J. COMMUN. DISORD. 33 (2000), 227–240
© 2000 by Elsevier Science Inc. All rights reserved. 0021-9924/00/$–see front matter
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DYSFLUENCY AND PHONIC TICS
IN TOURETTE SYNDROME:
A CASE REPORT
JOHN VAN BORSEL
Ghent University Hospital, Ghent, Belgium
University of Central Florida, Orlando, Florida
Tourette syndrome, a condition first recognized in 1825, is characterized by the presence of
multiple motor tics and one or more phonic tics. Individuals with Tourette syndrome may
also demonstrate fluency failures in their speech. This study investigated the disfluencies
and phonic tics in an 18-year-old affected male before and after a three week period of
speech therapy. It was found that the speech pattern displayed by this subject did not com-
pletely conform to the classic pattern of stuttering but did bear more resemblance to clutter-
ing. A limited number of therapy sessions resulted in a significant improvement of
speech. © 2000 by Elsevier Science Inc.
The reader will learn (1) about the tics and disfluency types that
might be present in people with Tourette syndrome; and (2) that the fluency failures associ-
ated with this syndrome are not characteristic of stuttering.
Tourette syndrome; Stuttering; Cluttering; Disfluency, Tics
Tourette syndrome (TS) is a condition that was first described in 1825 by the
French physician J.M. Itard (Itard, 1825), who reported on the presence of
tics, barking sounds, and uncontrollable utterances of obscenities in a French
noblewoman, Marquise de Dampierre. A more detailed description of eight
additional cases was published in 1885 by another French physician, George
Gilles de la Tourette (Gilles de la Tourette, 1885), after whom the disorder was
According to the DSM-IV (American Psychiatric Association, 1994), the
essential feature of TS is the presence of multiple motor tics and one or more
vocal tics that occur many times a day, recurrently throughout a period of
Address correspondence to John Van Borsel, Ph.D., UZ Gent, 2P1, Centrum voor Gehoor- en
Spraakrevalidatie, De Pintelaan 185, B-9000 Gent, Belgium. Tel:
32 9 240 22 96; Fax:
32 9 240 49
228 VAN BORSEL and VANRYCKEGHEM
more than one year, and cause marked distress or significant impairment in
social, occupational, or other important areas of functioning. TS has its onset
before the age of 18 years, and is not due to the direct physiological effects of
a substance or a general medical condition.
Two studies conducted in the 1980s (Kurlan, Behr, Medved, Shoulson,
Pauls, & Kidd, 1987; Rassas Cohn, Shames, McWilliams, & Ferketic, 1983)
estimated the prevalence of TS to be between a low of .01% and a high of
1.6%. The percentage prevalence at the high end of this range was, however,
not confirmed by more current studies that report a prevalence ranging from
.03% to 1% (Cardoso, Veado, & Teotoino de Oliveira, 1996; Van de Weter-
ing, Cath, & Buitelaar, 1996; Woods & Miltenberger, 1995). It is generally
agreed that TS is three to four times more likely among males than females
(Breakfield & Bressman, 1987; Cardozo, Veado, & Teotonio de Oliveira,
1996; Colligan, 1989; Rassas Cohn, Shames, McWilliams, & Ferketic,1983;
Singer & Walkup, 1991).
Research relative to the etiology and pathogenesis of TS has made it clear
that in most cases the disorder is genetically determined (Duffy, 1995). Most
likely there is an autosomal dominant inheritance with sex-specific penetrance
and variable expression (Pauls & Leckman, 1986; Van de Wetering & Pauls,
1996). It has been suggested that TS is caused by a dysfunction of central neu-
rotransmitter systems. Dopaminergic, serotonergic, noradrenergic, cholin-
ergic, GABAergic, as well as opoid systems have been found to show abnor-
malities in individuals with TS (Kurlan, Behr, Medved, Shoulson, Pauls,
Kidd, & Kidd, 1986; Malison, McDougle, Van Dyck, Scahill, Baldwin,
Seibyl, Price, Leckman, & Iniis, 1995; Singer, 1992; Singer & Walkup, 1991).
