Brain and Cognition 53 (2003) 185–189
www.elsevier.com/locate/b&c

Acquired stuttering following right frontal and bilateral
pontine lesion: A case study
Venu Balasubramanian,a Ludo Max,b John Van Borsel,c Kathleen O. Rayca,d
and Donald Richardsond
b

a
Seton Hall University, NJ, USA
University of Connecticut and Haskins Laboratories, New Haven, CT, USA
c
University of Ghent, Ghent, Belgium
d
VAMC, Philadelphia, PA, USA

Accepted 7 May 2003

Abstract
We report neurological information and experimental data regarding acquired neurogenic stuttering in a 57-year-old male
following ischemic lesion to the orbital surface of the right frontal lobe and the pons. The experimental data consist of stuttering
frequency measures under various conditions that are well known to enhance fluency in most individuals with developmental
stuttering. Specifically, we report data for adaptation, unison reading, delayed auditory feedback (DAF), and frequency altered
feedback (FAF). This work is the first published report of such a comprehensive examination of a variety of fluency-enhancing
conditions in acquired stuttering. The patient read six 200-word texts under different conditions: Six solo readings (Text 1), five
unison readings followed by five solo readings (Text 2), five readings with non-altered auditory feedback (Text 3), five readings with
50 ms delayed auditory feedback (Text 4), five readings with increased FAF (Text 5), and five readings with decreased FAF (Text 6).
Results indicate that, unlike the typical situation for developmental stuttering, this individual with acquired neurogenic stuttering
did not show increased fluency during an adaptation paradigm or under unison, DAF, and FAF conditions. We discuss possible
implications of these findings and emphasize the need for further research on acquired neurogenic stuttering.
Ó 2003 Elsevier Inc. All rights reserved.

1. Introduction
Recently, sophisticated experimental methods have
been applied (e.g., Salmelin, Schnitzler, Schmitz, &
Freund, 2000) to examine some hypotheses regarding
the neural bases of developmental stuttering that had
been formulated several decades ago (Orton, 1927;
Travis, 1931). Unlike the situation for developmental
stuttering, the neural bases of acquired neurogenic
stuttering are matter of certainty. The literature contains several case reports on acquired neurogenic
stuttering following heterogeneous lesion sites in the
left hemisphere (Orton, 1927; Canter, 1971; Carluer,
Lambert, Defer, Coskun, & Rossa, 2000), the right
hemisphere (Ardila & Lopez, 1986; Fleet & Heilman,
1985; Horner & Massey, 1983; Lebrun & Leleux, 1985;
Soroker, Bar-Israel, Schechter, & Solzi, 1990), or both
hemispheres (Balasubramanian & Hayden, 1996;
Helm-Estabrooks, 1993). Although lesions of the net0278-2626/$ - see front matter Ó 2003 Elsevier Inc. All rights reserved.
doi:10.1016/S0278-2626(03)00106-4

work of brain structures supporting motor speech can
lead to a variety of speech disorders, including acquired neurogenic stuttering, cases have also been reported in which neurological lesions led to the
disappearance or reduction of stuttering (Andy &
Bhatnagar, 1992) or to the re-emergence of childhood
stuttering from which the person had recovered in
early years (Helm-Estabrooks, Yeo, Geschwind,
Freedman, & Weinstein, 1986; Mouradian, Paslawski,
& Shauib, 2000).
Several investigators have observed striking similarities in symptomatology between developmental and
acquired neurogenic stuttering. Van Borsel and Taillieu
(2001) reported that even professionals were unable to
differentiate between these two disorders on the basis of
conversational speech samples. Van Borsel (1997) further pointed out that, based on such similarities, one
may be tempted to conclude that developmental stuttering is also due to neurogenic dysfunction. In addition,

