Theoretical Perspectives on the
Cause of Stuttering
Nicoline Grinager Ambrose
University of Illinois at Urbana-Champaign
F or some strange reason, we have never been able
to devise an agreeable definition of stuttering.
Demosthenes did not seem to have a problem
identifying stuttering—he knew that he did, and he knew
what could relieve it. Perhaps those seaside walks along the
crashing waves kept his head clear. And, philosophers of that
time had heavier thoughts on their minds. But, I will not
repeat here a review of the numerous commentaries of
Wingate (1964), Perkins (1990), and others on the definition
of stuttering and presence, or lack of, adequate theoretic
underpinnings. I will leave the philosophizing to the ancient
Greeks and others. Instead of trying to determine who is
right and who is wrong, I will try to connect the disparate
points of view about what type of disorder stuttering is.
Anyway, Demosthenes enjoyed his fluent walks along the
beach and enjoyed experimenting with talking with pebbles
in his mouth. He went home, and who should be there but
ABSTRACT: The many theories of the cause of stuttering
are too numerous to mention. Instead, this article
presents a brief background of theories in the realms of
psychology, learning theory, and biology. A representative
sampling of older literature is discussed, followed by a
more detailed consideration of a few state-of-the-art
studies. The article concludes that previously presented
general models can provide a basis for testable hypoth-
eses. Current research appears to indicate that there is a
genetic basis for stuttering, affecting both motor and
sensory systems in the brain in subtle ways, and that
deficits are exacerbated by a host of both other genetic
as well as environmental factors. Genetic, physiologic,
psychologic, and environmental influences guide the
developmental pathway of stuttering.
KEY WORDS: stuttering, etiology, theory, speech disorder,
childhood stuttering
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Freud, who immediately interpreted the ocean as his
mother’s womb and the pebbles as an oral fixation. Soon
after, Skinner came knocking at the door. He laughed at
Freud. How ridiculous. It is obvious, he said, that our
friend Demosthenes here has practiced fluency with the
noise of the waves in his ears, and now the stimulus of the
waves evokes a learned response and voila, fluent speech.
But Demosthenes was skeptical, thinking that he had
merely been walking and talking, nothing more. He
grabbed his sandals and strode into town. Later that
evening, at his Philosophy of Stuttering Support Group
meeting, he repeated the events of the day to his fellow
group members Moses and Darwin, and as the reader can
imagine, the issue of the cause of stuttering was far from
being resolved. Let’s leave them and return to reality.
Which one of the above gentlemen was correct in his
views? That is not an easy question to answer. It is not the
case that one must be right and the others wrong—any
number of them could be onto the truth, just different
aspects of it. How much we know about something drives
our thinking about its causes. Before Van Leeuwenhoek
discovered bacteria, or “animalcules,” in 1677, people had
other ideas about the causes of illness. Before the design of
DNA was discovered, understanding of the biologic
transmission of traits was limited.
Humans have always wondered about their world, but it
is more than simple curiosity. Our development and
survival as a species has in large part been due to our
unique capabilities for mental reflection. This fundamental
drive to explain, understand, predict, and control our
universe as we know it is strong. Long ago, natural
phenomena were explained as the work of deities. Greek
and Roman, African, Chinese, Native American, Egyptian,
and Scandinavian people—all had belief systems that
explained how the world worked. We think of these ideas
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as interesting and powerful, but many of them certainly not
“true” and certainly not “scientific” to our modern way of
thinking. But, given the observations that were available at
the time, these theories made sense. Theoretical invention
tries to suit the data. Perhaps in a millennium or two, what
we now believe to be “real truth” will seem ridiculous,
naïve, outdated, or wrong.
People use whatever resources they have to explain
occurrences of an almost infinite number of phenomena. It
has even been said that perhaps many beliefs come from the
left brain trying to explain what the right brain is experienc-
ing. And after all, truth is relative. Think of patients with
various brain malfunctions. Sometimes people with aphasia
have very interesting ideas about why they have difficulty
with language. Children have interesting explanations for
their behavior. The combination of natural curiosity and the
need to explain is perhaps at the root of science.
It follows that the history of ideas about the cause and
development of stuttering has undergone many develop-
ments as our knowledge base and technology have im-
proved. It is also important to remember that science goes
in circles. In other words, history repeats itself. Theories of
stuttering have gone from biologic to psychologic to
behaviorist and back to biologic to all three combined.
Regardless, several unusual phenomena must be incorpo-
rated into, or must not contradict, any theory of the cause
of stuttering; namely, those that ameliorate stuttering.
Stuttering diminishes, or even disappears, under a host of
conditions—singing, speaking in unison/choral reading,
talking with a metronome, talking with noise or delayed
auditory feedback, and talking to pets or babies (quite
similar, really, in that neither have read treatises on
stuttering and do not realize that their caretakers talk
differently than others). Conversely, stuttering tends to
worsen under various types of pressure (e.g., time) and
more complex linguistic demands. These facts need to be
taken into account when we attempt to answer the follow-
ing questions: What are we trying to explain? Where, in
the fluency-generating system, does the breakdown occur?
Do breakdowns occur at multiple sites? Is it components or
connections that are aberrant?
ASPECTS OF CAUSATION
From early on, professionals in speech-language pathology
had very different views on the cause of stuttering.
Stuttering has, at various points in time, been considered to
be caused by deep-seated neuroses arising in infancy,
purely by learning, and from a strictly structural flaw.
There is general agreement today, however, that the
ultimate origin of stuttering is in large part biologic, shaped
by additional biologic, psychologic, and behavioral influ-
ences. We begin the review of the various aspects of
causation of stuttering with a brief presentation of psycho-
logic and learning perspectives so as to provide a full view
of how far the field has come in its pursuit of truth in the
name of science. This is followed by a more in-depth
presentation of possible causative biologic factors. We shall
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not attempt to review all of the relevant literature; rather,
major trends are highlighted and supported by a few
samples of relevant studies.
Psychologic Causes
The writings of Sigmund Freud were in ascendance in the
early decades of the 1900s. In the 1920s and 1930s, one
line of thinking regarding the origins of stuttering focused
on personality conflict of the individual, referencing
Freud’s theory of psychoanalysis. Basically, this approach
viewed stuttering as merely an overt symptom of something
else—unconscious, deep-seated neurotic disorder(s). Authors
purporting this point of view, however, differed in what they
understood to be the specific nature of the conflict. Whereas
Coriat (1928) asserted that the problem is characteristic of
libido fixation at the oral stage of infant psychosexual
development, Fenichel (1945) maintained that the conflict
originally occurred during the anal stage, lending it more
aggressive characteristics. Blanton (1931) wrote that children
who began to stutter experienced fixation of the libido,
thereby making the child overly sensitive and anxious. He
agreed, however, that there were physiologic factors in
addition to psychologic ones, such as being left-handed or
having weak muscles in the tongue and throat area. Brill
(1923) discussed stuttering as a psychoneurosis, although
he also referred to physiologic factors as “hereditary
burden” (p. 135). These authors stressed family environ-
ment as shaping stuttering. Although Brill claimed consider-
able treatment success using classical Freudian psycho-
analysis as the main vehicle of therapy, he conceded that a
large number of his former patients eventually relapsed.
The psychoanalytic point of view continued to be active,
however, and in 1957, Travis wrote about “the unspeakable
feelings of people” who stutter. This was a complete
change from his earlier views on cerebral laterality. Travis
described stuttering as a vehicle that acts to inhibit
unconscious needs, or unacceptable statements of true inner
thoughts and feelings. The child wants to communicate,
but, being afraid of revealing unspeakable thoughts and
feelings, he emits stuttered speech that conceals them. Any
discomfort caused by the stuttering was, allegedly, more
than overcome by the relief of hiding unmentionables.
Glauber (1958) also saw stuttering as a neurotic disorder, a
personality disturbance reflected in speech. Even the
preponderance of stuttering in males was explained in
psychologic terms in that boys faced more pressure to live
up to standards of aggression and had a greater ability to
provide and take action. Females, so it was said, had only
to be passive creatures (Schuell, 1946).