The exact neuroanatomic localization of the dysfunction is presently un-
known. Sites of pathogenesis that have been mentioned are the basal ganglia,
the limbic system, the (pre)frontal cortex, and the thalamus (Singer, 1997;
Singer & Walkup, 1991; Van Woerkom, Van de Wetering, & Buitelaar,
Motor and vocal tics are behaviorally at the core of TS. Motor tics consist
of intermittent movements. They are defined as simple if the movements are
brief and involve only one muscle group. They are considered complex if they
appear as longer, more purposeful sequential movements, such as hopping or
writing the same word over and over. Vocal tics consist of abnormal sounds
and noises. Because not all the abnormal sounds and noises made by patients
with tics are produced by the vocal cords, the term “phonic tics” is to be pre-
ferred over “vocal tics.” (Jankovic, 1997). Phonic tics are considered simple
when sudden, fast, single meaningless sounds or words are uttered. Linguisti-
cally meaningful utterances, on the other hand, are classified as complex
phonic tics. These are exemplified by rituals, unusual accents, and change in
speech intensity (Bruun, Cohen, & Leckman, 1997). Coprolalia and echolalia
also belong to the category of complex tics. They are defined, respectively, as
DYSFLUENCY IN TOURETTE SYNDROME 229
“obscene, aggressive, or otherwise socially unacceptable words or phrases”
(Bruun, Cohen, & Leckman, 1997) and “the involuntary repetition of all or
part of the speech partner’s utterance” (Lebrun, 1993).
Attention deficit disorder and obsessive compulsive behavior are com-
monly cited as being associated with TS. So, too, are alcoholism, drug abuse,
conduct disorders, anxiety, and eating as well as sleep disorders (Comings &
Comings, 1993). Recently, learning disabilities and speech disorders have
also been seen as part of TS. Individuals with TS have been described as hav-
ing delayed speech, poor diction, poor language expression, and as talking too
fast and too loud and exhibiting disfluent speech. The fluency failures de-
scribed range from “repetitions, hesitations, and false starts” (O’Quinn &
Thompson, 1980) and “interjections, whole-word repetitions, prolongations,
phrase and part-word repetitions, revisions” (Rassas Cohn, Shames, McWil-
liams,& Ferketic, 1983) to “stutter-like behavior” (Singer, Pepple, Ramage, &
Butler, 1978) and “stutter-like repetitions of sounds” (Aronson, 1980). Palila-
lia, a disorder of speech characterized by compulsive repetition of a phrase or
word that the patient often utters with increasing rapidity and with decre-
scendo of voice volume (Brain, 1961) has also been seen in persons with TS
(Cardoso, Veado, & Teotonio de Oliveira, 1996; Jankovic, 1997; Ludlow, Po-
linsky, Caine, Bassich, & Ebert, 1982).
Although the incidence of stuttering or at least stutter-like behavior among
those with TS is said to range from 15.3% (Pauls, Leckman, & Cohen, 1993)
to 31.3% (Comings & Comings, 1993), little knowledge exists relative to the
types of speech disruptions that they display. Data relative to the types of dis-
fluency, their frequency, and their locus are essentially nonexistent at this
time. Hard data as to the fluency failures of those with TS are critically needed
in order to study the variables that set the occasion for their occurrence and to
develop management procedures that will bring them under control. So, too, is
information relative to the affective and cognitive components which might be
associated with the fluency failures that they evidence. It would serve to make
differential diagnostic determination easier and therapeutic procedures more
appropriate and effective. The present case study of a person suffering from
TS is seen as a first step in the gathering of information on the speech-related
characteristics of this disorder.
CASE HISTORY AND INITIAL SCREENING
The subject of this study, G., was an 18-year-old right-handed male with a
clinical diagnosis of TS since the age of 12. He lived at home with his mother,
stepfather, one older sister, and a younger stepbrother. The stepfather joined
the family when G. was six years of age, two years after G’s parents divorced.
