medial tract / basal ganglia, by activating the lateral coordinated tract, one can bypass the "faulty circuit." In such a system, it would seem reasonable to observe more fluent speech, thus establishing the basis for understanding the therapeutic effects of choral reading and auditory feedback (DAF/FAF). By fluent speech we mean speech production that is even, rhythmic and not strained (Lind 2004).

Radiology

Some degree of support for Alm's theory can be found in a recent functional Magnetic Resonance Imaging (fMRI) study done on 16 adult stutterers. Images were taken before and after Kassel Stuttering Therapy (Giraud et al, 2007). Before treatment, the patients had increased activity in a portion of the basal ganglia (nucleus caudatus), while after successful treatment this activity was no longer present.

With the help of Positron Emission Tomography (PET) technology, support has been found for a number of etiological hypotheses of stuttering:

- Lack of development of left hemisphere dominance.

- Hyperactivity of the right hemisphere.

- Deactivation of the frontal-temporal system implicated in speech production.

- Hyperactivity of motor systems.

The hyperactivity was shown to be significantly reduced with the use of choral speech. In addition , there was a corresponding reactivation of the deactivated frontal-temporal systems. (Fox et al, 1996).

Considering that a PET scan is a picture of metabolic activity over elapsed time, we consider the functional findings of the type given above to be poorly suited for understanding the etiology of stuttering. The time that it takes from the time the dysfunction occurs until supplementary mechanisms are activated is so short that it is likely impossible with today's technology to expose the actual instant of dysfunction. The question then being; Which of the observed changes represent the point of error and which represent the brains secondary compensation mechanisms?

Dr. Chang (Schonfeld , 2007) has observed in both stuttering children and adults a reduction in white substance in areas that connect the frontal motor-speech region and the language understanding region. Dr. Chang expressed the following thoughts in Ped News (January 2007, s.34):

'Adults who stutter show the same tract abnormalities as do children, but also show asymmetry in gray-matter volume, suggesting that the gray-matter finding in adults reflect neuroplastic changes secondary to a lifetime of stuttering.'

This must be considered a significant find in that it represents an introduction of the brains plastic change in the pathology of stuttering .

Can therapy induce plastic change?

Under clinical testing of a DAF/FAF device, Henriksen and Solheim observed a technically induced spontaneous remission in a sever stuttering patient. The testing was conducted under controlled conditions at Rikshospital in Oslo Norway on November 4, 2003. Under great academic skepticism we ask; can such a remission in some cases be permanent?

In the last few years we have learned that the brain has enormous potential for plastic change throughout life, both as a result of normal learning and restitution after injury (see Dietrichs, 2007 for overview). Nevertheless it is in the first few years of life that the brain has its greatest potential for plastic change. During these years all of the important nerve tracts are being fully developed and those that are not in use are being gradually degraded. This re-modulation process is used in clinical medicine, for example in the treatment of children with astigmatism. Treatment involves a period of alternating patching of the aligned and nonaligned eyes, thus training the child to use both eyes. It is recommended this be done prior to age 7 for optimal effect. If this is not done, the brain will often suppress the vision and degrade the optic tract of the crossed eye potentially resulting in blindness.

Based on current knowledge of the brains enormous potential for plastic change and logical deduction from the empirical treatment of astigmatism, Henriksen and Solheim have developed the following hypothesis: If technical intervention against stuttering is initiated while the brain is in its most plastic phase (prior to age 7) it may be possible to induce a persistent fluency even after the device is removed. They have further theorized that technical intervention with DAF/FAF works by blocking the dysfunctional medial motor tract while activating the lateral tract. In doing so the dysfunctional tracts would be degradated during treatment. This in theory could result in a permanent fluency mediated by the lateral system.

A parallel hypothesis could be presented for evaluating the Lidcombe program's effect. An important element in the program involves the parents active participation in intervention. The parents are instructed to give direct feedback to the child (within very specific guidelines and procedures). The child is encouraged to repeat his or her utterance in a more controlled matter. According to Alms theory, the lateral system is more dominant when motion is consciously controlled. (Alm 2004) The question being can the brains plastic potential be exploited here? Can direct intervention via the Lidcombe program contribute to improved long term fluency?

There have been several effectiveness studies done on the Lidcome program with variable degrees of dependability and reliability. However, one of the more interesting studies should be considered. The study, which was randomized and controlled, was built on a considerable number of children that stuttered between the ages of 3 to 6 years (Randomexed Control Trials). The study consisted of two groups where one of the groups received intervention through the Lidcombe program. The groups were thereafter compared and the results showed a significant difference (Jones et al, 2005)

We are of the opinion that it is important to examine as well as initiate treatment at an early age. We hope that our thoughts and hypotheses can advance professional reflection and discussion both within the fields of speech pathology and medicine. We believe that a closer interdisciplinary collaboration and more research can contribute to an increased understanding of stuttering. Our aim is to give a more evidence based , academic anchored treatment. Our fundamental goal is to provide patients that stutter the best and most effective therapy.

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