Neuroscience and Biobehavioral Reviews 27 (2003) 339–347

www.elsevier.com/locate/neubiorev

Choral speech: the amelioration of stuttering via imitation

and the mirror neuronal system
Joseph Kalinowski*, Tim Saltuklaroglu
Stuttering Research Lab, Department of Communication Sciences and Disorders, East Carolina University, Oglesby Drive, Greenville,
NC 27858-4353, USA

Received 5 August 2002; revised 8 January 2003; accepted 30 May 2003

Abstract
‘Choral’ speech or speaking in unison is an undeniable phenomenon that immediately induces fluent and natural sounding speech in almost
all people who stutter, regardless of linguistic content, situation or audience size. We propose that the choral speech effect is a form direct
imitation, a primitive and innate human capacity that is possibly mediated at the neuronal level by ‘mirror neurons’. Mirror systems link
observations and actions are considered by many to be a neuronal substrate for gestural language acquisition, as well as forming the basis for
many learned behaviors, thus possibly playing a vital role in ensuring survival during infancy. The engagement of these systems allows
gestural sequences, including speech, to be fluently replicated. Choral speech and its permutations use the capacity for fluent imitation in
people who stutter via a ‘loose’ gestural matching system in which gestures in the external signal possessing cues found in the intended
utterance can serve as stuttering inhibitors. We suggest implementing these innate gestural mirrors to provide immediate and effective
amelioration for stuttering.
q 2003 Elsevier Ltd. All rights reserved.
Keywords: Stuttering; Fluency; Inhibition; Speech; Gestures; Perception

Contents
1. The choral speech phenomenon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 339
2. Neurological evidence for the ‘normalization’ of cerebral activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 340
3. Examining the behavioral data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341
4. Towards a gestural model of fluency enhancement. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342
5. ‘Mirror neurons’: necessary precursors for the imitation of gestures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342
6. Mirror neurons, imitation and the onset of stuttering . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343
7. Gestural mirrors for fluency enhancement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344
8. The flexibility of gestural mirrors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 344
9. From parlor game to therapeutic reality. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 345
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346

1. The choral speech phenomenon
To the best of our knowledge, with the exception of
stuttering, no other neurological pathology with extreme
overt symptomatology can be immediately neutralized via
the simple presentation of an external speech signal.
Stuttering, the debilitative disorder of communication is
* Corresponding author. Tel.: þ 1-252-328-1986; fax: þ1-252-328-4469.
E-mail address: kalinowskij@mail.ecu.edu (J. Kalinowski).
0149-7634/03/$ - see front matter q 2003 Elsevier Ltd. All rights reserved.
doi:10.1016/S0149-7634(03)00063-0
defined as a centrally originating involuntary block [8,54,66]
that manifests during speech production. Its core primary
symptoms consist of speech disruptions in the form of part-
word repetitions, sound prolongations and complete
blockages in the forward flow of speech. Ancillary behaviors
such as nostril flaring, facial grimacing, rolling of the eyes,
blinking, irregular breathing, and any number of other bodily
contortions may also accompany these primary speech
disruptions. Furthermore, the continued manifestations of
such overt symptomatology usually leads to the development
340 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
of secondary covert behaviors such as word, sound or
situational avoidances, word or phrase substitutions, or
circumlocutions around difficult words [8]. Simply put, the
fear of stuttering permeates almost every utterance of those
so afflicted, negatively impacting nearly every aspect of life.
