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Models of stuttering


Figure 1C illustrates Webster's Two-Factor Interference Model. Three elements comprise this model: i) we still assume normal left hemisphere ... – PowerPoint PPT presentation

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Title: Models of stuttering

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
  • 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
  • Physiological
  • Psychological
  • Environmental
  • Multifactorial

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

  • Refinement of genetic studies show a clear
    evidence of genetic contribution to many cases of
  • 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

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,
  • 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
  • Reaction time
  • Coordination
  • Time and visuospatial estimation
  • Laterality and cortical organization for language
  • Task interference (capacity limitations)
  • Most find some, but minor and inconsistent
    differences (see book).

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.

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

Lateralizationmodels (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
Orton-Travis (continued)
  • 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
  • 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
  • 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 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
  • 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.

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
  • 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

Data for dominance models
  • Handedness (inconclusive)
  • 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,
  • 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 (ad) and stuttering
subjects (eh) 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 (ad), and
for stuttering subjects in the bottom row (eh).
Effects of fluency therapy on brain activity
during single word reading
1 year
Source L. De Nil, Univ. Toronto
Neuropsycholinguistic models
  • 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
  • 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

Levelts model of speech production and
Covert Repair Hypothesis
  • Note that Levelts 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 models builders.
  • It is also unclear at which stage phonological
    encoding or monitoring is disturbed.

Covert Repair Hypothesis
Self-monitoring loops
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
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.

NPL (continued)
  • 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).

Other Higher Order deficit modelsInverse
Modeling Deficit Neilson Neilson
  • 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 doesnt 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
  • 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
  • What was the Monster Study?
  • Read more about the Monster Study
  • Discussion
  • What are the ethical obligations of researchers
    in communication disorders?
  • What data are required to support a model of

  • General principles
  • 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
  • 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 1960s 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
  • 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

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Learning theory (continued)
  • 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 modelBloodstein the continuity
  • Stuttering evolves from normal disfluency, and
    the childs responses that lead to tension and
  • These responses are self-generated and are not
    caused by parental reactions.

Multi-factorial models
  • 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., Smiths
    Multifactorial-Dynamic model vs. Demands and

Demands and Capacities (DCM)
  • Model popularized by Starkweather, Gottwald
    Halfond, 1990.
  • Based on earlier proposals by Andrews Neilson
  • 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

DCM (continued)
  • 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 childrens 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.

Multifactorial-Dynamic Model
  • 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
  • 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
  • Still a popular lay account, especially in other
  • 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
  • Psycho-sexual (Glauber, Freud) or
  • Inadequate interpersonal relationships (Barbara,
  • Most thoroughly summarized by Travis (1957)
  • 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?

Specific theories
  • Stuttering as manifestation of repressed need
    oral gratification (Coriat (1931)
  • Repressed desires to remain silent (Fenichel,
    1945), or withhold unspeakable thoughts (Barbara,
  • 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.

Freuds iceberg (compare to Sheehans)
Why teach about theories and models?
  • Discussion
  • 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
  • PubMed searches
  • http//
  • Try the tutorial http//
  • Consider your terms carefully!
  • Other good resources EBSCO

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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
  • http//
  • Do you have a research question youd like to
    ask? Come by, and lets talk!