G. received vocational education until the age of 17. At school, he was fre-
quently the victim of bullying because of the tics he exhibited. At the time the
230 VAN BORSEL and VANRYCKEGHEM
present study was undertaken, G. was unemployed. Testing at age 18 years 3
months revealed that G. was of low-normal intelligence, with a verbal IQ that
was significantly lower (p
5%) than the performance IQ (WAIS: TIQ
94). No history of TS or stuttering was reported in the family.
Disfluent speech was first observed, according to G.’s mother, at about the
age of 14. However, G. never received speech therapy. Medical records men-
tioned also the presence of coprolalia (which, according to his mother, was
also first noticed at age 14). Over the years, G. had been administered differ-
ent medicines, including Seroxat, Dipiperon, Risperidone, Risperdal, and In-
deral retard mitis. The medication was taken irregularly, however, or was
stopped prematurely. Between the ages of 18 and 20, G. was admitted to the
psychiatric ward of the Ghent University Hospital on three separate occasions
because of aggressive behavior, acting out, and amphetamine, cocaine, and al-
cohol abuse. During a period of hospitalization at age 18, he was referred to us
for a speech-language assessement with a request for possible therapy. An ini-
tial screening showed that G. had difficulties with verbal and graphic expres-
sion. He could not easily formulate ideas, sometimes halting and then again
speaking in short spurts. From time to time he also produced grammatical er-
rors, and his articulation was often slurred. Foremost, however, he showed a
great number of disfluencies in his speech, as well as many tics. His writing
was graphically irregular with many overwritings. G. did not use capitaliza-
tion, and spontaneous writing was characterized by chaining and repetition of
DATA COLLECTION AND ANALYSIS
Data were collected on two separate occasions: once during the initial assess-
ment and a second time six weeks later upon dismissal from the psychiatric
ward. Between these, G. had received speech therapy for a period of three
Data collected prior to therapy included: samples of automatized speech
(reciting days of the week and months of the year, and counting from 1 to 20);
word and sentence repetition (parts 2 to 5 of the subtest “Naspreken” from the
Dutch version of the Aachener Aphasie Test (Graetz, De Bleser, & Willmes,
1992); oral reading (Dutch version of
The North Wind and the Sun
tional Phonetic Association, 1974); conversational speech (about leisure ac-
tivities); semantic fluency (retrieval of names of animals, subtest of the Dutch
aphasia battery S.A.N.; Deelman, Koning-Haanstra, Liebrand, & Van De
Burg, 1981); final-word repetition (repeating the final word of sentences using
part 5 of the subtest “Naspreken”’ from the Dutch version of the Achener
Aphasie Test; (Graetz, De Bleser, & Willmes, 1992); and singing (G. sang a
non-standard version of a Dutch nursery song). In addition, the Erickson
S-scale of Communication Attitudes (Erickson, 1969) was administered. This
DYSFLUENCY IN TOURETTE SYNDROME 231
39-item questionnaire investigates a person’s attitude toward speech. Finally,
oral mechanism mobility was investigated, and inhibition of tics was probed
(The patient was asked to inhibit tics during two consecutive minutes of si-
The speech therapy following the initial assessment consisted of seven
half-hour sessions and was given by the first author. It focused on the use of
slowed and syllable-timed speech as well as on awareness training for the bi-
labial tics which G. demonstrated.
For the purpose of pre-post comparison, speech samples were once more
collected following the therapy sessions. G. orally read the text
Wind and the Sun
(International Phonetic Association, 1974) and engaged in a
conversation (on the topic of cooking and food preferences).
Both speech sampling sessions took place in a sound-protected room in the
ENT department of the University Hospital and were video-recorded (Sony
Video Hi 8 camera). The samples were subsequently subjected to an ortho-
graphic transcription of the recordings by both authors (consensus transcrip-
tion) and to an analysis of the number and type of disfluencies for each speech
task sampled as well as an analysis of type and number of phonic tics in the
various speech tasks. For all analyses, consensus was reached by both authors.