From the 1920s through the 1980s, a large number of
personality studies of stutterers were undertaken. The
findings were mixed, but overall, it became clear that
people who stutter (PWS) are not any more neurotic than
average (see reviews by Bloodstein, 1995; Goodstein, 1958;
Sheehan, 1958). The only areas identified as problematic
involved communication situations, difficulties that can be
explained as resulting from the stuttering rather than being
a cause of it. Although today it appears perhaps illogical to
consider stuttering part of a neurosis, amenable to
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psychoanalytic treatment, interest in personality, especially
anxiety, has been renewed, as seen in a number of recent
studies. Craig, Hancock, Tran, and Craig (2003) investi-
gated trait anxiety in a large sample of adults who stutter.
Trait anxiety is a stable attribute, as opposed to state
anxiety, which occurs in certain circumstances. The persons
who stutter did present higher trait anxiety levels, but the
anxiety appeared to have developed as a result of the
stuttering and so would not be considered a causal factor.
The issue is not that simple, however. As in the next study
described below, it is likely that some individuals have a
predisposition to develop trait anxiety, and it is not known
how this tendency might interact with other factors that
contribute to a predisposition to stutter.
Recently, there has been another shift of interest in
psychosocial aspects of stuttering, with a focus on tempera-
ment. Anderson, Pellowski, Conture, and Kelly (2003)
investigated temperament factors in young children who
stutter through a norm-referenced parent questionnaire. The
temperament scale used contains nine subscales: activity,
adaptability, approach or withdrawal, quality of mood,
intensity of reaction, distractibility, attention span, sensory
threshold, and rhythmicity of physiologic functions. Com-
pared to the normally fluent children, the stuttering children
were less adaptable to novel situations, less distractible, and
less regular in daily physiologic functions. The differences
were statistically significantly different, but the mean scale
scores for both groups on all nine scales were within normal
limits. More children in the stuttering group had individual
scores that exceeded 1 SD. The study also reported that there
was no direct relationship between the time since onset of
stuttering and scale scores, which indicates that the tempera-
ment qualities measured may be relatively stable. The point
of interest to the discussion here, however, lies in a chicken
and egg question: Do the differing temperament dimensions
precipitate or exacerbate stuttering, or does the stuttering
reinforce the temperamental proclivities of the child? The
authors concluded that “temperamental characteristics…could
potentially contribute, in some as yet unknown fashion, to
the onset and development of stuttering” (Anderson et al.,
2003, p. 1230). Although their stipulations have not yet been
substantiated, the fact that there are differences means that
we cannot yet rule out that possibility.
We have come a long way from thinking that neuroticism
causes stuttering, but this does not mean that psychosocial
factors must be relegated only to the shaping of stuttering
independent of causative factors. As the genetic and
environmental bases of personality reveal themselves, it
may become obligatory to add them to the complex
equation for the etiology of stuttering. Psychologic causes
of a disorder are no longer necessarily distinct from
organic causes. Overall, the renewed interest in this aspect
is a welcome development. It would seem to be particularly
profitable to study the interaction of personality/tempera-
ment with other factors.
Behaviorism and Learning Theory
The idea that stuttering is a learned behavior or a “bad
habit” is quite old. Bloodstein (1995) provided an excellent
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overview of theories of stuttering that covers behaviorism
and learning. Any discussion of behaviorism and learning
theory in relation to stuttering must mention Wendell
Johnson’s diagnosogenic theory (Johnson et al., 1959),
stating that stuttering begins in the ears of the parents when
they overreact to their child’s normal disfluencies. The child
attempts to avoid the disfluencies and, in the struggle,
stuttering develops. Along similar lines, Wischner (1950)
portrayed stuttering as emerging in accordance with a more
formal learning theory. Stuttering originates from a painful,
anxiety-producing stimulation in the form of parental
disapproval of normal disfluency. In other words, the child
anticipates negative, painful reactions to his or her stuttering
and so tries to avoid them. Initial successful avoidance
reduces the anxiety drive and thus reinforces the behavior
that eventually becomes more complicated stuttering.
Another concept is that stuttering results from an
approach–avoidance drive (Sheehan, 1953). In this concept,
the desire to communicate collides with the drive to avoid
speech anxiety, which may have roots in either or both
personality and conditioning from prior negative experi-
ences with stuttering. Bloodstein’s (1958) notion that
stuttering is an anticipatory struggle arising from the belief
that speech is difficult contains some similar elements.
Stuttering is seen as a reflection of tension and fragmenta-
tion in speech when the complexity of the act causes
concern and feelings of being overwhelmed.
Still another view explains stuttering as a behavior that
is acquired through operant conditioning, that is, a behavior
that is shaped by its own consequences. In a pioneer,
controlled experiment, Flanagan, Goldiamond, and Azrin
(1958) demonstrated that stuttering was reduced when
stuttered events were immediately followed by punishment
(loud noise); it was increased when stuttered events were
immediately followed by the removal of punishment
(continuous tone). Later, Shames and Sherrick (1963)
theorized that stuttering was shaped out of normal dis-
fluency as operant behavior, subject to a combination of
punishment, positive reinforcement, and negative reinforce-
ment. Normal repetitions are reinforced when a parent
eventually heeds the child’s request. But as repetitions
become aversive, the parent indicates displeasure at
disfluency (in terms of operant behavior, punishment).
When the consequences of disfluency are negative reac-
tions, the child may change disfluencies into struggle
behavior or silence in order to avoid the aversive conse-
quences (negative reinforcement for the parent). Thus,
stuttering emerges and is maintained by complex interaction
of positive and negative reinforcement. Brutten and
Shoemaker (1967) developed a two-factor theory of
stuttering. They believe that stuttering is initially estab-
lished through classical conditioning of emotional learning,
when anxiety causes disruptions in speech. Through
generalization, many stimuli acquire the capability of
triggering anxiety that results in fluency breakdowns—
stuttering. Secondary characteristics of stuttering designed
to cope with the disfluencies are then developed through
operant conditioning.
In general, these ideas have been discarded as ultimate or
sufficient causes of stuttering. Instead, they are now viewed
DISORDERS • Volume 31 • 80–91 • Spring 2004
as forces in its development (see Wingate, 1997, for a
thorough discussion of the matter). The idea that stuttering
develops out of normal disfluencies along a continuum
remains prevalent, although not supported by data, as
repeatedly pointed out in the Illinois studies by Yairi,
Ambrose, and colleagues (e.g., Ambrose & Yairi, 1999;
Yairi & Ambrose, 1999). Nevertheless, stuttering therapies
reflecting various learning models have been shown to be
rather promising (Onslow, Packman, & Harrison, 2001;
Ryan, 2001).
Biologic Causes
Bloodstein (1995) wrote that Aristotle believed that
stuttering stemmed from a problem with the tongue, and in
the 1840s, tongue reduction surgery was performed to
alleviate stuttering. The better known early biologic
theories of stuttering, however, come from the 1920s and
1930s. The first three years of the Journal of Speech
Disorders, 1936–1938, contained no fewer than nine
articles devoted to physiologic aspects of stuttering. Topics
included conditioned reflexes (Moore, 1938), twinning
(Berry, 1938), and heart rates (Palmer & Gillette, 1938;
Travis, Tuttle, & Cowan, 1936). There are a plethora of
publications regarding anatomic and physiologic bases of
stuttering; only a representative few will be touched on
here as a reflection of past and current work. They are
grouped loosely into four sections: sensory, central process-
ing, motor, and genetics. For each section, a brief back-
ground will be presented, and a few current studies will be
discussed in more detail to indicate the general direction of
cutting-edge research.
The sensory side of the picture. The role of auditory
function has long been discussed in the field of stuttering.
Stuttering tends to be reduced in noisy environments (as
Demosthenes knew), and it may be reduced or even
eliminated with delayed auditory feedback or white noise in
one or both ears. This effect is even more curious in that
when normally fluent speakers have delayed auditory
feedback played, their speech tends to become disrupted. In
1946, Shane (1955) demonstrated that stuttering was
reduced with high levels of binaurally applied noise. She
concluded that when PWS cannot hear themselves, speech
anxiety is reduced and so is the stuttering. A decade later,
Cherry and Sayers (1956) conducted a series of experi-
ments using both air- and bone-conducted noise of different
frequency ranges to identify which one of many possible
combinations is the most effective in ameliorating stutter-
ing. Based on their results, Cherry and Sayers theorized
that PWS have abnormal auditory feedback. They thought
that the noise works because it neutralizes the defective
auditory feedback. Therefore, they concluded, stuttering is a
perceptual problem. On the other hand, Wingate (1969)
suggested that noise reduces stuttering because it causes
motoric alterations, such as changes in vocalization. Yairi
(1976) compared monaural and binaural noise and con-
cluded that the psychologic explanation does not hold, that
the motor explanation receives some support, and that
perceptual difficulties are possible factors. Hall and Jerger
(1978) administered a number of auditory function tests to
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PWS or were normally fluent and reported subtle evidence
of a central auditory problem in stuttering at the level of
the brainstem.
