choral speech and the amelioration of stuttering via imitation

7/28/2019 Choral Speech and the Amelioration of Stuttering via Imitation

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Choral speech: the amelioration of stuttering via imitationand 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

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 symptomatologyusually leads to the development

0149-7634/03/$ - see front matter q 2003 Elsevier Ltd. All rights reserved.

doi:10.1016/S0149-7634(03)00063-0

Neuroscience and Biobehavioral Reviews 27 (2003) 339347www.elsevier.com/locate/neubiorev

* Corresponding author. Tel.:1-252-328-1986; fax:1-252-328-4469.

E-mail address: [email protected] (J. Kalinowski).
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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 ofany 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 tostuttering that is seldom observed elsewhere. By invulner-

ability, we imply that the possibility of stuttering will likelynot 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 stutterers 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 associatedwith 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 neuroimagingstudies 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 Brocas and

Wernickes 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 speechmonitoring [13,42], a notion that finds additional credibility

J. Kalinowski, T. Saltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339347340


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in magnetoencephalography (MEG) studies [52,53] and in

behavioral studies using altered auditory feedback[5860].

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 relativenormalization 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 ofcurrently 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 totemporary 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 almostcomplete removal of stuttering symptoms is unmatched,

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], thisparadigm 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 speakers 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, sensorychanges caused by alteration to auditory feedback create

the illusion of a second speaker producing similarlinguistic 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 asless 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 theintended speech stream.

J. Kalinowski, T. Sa ltuklaroglu / Neuroscience and Biobehavioral Reviews 27 (2003) 339347 341


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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 productionare 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 wouldmeet 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 ofgestures, 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 directedimitation 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 matchmakersduring 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 looselydefined temporal window. The imitative ability of humans

may have its genesis in the mirror neuronal system [24,47,

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, includingcircuits within Brocas motor speech area [6,22,43,44,50,



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51]. Interestingly, Brocas 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 fromgross 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 earlydevelopmental 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 immediatelink between an observation and an action. At this

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 observationaction 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 duringthe 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 thesequence in question is represented within the individuals

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 inputoutput 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 Piagets pre-operational stage. We

suggest that with an increased gestural repertoire and

cognitive abilities, a childs reliance on mirror drivenimitative 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 wouldalmost ensure the continuation of fluent speech, possibly



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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

systems most efficacious means of counteracting thestuttering 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 imitateinternal 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 tobe 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 ofcognitive or linguistic [56] ability suggests that the choral

speech phenomenon operates at thecentral level of phonemic

execution (i.e. enactment of the motor speech plan), rather

thanimpactingencoding 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 beone and the same. Suchis the parallelnature

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 notimpose anymotoric control over productionduring 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. Simplyput, the choral speech effect is a simple inputoutput 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 methodover even the most severeof stutteringsymptoms

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

systemsif thedrive or goal issufficient. Forexample, 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 tofluently imitate speech gestures and their role in choral



7/9

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. Thisflexibility 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 isobserved in people who stutter when linguistically incon-

gruous second speech signals are presented concomitantlywith 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 ones own voice; why reading, once initiated isan easier task than conversational speech for many people

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 tobest 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, thesepermutations 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 ofinconspicuous 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 tooptimal 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 neuronalsystem for action recognition. In people who stutter this



8/9

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 natures 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 Harvardon The Evolution of Language in 2002, it bore fruit.

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