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some have argued that acquired stuttering may be influenced by the same variables that have been documented to have an influence on the symptoms of
developmental stuttering. However, studies examining
the role of such variables in acquired neurogenic stuttering have yielded inconsistent results (Van Borsel &
Taillieu, 2001; Ringo & Dietrich, 1995). For example,
most studies have reported an absence of the adaptation
effect (i.e., decreased dysfluency on successive readings
of the same text) in acquired neurogenic stuttering.
However, the method of measuring adaptation in these
studies was often unclear (Ringo & Dietrich, 1995).
Similarly, one cannot generalize the available data regarding the effects of delayed auditory feedback (DAF)
on acquired stuttering. DAF appears to have been applied only to four cases associated with traumatic brain
injury and degenerative diseases (Van Borsel, 1997).
Replicating such work, and extending it to other fluency
enhancing conditions such as frequency altered feedback
(FAF), may provide additional information regarding
differences and similarities between developmental and
acquired stuttering. One group of investigators has reported FAF to be very effective in reducing stuttering
for most cases of developmental stuttering (Stuart, Kalinowski, Armson, Stenstrom, & Jones, 1996) although
others have obtained less consistent findings (Ingham,
Moglia, Frank, Ingham, & Cordes, 1997). To the best of
our knowledge, FAF has not been investigated with
acquired neurogenic stuttering.
The present work reports a case of acquired neurogenic stuttering following ischemic lesion of the
right orbital frontal surface and bilateral attenuation
of the pons. In addition to the neurological background, we present stuttering frequency data collected
in each of the aforementioned fluency-enhancing
conditions (i.e., adaptation, unison reading, DAF, and
FAF).

2. Method
2.1. Subject
CP, a 57-year-old male with a medical history of noninsulin dependent hyperglycemia, hypertension, and
ischemic disease, had a cerebro-vascular accident on 124-2000. A CT scan evaluation on 12-13-2000 revealed a
new subcortical ischemia involving the right hemisphere
and bilateral hypodensity of the pons (see Fig. 1). The
subject was evaluated by a speech–language pathologist
and was found to have dysphagia and occasional deficits
in naming. Since onset of the CVA, CPÕs speech had
reportedly become non-fluent. Family members reported that the symptoms resembled those of the
childhood stuttering that the patient had shown, but
outgrown, at a young age. CP and his brother claimed

Fig. 1. CPÕs CT scans showing right hemisphere orbital surface lesion.

that CP had been free from symptoms of stuttering for
well over four decades.
During oral reading of a 200-word passage, CP
stuttered on 5% of the words. For this evaluation as well
as all experimental conditions, stuttering was defined as
part-word repetitions, audible and inaudible prolongations, broken words, and monosyllabic whole word
repetitions.

V. Balasubramanian et al. / Brain and Cognition 53 (2003) 185–189

187

2.2. Materials
The present study used six different 200-word texts.
These texts were chosen from current issues of ReadersÕ
Digest to have neutral content, and they were used for
different oral reading tasks. Instrumentation involved in
this study included a Korg digital signal processor used
for FAF (Pandora 28086), a Kay Elemetrics Facilitator
(Model 3500) used for DAF, a digital minidisk audio
recorder (Sharp MD-MS722), and a digital video camcorder (JVC GR-DV2000).
2.3. Procedures
CP was seen twice, with a one-month interval between the sessions. Each session lasted approximately
one hour. In the first session, CP was tested in an adaptation/unison reading paradigm previously described
by Max, Caruso, and Vandavenne (1997). This paradigm included an adaptation condition with six solo
readings of a 200-word passage (Text 1) and a chorus
reading condition in which the subject read another 200word passage five times in unison with a speech–language pathologist and then five times solo (Text 2).
In the second session, CP was tested using altered
auditory feedback conditions. A non-altered auditory
feedback condition served as a control condition. In this
control condition, CP was wearing headphones while
reading a 200-word passage (Text 3) but his speech was
fed back to his ears without any modification. It was
followed by a DAF condition during which CPÕs speech
was fed back to his ears through the headphones with a
delay of 50 ms. During this task, CP read another 200word passage (Text 4). For an increased FAF condition,
CPÕs speech was altered by increasing the frequencies of
his speech spectrum by 1/2 octave prior to feeding the
speech signal back to his ears through the headphones.
Another 200-word passage (Text 5) was read in this
condition. For a decreased FAF condition, CPÕs speech
was altered by decreasing the frequencies in the acoustic
signal by 1/2 an octave before it was fed back to his ears
through the headphones. As with all other conditions,
CP read a different 200-word passage (Text 6). For each
reading in each condition, both audio and video signals
were recorded.

3. Results and discussion
All adaptation/unison and altered auditory feedback
results for CP are shown graphically in the middle and
bottom panels, respectively, of Fig. 2. For comparison,
the top panel of the figure also shows the stuttering frequency group data for adults with developmental stuttering during solo reading and unison reading followed by
solo reading as previously reported by Max et al. (1997).

