Models of stuttering Why develop a model of stuttering?Presentation Transcript
Models of stuttering
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?
What is a model of stuttering?
In trying to explain stuttering, we must try to account for:
What initially causes stuttering
“ triggers” vs. causes?
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
A historical perspective
Stuttering is one of the oldest recorded communication disorders
Theories can be divided into those that view stuttering as:
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.
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 don’t, 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).
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 1960’s and 1970’s.
By far, the most common modern physiological models focus on cortical representation of, and control of, speech and language functions.
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?
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
SUPPORTING DATA : 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.
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 the amount of overflow from the right to left hemispheres.
Figure 1C illustrates Webster’s 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 activity in 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).
Other cerebral lateralization models:
Geschwind-Galaburda model (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.
Data for dominance models
Wada test (inconclusive)
Dichotic listening and CAP batteries (variable)
Neuroimaging (more promising)
Structural (e.g., CT, MRI)
Functional (e.g., fMRI, EEG, EPs)
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 of Foundas ’ 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; Ingham, Fox & Ingham, 1994)
PET (Wu, et al., 1995; Braun, et al., 1997; DeNil, et al., 2000; Fox et al, 1996 – differences found; Ingham, et al., 1996 – no support for cerebral asymmetries)
(See Fox et al. data here)
Some studies suggest that observed differences in cortical function between PWS and NS may diminish following intensive fluency therapy (DeNil, et al., 2000).
Example: Braun, et al., 1997 Fig. 2 Brain map illustrating focal rCBF activation during the formulation and expression of language in controls ( a – d ) and stuttering subjects ( e – h ) during tasks in which stuttering subjects were dysfluent. Language tasks are contrasted with the oral motor task as a baseline, in order to highlight regions involved in linguistic processing. Data for control subjects are displayed in the top row ( a – d ), and for stuttering subjects in the bottom row ( e – h ).
Effects of fluency therapy on brain activity during single word reading Controls Pre Post 1 year Source: L. De Nil, Univ. Toronto L R
Neuroimaging data support but do not constitute a model of what deficits underlie stuttering
For a terrific review of the problems in interpreting recent neuroimaging studies, see the recent presentation by Luc De Nil (be patient, it has wonderful graphics and can take a while to load).
Neuropsycholinguistic models are more abstract and provide a more schematic view of the underlying deficit in stuttering; they tend to be grounded in psycholinguistic models of the normal speech/language production process.
Among the more popular are the Covert Repair Hypothesis (Postma & Kolk) and the Neuropsycholinguistic Model (Perkins, Kent & Curlee).
Levelt’s model of speech production and comprehension
Covert Repair Hypothesis
Note that Levelt’s model of speech production contains a pre-articulatory monitoring stage,
for which there is considerable evidence.
The CRH states that people who stutter have a temporal impairment in phonological encoding (it is slowed). When the phonetic plan cannot proceed normally, this impairment is adapted to by covert repairs, restarts and postponements, which result in the surface or overt behavior of stuttering. Thus stuttering is seen as a by-product or side-effect of self-repairs.
Evidence to support the model is building, but is primarily being gathered by the model’s builders.
It is also unclear at which stage phonological encoding or monitoring is disturbed.
Covert Repair Hypothesis
Spreading activation and phonological error
Connectionist models (e.g., Dell, 1988), which describe speech production and comprehension in terms of activation of representations and their spread (spreading activation) may account for mis-selections or poorly timed phonetic plans.
Spreading activation: the general concept and an illustration
A potential model of delayed phonological encoding from Yaruss & Conture, 1996 ).
Components of the NPL model:
This is basically a temporal dis-synchrony model
Disfluencies occur due to a disruption in timing among various linguistic formulation and motoric execution demands
Stuttering is perceived as a loss of control; the speaker cannot proceed but does not know why; internally imposed time pressure pushes the incomplete phonetic plan forward.
For an excellent review of the Covert Repair and NPL models and their implications, visit Scott Yaruss's supercourse on this topic .
SUPPORTING DATA : most linguistic and motor differences noted between PWS and fluent speakers, including imaging and ERP studies (e.g., Weber-Fox, 2001); linguistic regularities in stutter events.
CONFLICTING DATA : the theory places stuttering on a continuum with normal disfluencies, and thus stutter events should conform to patterns of normal disfluency, which they do not in advanced stuttering (Silverman & Bernstein Ratner, 1997).
MISSING DATA : weak evidence for subjective time pressure and loss of control (although some data do exist: Ezrati-Vinecour & Levin, 2001; Barasch, et al., 2000).
Some concepts have been lifted into the Demands and Capacities Model (later), but are based on cybernetic theory.
Summary: There is a deficit in the persons ability to make and use Inverse internal models of the speech production system. the child has a sensory-motor model for speech (it inverts sensory targets into motor commands) Children plan an utterance based on what it should sound like. They generate the motor commands. The motor commands are sent to the muscles which are stored in the brain as models. The actual speech is compared to the model expected. The child has a weakness in making transformations between what they want to say and the motor movements required to say them: the sensory to motor and motor sensory transformation. If the demands are not great, stuttering doesn’t occur because the child can compensate for the weakness.
