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What Causes Stuttering?
Christian Büchel and Martin Sommer
tuttering, with its characteristic
disruption in verbal ﬂ uency, has
been known for centuries; earliest
descriptions probably date back to the
Biblical Moses’ “slowness of speech
and tongue” and his related avoidance
behavior (Exodus 4, 10–13). Stuttering
occurs in all cultures and ethnic groups
(Andrews et al. 1983; Zimmermann et
al. 1983), although prevalence might
differ. Insofar as many of the steps in
how we produce language normally are
still a mystery, disorders like stuttering
are even more poorly understood.
However, genetic and neurobiological
approaches are now giving us clues to
causes and better treatments.
What Is Stuttering?
Stuttering is a disruption in
the ﬂ uency of verbal expression
characterized by involuntary, audible
or silent, repetitions or prolongations
of sounds or syllables (Figure 1). These
are not readily controllable and may be
accompanied by other movements and
by emotions of negative nature such
as fear, embarrassment, or irritation
(Wingate 1964). Strictly speaking,
stuttering is a symptom, not a disease,
but the term stuttering usually refers to
both the disorder and symptom.
Developmental stuttering evolves
before puberty, usually between two
and ﬁ ve years of age, without apparent
brain damage or other known cause
(“idiopathic”). It is important to
distinguish between this persistent
developmental stuttering (PDS),
which we focus on here, and acquired
stuttering. Neurogenic or acquired
stuttering occurs after a deﬁ nable brain
damage, e.g., stroke, intracerebral
hemorrhage, or head trauma. It is
a rare phenomenon that has been
observed after lesions in a variety of
brain areas (Grant et al. 1999; Ciabarra
et al. 2000).
The clinical presentation of
developmental stuttering differs
from acquired stuttering in that it is
particularly prominent at the beginning
of a word or a phrase, in long or
Figure 1. Speech Waveforms and Sound Spectrograms of a Male Speaker Saying “PLoS Biology”
The left column shows speech waveforms (amplitude as a function of time); the right
column shows a time–frequency plot using a wavelet decomposition of these data. In the
top row, speech is ﬂ uent; in the bottom row, stuttering typical repetitions occur at the
“B” in “Biology.” Four repetitions can be clearly identiﬁ ed (arrows) in the spectrogram
Copyright: © 2004 Büchel and Sommer. This is an
open-access article distributed under the terms of
the Creative Commons Attribution License, which
permits unrestricted use, distribution, and reproduc-
tion in any medium, provided the original work is
Abbreviations: CNS, central nervous system; DTI,
diffusion tensor imaging; fMRI, functional magnetic
resonance imaging; MEG, magnetoencephalography;
MRI, magnetic resonance imaging; PDS, persistent
developmental stuttering; PET, positron emission
Christian Büchel is at NeuroImage Nord in the De-
partment of Neurology at the University of Hamburg
in Hamburg, Germany. Martin Sommer is at the
Department of Clinical Neurophysiology at the Uni-
versity of Göttingen in Göttingen, Germany. E-mail:
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meaningful words, or syntactically
complex utterances (Karniol 1995;
Natke et al. 2002), and the associated
anxiety and secondary symptoms are
more pronounced (Ringo and Dietrich
1995). Moreover, at repeated readings,
stuttering frequency tends to decline
(adaptation) and to occur at the
same syllables as before (consistency).
Nonetheless, the distinction between
both types of stuttering is not strict. In
children with perinatal or other brain
damage, stuttering is more frequent
than in age-matched controls, and
both types of stuttering may overlap
(Andrews et al. 1983).
Who Is Affected?
PDS is a very frequent disorder,
with approximately 1% of the
population suffering from this
condition. An estimated 3 million
people in the United States and 55
million people worldwide stutter.
Prevalence is similar in all social
classes. In many cases, stuttering
severely impairs communication,
with devastating socioeconomic
consequences. However, there are
also many stutterers who, despite
their disorder, have become famous.
For instance, Winston Churchill had
to rehearse all his public speeches to
perfection and even practiced answers
to possible questions and criticisms to
avoid stuttering. Charles Darwin also
stuttered; interestingly, his grandfather
Erasmus Darwin suffered from the
same condition, highlighting the fact
that stuttering runs in families and is
likely to have a genetic basis.
