Neuroscience Letters 293 (2000) 115±118
www.elsevier.com/locate/neulet
Stutter-free and stutter-®lled speech signals and their role in
stuttering amelioration for English speaking adults
Joseph Kalinowski a,*, Vikram N. Dayalu a, Andrew Stuart a,
Michael P. Rastatter a, Manish K. Rami b
a
Department of Communication Sciences and Disorders, School of Allied Health Sciences, East Carolina University,
Greenville, NC 27858-4353, USA
b
Department of Communication Sciences and Disorders, University of North Dakota, Grand Forks, ND-58202-8040, USA
Received 1 June 2000; received in revised form 30 August 2000; accepted 31 August 2000
Abstract
This study examined the power of an exogenously generated stuttered speech signal on stuttering frequency when
compared to an exogenously generated normal speech signal. In addition, we examined the speci®c components of the
second speech signal, which might be responsible for the inducement of ¯uency in people who stutter. Eight males and
two females who stuttered participated in this study. Experiment I involved meaningful speech: normal continuous
speech, normal interrupted speech, stuttered continuous speech, and stuttered interrupted speech, whereas Experiment
II involved vowels and consonants: /a/, /a-i-u/, /s/, /s-sh-f/. The results indicated that stuttered and normal speech signals
were equally effective in reducing stuttering frequency. Further, the vowels were more powerful than consonants in
inducing ¯uency for people who stutter. It is suggested that acoustic manifestations of stuttering, rather than a problem,
may be a natural compensatory mechanism to bypass or inhibit the `involuntary block' at the neural level. q 2000
Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Stuttering; Auditory signals; Auditory feedback; Speech gesture; Choral speech
A second speech signal comes from another speaker in
unison, choral, semi-choral, or shadow forms, where the
speech signal from the other speaker is temporally either
ahead, behind, or in perfect synchronization with the person
who stutters. In terms of probability, perfect synchronization of two speech signals is relatively rare. In its electronic
manifestations, a second speaker is `derived' via electronic
means to produce a signal, which is temporally out of phase
and oftentimes shifted in frequency. A substantial number
of replicated empirical reports coupled with the near total
absence of opposing reports indicate that endogenous alterations of the speech signal output (e.g. prolonged or slowed
speech, rhythmic speech, singing, and lipped speech) or
exogenous alterations of speech signal input induces relatively ¯uent speech in people who stutter [6]. Exogenous
auditory speech signals in the form of a `second speech
signal' (e.g. chorus reading, shadow speech, delayed auditory feedback, frequency altered feedback) [2±6,8,14,15], or
* Corresponding author. Tel.: 11-252-328-1986; fax: 11-252328-4469.
E-mail address: kalinowskij@mail.ecu.edu (J. Kalinowski).
speech signals via the visual modality (e.g. visual choral
speech) [16], produce more powerful and natural-sounding
reductions in stuttering than incongruous non-speech auditory (e.g. masking noise, clicks) [1,8,10,19] or visual (e.g.
¯ashing lights) inputs [17,18]. All exogenous speech
signals, either produced by a second speaker or produced
via electronic means, should be considered as `second
speech signals'. In other words, when persons who stutter
are speaking in the presence of an exogenous second speech
signal, they always receive two speech signals due to the
impossibility of removing the bone conducted signal generated by the endogenous speech signal (i.e. the person's own
speech), and the incomplete masking of the air-borne speech
signal.
Generally, the reduction in stuttering frequency under
alterations of the second speech signal has been attributed
to such factors as entrained rhythm [14], distraction [5,6],
modi®ed vocalization, and rate reduction [20]. These explanations are based on the assumption that the peripheral
manifestations of stuttering (e.g. repetitions, prolongations,
and audible struggle behaviors) are the problem. There has
been, however, no examination as to the possibility that
0304-3940/00/$ - see front matter q 2000 Elsevier Science Ireland Ltd. All rights reserved.