Fig. 2. Top panel: Previously reported stuttering frequency group data
(N ¼ 10) for adults with developmental stuttering during solo reading
and unison reading followed by solo reading (Max et al., 1997). Middle
panel: Stuttering frequency for the individual with acquired neurogenic
stuttering during the same two conditions. Bottom panel: Stuttering
frequency for the individual with acquired neurogenic stuttering during
reading under normal auditory feedback (NAF), 1/2 octave up frequency-altered auditory feedback (FAF +1/2), 1/2 octave down frequency-altered auditory feedback (FAF )1/2), and 50 ms delayed
auditory feedback (DAF).

As shown in the middle panel of Fig. 2, CP showed no
evidence of an adaptation effect during six repeated solo
readings. Moreover, it can be seen that unison reading, a
strong fluency-enhancing condition for individuals with
developmental stuttering, had no beneficial effects on the
stuttering frequency of CP. As shown in the bottom panel
of Fig. 2, DAF and FAF also failed to enhance fluency in
CPÕs oral reading. In fact, in all three altered feedback
conditions, CPÕs stuttering frequency was slightly higher
than that observed during the control condition.

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Clearly, the results for CP, an adult with acquired
neurogenic stuttering, are inconsistent with those reported by Max et al. (1997) for adults with developmental stuttering. Comparing the lack of adaptation in
CPÕs solo reading with the presence of such an effect in
most cases of developmental stuttering, it may be the
case that individuals with developmental stuttering but
not individuals with acquired neurogenic stuttering
benefit from repeated practice (i.e., resulting in motor
learning) of a limited set of speech utterances. This may
suggest that the stuttering symptoms seen in acquired
neurogenic and developmental stuttering are not based
on the same neural dysfunction (Van Borsel, 1997). In
particular, this finding is in keeping with the hypothesis
that developmental stuttering may involve, at least in
part, a problem with the process of developing and refining internal models for speech motor control (i.e., the
neural mapping between motor commands and the
sensory consequences of those commands) during
speech development (Max, in press). It would seem
reasonable to speculate, then, that such a problem
would allow individuals with developmental stuttering
to obtain some benefits from repeated motor practice. In
acquired neurogenic stuttering, on the other hand, the
dysfluencies are the result of an actual lesion and shortterm practice such as provided during an adaptation
paradigm may be insufficient to result in improved
speech fluency.
The lack of enhanced fluency under DAF and FAF
conditions also suggests that the mechanisms underlying
CPÕs non-fluent speech are different from those involved
in individuals with developmental stuttering given that
the speech of the latter group typically becomes more
fluent under these conditions. Most certainly, CPÕs lesion in the right hemisphere orbital surface does not
suggest a causal role for the auditory system in this case.
However, the effects of DAF and FAF need to be further explored in acquired neurogenic stuttering to replicate the present findings. Indeed, individuals with
developmental stuttering also vary in terms of which
delay and frequency shifts are most optimal, and they do
not respond uniformly to FAF conditions (Ingham et
al., 1997). Hence, other DAF durations and FAF frequency shifts should be investigated in future studies on
acquired stuttering. There is clearly a need for further
study in this regard.
Interestingly, the role of right hemisphere in speech
production has become increasingly clear in recent research (Goulet, Joanette, & Van Dongen, 1997; Kurowski, Blumstein, & Mathison, 1998). The present
work documents a case of acquired neurogenic stuttering following lesions in both the right hemisphere and
the pons. Of course, this case study and the accompanying experimental data do not allow us to attribute the
patientÕs stuttering specifically to either of these two lesions. In order to gain a better understanding of the

differences and similarities between developmental and
acquired stuttering, and the neurological mechanisms
underlying each of these two disorders, more cases with
a variety of etiologies/sites of lesion resulting in acquired
neurogenic stuttering need to be studied using a large
number of tasks. We hope that the tasks and analyses
used in the present study will form a first step in this
direction.