However, these overt speech disruptions and concomi-
tant facial manifestations that have proven to be highly
resistant to behavioral treatments [11,12] are almost
invariably, immediately transformed into natural sounding,
smooth flowing, fluent speech when a second speaker
produces similar linguistic material in unison with the
person who stutters [8,10,30,54]. In the field of stuttering,
this phenomenon is known as ‘Choral Speech’ and is
considered a benchmark for all other methods of fluency
enhancement. Under choral conditions, that require no
training whatsoever to enable and are functional in front of
any sized audience [5], stuttering is inhibited to the extent
that speech is nearly indistinguishable from the speech of
those who do not stutter, a standard that is rarely met by any
other form of fluency enhancement. Witnesses to the choral
phenomenon often stare in wonderment as they observe
alternating patterns of fluent and stuttered speech with the
presentation and removal of the choral second speech
signal. They are truly witnessing neurological symptoma-
tology being turned ‘off’ and ‘on’ in the presence or absence
of the choral signal [25]. The true hallmark of this choral
speech phenomenon is a sense of invulnerability to
stuttering that is seldom observed elsewhere. By invulner-
ability, we imply that the possibility of stuttering will likely
not factor into speech production as long as the choral signal
is maintained, unlike in all other ameliorative strategies in
which this possibility remains a salient and constant fear. As
such, nearly all covert secondary behaviors (such as
avoidances, substitutions and circumlocutions) are also
removed. When a person who stutters speaks under choral
conditions, their speech behaviors become relatively
‘normalized’, making them almost indistinguishable from
normally fluent speakers as the discrete core symptoms and
compensatory strategies used to hide the disorder almost
cease to exist. For those who stutter this phenomenon is
undeniable and simply amazing. It represents everything
that an ameliorating condition should encompass.
Though its effects are undeniable and well documented,
choral speech has never achieved clinical popularity.
Stuttering treatment paradigms have changed numerous
times over the last 75 years, from the use of psycho-
analysis to strict behavioral speech retraining, which has
dominated for the last 30 years [8,26]. Under each reigning
paradigm, choral speech was seen as no more than a
‘parlor’ game to demonstrate the stutterer’s capacity for
producing fluent speech and the idealized potential of the
therapy du jour [1,27,29]. Various explanations for the
immediate and spontaneous fluency enhancement derived
from choral speech have been offered. These have
included the reduction in communicative responsibility
[18], the inducement of novel patterns of vocalization [67],
and the provision of an external timing mechanism [57].
Yet attempts to confirm any of these postulated hypotheses
have essentially failed [25] and the choral speech
phenomenon has remained enigmatic. We will examine
the neurological and behavioral data and present an
explanation of choral speech founded in the presence of
a mirror neuronal system for action recognition and
imitation.
2. Neurological evidence for the ‘normalization’
of cerebral activity
Brain imaging studies over the last decade or so have
been conducted and continue to be conducted on those who
stutter in attempts to map regions of the brain associated
with stuttering and reveal possible neurophysiological
differences between those who stutter and normally fluent
speakers. Of particular interest are studies that have
employed choral speech as a means of inducing fluent
speech productions in those who stutter for the purposes of
comparing and contrasting levels of cerebral activation
when producing fluent versus stuttered speech. It should be
noted that the majority of neuroimaging studies that require
stutterers to speak fluently employ choral speech for its
unfailing effects and immediacy of inducement, over any
other method of fluency enhancement, behavioral or
otherwise [19,20,25]. The relative normalization that is
observed behaviorally is also observed in neuroimaging
studies that employ such designs. However, we caution that
brain mapping in the field of stuttering appears to still be in
its infancy and the implications of these studies appear to be
far from conclusive. Ingham [25] succinctly summarizes the
relatively consistent findings from positron emission
tomography studies that appear to be associated with
stuttering and its immediate amelioration via choral speech.
Overall, stutterers tend to show increased right side
activation [9,16,19,20,25,28,69], that may be considered to
be consistent with early theories of incomplete cerebral
dominance for speech [63,64]. However, prominent
researchers in this area tend to agree that the disorder
is much more complex than a simple question of laterality
[25,42,52].
Not surprisingly, stuttering appears to be associated with
the hyperactivation relative to normally fluent speakers in
motor regions such as the supplementary motor area,
superior lateral premotor area [16,19,20,28]. Abberant
activation patterns have also been found in the anterior
insula [16,19,20] and the anterior cingulate cortex [9,16].
Suppression or deactivation relative to normals has been
found in the primary auditory cortex as well as areas
involved in language processing such as Broca’s and
Wernicke’s areas [19,20,28] suggesting that stuttering may
in some way be related to deficits in sensory motor
integration, possibly related to auditory feedback and speech
monitoring [13,42], a notion that finds additional credibility
 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
in magnetoencephalography (MEG) studies [52,53] and in
behavioral studies using altered auditory feedback [58 – 60].