The incidence of PDS is about 5%,
and its recovery rate is up to about
80%, resulting in a prevalence of PDS
in about 1% of the adult population. As
recovery is considerably more frequent
in girls than in boys, the male-to-female
ratio increases during childhood
and adolescence to reach three or
four males to every one female in
adulthood. It is not clear to what extent
this recovery is spontaneous or induced
by early speech therapy. Also, there is
no good way of predicting whether an
affected child will recover (Yairi and
The presence of affected family
members suggests a hereditary
component. The concordance rate
is about 70% for monozygotic twins
(Andrews et al. 1983; Felsenfeld et al.
2000), about 30% for dizygotic twins
(Andrews et al. 1983; Felsenfeld et al.
2000), and 18% for siblings of the same
sex (Andrews et al. 1983). Given the
high recovery rate, it may well be that
the group abnormalities observed in
adults reﬂ ects impaired recovery rather
than the causes of stuttering (Andrews
et al. 1983).
Over the centuries, a variety of
theories about the origin of stuttering
and corresponding treatment
approaches have been proposed. In
ancient Greece, theories referred
to dryness of the tongue. In the
century, abnormalities of the
speech apparatus were thought to
cause stuttering. Thus, treatment
was based on extensive “plastic”
surgery, often leading to mutilations
and additional disabilities. Other
treatment options were tongue-
weights or mouth prostheses (Katz
1977) (Figure 2). In the 20th century,
Figure 2. Two Different Apparatuses to Prevent Stuttering
On the left is a device by Gardner from 1899 to artiﬁ cially add weight to the tongue (United States patent number 625,879). On the
right is a more complex speech apparatus by Peate from 1912 (United States patent number 1,030,964).
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stuttering was primarily thought to be
a psychogenic disorder. Consequently,
psychoanalytical approaches and
behavioral therapy were applied
to solve possible neurotic conﬂ icts
(Plankers 1999). However, studies
of personality traits and child–
parent interactions did not detect
psychological patterns consistently
associated with stuttering (Andrews et
Other theories regard stuttering
as a learned behavior resulting
from disadvantageous external,
usually parental, reactions to normal
childhood dysﬂ uencies (Johnson
1955). While this model has failed to
explain the core symptoms of stuttering
(Zimmermann et al. 1983), it may
well explain secondary symptoms
(Andrews et al. 1983), and guided early
parental intervention may prevent
persistence into adulthood (Onslow et
al. 2001). The severity of PDS is clearly
modulated by arousal, nervousness, and
other factors (Andrews et al. 1983).
This has led to a two-factor model of
PDS. The ﬁ rst factor is believed to
cause the disorder and is most likely a
structural or functional central nervous
system (CNS) abnormality, whereas the
second factor reinforces the ﬁ rst one,
especially through avoidance learning.
However, one should be careful to
call the latter factor “psychogenic” or
“psychological,” because neuroscience
has shown that learning is not simply
“psychogenic” but leads to measurable
changes in the brain (Kandel and
In some cases, arousal actually
improves stuttering instead of making
it worse. Consequently, some famous
stutterers have “treated” their stuttering
by putting themselves on the spot.
Anecdotally, the American actor Bruce
Willis, who began stuttering at the age
of eight, joined a drama club in high
school and his stuttering vanished in
front of an audience.
Is Stuttering a Sensory, Motor, or
Stuttering subjects as a group
differ from ﬂ uent control groups by
showing, on average, slightly lower
intelligence scores on both verbal
and nonverbal tasks and by delays in
speech development (Andrews et al.
1983; Paden et al. 1999). However,
decreased intelligence scores need to
be interpreted carefully, as stutterers
show a schooling disadvantage of
several months (Andrews et al. 1983).
Associated symptoms comprise delays
in tasks requiring a vocal response
(Peters et al. 1989) and in complex
bimanual timed tasks such as inserting
a string in the eye of a needle (Vaughn
and Webster 1989), whereas many
other studies on sensory–motor
reaction times yielded inconsistent
results (Andrews et al. 1983).
Alterations of auditory feedback (e.g.,
delayed auditory feedback, frequency-
altered feedback), various forms of
other auditory stimulation (e.g., chorus
reading), and alteration of speech
rhythm (e.g., syllable-timed speech)
yield a prompt and marked reduction
of stuttering frequency, which has
raised suspicions of impaired auditory
processing or rhythmic pacemaking
in stuttering subjects (Lee 1951; Brady
and Berson 1975; Hall and Jerger 1978;
Salmelin et al. 1998). Other groups
have also reported discoordinated and
delayed onset of complex articulation
patterns in stuttering subjects (Caruso
et al. 1988; van Lieshout et al. 1993).