PII: S03 04 - 394 0( 0 0) 01 50 9- 3
116
J. Kalinowski et al. / Neuroscience Letters 293 (2000) 115±118
stuttering behaviors may be a natural compensatory
mechanism for an `involuntary block' at the central level,
rather than a manifestation of a mechanistic problem at the
peripheral level. If so, then the immediacy and naturalness
of the ¯uency enhancement via the second speech signal
may be explained in a dramatically different manner.
In order to investigate these notions, we examined the
power of an exogenous stuttered speech signal on stuttering
frequency when compared to an exogenous normal speech
signal. We used incongruent second speech signals in order
to compare the inherently incongruent nature of exogenous
stuttered speech to that of the disconsonant ¯uent speech (in
incongruent or disconsonant speech, the second speech
signal contains different phonemic material than that read
aloud by the participants). If ¯uency reduction was observed
as would be expected in the aforementioned compensatory
mechanism model, it would be essential to determine the
speci®c components of the incongruent second speech
signal, which might be responsible for the inducement of
¯uency. Speci®cally, the natural classi®cation scheme of
vowels and consonants were examined in both dynamic
and relatively static vocal tract positions as this provides
an appropriate continuum for examination.
Ten normal-hearing adults who stutter (eight males, two
females, mean ˆ 27.9 years, SD ˆ 9.4) participated in both
experiments. Participants did not present with any other
speech and language disorders. All participants had a
history of therapy, but were currently not receiving any
formal therapeutic intervention. Participants read different
junior-high level passages of 300 syllables with similar
theme and syntactic complexity in both experiments.
Based on informal clinical measures, severity of stuttering
for the participants in this study ranged from moderate to
severe. The two experiments were counterbalanced while
the experimental conditions and the passages were randomized. They were instructed throughout the experiment to
read at a normal rate and not to use any controls to reduce or
inhibit stuttering. In both experiments participants listened
to the exogenous auditory speech signals via supra-aural
earphones (headphones that completely cover the external
ear) at a most comfortable listening level. The participants
listened to the exogenous speech signals during the various
reading tasks in both experiments. It should be reiterated
that the auditory signals used in these experiments did not
fully mask the auditory feedback generated by the participants' own speech. Participants would perceive their endogenously produced speech via bone conduction as well as
portion of the airborne signal due to the incomplete masking
capabilities of the exogenous speech signal.
The ®rst experiment required participants to listen to
incongruous ¯uent or stuttered speech samples presented
continuously or intermittently (50% duty cycle). Both
speech samples were incongruent recorded text. The stuttered speech sample contained discrete stuttering acts on all
words. Thus in total, there were four listening conditions. In
the second experiment, participants listened to four contin-
uous speech signals: a steady state neutral vowel /a/, a three
vowel train representing the three corners of the vowel
triangle /a-i-u/, a steady state consonant /s/, and a three
consonant train /s-sh-f/. The consonants were selected as
these could be presented in the absence of a vowel. Steady
vowels and consonants and trains of each were used to
represent different levels of proximity with the speech act.
Participants also read a control passages for each experiment. This was the non-altered auditory feedback (NAF)
condition, wherein the participants read a passage in the
absence of any external auditory stimuli other than the auditory feedback normally received while speaking (i.e. no
exogenous speech signals).
The stimuli for these samples were recorded in a soundtreated room with a digital tape-recorder (Sony model
8819). A normal ¯uent American-English speaking adult
male produced the vowel, consonant, and ¯uent speech
samples for both experiments. An American-English adult
male who stutters produced the stuttered speech sample for
the ®rst experiment. Both speakers produced speech
samples at a normal vocal effort. The text for the ®rst experiment was junior-high level passages with similar theme and
syntactic complexity as that read by the participants of the
experiments.