One point of concern when interpreting the data from
neuroimaging studies in stuttering is the separation between
state-induced effects and trait-induced effects [42]. During
periods of silence, the regional cerebral blood flow (rCBF)
data collected from people who stutter cannot be differ-
entiated from those who are fluent [25] suggesting that at
least some of the differences in activation levels (we suggest
those associated with motor areas) may be the neurological
by-products of the covert anticipatory reactions and overt
manifestations of stuttering. Simply put, they may reflect
stuttering at the neurological level and not is neural cause.
Regardless of the neurophysiological discrepancies
found during stuttering, to us the most impressive finding
from neuroimaging studies seems to be the relative
normalization of cerebral activity under choral conditions.
When fluency is immediately induced using choral speech,
rCBF studies indicate that speech immediately becomes
normally lateralized in the left hemisphere, hyperactivity in
the motor areas subsides and activation levels are increased
in the primary and association auditory cortices [19,20,25,
52]. However, at a behavioral level, this normalization of
activity is implicit. Gone are the aberrant speech patterns,
facial tension and excessive effort. These communicative
anomalies are immediately replaced by smooth flowing,
natural sounding speech. The question remains as to why.
Neuroimaging data alone have yet to answer this question as
the combined spatial and temporal resolving capacities of
currently available technology seem to fall short of
capturing the true essence of stuttering at a neuronal level.
We are optimistic that future technological advances will
solve this problem, yet at present we suggest that these data
be assimilated with behavioral data from stuttering research
and contemporary theories of speech perception and
language acquisition to produce a compelling explanation
for the choral speech effect.
3. Examining the behavioral data
Stuttering is a complex disorder that is amenable to
temporary overt symptom reduction by almost any form of
sensory or motoric change. Behavioral speech therapy makes
use of motoric changes to induce novel speech patterns.
Unfortunately, these speech patterns are often highly
unnatural, require a great deal of effort to produce, and are
subject to breakdown [14]. Sensory modalities have also
been targeted for stuttering inhibition. The introduction of
masking noise and pure tones has resulted in significant
improvements in fluency, yet these sensory stimuli fail to
meet the levels of fluency enhancement induced by choral
speech when attacking the disorder through the auditory
modality [8]. Choral speech is and always has been the most
potent of stuttering inhibitors. Its immediacy and almost
complete removal of stuttering symptoms is unmatched,
341
suggesting that it provides the most potent sensory input that
somehow compensates for any presumed sensory motor
deficits in those who stutter. Behavioral studies involving
permutations of choral speech cast significant light onto the
choral speech phenomenon. Shadowed speech (direct
imitation) also induces almost complete stuttering inhibition
[10,23], thus implicating the power of imitation in fluency
enhancement. More recently, a series of studies by
Kalinowski and colleagues, using various other permutations
of choral speech or ‘second speech signals’ leads to the
parsimonious explanation involving mirror neuronal systems
in humans that are predisposed for the imitation of gestures.
Delayed auditory feedback (DAF) has been used in the
amelioration of stuttering for over 50 years. Originally
used to establish a reduced speech rate deemed necessary
for those who stutter to produce fluent speech [45], this
paradigm was essentially discarded when it was proven
that people who stutter could speak just as fluently at
fast rates as at slower rates while under the effects of DAF
[31,35]. Frequency altered feedback (FAF) makes use of
digital signal processing (DSP) to create online perceived
pitch changes to a speaker’s own voice, allowing people
who stutter to listen to themselves at higher or lower pitch,
without making motoric changes to their speech patterns
[24,61]. The use of DAF and FAF induce similar levels of
stuttering inhibition [21,24,32,54]. Hence we suggest that,
rather than inducing novel motor speech patterns, sensory
changes caused by alteration to auditory feedback create
the illusion of a second speaker producing similar
linguistic material, mimicking choral speech. In a some-
what similar vein, stuttering was reduced by over 70% in
the presence of auditory stimuli consisting of a continuous
vowel /a/ or a vowel train /a-i-u/, yet no significant
improvement was noted when a more noise-like, fricative /
s/ was presented [33], suggesting that a voiced feature in
the external signal may be sufficient for significant
stuttering inhibition. These data seem to suggest that
sensory stimuli most associated with the immediate
amelioration of stuttering contains speech or speech-like
properties. In this case, the acoustic properties of the
isolated continuous voiceless fricative /s/, devoid of
contextual information, were deemed to be perceived as
less speech-like than those of the vowels. To further
expound on this theory, a study in which a person who
stuttered spoke while watching another person silently
mouth the linguistic material yielded reductions in
stuttering of approximately 80%, a level of stuttering
inhibition that is more impressive than those achieved by
non-speech signals (such as oscillating light sources)
presented through visual modalities [34]. This ‘visual
choral’ effect demonstrated that sensory input need not
even be presented via the auditory modality for it to be
effective in enhancing fluency. In this study, the fluency
enhancing condition was the presence of frontal, dynamic
articulatory gestures that were congruous with the
intended speech stream.