The assumption that stuttering might
be a form of dystonia—involuntary
muscle contractions produced by the
CNS—speciﬁ c to language production
(Kiziltan and Akalin 1996) was not
supported by a study on motor cortex
excitability (Sommer et al. 2003).
Neurochemistry, however, may link
stuttering with disorders of a network
of structures involved in the control
of movement, the basal ganglia. An
increase of the neurotransmitter
dopamine has been associated with
movement disorders such as Tourette
syndrome (Comings et al. 1996;
Abwender et al. 1998), which is a
neurological disorder characterized
by repeated and involuntary body
movements and vocal sounds (motor
and vocal tics). Accordingly, like
Tourette syndrome, stuttering improves
with antidopaminergic medication,
e.g., neuroleptics such as haloperidol,
risperidone, and olanzapine (Brady
1991; Lavid et al. 1999; Maguire et al.
2000), and anecdotal reports suggest
that it is accentuated or appears
under treatment with dopaminergic
medication (Koller 1983; Anderson
et al. 1999; Shahed and Jankovic
2001). Hence, a hyperactivity of the
dopaminergic neurotransmitter system
has been hypothesized to contribute to
stuttering (Wu et al. 1995). Although
dopamine antagonists have a positive
effect on stuttering, they all have
side effects that have prevented them
from being a ﬁ rst line treatment of
Lessons from Imaging the Brain
Given reports on acquired stuttering
after brain trauma (Grant et al. 1999;
Ciabarra et al. 2000), one might think
that a lesion analysis (i.e., asking the
question where do all lesions that lead
to stuttering overlap) could help to
ﬁ nd the location of an abnormality
linked to stuttering. Unfortunately,
lesions leading to stuttering are
widespread and do not seem to follow
an overlapping pattern. Even the
contrary has been observed, a thalamic
stroke after which stuttering was
“cured” in a patient (Muroi et al. 1999).
In ﬂ uent speakers, the left language-
dominant brain hemisphere is most
active during speech and language
tasks. However, early studies on EEG
lateralization already strongly suggested
abnormal hemispheric dominance
(Moore and Haynes 1980) in stutterers.
With the advent of other noninvasive
brain imaging techniques like positron
emission tomography (PET) and
functional magnetic resonance imaging
(fMRI), it became possible to visualize
brain activity of stutterers and compare
these patterns to ﬂ uent controls.
Following prominent theories that
linked stuttering with an imbalance
of hemispherical asymmetry (Travis
1978; Moore and Haynes 1980), an
important PET study (Fox et al. 1996)
reported increased activation in the
right hemisphere in a language task in
developmental stutterers. Another PET
study (Braun et al. 1997) conﬁ rmed
this result, but added an important
detail to the previous study: Braun
and colleagues found that activity in
the left hemisphere was more active
during the production of stuttered
speech, whereas activation of the
right hemisphere was more correlated
with ﬂ uent speech. Thus, the authors
concluded that the primary dysfunction
is located in the left hemisphere and
that the hyperactivation of the right
hemisphere might not be the cause of
stuttering, but rather a compensatory
process. A similar compensatory
process has been observed after
stroke and aphasia, where an intact
right hemisphere can at least partially
compensate for a loss of function
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(Weiller et al. 1995). Right hemisphere
hyperactivation during ﬂ uent speech
has been more recently conﬁ rmed with
fMRI (Neumann et al. 2003).
PET and fMRI have high spatial
resolution, but because they only
indirectly index brain activity
through blood ﬂ ow, their temporal
resolution is rather limited.