Another method used to study the auditory system in
stuttering is dichotic listening, where competing stimuli are
presented to the left and right ears. Most normal right-
handers show a right ear advantage for speech stimuli.
Some studies showed that PWS had the expected right ear
advantage, but Rosenfield and Goodglass (1980) found that
more stutterers than controls failed to have the expected
advantage, and Blood and Blood (1984) reported that the
magnitude of right ear preference was greater for those who
were normally fluent. A note of caution, however, must be
heeded. Dichotic listening has been described as having low
test–retest reliability; in fact, in a second report, Blood and
Blood (1989) reanalyzed the same data using different
analysis methods and came up with varying results.
Older studies with conflicting findings have been
replaced by current work with state-of-the-art technology
yet again revealing a variety of differences, not always
consistent, in at least some groups of speakers. Probably
among the most enlightening of the newer technologies is
brain imaging. Magnetic resonance imaging (MRI) can be
used to create a detailed view of brain morphology, and
functional MRI and positron emission tomography (PET)
give an eye to function in the brain. Another promising
methodology involves magnetoencephalography (MEG).
Although imaging yields poor resolution in time, but
excellent resolution in space, MEG is not as accurate in
terms of place but gives much improved resolution in the
time dimension. A few studies with findings relating to the
auditory system are mentioned here.
In normal speakers, the left planum temporale, part of
the auditory association cortex, is larger in the left than the
right hemisphere. In some individuals who stutter, however,
this structural difference is reduced (Foundas, Bollich,
Corey, Hurley, & Heilman, 2001). Functional studies have
also found differences in auditory association cortex (in the
temporal lobe, which includes Wernicke’s area) in adults
who stutter as compared to those who are normally fluent.
Both Braun et al. (1997) and Fox, Ingham, and colleagues
(Fox et al., 1996; Ingham, Fox, Ingham, & Zamarripa,
2000) reported deactivation in this area, especially in the
right hemisphere, in stuttering speakers.
One relatively recent study of particular interest used
MEG to compare and contrast left versus right auditory
association areas of the brain (Salmelin et al., 1998).
Participants were asked to read silently, read while mouth-
ing but silent, read aloud individually, and read in chorus.
The stuttering speakers were disfluent during reading aloud
alone but fluent during choral reading. Brain activation
levels (and latencies) in the right and left hemispheres in
response to tones delivered to each ear during these tasks
were monitored. Higher activation typically occurs opposite
to the ear being stimulated, providing a contralateral
response. Both groups performed similarly in terms of
timing of activation (latency). But, the pattern of activation
of left and right auditory association areas differed between
the stuttering and the normally fluent speakers. As ex-
pected, all speakers showed higher contralateral responses
83
in general, and during the speaking tasks, there was
reduced activation. For all of the tasks, however, there was
higher activation in the stuttering speakers, with the excep-
tion of right hemisphere activation to right ear stimuli. The
second notable difference occurred in the reading aloud
condition, the only task where stuttering speakers were
disfluent. During this task, the balance of left hemisphere
activation by the left stimulus (left ipsilateral) was de-
creased, and approached the level of the control group. The
authors concluded that interhemispheric balance in the
auditory cortex appears to be unstable in PWS.
As studies have become more and more specific and
sophisticated, differences in the auditory systems of PWS
have continued to be evident. All of the studies to date
have been conducted with adults, and so it is not possible
to separate what may be effects due to having stuttered for
years from brain function as it was at the onset of stutter-
ing. In addition, it is always important to remember that
there is no evidence that stutterers form a homogeneous
group, and perhaps future studies may reduce or eliminate
some of the contradictions found in studies by identifying
subtypes of stuttering. Any theory of stuttering, then, must
take the auditory system into account.
Central processing and sensorimotor integration:
A look inside the brain.
Differential hemispheric activation. In the 1930s, Travis
(1931/1978) expounded on a theory of the involvement of
the brain in stuttering, claiming that stuttering resulted
from incomplete cerebral dominance or, more precisely,
from “general reduction in cortical lead control” (p. 276).
The brains of PWS have been under scrutiny continuously
from that time. As technology has improved, documentation
of functional differences in brain activity in normally fluent
speakers versus those who stutter has become available,
although results were often conflicting and thus inconclu-
sive. For example, some EEG studies showed abnormalities
in hemispheric processing in stutterers in that they used the
right hemisphere more than normally fluent speakers did
(Fitch & Batson, 1989; Moore & Haynes, 1980); other
studies had negative results (Pinsky & McAdam, 1980).
Age of participants and stimuli varied from study to study,
which may explain the conflicting findings. A better
explanation may be that PWS are a heterogeneous group,
and not knowing how to subgroup them leads to very
inconclusive findings.
Differences in hemispheric activation have been docu-
mented more recently with imaging techniques. Several
independent research groups have reported greater use of
the right hemisphere in speech and language in PWS as
compared to normally fluent speakers (see Ingham, 2001
for a review of findings); that is to say, language is more
bilaterally represented. Although an early study (Pool,
Devous, Freeman, Watson, & Finitzo, 1991) reported that
left blood flow in the left hemisphere was overall reduced
compared to the right, areas of greatest difference were
those of auditory association and motor planning.
Language. Another area within the purview of central
processing is the involvement of language in stuttering.
There have been investigations of phonology, syntax,
semantics, and cognitive processing. It has been noted that
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there seems to be a higher incidence of the co-occurrence
of stuttering and phonological disorders, which led to
speculations about a mechanism explaining both. Postma
and Kolk (1993) introduced the covert repair hypothesis,
which explains not just stuttering, but all types of dis-
fluencies, as self-repairs. Monitoring and error detection
can occur at the prearticulatory level. Disfluencies are seen
as by-products of covert repairs of internal speech errors, at
the level of phonological encoding. When correction is
successful, no error appears, but it may impede progress of
an utterance, thereby leading to disfluency. Normal speakers
perform covert repairs of phonological encoding. Therefore,
PWS may have a deficit in phonological encoding, leading
to more frequent phonological encoding errors, which must
frequently be repaired, which leads to stuttering. More recent
work has argued this theory (Yaruss & Conture, 1996). Other
work has been directed toward linguistic complexity. As
mean length of unit (MLU) and syntactic complexity
increase, stuttering is more frequent (Logan & Conture,
1995; Yaruss, 1999). It has also been shown that adults
who stutter may have more difficulty producing unfamiliar
vocabulary fluently (Hubbard & Prins, 1994).
Bosshardt (2002) designed a study to measure the effects
of cognitive interference on the speech of PWS. Two
groups, normally fluent and stuttering participants, were
asked to repeat sequences of three words as fast as possible
(primary task) while simultaneously reading or memorizing
two additional words presented visually (secondary task).
The additional words were either phonologically similar or
dissimilar to those of the primary task. They were then
asked to recall those words. Accuracy was measured for
recollection of the similar and dissimilar words that had
been presented visually. For repetition of the sequence of
three words, accuracy and frequency of disfluency were
measured. For the control group, the concurrent reading
task had no significant effect on the fluency of their
repetitions, but the stuttering group had significantly more
disfluencies when reading the list of similar words. In other
words, their fluency-generating system was more easily
perturbed by, or subject to interference from, the concurrent
cognitive task. The elegant design of the study provided a
way to isolate the effect of a very specific element—that of
phonological similarity. This does not rule out, however,
susceptibility to interference of a host of other cognitive,
auditory, motor, or affective processes. Some of the brain
imaging studies lend support to the hypothesis that phono-
logical planning is aberrant in PWS, or at least in a sub-
group of them. DeNil, Kroll, Kapur, and Houle (1998), and
Ingham et al. (2000) reported clear differences in activation
of the anterior insula in the frontal lobe, which is presumed
to involve phonological planning. Another study, however,
did not find such differences (Braun et al., 1997).