342 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
The common element in sensory based stuttering
inhibition seems to be presence of an external speech signal
that allows gestures in the intended utterance to be loosely
matched to those in the external signal [54]. Though choral
speech presents the optimal signal, the effectiveness of its
many permutations suggests high levels of flexibility in the
temporal and linguistic parameters of the exogenous signal
for the purposes of stuttering inhibition. Furthermore, the
absence of an ‘invariant’ cue or feature that is necessary and
sufficient to inhibit stuttering alludes to a gestural model of
stuttering inhibition based on the Motor Theory of Speech
Perception [40,41].
4. Towards a gestural model of fluency enhancement
The Revised Motor Theory of Speech Perception [40,41]
states that the invariant objects of both speech perception
and production are gestures representative of the coarticu-
lated dynamic trajectories of the human vocal tract.
However, no single speech cue, acoustic or otherwise has
been found to be both necessary and sufficient for gestural
speech perception. Rather, a specialized phonetic or
linguistic ‘module’ allows communicative messages to be
shared between senders and receivers by working efficiently
in a parallel manner, transposing between invariant speech
percepts and speech products that are defined according to
vocal tract trajectories for specific patterns of coarticulation.
Thus, at a central level, speech perception and production
are tightly linked and share the same encoding and decoding
mechanism.
The behavioral evidence for sensory derived stuttering
inhibition also converges on a gestural model. Regardless of
the modality of presentation, choral speech and its
derivatives, working in parallel with speech production,
provide an external matrix of speech gestures that is rich in
redundant speech cues. As long as the external signal is
perceived as speech, the presence of a particular cue (e.g.
voicing, place of articulation, manner of articulation,
intonation or temporal pattern) in the external gestural
sequence that is complimentary and therefore, may be
matched to one of cues found in the intended utterance,
within a loosely defined temporal window, appears to be
sufficient to inhibit stuttering [54]. An exact match between
external signal and intended utterance is not required and
the inhibitory system is endowed with the observed
flexibility. However, we can predict with relative confi-
dence that the closer the external gestural representation is
to the intended utterance, the more likely it will be to
enhance fluency (explaining why true choral speech is
unsurpassed as a stuttering inhibitor). For example, if a
person who stutters produces the utterance, I am i-i-i-in
trouble (stuttering and showing increased tension on the
word ‘in’), the external presentation of the word ‘in’
immediately prior to or while in the stuttering block would
meet the gestural demands for the block to be released and
allow the remainder of the sentence to be uttered. Yet, It is
also highly likely that that the percept of other similar
gestural sequences (such as ‘on’, ‘an’ ‘it’, etc.) may
accomplish this block release as these gestural sequences
possess some of the same speech cues (e.g. voicing) found
in the word ‘in’. Block release becomes less likely to occur
when the externally provided gestures deviate significantly
from the intended utterance. However, if linguistically
equivalent external gestures were presented in unison
(chorally) from the onset of the utterance, it is most likely
that stuttering would not even factor into the production of
this sentence. It follows that in more severe cases of
stuttering in which stuttering is prone to extend across
several words, the external inhibitory gestural sequence
would be required to be a better match to the intended
utterance providing an extended inhibitory framework of
gestures, from which the speaker may continually draw
salient cues to inhibit stuttering.
The question that remains is how salient cues from
exogenous speech gestures allow for stuttering to be
centrally inhibited without the use of any cognitive
strategies or the volitional imposition of motoric control.