Stuttering as a timing disorder
Van Riper (1982) favored the view that stuttering represented mis-coordination of the timing gestures needed for speech. Elaborated on by Kent (1984), who also relates earlier theories of cerebral organization to this theory: the left hemisphere is specialized for processing of brief, rapidly changing acoustic/motoric events, and may be impaired in carrying out this function in PWS. Finally, Kent notes the possible interference with effective function by overactivity in the right hemisphere stemming from emotional arousal.
SUPPORTING DATA : Evidence of poorly coordinated gestures during speech production in PWS (e.g., Caruso, Abbs & Gracco, 1988); acoustic measures showing abnormalities in speech timing for VOT and other parameters of speech (e.g., Zimmerman, 1980 and many others). Slowed RT data are plentiful for PWS for a variety of targeted behaviors, both motoric and linguistic (Bosshardt & Frandsen, 1996).
CONFLICTING DATA : Few, although mistimed segments are not well-coordinated with stutter events (see Smith, 1998); variety of stuttered types not well accounted for (by any theory).
MISSING DATA : more data needed from very young children, to show that timing problems are not result of stuttering, or ancillary to stuttering.
Stuttering as an auditory feedback disorder
Stromsta (1965) suggested that stutterers have an built-in “DAF”-like defect in their auditory feedback systems; Tomatis (1963) believed that stutterers suffered from a hearing loss in the dominant ear used to monitor speech. While changes in feedback (DAF, FAF) does produce increased fluency for many persons who stutter, neither theory is highly regarded at this time.
Stuttering as learned behavior
Many of the models in this category can be termed “anticipatory struggle” hypotheses.
Some of the earliest models developed in this century by the first professional speech-language pathologists fit under this rubric.
The “Iowa” school of research
Diagnosogenic theory (Johnson, 1959)
A popular reduction of this theory into few words is that stuttering is in the “ear of the parent”
Parents react poorly to normal disfluencies in children; this reaction is perceived and responded to with anxiety and avoidance by the children, setting up a cycle of fluency failure, anxiety, and more fluency failure.
What types of evidence would be required to validate this theory?
Still a popular theory with broad implications for advisement to parents, even though most of its principal tenets have been disproven.
Diagnosogenic theory (continued)
SUPPORTING DATA : Early studies showing high levels of demand in parents of CWS; high sensitivity to normal disfluencies as pathological.
CONFLICTING DATA : Almost all studies done in recent years. In general, there are few differences between parents of CWS and their fluent peers (see Bernstein Ratner & Silverman, 2000); it is virtually impossible to tell, when attitudes differ, which came first: the attitude or the stuttering?
Finally, effectiveness of some operant, parent-administered programs, such as Lidcombe, are in direct conflict with predictions flowing from the diagnosogenic theory.
Ethics and stuttering research: the “Monster Study”
What was the “Monster Study”?
Read more about the “Monster Study”
What are the ethical obligations of researchers in communication disorders?
What data are required to support a model of stuttering?
Conflict occurs when a person experiences demands or desires that are incompatible with each other. In approach-approach conflict we are attracted to two equally desirable goals. In avoidance-avoidance conflict we must choose between two equally undesirable demands. In approach-avoidance conflict we have one goal that has positive and negative aspects. And in double approach-avoidance conflict we experience two or more goals, both of which have positive and negative aspects.
How would this apply to speaking and stuttering?
Read Joe Sheehan's "Message to a stutterer "
Approach-Avoidance (Sheehan, 1953, 1958) in more detail
Stuttering results from the conflict between the opposed drives to speak and to avoid speaking. When the desire to speak is stronger than the desire not to speak, speakers can be fluent. When the desires to speak and not to speak are equal, stuttering results. Speech avoidance might result from: 1) reactions to specific words, stemming from conditioned responses to phonetic factors, 2) reactions to threatening speaking situations, 3) guilt or anxiety about message content, 3) anxiety about relationship between the speaker and listener, and 5) the need of the ego to avoid competitive situations that might result in failure. This theory is a hybrid of learning theory and personality factors as primary components in stuttering development.
Approach-avoidance conflict may have its roots in generalized emotions about speaking, but quickly develops strong ties to feelings about fluency and stuttering itself.
The approach-avoidance gradient
The Iceberg of Stuttering
More recent views of learning and stuttering
In the 1960’s more formal accounts of how stuttering could be described in terms of classical (instrumental) and operant (respondant) conditioning were advanced.
In classical conditioning, the child learns to associate speaking with an emotional response
In operant conditioning, fluency failures are shaped by the responses they elicit.
This account explains development better than onset
Example of such a model: Brutten & Shoemaker (1967) two-factor model:
Stuttering is the involuntary disruption of speech resulting from negative emotional responses that are classically conditioned, while secondary behaviors are instrumentally conditioned
Learning theory (continued)
SUPPORTING DATA :
Interventions in which the techniques of operant conditioning are effective suggest some support for learning theory in stuttering (e.g., punishment, negative reinforcement, time-out, positive reinforcement of fluency, etc.) Ingham notes that no intervention has managed to increase stuttering by rewarding it, an imbalance for a full-fledged model of stuttering as a conditioned behavior.