References
Andy, J. O., & Bhatnagar, S. C. (1992). Stuttering acquired from
subcortical pathologies and its alleviation from thalamic perturbation. Brain and Language, 42, 385–401.
Ardila, A., & Lopez, M. V. (1986). Severe stuttering associated with
right hemisphere lesion. Brain and Language, 27, 239–246.
Balasubramanian, V., Hayden, P. A., 1996. Acquired stuttering
following bilateral parietal lobe lesion: A case report. In: C. W.
Starkweather & H. F. M. Peters (Eds.), Proceedings of the first
world congress of fluency disorders (pp. 617–620). Nijmegen:
University Press, The International Fluency Association.
Canter, G. (1971). Observations on neurogenic stuttering: A contribution to differential diagnosis. British Journal of Disorders of
Communication, 6, 139–143.
Carluer, L., Lambert, J., Defer, G. L., Coskun, O., & Rossa, Y. (2000).
Acquired and persistent stuttering as the main symptom of striatal
infarction. Movement Disorder, 15, 343–346.
Fleet, W. S., & Heilman, K. M. (1985). Acquired stuttering from a
right hemisphere lesion in a right hander. Neurology, 35, 1343–
1346.
Goulet, P., Joanette, Y., & Van Dongen, H. (1997). Word fluency after
right hemisphere lesion. Neuropsychologia, 35, 1565–1570.
Helm-Estabrooks, N. (1993). Stuttering associated with acquired
neurological disorders. In: R. Curlee (Ed.), Stuttering and related
disorders of fluency. New York: Thieme Medical Publishers.
Helm-Estabrooks, N., Yeo, R., Geschwind, N., Freedman, M., &
Weinstein, C. (1986). Stuttering: Disappearance and reappearance
with acquired brain lesions. Neurology, 36, 1109–1112.
Horner, J., & Massey, E. W. (1983). Progressive dysfluency associated
with right hemisphere disease. Brain and Language, 18, 71–85.
Ingham, R. J., Moglia, R. A., Frank, P., Ingham, J. C., & Cordes, A.
K. (1997). Experimental investigation of the effects of frequencyaltered feedback on speech of adults who stutter. Journal of Speech,
Language, and Hearing Research, 40, 361–372.
Kurowski, K. M., Blumstein, S. E., & Mathison, H. (1998). Consonant
and vowel production of right hemisphere patients. Brain and
Language, 63, 276–300.
Lebrun, Y., & Leleux, C. (1985). Acquired stuttering following right
brain damage in dextrals. Journal of Fluency Disorders, 10, 137–
141.
Max, L. (in press). Stuttering as a neuromotor disorder: Identifying the
mechanisms. In: B. Maassen, R. Kent, H. F. M. Peters, P. Van
Lieshout & W. Hulstijn (Eds.), Speech motor control in normal and
disordered speech. Oxford University Press.
Max, L., Caruso, A. J., & Vandavenne, A. (1997). Decreased stuttering
frequency during repeated readings: A motor learning perspective.
Journal of Fluency Disorders, 22, 1–17.
Mouradian, M. S., Paslawski, T., & Shauib, A. (2000). Return of
stuttering after stroke. Brain and Language, 73, 120–123.
Orton, S. T. (1927). Studies in stuttering: Introduction. Archives of
Neurology and Psychiatry, 18, 671–672.
Ringo, C. C., & Dietrich, S. (1995). Neurogenic stuttering: An analysis
and critique. Journal of Medical Speech Language Pathology, 3,
111–122.

V. Balasubramanian et al. / Brain and Cognition 53 (2003) 185–189
Salmelin, R., Schnitzler, A., Schmitz, F., & Freund, H. J. (2000). Single
word reading in developmental stutterers and fluent speakers.
Brain, 123, 1184–1202.
Soroker, N., Bar-Israel, Y., Schechter, I., & Solzi, P. (1990). Stuttering
as a manifestation of right hemisphere subcortical stroke. European
Neurology, 30, 268–270.
Stuart, A., Kalinowski, J., Armson, J., Stenstrom, R., & Jones, K.
(1996). Fluency effect of frequency alterations of plus/minus onehalf and one-quarter octave shifts in auditory feedback of people

189

who stutter. Journal of Speech and Hearing Research, 39, 396–
401.
Travis, L. E. (1931). Speech pathology. Englewood Cliffs, NJ: PrenticeHall.
Van Borsel, J., & Taillieu, C. (2001). Neurogenic stuttering versus
developmental stuttering: An observer judgment study. Journal of
Communication Disorders, 34, 1–11.
Van Borsel, J. (1997). Neurogenic stuttering: A review. Journal of
Clinical Speech and Language Studies, 7, 16–33.