Sensorimotor integration. Brain activation levels can be
studied using functional imaging techniques such as PET
and functional MRI. These types of studies require a
complex design and can be difficult to interpret. Tasks must
be clearly differentiated theoretically and physiologically—a
resting state, or baseline, is needed from which to measure
activation or deactivation. It is not easy to determine
exactly what strategies are used or what functions are
DISORDERS • Volume 31 • 80–91 • Spring 2004
accessed or taxed when someone is instructed to view a
shape versus read a word silently versus read a word aloud
versus generate a synonym and so on. A newer technique
yields indirect information on function through visualization
of structure. Diffusion tensor imaging (DTI) allows
measurement of the degree of organization of white matter,
or myelin tracts, in the brain. The myelin sheaths are what
neural impulses are conducted through, and the more white
matter and higher organization, the better the signal. A
strong signal indicates a high degree of connectivity. Areas
used for comprehension, planning, and production of speech
typically show a high degree of connectivity in the left
hemisphere for normal speakers. Sommer, Koch, Paulus,
Weiller, and Buchel (2002) studied the brains of 15 adults
who stutter and 15 control speakers. They reported that the
stuttering group showed significantly less fiber coherence,
or myelin organization, in the area of the left rolandic
operculum, which contains connections from the temporal
to frontal lobes in areas subserving speech. The arcuate
fasciculus, simplistically identified decades ago as the
bridge between Wernicke’s and Broca’s area, is included in
this area. If indeed it were such a connection that fails to
perform smoothly and automatically in PWS, one would
expect that the areas that it connects might show lower
activation than normal. The authors further speculated that
overactivation of the right hemisphere in PWS may
represent a compensatory strategy.
Motor planning and execution. Could stuttering be due
to a strictly motoric deficit? Zimmermann (1980) conducted
articulatory dynamics experiments to explore this question.
In the speech of adults who stutter, he described slower
and asynchronous movements in their fluent speech, and
aberrant positioning of articulators during stuttered speech.
Zimmermann concluded that stuttering was a disorder of
movement, and explained that as we speak, there is a
temporal and/or spatial range of movement that is tolerable
to the system. As long as the speaker remains within that
range, there is no fluency breakdown. If, however, the
range is exceeded, due to emotional, perceptual, and/or
physiological events, the system is thrown off balance with
conflicting signals to and from the brain at a reflex level,
leading to oscillations (repetitions) and fixations (blocks
and prolongations).
Additional studies examined the motor system as
reflected in the planning, initiation, and execution stages of
speech. A broad range of studies generally found slower
reaction times for individuals who stutter as compared to
normally fluent speakers for at least some tasks. Prosek,
Montgomery, Walden, and Schwartz (1979) found differ-
ences in acoustic, but not manual or laryngeal, reaction
times. Similarly, Reich, Till, and Goldsmith (1981) con-
cluded that PWS had longer initiation times for speech
vocalization, but not for nonspeech vocalization, or manual
tasks. Borden (1983) had participants count out loud and
count silently using their fingers and also found those who
stutter to be slower, but in the execution stage, rather than
the initiation stage. In Peters, Hulstijn, and Starkweather’s
(1989) study of acoustic and physiological reaction times,
the conditions under which normally fluent and stuttering
people spoke were varied. By changing conditions, they
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were better able to discern the complexities of response
differences. Their results indicated that reaction times for
both stuttering and control groups increased with either
longer utterances or minimal preparation time, but in-
creased more for the stuttering group. They concluded that
a difficulty in motor programming for speech might
underlie stuttering.
Other recent studies have begun to examine aspects of
reaction time. Van Lieshout, Hulstijn, and Peters (1996)
tested whether or not PWS have difficulty assembling an
abstract motor plan by having speakers name pictures
representing one-, two-, and three-syllable words. They
measured reaction time as well as duration of the spoken
word. If PWS have difficulty in building a motor plan, then
they should take more time for words that are longer, as
compared to normally fluent speakers. They found that the
stuttering speakers had slower reaction times for all of the
words, but the gap between their reaction times and those
of the fluent speakers remained static—that is, in both
groups, performance did not appreciably change as word
length grew. This evidence refutes the motor plan assembly
hypothesis, and so contrasts with studies described in the
previous section that reported that central processing load
interferes with speech output. Overall, most studies point to
generally slower laryngeal, oral, and manual reaction times
for stutterers, although there are inconsistencies.
Execution of speech, as opposed to reaction times, has
also been examined in PWS. Many methods have been
used. Muscle activity and movement can be examined via
electromyography (EMG), or second formant (F2) transi-
tion, where articulator movement is indirectly represented
in the acoustic signal. Voice onset time (VOT) can be used
to measure laryngeal movement. In studies of speech
execution, investigators can choose to examine either
stuttered or fluent speech of PWS and compare it to the
speech of people who are normally fluent. Freeman and
Ushijima (1978) and Shapiro (1980) found evidence of
muscle activity of antagonistic pairs of laryngeal muscles
during stuttering. This was thought to be at the root of
moments of stuttering involving laryngeal closure. Smith,
Denny, and Wood (1991), however, looked at the speech of
normally fluent individuals and, surprisingly, found that they
too showed activation of both adductor and abductor
laryngeal muscles, negating the findings of the earlier
studies. Conture, Schwartz, and Brewer (1985) also exam-
ined laryngeal behavior during stuttering using fiber optics,
finding inappropriate opening and closing of vocal folds
during repetitions and prolongations, indicating difficulty in
motor control of the larynx during stuttering. Another
interesting set of studies (Alfonso, 1991) focused on the
spatial and temporal dynamics of articulator (lip, tongue,
and jaw) movements in the fluent speech of PWS. Results
indicated that articulatory targets were accurately reached,
but articulators attained targets in a less than efficient
manner in terms of the relative timing of their movements.
Webster (1988, 1989) looked at manual motor perfor-
mance of PWS, their ability both to write with both hands
simultaneously and to perform finger-tapping tasks. In
general, he found that the participants who stutter made
more errors and were slower in their performance than
85
normally fluent participants, and in addition they were
more susceptible to interference when they were asked to
perform a second manual motor task simultaneous with
finger tapping. Thus, these conclusions, similar to motor
speech studies, give an indication that more than just
speech is involved.
Most recently, Max, Caruso, and Gracco (2003) contin-
ued to examine neuromotor skills in speech and across
other motor systems. This study combined features of a
number of earlier studies. Data were obtained for three
motor systems—speech, orofacial nonspeech, and finger
movement—and in each system, four movement sequences
varying in length and complexity were tested. The use of
nonspeech domains allows examination of skill levels that
would not have been affected by either treatment for
stuttering or years of adaptation to the disorder. If the
deficit underlying stuttering extends to more than speech,
then PWS would be expected to perform more poorly
across the motor systems as compared to normally fluent
speakers, and, as the task conditions become more difficult,
their performance might be expected to deteriorate more
quickly. The movements were motorically comparable and
involved both flexion (closing) and extension (opening).
Kinematic analyses revealed sharp contrasts in the closing
versus opening movements for the stuttering versus the
fluent participants. For closing movements, in the speech
and finger movement tasks, the group who stutter had
statistically significantly longer duration and longer peak
velocity latency than the fluent group. Opening movements
were not significantly different between the groups. In
orofacial nonspeech movements, the same trend appeared
but was not statistically significantly different. The analysis
of subcomponents of the movements allowed the distinct
differences to be observable without being watered down
by components that were not different.
When adults who stutter are examined, it is not possible
to tell if any differences found represent a deficit that
caused stuttering or are due to having stuttered for years,
or even are unrelated to stuttering at all. Most past
investigations of young children’s speech production
concluded that if differences exist between children who
stutter and nonstuttering children in motor speech produc-
tion, they must be subtle (see review by Conture, 1991).
Some differences, however, were observed in comparisons
of temporal relationships between and among related events
rather than for singular speech variables (Zebrowski,
Conture, & Cudahy, 1985). Recent research among very
young stuttering children has provided additional indica-
tions of possible speech motor difficulties present close to
stuttering onset. Hall and Yairi (1992) reported that
stuttering children differed from normally fluent peers in
the shimmer and jitter parameters of vocal fold vibration.