For the analysis of disfluencies, an adaptation of the taxonomy of Johnson &
Associates (Johnson & Associates, 1959) was used. For the analysis of phonic
tics, an ad hoc procedure was adopted, distinguishing categories of tics ac-
cording to their acoustic and visual characteristics as they occurred in the
speech samples rather than by classifying them according to a predetermined
closed set of phonic tics.
Results of the analysis of G.’s disfluencies are shown in Table 1. The upper
part summarizes the results from the initial assessment, whereas the lower part
presents the results during oral reading and conversation after therapy. As can
be seen from this table, during the initial assessment, 450 of the 1770 syllables
uttered across different speech tasks (i.e., 25.4%) showed some type of disflu-
ency. This high number of disfluent syllables relative to the number of disflu-
encies stems from the fact that one disfluency might involve several syllables
(e.g., “he came came came home”
1 word repetition involving 3 syllables).
Disfluencies were most frequent during semantic fluency (46.3% of the sylla-
bles uttered) and conversation (32.3% of the syllables uttered). Disfluencies
were also observed during word repetition and automatic series but to a much
lesser degree (involving, respectively, 7.4% and 1.2% of the syllables ut-
tered). No disfluencies were observed during sentence repetition, oral reading,
final word repetition, and singing.
Overall, interjections were the predominant type of disfluency, accounting
232 VAN BORSEL and VANRYCKEGHEM
Type and Number of Disfluencies in Different Speech Tasks
TH # Syll Disfl
Syll PWR WR
Multi INTJ PR REV IP PROL BLOCK
series 81 1
(1.2%) —— — 1 — ——— —
repetition 68 5
(7.4%) —— — 3 —1 —— —
repetition 99———— — —————
Oral reading 182 — — — — — — — — — —
Conversation 1043 337
(32.3%) 13 12 12 51 30 18 6 — —
fluency 231 107
(46.3%) 54 3 53 9 3 ———
repetition 15———— — —————
Singing 51 — — — — — — — — — —
Oral reading 182 — — — — — — — — — —
Conversation 369 27
(7.3%) 11 —5 4 2 ———
Number of Syllables Uttered, Disfl Syll
Number of Disfluent Syllables, PWR
Part Word Repetition, WR Mono
Word Repetition of a Monosyllabic Word, WR Multi
Word Repetition of a Multisyllabic Word, INTJ
Phrase Repetition, REV
Incomplete Phrase, PROL
DYSFLUENCY IN TOURETTE SYNDROME 233
for 48.2% of all disfluencies demonstrated. Also, phrase repetitions occurred
with a relatively high frequency (17.4%). Revisions (9.8%), part-word repeti-
tions (8%), repetition of monosyllabic words (7.1%), repetition of multi-syl-
labic words (6.7%), and incomplete phrases (2.7%) were less frequently emit-
ted speech disruptions. Prolongations and blocks did not occur at all.
The lower part of Table 1 shows that, post therapy, the overall number of
disfluent syllables demonstrated during conversation dropped dramatically
from 32.3% to 7.3%. Again, interjections and phrase repetitions were the
types of disfluency that occurred most frequently.
Table 2 summarizes the results of the analysis of phonic tics. Across all
speech tasks sampled during the initial session (left part of Table 2), G. pro-
duced a sum total of 52 phonic tics. More than one-third of these (34.6%) were
demonstrated during conversation. Another 21.2% and 19.2% were produced
during word repetition and the semantic fluency test, respectively. The vast
majority of the phonic tics (24/52, i.e., 46%) were simple tics involving the bi-
labial area, namely, sputtering, spitting, and smacking. Another category of tics
that was seen rather frequently (8/52, i.e., 15.4%) involved the laryngeal area
and consisted of an audible egressive or ingressive sound produced with open
mouth or an audible egressive, somewhat humming-like sound. Still other tics
included inhalation or exhalation, sniffing, slurping, and throat clearing.