CONFLICTING DATA : generally low level of success of such interventions with adults who stutter; genetic factors, motor factors, linguistic factors that unite many PWS.
MISSING DATA : Plots of events that might have conditioned onsets; mechanisms by which operant techniques appear to achieve results (Bonelli, Dixon, Ratner & Onslow, 1998).
Related model: Bloodstein: the continuity hypothesis
Stuttering evolves from normal disfluency, and the child’s responses that lead to tension and fragmentation.
These responses are self-generated and are not caused by parental reactions.
Multi-factorial models attempt to integrate physiology, learning and the environment in the etiology and development of stuttering
Because they involve multiple factors, they are hard to test and validate, although some are more empirically testable than others (e.g., Smith’s Multifactorial-Dynamic model vs. Demands and Capacities).
Demands and Capacities (DCM)
Model popularized by Starkweather, Gottwald & Halfond, 1990.
Based on earlier proposals by Andrews & Neilson (1981)
Genetically conditioned weaknesses in systems that support fluency (language, motor, emotional, cognitive, etc.) interact with environmental factors (external and internal demands) to precipitate and maintain fluency failure
Consistent with recent advances in the genotype/phenotype, nature/nurture controversy
The model has intuitive appeal to many clinicians, but has been criticized as circular and untestable (see recent issue of JFD (2000) devoted entirely to this debate).
However, there is clear evidence of a series of “trading relationships” among language, motor coordination and fluency (Smith & colleagues; Ratner & colleagues) that provide some level of support for the model.
These will be explored more fully in a later lecture.
SUPPORTING DATA : Stuttering arises during the most dynamic period of speech, language and fluency development, a time in which trade-offs are readily noted in children’s speech (Crystal, 1987, Ratner, 1997). Some environmental modifications to reduce parental speech rate and demand on children appear to facilitate fluency (but complicated by normal patterns of remission to be expected in 80% of CWS).
CONFLICTING DATA : No evidence that parents of CWS are more demanding than other parents (Bernstein Ratner & Silverman, 2000; Miles & Bernstein Ratner, 2001)
MISSING DATA : The notion that individual children may have capacity limitations that can be stressed by normal levels of demand essentially make the model untestable. Ingham & Cordes (1997) rightfully critique the current model as circular. Data to suggest that given parental behaviors affect fluency patterns in a systematic fashion might address this problem.
The symptoms of stuttering are like smoke coming out of a volcano; they tell us little about the underlying processes that produce the phenomenon.
Stuttering evolves from essentially normal systems that interact poorly;
Neural pathways are dynamic and self-learning; abnormal patterns can self-perpetuate and become stabile.
Problems integrating systems are apparent in PWS; linguistic and cognitive demands impair their motor functioning more obviously than in PWDNS.
Similar to DeNil and colleagues’ Neurophysiological Model, in which learning of new skills is seen to change physiological markers of speech/language processing
Stuttering as an emotional or psychological problem
Still a popular lay account, especially in other cultures
Stuttering is still classified as a neurosis in the DSM-IV ( Diagnostic and Statistical Manual of the APA)
Ex: repressed need hypothesis: stuttering is the result of a repressed neurotic conflict
No evidence to support the theory (e.g., Yairi, 1997); no evidence to suggest that psychotherapy is effective in managing or curing stuttering (Andrews, et al., 1983).
Distinguishing cause from effect in psychological involvement in stuttering
What data would be required to support such models? What data exist to weaken them?
Stuttering as manifestation of repressed need: oral gratification (Coriat (1931)
Repressed desires to remain silent (Fenichel, 1945), or withhold unspeakable thoughts (Barbara, 1954)
Response to childhood stress and trauma (e.g., Wyatt, 1958)
SUPPORTING DATA : Early studies showing levels of personality disorder and maladjustment in PWS.
CONFLICTING DATA : Most, if not all, recent research. Genetics, motor data, linguistic data. Lack of effectiveness of psychotherapy in treating stuttering symptoms. Obvious difficulty in determining the directionality of any differences between personality attributes of people who stutter and comparison groups.
MISSING DATA : Genetic contributions of some personality traits.
FOR BEST DISCUSSIONS, SEE BLOODSTEIN’S HANDBOOK, 1995.
Freud’s iceberg (compare to Sheehan’s)
Why teach about theories and models?
How relevant are they to treatment?
Can good treatment occur in the absence of a good model or theory?
What will you say when a client or parent asks (or tells you) what causes stuttering?
It might be on the ASHA exam!
Evaluating research in stuttering
Using the internet to do research
Try the tutorial: http://www.nlm.nih.gov/bsd/pubmed_tutorial/m1001.html
Consider your terms carefully!
Other good resources: EBSCO
Department research on stuttering
Work in the department can be used to support neurospycholinguistic and multifactorial models of stuttering. Read some recent work, including our published articles, at
Do you have a research question you’d like to ask? Come by, and let’s talk!