The recorded signals were then fed into a personal
computer (Apple Power Macintosh 9600/300) via an apple
sound input port. Sampling was at 44 kHz. Sound analysis
software (Sound Edit version 2) was used to introduce the
silence, select the various stuttering moments, and loop the
signals. Silent intervals randomly varied from 2±5 s. These
were then recorded onto a compact disk that would be used
to deliver the signal via a compact disk player (Sony model
CFD-S28). The signals were delivered binaurally via headphones (Optimus model PRO.50MX) at the participants'
most comfortable level. All participants spoke into a lapel
microphone (Radio Shack model 33-3003) af®xed no more
than 15 cm from their mouths with an approximate orientation of 08 azimuth and 21208 altitude. The microphone
output was fed into a video camera (Sony model CCDTVR 75).
Stuttering episodes were calculated from the participants'
videotape recorded passages. Stuttering was de®ned as partword repetitions, part-word prolongations, and/or inaudible
postural ®xations. Interjudge syllable-by-syllable agreement, as indexed by Cohen's kappa [9] was 0.79. Intrajudge
Cohen's kappa syllable-by-syllable agreement was 0.81.
Kappa values above 0.75 represent excellent agreement
beyond chance [12].
The means and standard deviations for stuttering
frequency as a function of the exogenous auditory
speech signals delivered in Experiment I are as follows:
(a) NAF (mean ˆ 35.4, SD ˆ 25.11), (b) ¯uent interrupted
(mean ˆ 15.4, SD ˆ 17.11), (c) stuttered interrupted (mean
ˆ 14, SD ˆ 15.59), (d) stuttered continuous (mean ˆ 10.4,
SD ˆ 10.09), and (e) ¯uent continuous (mean ˆ 8.6,
SD ˆ 13.2). A one-factor-repeated-measure-analysis-of-
J. Kalinowski et al. / Neuroscience Letters 293 (2000) 115±118
variance revealed a signi®cant main effect of exogenous auditory speech signal on stuttering frequency
(F(4,36)ˆ14.35, Greenhouse-Geiser P ˆ 0.0004, h 2 ˆ 0.62).
A post hoc single-d.f. comparison revealed there was a
signi®cant reduction in stuttering frequency for all forms
of exogenous auditory speech signals relative to NAF
(P , 0:0001). No statistically signi®cant differences were
observed between ¯uent and stuttered speech signals
(P ˆ 0:76), or continuous and interrupted speech signals
(P ˆ 0:10).
The means and standard deviations for stuttering
frequency as a function of exogenous auditory speech
signals delivered in Experiment II ± are as follows: (a)
NAF (mean ˆ 37.5, SD ˆ 27.23), (b) /a/ (mean ˆ 10.3,
SD ˆ 15.98), (c) /a-i-u/ (mean ˆ 8.2, SD ˆ 11.92), (d) /s/
(mean ˆ 18, SD ˆ 20.49), and (e) /s-sh-f/ (mean ˆ 24.9,
SD ˆ 25.53). A one factor repeated measure analysis of
variance reveled a signi®cant main effect of the exogenous
auditory speech signal on stutter-ing frequency
Greenhouse±Geiser
P ˆ 0:0001,
(F…4;36† ˆ 17:77,
h2 ˆ 0:66). A post hoc single-d.f. comparison revealed
there was a signi®cant reduction in stuttering frequency
for all forms of exogenous auditory speech signals relative
to NAF (P , 0:0001). There were also statistically signi®cant fewer stuttering episodes when the exogenous auditory
signals were vowel(s) vs. consonant(s) (P , 0:0001). Nonsigni®cant differences in stuttering frequencies were found
between single versus trains of speech signals (P ˆ 0:40).