Also, Hall, Amir, and Yairi (1999) found that preschool
children near onset of stuttering had slower speaking rates
in comparison with normally fluent controls. In fact, other
investigators reported that even 1 year before stuttering
onset, children’s speech contained imperceptible speech
aberrations such as faster speaking rate than children who
did not develop stuttering (Kloth, Janssen, Kraaimaat, &
Brutten, 1995). Perhaps young children who stutter, as a
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group, do not exhibit pervasive deficits in speech motor
function, but instead may exhibit different thresholds for
perturbation.
Ideally, we would like to follow children from birth
through their stuttering development, but this is extremely
difficult. Another method of getting at such information is
to compare traits of people who stuttered only as children
with those of individuals who continue to stutter in
adulthood. Traits that are the same would likely have been
present close to onset of stuttering, and those that are
absent in the recovered people but present in the persistent
people may represent traits that normalized during recovery
from stuttering. Forster and Webster (2001) used this logic
to explore the idea that those who recovered from stutter-
ing outgrew a deficit in speech motor control. (They also
addressed interhemispheric anomalies, as discussed in the
previous section on central processing.) The authors
designed tasks to test the function of the supplementary
motor area (SMA), which has been implicated as being
involved in stuttering. Three groups of 24 adults partici-
pated—PWS, people who stuttered only in childhood, and
people who never stuttered. There were two procedures
designed to test the integrity of the SMA—a finger-tapping
task and a bimanual crank turning task. The recovered
group performed similarly to the control group, but the
persistent group had poorer skills. The authors interpreted
this to mean that for those who recovered, the SMA had
matured, but the SMAs of the persistent individuals
continued to function less than optimally. This type of
information leads us much further into the realms of
possible mechanisms not only at the root of stuttering, but
also those prompting recovery.
The Fox et al. (1996) study, mentioned earlier in the
section concerning central processing, found overactivation
across wide areas in the right hemisphere of PWS during
speaking, notably in the SMA, premotor areas, and cerebel-
lum. When the individuals who stutter read in chorus and
were fluent, many of the differences in their brain activa-
tion patterns were reduced or even disappeared. Other
imaging studies have confirmed activation abnormalities in
motor planning areas (see Ingham, 2001).
The motor component of stuttering clearly must be
central to any theory of stuttering, as the cardinal symptom
of stuttering is motoric. It would appear that PWS have a
generalized motor deficit, extending to more than speech,
but not perceptible in any behavior other than speech.
Studies have documented slower reaction times, longer
durations of motor behaviors, and effects becoming more
apparent in more difficult behaviors, such as closing versus
opening movements.
Genetics. Woven through some of the literature on
physiologic and biologic aspects of PWS and stuttering are
references to genetics (see a brief review by Yairi &
Ambrose, 2002). Published research first appeared in the
1930s, when Bryngelson and Rutherford (1937) reported
that the incidence of stuttering among relatives of stuttering
probands is higher than in the population at large. Early
studies focused on family incidence and personal character-
istics, such as handedness, of PWS (Bryngelson & Ruther-
ford, 1937). From the 1930s to 1990s, a number of
DISORDERS • Volume 31 • 80–91 • Spring 2004
investigations (e.g., Andrews, Morris-Yates, Howie, &
Martin, 1991; Felsenfeld et al., 2000; Godai, Tatarelli, &
Bonanni, 1976; Howie, 1981) explored twinning and
stuttering. In all, the rate of concordance for stuttering
(both stuttered) was higher for monozygotic (identical) than
dizygotic (fraternal) twins, indicating a strong genetic
factor. But, if stuttering was completely governed by
genetics, then if one identical twin stuttered, his or her
twin would also stutter, and that is not the case—the rate is
considerably less than 100, revealing the existence of
strong environmental factors.
Andrews and Harris (1964) published the first statistical
analysis of the pattern of expression of stuttering in
families. They found a higher risk of stuttering for relatives
of females who stutter, and documented that more males
than females stutter. Kidd (1984) confirmed these findings,
determining that susceptibility to stuttering was transmitted
vertically, that is, generation to generation, with sex-
modified expression, consistent with genetically controlled
traits. They concluded that males are more susceptible to
stuttering, with females having a higher threshold requiring
more factors for stuttering to be expressed. Ambrose, Yairi,
and Cox (1993) reported different conclusions, finding that
the risk to relatives of males and females who stutter is
equal. Their sample, however, was very different from that
of the Yale study (Kidd, 1984) in that it consisted of very
young children who stutter who were followed for a period
of years. Thus, the sample was representative of popula-
tions of both those who recovered and those who persisted
in stuttering.
Several studies have used statistical analyses (segregation
analyses) to predict what genetic model of transmission fits
the observed data best. There are several models to be
tested:
• nongenetic, random, or only environmental
• major contribution of one gene: single major locus
(SML)
• polygenic (many genes)
• multifactorial–polygenic (MFP): several or many genes
AND environmental factors
Andrews and Harris (1964) found that stuttering was
most likely accounted for either by polygenic inheritance or
by a dominant gene in conjunction with MFP components.
The Yale studies by Kidd and colleagues (Cox, Kramer, &
Kidd, 1984; Kidd, 1984) reported that the data were most
consistent with either an MFP model or an MFP plus major
locus model. More recently, Andrews et al. (1991) and
Felsenfeld et al. (2000), using the Australian Twin Registry,
determined that 70% of the heritability was due to additive
genetic effect and 30% to nonshared environmental effect.
Contributing environmental factors are those that are
nonshared, or unique to the individual, rather than those
that are shared by the family.
All of the studies discussed above were based almost
exclusively on adults with persistent stuttering. The genetic
studies conducted by the Illinois group (Ambrose, Cox, &
Yairi, 1997; Ambrose, Yairi, & Cox, 1993) used a unique
sample in that it is truly representative of stuttering in
general by including both persistent and recovered
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stuttering. Ambrose et al. (1997) focused on possible
subtypes of stuttering and performed separate segregation
analyses for the families of children who recovered from
stuttering (excluding persistent stuttering relatives) and the
families of children who persisted in stuttering (excluding
recovered stuttering relatives). Both analyses yielded the
single highest likelihood for the presence of a major gene
component (SML) in addition to MFP contributions.
Two additional findings were remarkable. First, the
parameters for the SML were almost identical in each
analysis, indicating that this component involves (at least)
one major gene that is present in both forms of stuttering,
persistent and recovered. But, for the MFP parameters, the
heritability component (phenotypic variation attributed to a
polygenic, additive effect) differed. Thus, the Ambrose et al.
1997 study advanced knowledge about the role of genetics a
step further. The results showed that not only does the initial
expression of stuttering have strong genetic components,
but also that its developmental course is influenced by
genetics. Specifically, the authors showed that children who
stutter and who have a familial history of chronic stuttering
would tend to follow that same pattern. And vice versa,
children who stutter but have a familial tendency of
recovered stuttering would tend to follow that pattern.
In summary, it is very likely that both forms of stuttering
share a common major gene, contributions of additional
genes, and environmental factors that are unique to the
individual. It may be that persistent stuttering arises more
from additional genetic components, whereas recovered
stuttering may be less genetically controlled, with evident
but less prominent family history. In addition, it is important
to remember that the division of stuttering into persistent
and recovered subtypes could be a false dichotomy, and that
there might be a better way to classify types of stuttering.
Currently, however, this appears to be the best lead.
The statistical evidence described above has laid the
groundwork for linkage analysis. Linkage analysis works by
identifying alleles for certain known marker genes on each
chromosome that are co-inherited with the disorder in
question. When a marker gene is co-inherited with stutter-
ing, it means that the gene contributing to stuttering is on
the same chromosome as the marker gene; in fact, very
close to it. These regions can then be studied further to
identify specific genes involved in the transmission of
stuttering. Cox (2000) reported the results of the first
complete standard genome-wide screen of DNA markers for
analysis of stuttering performed on members of the
Hutterite population in North Dakota, all descendants of a
single genealogy. In this groundbreaking study, Cox
mentioned sites on chromosomes 1, 13, and 17 as possible
locations of genes underlying stuttering. One other linkage
study has been published with weak evidence for linkage to
several chromosomes (Shugart et al., 2003), and a third one
by the Illinois group is currently close to completion.
DISCUSSION AND CONCLUSIONS
The question used to be, Is stuttering a motor disorder? A
motor speech disorder? A language disorder? A genetic
87
disorder? A psychologic disorder? A learned behavior?