The argument that follows is founded in the notion that
the choral speech effect is simply a goal directed
imitation of speech gestures. We posit that the presence
of a mirror neuronal system in humans, predisposed for
action recognition and paramount to imitation, is
activated in people who stutter during choral speech.
Mirror neurons may act as the ‘gestural matchmakers’
during choral speech, bridging the gap between incoming
speech gestures and the production of fluent speech,
temporarily restoring central integrity during speech
production.
5. ‘Mirror neurons’: necessary precursors
for the imitation of gestures
What is choral speech if not a form of direct imitation?
When two people speak in unison, two very similar
sequences of overlapping fluent speech gestures are
produced, with one signal imitating the other in a loosely
defined temporal window. The imitative ability of humans
may have its genesis in the mirror neuronal system [2 – 4,47,
65,68]. Evidence for this system began to mount when it
was observed that neurons in the rostral inferior premotor
cortex (F5) of monkeys were activated upon the execution
of specific goal directed actions [48]. Later these neurons
were observed firing, not just when the specific actions were
executed but also when they were observed [17,36,49]
establishing a ‘link’ between sender and receiver [47],
possibly forming the basis for primitive forms of communi-
cation [2,3,47]. The communicative function of mirror
neurons has been further supported by discovery of mirror-
like properties in numerous human cortical areas, including
circuits within Broca’s motor speech area [6,22,43,44,50,
 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
51]. Interestingly, Broca’s area in humans is considered to
be the homolog of the F5 region in monkeys, laying the
ground for a compelling gestural theory of language
acquisition in humans [2,3,43,47]. Simply put, the import-
ance of mirror neurons in our ability to communicate may
be that they represent the neuronal substrate that links the
perception and production of speech gestures under the
tenets of Motor Theory [47].
However, monkeys generally do not imitate or speak and
apes are only capable of imitating simple sequences. The
ability to imitate seems specialized to humans and is
paramount in the acquisition of complex motor sequences
required for many artistic and athletic endeavors, as well as
speech. Thus, speech seems to reflect an evolutionary
capitalization of the mirror system [3]. In other words, with
enhanced cognitive abilities and via the mirror system,
humans appear to have gained the ability to dissect motor
sequences and reassemble them from an acquired gestural
repertoire into meaningful actions that form the basis for
language, social interactions and culture [2,3]. Thus, while
the ability to imitate cannot be solely linked to the presence
of a mirror neuronal system, increasing evidence suggests
that it plays an integral role in this evolutionary landmark.
Imitation of gestures seems to dominate the earliest
phases of language acquisition, ‘forging the link between
[speech] perception and production’ [37,38]. However,
even throughout this stage, imitative actions progress from
gross to fine motor movements as the infant gains
increased coordination over the peripheral musculature.
By 6 months of age, most infants are capable of
‘babbling’, replicating the intonation patterns of their
caregivers [38,39]. At approximately a year old, parents
are often awed when their infant gains sufficient labial
coordination to fluently produce the gestural sequence
‘mama’, a gestural action sequence that appears to have
been readily primed for production at the level of the
mirror neurons by repeated observations of the sequence.
It appears that speech gestures generally emerge in infants
as soon as the peripheral speech motor system develops
sufficiently to at least approximate articulatory targets of
stored representations, even if the representation is not
completely accurate (as may be the case during early
developmental stages), allowing us to marvel at the rapid
increase in phonemic repertoire and the concurrent
exponential vocabulary growth. Gestural representations
appear to have been stored and primed for production
since birth via the duality of mirror neuronal circuitry that
strengthens the link between perception and production
[38]. Although developmental sequences show some
variation and initial productions may not be completely
accurate, the refinement of gestural representations and
motor sequences is generally forthcoming.
It is almost inconceivable to imagine a form of learned
behavior that could be more elementary than a simple
input –output neuronal system that creates an immediate
link between an observation and an action. At this
343
elementary level, the activation of mirror neurons appears
to be innate and reflexive [46], requiring no training of any
form, yet showing specific patterns of activation pertaining
to the motoric goal it intends to accomplish. Any imitative
behaviors that consist of observation –action sequences that
communicate vital goal oriented [7] needs such hunger or
thirst seem to be strengthened by repeated exposures. At
this basic level, a neuronal link between observation and
action may be strengthened if the gestural sequence being
observed or produced helps to ensure the survival of the
infant.