Before this set of experiments, to the best of our knowledge, there has been no empirical documentation that both
exogenously generated stutter-®lled and stutter-free incongruous speech signals could induce same levels of ¯uency
enhancement in people who stutter. Our results indicated
that stuttering frequency was substantially reduced, irrespective of whether the exogenous auditory speech signal
were stuttered or stutter free. What are the possible mechanisms that could be involved in the generation of true ¯uency
via the incongruous auditory speech signal presented in the
form of a second speech signal? The ¯uency enhancement
produced by a congruent but temporally shifted speech
signal might suggest a timing or entraining support mechanism (i.e. choral speech, DAF, FAF). However, asynchronous speech signals (i.e. signals used in this study)
produce the same level of ¯uency enhancement as the
signals mentioned above, suggesting some form or type of
`inhibitory response'. That is, the second speech signal
provides the required compensation to aid the system in
effectively executing the motor plan and generates ¯uent
speech in persons who stutter. Our data suggests that a
sonorant, voiced speech signal, stuttered or ¯uent, intermittent or continuous, is an effective acoustic mechanism to
release the system from the involuntary block at the neural
level. However, these second speech signals do not totally
eliminate the involuntary block as they only occur in
compensation to the formation of a `neural block' that has
already occurred. For a second signal to be a prophylaxis to
117
the overt manifestations of stuttering, it must impact the
neural system before the block occurs- as is evidenced in
identical choral speech.
We also suggest that this data might illuminate the
purpose of producing oscillations and sustained vowel
gestures by a person who stutters (i.e. repetitions and
prolongations). It is hypothesized that the person produces
the overt manifestations of stuttering (i.e. repetitions and
prolongations), in an attempt to generate an auditory release
mechanism from an `involuntary block' in speech execution
at the neural level. Simply put the overt manifestations of
stuttering are an attempt to compensate at the peripheral
level for a loss of control at the central level-albeit a
conspicuous compensation. Thus the overt stuttering manifestations are hypothesized to be a form of compensation
rather than a problem in itself. The overt manifestations of
stuttering appear to be analogous to the role of fever in an
infectious disease state. Oftentimes, the fever has been
confused as the problem, when in fact it is an inherent
compensatory mechanism of the body to a disease state.
Thus, a lack of an appropriate ¯uency enhancing gesture
is hypothesized to be the predominate etiological factor that
is exhibited or manifested due to a lack of inhibition on the
part of the auditory cortex in assimilating the appropriate
plan required for the smooth execution of the speech act.
Recent brain imaging procedures have employed choral
speech condition to induce ¯uent speech in adults who stutter and have compared the brain images obtained, to those
attained during the stuttering behavior [13,21]. A lack of
activation in the auditory areas during the motor planning
of stuttered speech was observed, but an essential normalization under the choral speech condition was noted, indicating its inherent ¯uency enhancing capabilities. Simply
put, the second speech signals provide the required inhibition that is essential for the system of a person who stutters,
to smoothly execute the speech act. The resultant inhibition
via the second speech signal eliminates the system from
requiring the production of oscillations or stuttering manifestations (i.e. repetitions and prolongations) that was
previously required to produce speech. Thus the resultant
speech is almost free of the overt manifestations of stuttering.
It should be noted that a parallel between the manifestations of stuttering and that of expressive aphasia has been
identi®ed previously and appears to be support, at least in
part in the data revealed in these experiments [7,11]. That is,
the stuttering and expressive aphasia may exist on a functional-morphological continuum and have similar central
explanations. The power of auditory cueing or priming in
both disorders provides an impetus for further investigation
of the possible parallels of these disorders.
[1] Adams, M.R. and Moore Jr., W.H., The effects of auditory
masking on the anxiety level, frequency of dys¯uency, and
selected vocal characteristics of stutterers, J. Speech Hear.
Res., 15 (1972) 572±578.
118
J. Kalinowski et al. / Neuroscience Letters 293 (2000) 115±118
[2] Andrews, G., Craig, A., Feyer, A., Hoddinott, S., Howie, P.
and Neilson, M., Stuttering: a review of research ®ndings
and theories circa 1982, J. Speech Hear. Disord., 45 (1983)
226±246.