Well, the answer is probably yes, to all. It all depends on
what you are trying to explain. More simply put, What is
stuttering a symptom OF? There has been great progress in
many areas, and soon researchers will begin to link up
their findings. The multidisciplinary approach is absolutely
necessary, although contributions can be made within any
specific field. How can we put all of this information
together to devise a well-formed theory? We strive to
delineate the necessary and sufficient factors, differentiating
cause versus contributing factor versus result. It has become
clear that we cannot account for the existing data using one
schema over another, but we must integrate them. Previous
comprehensive frameworks, such as Smith and Kelly’s
(1997) multifactorial dynamic model, the demands and
capacities model (Starkweather & Gottwald, 1990), or
Bernstein Ratner’s (1997) trade-off hypothesis, have much to
offer but do not incorporate specifics as described in many
of the studies discussed here. The Smith and Kelly model
posits that it is the interaction of a number of components
that underlies fluency breakdown, and that the contribution
of each component will vary from individual to individual
and over time within an individual. The demands and
capacities model merely states that when demands exceed
capacities, breakdown occurs, whereas the trade-off
hypothesis is based on uneven resource allocation, so that
if resources are diverted for a challenging task, other
functions may suffer. Because these models are general,
they lack explanatory relevance and are difficult to test.
They were not devised to answer specifics but to provide a
framework for more intricate and testable hypotheses.
We are not yet at a point to propose an encompassing
detailed model of the cause of stuttering. It is safe to say
that stuttering involves, at its ultimate origin, a complex
but strong genetic component affecting the fluency-
generating system of the brain, but this does not narrow the
possibilities as much as one might think. Unfortunately, we
do not yet know what such genes actually do, how they
interact with each other, or how they interact with the
environment. The ultimate question is, What are the types
of genes that could cause the types of effects in the brain
that could cause the types of aberrant brain activity that
could cause the types of stuttering symptoms? Researchers
in fluency are trying determine how we go from a major
gene or two, some additional genes, and nonshared environ-
mental factors to a fragile fluency-generating system that is
susceptible to breakdowns related to/from factors in the
spheres of linguistic complexity, time pressure, excitement
or anxiety, among a host of other specifics, susceptible to
interference. This mechanism must also explain how so
many children stutter even severely and yet recover
completely without formal intervention, whereas others
stutter lifelong in spite of treatment.
Is there a specific location, or specific locations, where the
process goes awry? Are all of the components in good
working order, but their intercommunication does not
proceed smoothly enough to allow fluent speech? Does the
most primal deficit lie in auditory processing, or central
processing, or speech planning? It is not easy, and probably
not overly important, to determine where auditory processing
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becomes central processing-language-cognitive processes
and where motor planning begins. All of these areas are
interconnected, and a problem at one site will create a
cascade effect prompting aberrancies downstream. It is not
as simple as finding an electrical problem in a motor,
where one can systematically check the battery, the
generator, the distributor, the spark plugs, and the wiring
that connects them.
Although there may be, and probably are, subtypes of
stuttering, there does appear to be commonality in the
underlying genetically orchestrated deficit. In PWS, perhaps
neural development, under genetic influence, is uneven, and
systems subserving speech and language do not mature in
the right order at the right time. It is known that the two
hemispheres of the brain proceed differently in their
maturation (Kent, 1999). The best bet may be that there is
a deficit in the left hemisphere affecting both auditory and
motor functions, and that the right hemisphere perhaps
attempts to compensate, and one or more parts (subsystems)
of the complex multilevel sensory and motor system
responsible for the planning and orderly execution of fluent
speech are fragile and easily perturbed. In persistent
stuttering, the left hemisphere system may be wired
differently and less efficiently, but may attempt to develop
coping strategies, compensating with the right hemisphere.
Those who stutter mildly and/or occasionally have success-
fully developed organized wiring mechanisms to circumvent
the problem areas. Those who stutter consistently and/ or
severely manage to use available pathways but cannot
maintain and/or develop consistent new efficient wiring.
(See discussion in Yairi and Ambrose, in press). The neural
system of a child who fully and naturally recovers from
stuttering may develop unevenly but become indistinguish-
able from that of a child who is normally fluent. The
challenge now is to create testable hypotheses to continue
to narrow down specifics. It is an exciting time, and it is
not unreasonable to expect to see exciting results around
the corner.
Science has come full circle, but the spiral has tightened.
In his discussion of the cerebral dominance theory, Travis
(1931/1978) wrote that stuttering “reflects a certain lack of
maturation of the central nervous system which either does
not afford integration of the highest neurophysiologic levels
involved in speech or predisposes these levels to disintegra-
tion by various types of exogenous or endogenous stimuli”
(p. 277). This sounds very much like the current position
on the etiology of stuttering—but now we are accumulating
the concrete evidence to support it.
Relevance to Evidence-Based Practice
One’s perspective on the cause of stuttering perforce drives
one’s therapeutic approach. The current thrust toward
evidence-based practice demands that clinicians take a
position and provide an objective rationale for their
treatment regimens. This does not mean that the art of
clinical judgment or client desires must be replaced by
scientific findings, as Bothe (2003) pointed out. Art and
science are not in opposition; rather, they should be
incorporated into a unity, or consilience, of knowledge (cf.
DISORDERS • Volume 31 • 80–91 • Spring 2004
Starkweather, 2002). Not only is the nature–nurture debate
pointless and artificial, the division between researchers and
clinicians is equally fruitless. As Wilson (1998) stated, in
reference to science and literature, “the way to unite…is to
view the boundary…not as a territorial line but as a broad
and mostly unexplored terrain awaiting cooperative entry
from both sides” (p. 137). Demosthenes was a philosopher
and did not write a treatise on the amelioration of stutter-
ing in the presence of noise, nor did he conduct a scientific
experiment in this regard. But, his self-therapy could still
be considered evidence based, using the best quality
information available.
Understanding the present state of affairs of stuttering
etiology theories is not a dry mental exercise, nor a mandate
from the American Speech-Language-Hearing Association. As
a scientist, it is a privilege and a duty to provide objective
insight that might drive treatment strategies, and as a
clinician, it is a privilege and a duty to artfully incorporate
scientific findings for the benefit of PWS.
ACKNOWLEDGMENT
A portion of the research described here was supported by the
National Institute on Deafness and Other Communication Disorders
Grant R01 DC05210, Principal Investigator: Ehud Yairi.
REFERENCES
Alfonso, P. (1991). Implications of the concepts underlying task-
dynamic modeling on kinematic studies of stuttering. In H.
Peters, W. Hulstijn, & C. W. Starkweather (Eds.), Speech motor
control and stuttering (pp. 79–100). Amsterdam: Elsevier
Science.
Ambrose, N., Cox, N., & Yairi, E. (1997). The genetic basis of
persistence and recovery in stuttering. Journal of Speech,
Language, and Hearing Research, 40, 567–580.
Ambrose, N., & Yairi, E. (1999). Normative disfluency data for
early childhood stuttering. Journal of Speech, Language, and
Hearing Research, 42, 895–909.
Ambrose, N. G., Yairi, E., & Cox, N. (1993). Genetic aspects of
early childhood stuttering. Journal of Speech and Hearing
Research, 36, 701–706.
Anderson, J., Pellowski, M., Conture, E., & Kelly, E. (2003).
Temperamental characteristics of young children who stutter.
Journal of Speech, Language, and Hearing Research, 46,
1221–1233.
Andrews, G., & Harris, M. (1964). The syndrome of stuttering:
Clinics in developmental medicine, No. 17. London: Spastics
Society Medical Education and Information Unit in association
with Wm. Heinemann Medical Books.
Andrews, G., Morris-Yates, A., Howie, P., & Martin, N. G.
(1991). Genetic factors in stuttering confirmed. Archives of
General Psychiatry, 48, 1034–1035.
Bernstein Ratner, N. (1997). Stuttering: A psycholinguistic
perspective. In R. F. Curlee & G. M. Siegel (Eds.), Nature and
treatment of stuttering: New directions (2nd ed., pp. 99–127).
Boston: Allyn & Bacon.
Berry, M. F. (1938). A common denominator in twinning and
stuttering. Journal of Speech Disorders, 3, 51–57.