6. Mirror neurons, imitation and the onset of stuttering
According to Piaget, early infant communication during
the ‘pre-operational’ stage between birth and 2 years is
characterized by being reflexive and imitative [46]. We
suggest adding one further characteristic pertaining to
speech. It is a period of fluency. Simply put, ‘reflexive
imitation is fluent’ [56]. The presence of mirror neurons
may ensure that the motoric sequences of speech gestures
are faithfully and fluently replicated. This fluent imitation
may be observed regardless of linguistic knowledge or
cognitive development. It is found in communicatively
disabled populations such as those with autism and mental
retardation, suggesting that the ability to immediately
imitate a sequence of coarticulated speech phones is not
dependent on higher cognitive functions, assuming that the
sequence in question is represented within the individual’s
gestural repertoire. During this preliminary linguistic stage,
speech gestures are observed and fluently reproduced in a
reflexive manner to the extent that is motorically possible
[38] by virtue perhaps, of simple input –output neuronal
circuits that are the mirror neurons.
Considering that the earliest phases of language devel-
opment are characterized by reflexive fluency, it should not
be surprising that stuttering generally develops in children
between the ages of 2 and 6 years [8] loosely coinciding
with the termination of Piaget’s pre-operational stage. We
suggest that with an increased gestural repertoire and
cognitive abilities, a child’s reliance on mirror driven
imitative linguistic forms for communicative purposes
diminishes [46]. With the continued neuronal development
and increased mental capacities, children generally become
capable of forming more complex utterances and using
increasingly more complex linguistic forms, while at the
same time relinquishing the use of imitation for the purposes
of speech and language acquisition. It is during this later
phase that any predisposition to stutter may be exposed in
children. Without the use of fluent imitation, speech
disruptions that characterize stuttering are free to surface.
It may also be fair to state that if cognitive and linguistic
development never surpassed the stage of reflexive imita-
tion, the mirror neurons that seem to drive this system would
almost ensure the continuation of fluent speech, possibly
344 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
preventing the chronic disorder from ever manifesting in
those who are later susceptible.
Of considerable interest are the early symptoms of
stuttering. Incipient stuttering is generally marked by the
presence of easy, part-word or syllabic repetitions [8,15]
that are free from tension and sometimes go unnoticed by
the child producing them. It is not until later in the
developmental course that sound prolongations, silent
blocking, ancillary and secondary behaviors develop. As
such, these elementary syllabic repetitions seem to
represent the canonical form of stuttering. At this early
stage, the involuntary stuttering block seems to be most
easily overcome by the simple self-generated syllabic
repetitions or the canonical forms of stuttering. Hence, the
production of syllabic repetitions appears to be the
system’s most efficacious means of counteracting the
stuttering block [15]. This leads us to speculate: why a
syllabic repetition? Could the involuntary repeated pro-
ductions of these simple dynamic speech gestures be an
attempt to access circuitry responsible for fluent imitation?
Could it be an attempt to reengage a mirror system of
neurons? Surely it is not coincidental that these preliminary
symptoms of stuttering are repetitive or imitative in nature.
We suggest that they are endogenous attempts to imitate
internal gestural speech representations by reengaging
mirror driven imitative circuitry.
7. Gestural mirrors for fluency enhancement
Mirror systems appear to drive the period of reflexive
fluency during the initial phases of language development
[46] and their relatively diminished use at later stages may
expose a predisposed vulnerability to stuttering. However,
simply because these primitive neuronal circuits no longer
reflexively predominate over cognitive and linguistic
acquisition processes at later stages, does not imply that
they are inactive and cannot be reengaged. Even in later
years, people learn by observing others and imitating their
actions [2,3]. This is evident in athletic, musical and artistic
endeavors, as well as the learning foreign languages. When
needed, at almost any stage in life, mirror systems appear to
be available and provide the inherent capability to fluently
imitate motoric actions. Obviously, every action recognition
does not lead to an imitation, suggesting that this mirror
circuitry can be cognitively mediated [2,3] and called to
action when required to either learn novel gestural
sequences or facilitate ingrained motoric gestural sequences
that are prone to breakdown. We suggest that the latter
explains the effects of choral speech. When a person who
stutters speaks in unison with another speaker, a goal
directed imitation of speech gestures is once again being
implemented that allows these gestures to be fluently
replicated.