Magnetoencephalography (MEG) is
the method of choice to investigate
ﬁ ne-grained temporal sequence of
brain activity. Consequently, MEG was
used to investigate stutterers and ﬂ uent
controls reading single words (Salmelin
et al. 2000). Importantly, stutterers
were reported to have read most single
words ﬂ uently. Nevertheless, the data
showed a clear-cut difference between
stutterers and controls. Whereas ﬂ uent
controls activated left frontal brain
areas involved in language planning
before central areas involved in speech
execution, this pattern was absent, even
reversed, in stutterers. This was the
ﬁ rst study to directly show a neuronal
correlate of a hypothesized speech
timing disorder in stutterers (Van
Thus, functional neuroimaging
studies have revealed two important
facts: (i) in stutterers, the right
hemisphere seems to be hyperactive,
and (ii) a timing problem seems
to exist between the left frontal
and the left central cortex. The
latter observation also ﬁ ts various
observations that have shown that
stutterers have slight abnormalities in
complex coordination tasks, suggesting
that the underlying problem is located
around motor and associated premotor
Are there structural abnormalities
that parallel the functional
abnormalities? The ﬁ rst anatomical
study to investigate this question used
high-resolution MR scans and found
abnormalities of speech–language
areas (Broca’s and Wernicke’s
area) (Foundas et al. 2001). In
addition, these researchers reported
abnormalities in the gyriﬁ cation
pattern. Gyriﬁ cation is a complex
developmental procedure, and
abnormalities in this process are an
indicator of a developmental disorder.
Another recent study investigated
the hypothesis that impaired cortical
connectivity might underlie timing
disturbances between frontal and
central brain regions observed in MEG
studies (Figure 3). Using a new MRI
technique, diffusion tensor imaging
(DTI), that allows the assessment
of white matter ultrastructure,
investigators saw an area of decreased
white matter tract coherence in the
Rolandic operculum (Sommer et al.
2002). This structure is adjacent to
the primary motor representation of
tongue, larynx, and pharynx (Martin
et al. 2001) and the inferior arcuate
fascicle linking temporal and frontal
language areas, which both form
a temporofrontal language system
involved in word perception and
production (Price et al. 1996). It is
thus conceivable that disturbed signal
transmission through ﬁ bers passing
the left Rolandic operculum impairs
the fast sensorimotor integration
necessary for ﬂ uent speech production.
This theory also explains why the
normal temporal pattern of activation
between premotor and motor cortex
is disturbed (Salmelin et al. 2000)
and why, as a consequence, the right
hemisphere language areas try to
compensate for this deﬁ cit (Fox et al.
These new data also provide a theory
to explain the mechanism of common
ﬂ uency-inducing maneuvers like chorus
reading, singing, and metronome
reading that reduce stuttering
instantaneously. All these procedures
involve an external signal (i.e., other
readers in chorus reading, the music
in singing, and the metronome
itself). All these external signals feed
into the “speech production system”
through the auditory cortex. It is thus
possible that this external trigger
signal reaches speech-producing
central brain areas by circumventing
the frontocentral disconnection and
is able to resynchronize frontocentral
decorrelated activity. In simple terms,
these external cues can be seen as an
Future Directions in Research
There are numerous outstanding
issues in stuttering. If structural
changes in the brain cause PDS, the key
question is when this lesion appears.
Although symptoms are somewhat
different, it would be interesting to ﬁ nd
out to what extent transient stuttering
(which occurs in 3%–5% in childhood)
is linked to PDS. It is possible that all
children who show signs of stuttering
develop a structural abnormality during
development, but this is transient in
those who become ﬂ uent speakers.
If this is the case, it is even more
important that therapy starts as early
as possible if it is to have most impact.
This question can now be answered
with current methodology, i.e.,
noninvasive brain imaging using MRI.
Figure 3. Decreased Fiber Coherence
Decreased ﬁ ber coherences, as observed with DTI, in persistent developmental
stutterers compared with a ﬂ uent control group. A red dot indicates the peak
difference in a coronal (top left), axial (top right), and a sagittal (bottom) slice.
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Given that boys are about four
times less likely to recover from
stuttering than girls, it is tempting
to speculate that all stutterers have
a slight abnormality, but only those
that can use the right hemisphere
for language can develop into ﬂ uent
speakers. Language lateralization
is less pronounced in women
(McGlone 1980) and might therefore
be related to the fact that women
show an overall lower incidence in
PDS. Again, a developmental study
comparing children who stutter with
ﬂ uent controls and, most importantly,
longitudinal studies on these children
should be able to answer these
It is unlikely that stuttering is
inherited in a simple fashion.
Currently, a multifactorial model for
genetic transmission is most likely.
Moreover, it is unclear whether a
certain genotype leads to stuttering
or only represents a risk factor and
that other environmental factors are
necessary to develop PDS. Again, this
question might be answered in the near
future, as the National Institutes of
Health has recently completed the data
collection phase of a large stuttering
sample for genetic linkage analysis.
We thank Tobias Sommer and Andreas
Starke for fruitful discussions and the
Volkswagen Foundation as well as the
Deutsche Forschungsgemeinschaft for
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