2. Why develop a model of stuttering?
- What does a model of stuttering give us
- In terms of guiding treatment?
- In terms of guiding research?
- For one other good reason to study models of stuttering, stay awake til the end of this presentation!
- What must a good model of stuttering account for?
3. What is a model of stuttering?
- In trying to explain stuttering, we must try to account for:
- What initially causes stuttering
- What the basis for fluency breakdown is
- How stuttering develops over the lifespan (how it is maintained and perpetuated)
- Some models are not mutually exclusive
- (e.g., genetics and learning)
- Etiology model, but can help build one
- A good model must explain:
- The phenomenology of stuttering
- When and how stuttering develops
- How fluency breakdown fits within known facts about speech production
4. A historical perspective
- Stuttering is one of the oldest recorded communication disorders
- Theories can be divided into those that view stuttering as:
5. The nature vs. nurture controversy
- Models of stuttering tend to divide in their emphasis on whether stuttering is primarily due to physiological bases, environmental influences, or a mixture of both.
- Virtually no models ignore some component of learning in the DEVLOPMENT of the disorder
- Before discussing models, we will examine studies that have contrasted PWS and normally fluent speakers on physiological and environmental features.
- Refinement of genetic studies show a clear evidence of genetic contribution to many cases of stuttering;
- such studies weaken environmental accounts when affected family members cannot serve as models, or demonstrate patterns of stuttering that differ from that of the affected child.
- Conversely, discordant twins show some impact of non-genetic factors on the emergence of stuttering.
7. Genetic factors in stuttering .
- At this point, few disagree that stuttering has a genetic component. This component appears to predict chronicity and recovery better than it predicts severity, and the model of the genetic transmission is still under discussion. Cases in which monozygotes differ in stutter symptoms are problematic, although such situations are found in other disorders having clear genetic roots. Cases in which adopted children who stutter show family histories of stuttering in the adopting family suggest an environmental contribution to stuttering to some researchers (Bloodstein, 1995).
- MISSING DATA : Although genetic factors can remove weight from some hypotheses about the nature of stuttering, they do not explain the mechanism by which stuttering physically arises or is best treated. Moreover, because stuttering is at least partially predicted by genetic background, studies of parents of CWS should, but usually dont,segregate reports of adult parenting styles by fluency status of parent.
- Most studies of physiological function in stuttering divide into the following topic areas:
- Time and visuospatial estimation
- Laterality and cortical organization for language
- Task interference (capacity limitations)
- Most find some, but minor and inconsistent differences (see book).
9. Physiological models
- Perhaps the first models of all models (excluding religious explanations): Older models tended to localize stuttering to weaknesses in specific peripheral systems, particularly the tongue, from Greco-Roman times through the last century
- Other parts of the vocal tract, e.g., the larynx, were investigated during the 1960s and 1970s.
- By far, the most common modern physiological models focus on cortical representation of, and control of, speech and language functions.
10. Challenges to studies of physiological limitations in stuttering
- Do such limitations exist at stuttering onset or do they result from adaptation to stuttering?
- Could transient limitations early in development yield persistent symptoms?
- Do observed patterns predict the behavioral symptoms of stuttering?
- Are aberrant physiological patterns amenable to treatment?
11. Lateralization models ( Webster, 1996 )
- Orton-Travis: In normal speech/language production, a dominant hemisphere takes primary responsibility for linguistic functions. In stuttering, dominance fails to occur, causing competing commands to speech/language functions.
From W. Webster 12. Orton-Travis (continued)
- SUPPORTINGDATA : Differences between lateralization of language functions in PWS and fluent speakers, as revealed through numerous tasks: EEG (e.g., Moore & Haynes, 1980), dichotic listening (e.g., Gregory & Curry, 1967), PET, fMRI (current work by teams such as DeNil & Kroll (1995), Fox, Ingham & Ingham (1996), Braun, et al. (1996), more each month.
- CONFLICTING DATA : No evidence of changed handedness history in majority of PWS. No evidence that reverting handedness effects fluency.
- MISSING DATA : Whether lateralization differences are primary or the result of experience with stuttering; lateralization theories are particularly vulnerable to this challenge, as therapy (particularly those that deal with speech planning and pacing) and emotional reactions are logically presumed to elicit changes in right hemisphere function.
13. Other hemispheric organization models(from Webster):
- As illustrated in Figure 1B, the interhemispheric interference model has three major features to it: i) normal left hemisphere lateralization; ii) normal right hemisphere functioning; but iii) interference with the left hemisphere coming from the right hemisphere through a "slop-over" of activity (the large arrow). Within this model, variations in stuttering severity would reflect variations in theamount of overflow from the right to left hemispheres.
- Figure 1C illustrates Websters Two-Factor Interference Model. Three elements comprise this model: i) we still assume normal left hemisphere specialization for speech and motor sequencing; ii) we see a left hemisphere system for speech and motor sequencing that is inefficient and unusually susceptible to interference (illustrated by the larger number of "pores"), not just from activityin the right hemisphere, but also the left (illustrated with arrows from both hemispheres impinging on the speech mechanisms); and iii) a lack of what we call "left hemisphere activation bias" (illustrated with equal rather than unequal sized arrows coming from the mid-and hind-brain activating system).
14. Other cerebral lateralization models:
- Geschwind-Galaburdamodel (1985): a variety of speech-language disturbances (dyslexia, stuttering, autism) may arise from delays in left hemisphere development during gestation. Such delays lead to inefficient right hemisphere dominance for language functions. Because of the loading of such disorders in males, the authors hypothesized a role of fetal exposure to high levels of testosterone.
- SUPPORTING DATA : Sex-bias in stuttering incidence; other data supporting Orton-Travis; recent anatomical data from Foundas, et al.
- CONFLICTING DATA : No obvious conflicts, but theory leaves stuttering in girls somewhat unresolved
- MISSING DATA : Mechanisms by which the different disorders arise; evidence of actual testosterone influences during development, lack of known association between stuttering and developmental conditions characterized by hormonal abnormalities.
15. Data for dominance models
- Handedness (inconclusive)
- Dichotic listening and CAP batteries (variable)
- Neuroimaging (more promising)
- Structural (e.g., CT, MRI)
- Functional (e.g., fMRI, EEG, EPs)
16. More on neuroimaging
- Previous work found few structural differences between PWS and NS; however, work in the past year by Foundas, et al. (2001) and Sommer, et al.(2002), have shown anatomical variation between the groups.
- (See a short summary ofFoundas work) ; Sommer et al. is on your reading list and linked.
- Work examining functional differences in processing has been much more promising:
- rCBF (Watson, et al., 1994