The human propensity for fluent imitation regardless of
cognitive or linguistic [56] ability suggests that the choral
speech phenomenon operates at the central level of phonemic
execution (i.e. enactment of the motor speech plan), rather
than impacting encoding and decoding strategies at semantic,
syntactic, or phonological levels. Thus, when choral speech
operates, linguistic representation is not affected at these
higher levels. Simply put, the compromise in the system
during stuttering, and hence, the facilitation of fluency via
choral speech occurs at the central level of execution.
Transition form speech percept (gestural representation) to
speech product is immediate, since at a neuronal level, these
two tasks may be one and the same. Such is the parallel nature
of the specialized phonetic or linguistic ‘module’, as
described by the Motor Theory [40,41]. During choral
speech, this transition seems to be aided by mirror driven
imitative circuitry. Furthermore, the recruitment of mirror
neurons does not impose any motoric control over production
during choral speech. Mirror neurons simply allow for an
external speech model to serve as a loose framework for
fluent imitation, temporarily rectifying the possible compro-
mise in sensory motor integration in those who stutter [55].
As the external model is more closely matched to the
intended production with respect to the presence of common
speech cues, the chances improve for engaging the mirror
system and inhibiting stuttering by fluent imitation. Simply
put, the choral speech effect is a simple input – output reflex
taking place in a specialized phonetic module and mediated
by mirror neurons. The only cognitive tasks required are
perceiving and attending to the external signal during speech
production.
Reengaging mirror systems via choral speech to induce
fluency in people who stutter seems logical. The primacy of
this method over even the most severe of stuttering symptoms
is apparent. Perhaps it is the fact that these systems are
primitive that they usually override the later developing
involuntary stuttering block. Human and animal nature
dictates that primordial systems override later developing
systems if the drive or goal is sufficient. For example, since the
dawn of time, our innate, primordial drive to feed and
reproduce seems to overpower any cognitive, religious,
spiritual, behavioral, psychoanalytical, or other psychologi-
cal needs that have been created. By the same token, by
simply perceiving speech gestures from the second signal,
choral or imitated speech provides gestural mirrors that when
employed in a manner that is directed towards imitating
speech gestures seem to almost invariably preclude the
occurrence of the central involuntary stuttering block. Simply
put, gestural imitation via choral speech seems to inhibit
stuttering by supplanting the disorder, at least to some extent.
However, once the signal is removed, fluency is revoked and
stuttering once again permeates the speech output.
8. The flexibility of gestural mirrors
We have discussed the ability of mirror neurons to
fluently imitate speech gestures and their role in choral
 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
speech. It is at this point that the flexibility of this fluency
enhancing mechanism should be noted, accounting for the
effects of choral speech derivatives such as DAF or
incongruous linguistic material, in which the imitative
process may not be overtly apparent. First, the term ‘choral’
speech is truly a misnomer. Rarely, if ever during a unison
production of the same linguistic material are the two
speakers in temporal synchrony. The two speakers may take
turns leading the speech production. The two signals
become intertwined. The originator may become the
imitator and vice versa. Even though the choral signal
may be out of phase, the flexibility of the system ensures
that stuttering inhibition is constant and generally unfailing.
Thus, the temporal inconsistencies in the choral signal
suggest some flexibility in the proposed mirror neuronal
architecture for accommodating imitation of speech. This
flexibility should be somewhat expected in a system that
may initially function to ensure the survival of the infant. In
developing children, actions may not always directly follow
observations, observation and action may overlap, or after
continued exposures, an action may even precede the
expected observation. We suggest that each of these
scenarios would serve the imitative purpose and engage
the direct input – output mirror neuronal circuitry. Not only
is flexibility observed in the temporal domain under choral
conditions, but it may also be extended to the linguistic
domain. As previously stated, fluency enhancement is
observed in people who stutter when linguistically incon-
gruous second speech signals are presented concomitantly
with speech, as long as relevant speech cues are extracted
from the gestural sequence. This generalization of effects
may be loosely analogous to the generalization shown by
the mirror neurons in monkeys that show visual generaliz-
ation for the proximity of the intended action and size of the
agent (e.g. hand) performing the action [3].