Ambrose: Theoretical Perspectives on the Cause of Stuttering
Downloaded from: https://pubs.asha.org 85.153.205.87 on 12/10/2021, Terms of Use: https://pubs.asha.org/pubs/rights_and_permissions
Blanton, S. (1931). Stuttering. Mental Hygiene, 15, 271–282.
Blood, G., & Blood, I. (1984). Central auditory function in young
stutterers. Perceptual & Motor Skills, 59, 699–705.
Blood, G., & Blood, I. (1989). Multiple data analysis of dichotic
listening advantages of stutterers. Journal of Fluency Disorders,
14, 97–107.
Bloodstein, O. (1958). Stuttering as anticipatory struggle reaction.
In J. Eisenson (Ed.), Stuttering: A symposium (pp. 1–70). New
York: Harper & Row.
Bloodstein, O. (1995). A handbook on stuttering (5th ed.). San
Diego, CA: Singular.
Borden, G. (1983). Initiation vs. execution time during manual
and oral counting by stutterers. Journal of Speech and Hearing
Research, 26, 389–396.
Bosshardt, H.-G. (2002). Effects of concurrent cognitive process-
ing on the fluency of word repetition: Comparison between
persons who do and do not stutter. Journal of Fluency Disor-
ders, 27, 93–114.
Bothe, A. (2003). Evidence-based treatment of stuttering: V. The
art of clinical practice and the future of clinical research.
Journal of Fluency Disorders, 28, 247–258.
Braun, A. R., Varga, M., Stager, S., Schulz, G., Selbie, S.,
Maisog, J. M., et al. (1997). Altered patterns of cerebral
activity during speech and language production in developmental
stuttering: An H215O positron emission tomography study. Brain,
120, 761–784.
Brill, A. (1923). Speech disturbances in nervous and mental
diseases. Quarterly Journal of Speech Education, 9, 129–135.
Brutten, G. J., & Shoemaker, D. (1967). The modification of
stuttering. Englewood Cliffs, NJ: Prentice-Hall.
Bryngelson, B., & Rutherford, B. (1937). A comparative study of
laterality of stutterers and non-stutterers. Journal of Speech
Disorders, 2, 15–16.
Cherry, C., & Sayers, B. (1956). Experiments upon the total
inhibition of stammering by external control and some clinical
results. Journal of Psychosomatic Research, 1, 233–246.
Conture, E., Schwartz, H., & Brewer, D. (1985). Laryngeal
behavior during stuttering: A further study. Journal of Speech
and Hearing Research, 28, 233–240.
Conture, E. G. (1991). Young stutterers’ speech production: A
critical review. In H. F. M. Peters, W. Hulstijn, & C. W.
Starkweather (Eds.), Speech motor control and stuttering:
Proceedings of the 2nd International Conference on Speech Motor
Control and Stuttering (pp. 365–384). New York: Elsevier.
Coriat, I. (1928). Stammering: A psychoanalytic interpretation.
Nervous & Mental Disorders Monographs, Series #47, 1–68.
Cox, N. (2000, November). Genetics of stuttering: Insights and
recent advances. Paper presented at the annual convention of
the American Speech-Language-Hearing Association, Washing-
ton, DC.
Cox, N., Kramer, P., & Kidd, K. (1984). Segregation analyses of
stuttering. Genetic Epidemiology, 1, 245–253.
Craig, A., Hancock, K., Tran, Y., & Craig, M. (2003). Anxiety
levels in people who stutter: A randomized population study.
Journal of Speech, Language, and Hearing Research, 46,
1197–1206.
DeNil, L., Kroll, R., Kapur, S., & Houle, S. (1998). A positron
emission tomography study of silent and oral single word
reading in stuttering and nonstuttering adults. Journal of Speech,
Language, and Hearing Research, 43, 1038–1053.
89
Felsenfeld, S., Kirk, K. M., Zhu, G., Statham, D. J., Neale, M.
C., & Martin, N. G. (2000). A study of the genetic and
environmental etiology of stuttering in a selected twin sample.
Behavior Genetics, 30, 359–366.
Fenichel, O. (1945). The psychoanalytic theory of neurosis. New
York: W. W. Norton.
Fitch, J., & Batson, E. (1989). Hemispheric asymmetry of alpha
wave suppression in stutterers and nonstutterers. Journal of
Fluency Disorders, 14, 47–55.
Flanagan, B., Goldiamond, I., & Azrin, N. (1958). Operant
stuttering: The control of stuttering behavior through response-
contingent consequences. Journal of Experimental Analyses of
Behavior, 1, 173–177.
Forster, D., & Webster, W. (2001). Speech-motor control and
interhemispheric relations in recovered and persistent stuttering.
Developmental Neuropsychology, 19, 125–145.
Foundas, A. L., Bollich, A. M., Corey, D. M., Hurley, M., &
Heilman, K. M. (2001). Anomalous anatomy of speech-language
areas in adults with persistent developmental stuttering.
Neurology, 57, 207–215.
Fox, P. T., Ingham, R. J., Ingham, J. C., Hirsch, T. B., Downs,
J. H., Martin, C., et al. (1996). A PET study of the neural
systems of stuttering. Nature, 382, 158–162.
Freeman, F., & Ushijima, T. (1978). Laryngeal muscle activity
during stuttering. Journal of Speech and Hearing Research, 21,
538–562.
Glauber, P. J. (1958). Stuttering and personality dynamics. In J.
Eisenson (Ed.), Stuttering: A symposium (pp. 71–120). New
York: Harper & Row.
Godai, U., Tatarelli, R., & Bonanni, G. (1976). Stuttering and
tics in twins. Acta Geneticae Medicae et Gemellologiae, 25,
369–375.
Goodstein, L. (1958). Functional speech disorders and personality:
A survey of the research. Journal of Speech and Hearing
Research, 1, 359–376.
Hall, J., & Jerger, J. (1978). Central auditory function in stutterers.
Journal of Speech and Hearing Research, 21, 324–337.
Hall, K. D., Amir, O., & Yairi, E. (1999). A longitudinal
investigation of speaking rate in preschool children who stutter.
Journal of Speech, Language, and Hearing Research, 42,
1367–1377.
Hall, K. D., & Yairi, E. (1992). Fundamental frequency, jitter, and
shimmer in preschoolers who stutter. Journal of Speech and
Hearing Research, 35, 1002–1008.
Howie, P. M. (1981). Concordance for stuttering in monozygotic
and dizygotic twin pairs. Journal of Speech and Hearing
Research, 24, 317–321.
Hubbard, C., & Prins, D. (1994). Word familiarity, syllabic stress
pattern and stuttering. Journal of Speech and Hearing Research,
37, 564–571.
Ingham, R. (2001). Brain imaging studies of developmental
stuttering. Journal of Communication Disorders, 34, 493–516.
Ingham, R., Fox, P., Ingham, J., & Zamarripa, F. (2000). Is
overt stuttered speech a prerequisite for the neural activations
associated with chronic developmental stuttering? Brain and
Language, 75, 163–194.
Johnson, W., & Associates. (1959). The onset of stuttering:
Research findings and implications. Minneapolis: University of
Minnesota.
Kent, R. D. (1999). Motor control: Neurophysiology and
90 CONTEMPORARY ISSUES IN COMMUNICATION SCIENCE AND
Downloaded from: https://pubs.asha.org 85.153.205.87 on 12/10/2021, Terms of Use: https://pubs.asha.org/pubs/rights_and_permissions
functional development. In A. Caruso & E. Strand (Eds.),
Clinical management of motor speech disorders in children (pp.
46–62). New York: Thieme.
Kidd, K. K. (1984). Stuttering as a genetic disorder. In R. F.
Curlee & W. H. Perkins (Eds.), Nature and treatment of
stuttering: New directions (pp. 149–169). San Diego, CA:
College-Hill.
Kloth, S. A., Janssen, P., Kraaimaat, F. W., & Brutten, G. J.
(1995). Speech-motor and linguistic skills of young stutterers
prior to onset. Journal of Fluency Disorders, 20, 157–170.
Logan, K., & Conture, E. (1995). Length, grammatical complex-
ity, and rate differences in stuttered and fluent conversational
utterances of children who stutter. Journal of Fluency Disorders,
20, 35–61.
Max, L., Caruso, A., & Gracco, V. (2003). Kinematic analyses of
speech, orofacial nonspeech, and finger movements in stuttering
and nonstuttering adults. Journal of Speech, Language, and
Hearing Research, 46, 215–232.