[3] Andrews, G., Howie, P.M., Dozsa, M. and Guitar, B.E., Stuttering: speech pattern characteristics under ¯uency-inducing conditions, J. Speech Hear. Res., 25 (1982) 208±215.
[4] Armson, J., Kalinowski, J. and Stuart, A., A model of stuttering remediation: multiple factors underlying ¯uency
enhancement, In C.W. Starkweather and H.F.M. Peters
(Eds.), Stuttering: Proceedings from The First World
Congress on Fluency Disorders, University Press, Nijmegen, 1995, pp. 296±300.
[5] Barber, V., Studies in the psychology of stuttering: XV,
Chorus reading as a distraction in stuttering, J. Speech
Disord., 4 (1939) 371±383.
[6] Bloodstein, O., A Handbook on Stuttering, 5th edn., Singular, San Diego, CA, 1995.
[7] Boller, F., Vrtunski, P.B., Kim, Y. and Mack, J.L., Delayed
auditory feedback and aphasia, Cortex, 14 (1978) 212±226.
[8] Cherry, E. and Sayers, B., Experiments upon total inhibition
of stammering by external control and some clinical
results, J. Psychosom. Res., 1 (1956) 233±246.
[9] Cohen, J., A coef®cient of agreement for nominal scales,
Edu. Psychol. Meas., 20 (1960) 37±46.
[10] Conture, E.G., Some effects of noise on the speaking behavior of stutterers, J. Speech Hear. Res., 17 (1974) 714±723.
[11] Eisenson, J., Stuttering as preservative behavior, In J.
Eisenson (Ed.), Stuttering: A Symposium, Harper & Row,
New York, 1975, pp. 403±452.
[12] Fleiss, J.L., Statistical Methods for Rates and Proportions,
2nd edn., Wiley, New York, 1981.
[13] Fox, P.T., Ingham, R.J., Ingham, J.C., Hirsch, T.B., Downs,
J.H., Martin, C., Jerabek, P., Glass, T. and Lancaster, J.L., A
PET study of the neural systems of stuttering, Nature, 382
(1996) 158±161.
[14] Johnson, W. and Rosen, L., Studies in psychology of stuttering: VII. Effect of certain changes in speech pattern upon
frequency of stuttering, J. Speech Disord., 2 (1937) 105±109.
[15] Kalinowski, J., Armson, J., Roland-Mieszkowski, M., Stuart,
A. and Gracco, V.L., Effects of alterations in auditory feedback and speech rate on stuttering frequency, Lang.
Speech., 36 (1993) 1±16.
[16] Kalinowski, J., Stuart, A., Rastatter, M.P., Snyder, G. and
Dayalu, V., Inducement of ¯uent speech in persons who
stutter via visual choral speech, Neurosci. Lett., 281 (2000)
198±200.
[17] Kuniszyk-Jozkowiak, W., Smolka, E. and Adamczyk, B.,
Effect of acoustical, visual, and tactile reverberation on
speech ¯uency of stutterers, Folia Phoniatr. Logop., 48
(1996) 193±200.
[18] Kuniszyk-Jozkowiak, W., Smolka, E. and Adamczyk, B.,
Effect of acoustical, visual, and tactile echo on speech
¯uency of stutterers, Folia Phoniatr. Logop, 49 (1997) 26±34.
[19] May, A.E. and Hackwood, A., Some effects of masking and
eliminating low frequency feedback on the speech of stammerers, Behav. Res. Ther., 6 (1968) 219±223.
[20] Wingate, M.E., Stuttering: Theory and Treatment, Irvington,
New York, 1976.
[21] Wu, J.C., Maguire, G., Riley, G., Fallon, J., LaCasse, L., Chin,
S., Klein, E., Tang, C., Cadwell, S. and Lottenberg, S., A
positron emission tomography [18 F] deoxyglucose study
of developmental stuttering, NeuroReport, 6 (1995) 501±
505.