However, this flexibility in the fluency enhancing
mechanism, especially in mild to moderate stutterers may
also result from contributions made by a ‘normalization’ of
sensory to motor priming once fluent speech production has
been initiated. A recent MEG study showed a significant
delay and reduction in amplitude of the M100 response in
both auditory cortices (but more prominently in the left)
when normally fluent subjects produced vowels compared
to listening to replays of these self-produced vowels [13].
These data were interpreted as being indicative of motor to
speech priming resulting from inhibition of the auditory
cortices, a process that may be disrupted in people who
stutter [13,52,53,60]. Once fluent speech production is
initiated in people who stutter by engagement of the mirror
driven imitation system, it is possible that enhanced central
speech priming allows fluent speech to be self-sustained in
the presence of an asynchronous choral signal. This may
also explain why stuttering occurs most frequently during
the initiation of speech [8], prior to the possibility of speech
priming by one’s own voice; why reading, once initiated is
an easier task than conversational speech for many people
345
who stutter; and, why many people who stutter observe a
short period of ‘carry-over’ fluency following the removal
of a choral signal. Thus, the leeway in the choral fluency
enhancing mechanism may be an interactive effect of mirror
neuron flexibility and a central priming of the auditory
cortices for speech production once speech has been
initiated. Put simply, in people who stutter, fluency primes
fluency. However, from our clinical observations, it appears
that severe stutterers appear to be less susceptible to carry-
over. Here, flexibility may be compromised and therefore,
due to the relative frequency and potency of their
involuntary stuttering block, higher degrees of linguistic
and temporal synchrony in the choral signal may paramount
to the maintenance of fluent speech.
For practical purposes of enhancing fluency in people
who stutter, this leeway in the mirror system may be put to
best use by employing permutations of choral speech such
as DAF, FAF, reverberation, or echo speech [54]. These
choral speech derivatives rely on the production of speech
by the person who stutters to generate the choral effect. That
is, once speech is initiated, perceiving alterations to the
incoming auditory signal creates the illusion of a second
speaker and fools the brain into immediately engaging
gestural mirrors to inhibit stuttering. In the past, these
permutations of choral speech were acknowledged, but
never considered clinically viable. Nowadays, technological
advances in digital signal processing and miniaturization
have allowed the power of choral speech derivatives and the
engagement of mirror neurons to be accessed in the form of
inconspicuous self-contained, all in the canal, ear-level
devices, that produce combinations of DAF and FAF. For a
more complete description of this technology, see Ref. [62].
9. From parlor game to therapeutic reality
Clearly, the fluent speech derived from choral conditions
possesses qualities such as naturalness, spontaneity, and
stability that instill a sense of invulnerability to stuttering.
When incoming speech gestures are verbally mirrored by
the person who stutters, primitive neuronal circuitry that
perhaps once ensured the survival of the infant is put to
optimal use in the generation of fluent speech. After 75 years
of failed attempts to bring an involuntary neurological
disorder under voluntary motoric control by creating
tenuous and laborious speech patterns, is it not time to
simply endow the person who stutters with gestural mirrors
and allow them to exercise their innate ability for fluent
imitation? To the best of our knowledge, this innate and
flexible neuronal encoding stratagem is the only true means
of inducing invulnerability to stuttering that is paramount to
the complete removal of overt and covert symptomatolgy.
Humans are born with an innate capacity for fluent imitation
of complex gestural sequences, a capacity that seems to
have been refined through optimization of a mirror neuronal
system for action recognition. In people who stutter this
346 J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339–347
capacity may be gift that should not be overlooked. Mirror
neuronal systems appear to have served mankind in the
acquisition and development of language as well as other
motoric skills. Perhaps, it is time to let them ensure the
survival of those who stutter via the ameliorative use of
choral speech and its permutations. Parlor game? We think
not. Thanks to the evolution of our species, choral speech is
simply nature’s own fluency generator.
Acknowledgements
We would like to thank Alison Motluk of New Scientist
Magazine for suggesting that we examine a possible role for
mirror neurons in stuttering. Her suggestion lay dormant for
a year or two but after we attended a conference at Harvard
on The Evolution of Language in 2002, it bore fruit.
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