Moore, W. (1938). A conditioned reflex study of stuttering.
Journal of Speech Disorders, 3, 163–183.
Moore, W., & Haynes, W. (1980). Alpha hemispheric asymmetry
and stuttering: Some support for a segmentation dysfunction
hypothesis. Journal of Speech and Hearing Research, 23,
229–247.
Onslow, M., Packman, A., & Harrison, E. (2001). The Lidcombe
Program of Early Stuttering Intervention: A clinician’s guide.
Austin, TX: Pro-Ed.
Palmer, M., & Gillette, A. (1938). Sex differences in the cardiac
rhythms of stutterers. Journal of Speech Disorders, 3, 3–12.
Perkins, W. H. (1990). What is stuttering? Journal of Speech and
Hearing Disorders, 55(3), 370–382.
Peters, H., Hulstijn, W., & Starkweather, C. (1989). Acoustic
and physiological reaction times of stutterers and nonstutterers.
Journal of Speech and Hearing Research, 32, 668–680.
Pinsky, S., & McAdam, D. (1980). Electroencephalographic and
dichotic indices of cerebral laterality in stutterers. Brain &
Language, 11, 374–397.
Pool, K., Devous, M., Freeman, F., Watson, B., & Finitzo, T.
(1991). Regional cerebral blood flow in developmental stutterers.
Archives of Neurology, 48, 509–512.
Postma, A., & Kolk, H. (1993). The covert repair hypothesis:
Prearticulatory repair processes in normal and stuttered
disfluencies. Journal of Speech and Hearing Research, 36,
472–487.
Prosek, R., Montgomery, A., Walden, B., & Schwartz, D.
(1979). Reaction-time measures of stutterers and nonstutterers.
Journal of Fluency Disorders, 4, 269–278.
Reich, A., Till, J., & Goldsmith, H. (1981). Laryngeal and
manual reaction times of stuttering and nonstuttering adults.
Journal of Speech and Hearing Research, 24, 192–196.
Rosenfield, D., & Goodglass, H. (1980). Dichotic testing of
cerebral dominance in stutterers. Brain & Language, 11,
179–180.
Ryan, B. P . (2001). Programmed therapy for stuttering in
children and adults (2nd ed.). Springfield, IL: Charles C.
Thomas.
Salmelin, R., Schnitzler, A., Schmitz, F., Jancke, L., Witte, O.
W., & Freund, H-J. (1998). Functional organization of the
auditory cortex is different in stutterers and fluent speakers.
NeuroReport, 9, 2225–2229.
DISORDERS • Volume 31 • 80–91 • Spring 2004
Schuell, H. (1946). Sex differences in relation to stuttering: Part I.
Journal of Speech Disorders, 11, 277–298.
Shames, G. H., & Sherrick, C. E. (1963). A discussion of
nonfluency and stuttering as operant behavior. Journal of Speech
and Hearing Disorders, 28, 3–18.
Shane, M. (1955). Effect on stuttering of alteration in auditory
feedback. In W. Johnson & R. Leutenegger (Eds.), Stuttering in
children and adults (pp. 286–297). Minneapolis: University of
Minnesota Press.
Shapiro, A. (1980). An electromyographic analysis of the fluent
and dysfluent utterances of several types of stutterers. Journal of
Fluency Disorders, 5, 203–231.
Sheehan, J. (1953). Theory and treatment of stuttering as an
approach-avoidance conflict. Journal of Psychology, 36, 27–49.
Sheehan, J. G. (1958). Projective studies of stuttering. Journal of
Speech and Hearing Disorders, 23, 18–25.
Shugart, Y., Mundorff, J., Kilshaw, J., Doheny, K., Doan, B.,
Wanyee, J., et al. (2003). Results of a genome-wide linkage
scan for stuttering. American Journal of Medical Genetics, 124A,
133–135.
Smith, A., Denny, M., & Wood, J. (1991). Instability in speech
muscle systems in stuttering. In H. Peters, W. Hulstijn, & C. W.
Starkweather (Eds.), Speech motor control and stuttering:
Proceedings of the 2nd International Conference on Speech Motor
Control and Stuttering (pp. 231–242). New York: Elsevier.
Smith, A., & Kelly, E. M. (1997). Stuttering: A dynamic,
multifactorial model. In R. F. Curlee & G. M. Siegel (Eds.),
Nature and treatment of stuttering: New directions. (2nd ed., pp.
204–217). Boston: Allyn & Bacon.
Sommer, M., Koch, M. A., Paulus, W., Weiller, C., & Buchel, C.
(2002). Disconnection of speech-relevant brain areas in
persistent developmental stuttering. Lancet, 360, 380–383.
Starkweather, C. (2002). The epigenesis of stuttering. Journal of
Fluency Disorders, 27, 269–288.
Starkweather, C. W., & Gottwald, S. R. (1990). The demands
and capacities model: II. Clinical applications. Journal of
Fluency Disorders, 15(3), 143–157.
Travis, L. (1957). The unspeakable feelings of people, with special
reference to stuttering. In L. Travis (Ed.), Handbook of speech
pathology (pp. 1009–1033). New York: Appleton-Century-Crofts.
Travis, L. (1978). Neurophysiological dominance. Journal of
Speech and Hearing Disorders, 43, 275–277. (Original work
published 1931).
Travis, L., Tuttle, W., & Cowan, D. (1936). A study of the heart
rate during stuttering. Journal of Speech Disorders, 1, 21–26.
Van Lieshout, P., Hulstijn, W., & Peters, H. (1996). Speech
production in people who stutter: Testing the motor plan
Ambrose: Theoretical Perspectives on the Cause of Stuttering
Downloaded from: https://pubs.asha.org 85.153.205.87 on 12/10/2021, Terms of Use: https://pubs.asha.org/pubs/rights_and_permissions
assembly hypothesis. Journal of Speech and Hearing Research,
39, 76–92.
Webster, W. (1988). Neural mechanisms underlying stuttering:
Evidence from bimanual handwriting performance. Brain &
Language, 33, 226–244.
Webster, G. (1989). Sequence initiation performance by stutterers
under conditions of response competition. Brain & Language,
36, 286–300.
Wilson, E. O. (1998). Consilience: The unity of knowledge. New
York: Vintage Books.
Wingate, M. (1964). A standard definition of stuttering. Journal of
Speech and Hearing Disorders, 29, 484–489.
Wingate, M. (1969). Sound and pattern in “artificial” fluency.
Journal of Speech and Hearing Research, 12, 677–686.
Wingate, M. (1997). Stuttering: A short history of a curious
disorder. Westport, CT: Bergin & Garvey.
Wischner, G. J. (1950). Stuttering behavior and learning: A
preliminary theoretical formulation. Journal of Speech and
Hearing Disorders, 15, 324–335.
Yairi, E. (1976). Effects of binaural and monaural noise on
stuttering. The Journal of Auditory Research, 16, 114–119.
Yairi, E., & Ambrose, N. (1999). Early childhood stuttering I:
Persistency and recovery rates. Journal of Speech, Language,
and Hearing Research 42, 1097–1112.
Yairi, E., & Ambrose, N. (2002). Evidence for genetic etiology in
stuttering. Perspectives, 12(2), 10–15.
Yairi, E., & Ambrose, N. (in press). Early childhood stuttering.
Austin, TX: Pro-Ed.
Yaruss, J. S. (1999). Utterance length, syntactic complexity, and
childhood stuttering. Journal of Speech, Language, and Hearing
Research, 42, 329–344.
Yaruss, J. S., & Conture, E. G. (1996). Stuttering and phonologi-
cal disorders in children: Examination of the covert repair
hypothesis. Journal of Speech and Hearing Research, 39,
349–364.
Zebrowski, P. M., Conture, E. G., & Cudahy, E. A. (1985).
Acoustic analysis of young stutterers’ fluency: Preliminary
observations. Journal of Fluency Disorders, 10, 173–192.
Zimmermann, G. (1980). Stuttering: A disorder of movement.
Journal of Speech and Hearing Research, 23, 122–126.
Contact author: Nicoline Grinager Ambrose, University of
Illinois, Speech and Hearing Science, 901 S. Sixth St., Champaign,
IL 61820. E-mail: nambrose@uiuc.edu
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