Although G.’s records mentioned the occurrence of coprolalia and G. him-
self reported to us that he demonstrate coprolalia from time to time, no in-
stances were noted during data collection of the present study or during the
therapy sessions. Neither did we find any examples of echolalia. The only
complex phonic tic that was observed was a sudden increase in loudness. This
type of tic was observed five times.
When comparing the number of phonic tics per syllables uttered during the
initial session with the number of phonic tics produced after therapy (right
part of Table 2), a slight increase can be observed during conversation (from
18/1043, i.e., 1.7% to 8/369, i.e., 2.2%) and a decrease during oral reading
(from 4/182, i.e., 2.2% to zero). Qualitatively the tics were far less conspicu-
ous after therapy and were sometimes hardly audible.
On the Erickson S-scale, G. obtained a score of 28, which is almost two
standard deviations above the mean for non-stutterers and slightly above the
mean for stutterers. This indicates that G. exhibits a clinically significant neg-
ative attitude toward his speech. Oral mechanism mobility proved overall
good for tongue as well as for lip movements. Lateral movements of the
tongue, however, were associated with head movements. G. appeared capable
of inhibiting phonic tics for two consecutive minutes of silence, but he did
continue to show motor tics. While he was filling out the Erickson S-scale, it
was also observed that G. could not refrain from producing a word aloud now
and then, sometimes even with excessive loudness. The same tendency had
been noted during spontaneous writing and copying.
234 VAN BORSEL and VANRYCKEGHEM
Type and Number of Phonic Tics in Different Speech Tasks
Prior to Therapy After Therapy
Number Conversation Oral
Sputtering 1 4 1 1 8 1 3 19 4 —
Spitting 1 2 — 1 — — — 4 — —
Smacking 1 — — — — — — 1 — —
Ingressive — 2 — — 1 13
Egressive — — — — — — 1 1 — —
Inhalation — 1 — — 1 — 1 3 — —
Exhalation — 1 1 — — — — 2 — —
Sniffing — 1 1 — 1 — — 3 — —
Slurping — — — 2 4 — — 6 1 —
loudness ————3 —25 2 —
clearing ——1 — — ——1 — —
DYSFLUENCY IN TOURETTE SYNDROME 235
Several authors have reported the presence of disfluent speech in people with
TS (Aronson, 1980; O’Quinn & Thompson, 1980; Rassas Cohn, Shames,
McWilliams, & Ferketic, 1983; Singer, Pepple, Ramage, & Butler, 1978), and
at least some of them label this disfluent speech as stuttering (Comings &
Comings, 1993; Pauls, Leckman, & Cohen, 1993). The results of the present
study confirm that disfluent speech may be encountered in individuals with
TS. In the case described in this article, more than one-quarter of the syllables
in the speech sample collected prior to speech therapy were affected by disflu-
encies. However, whether the disfluent speech in our subject is genuine stut-
tering is less clear. Only 15% of the total number of disfluencies in the initial
assessment were of the kind that most researchers would consider to be char-
acteristic of stuttering (part-word repetitions, 8%; monosyllabic word repeti-
tions, 7%). The vast majority of the disfluencies (85%) were disfluencies that
are also seen in “normal” speakers. In this respect, our findings run parallel to
those of Rassas Cohn and colleagues (Rassas Cohn, Shames, McWilliams, &
Ferketic, 1983), who studied the disfluencies in a 25-year-old male with TS.
They reported that in spontaneous speech, 38% of the subject’s disfluencies
were interjections, 26% were whole-word repetitions, 9% were phrase repeti-
tions, and 6% were revisions. Only 21% of their subject’s fluency failures
were disfluencies characteristic of stuttering (prolongations, 15%; repetitions, 6%).
Evidently the speech pattern displayed by our subject does not completely
conform to the classic pattern of stuttering. It does, however, seem to bear
more resemblance to another type of fluency disorder, that of cluttering. As is
typically seen in cluttering, G. used many interjections and repeated whole
words and phrases. At times he also showed a rapid speech rate and spoke in
spurts. Furthermore, it had been observed during the initial screening that G.’s
wording was often disorganized and confused. Also, his grammar was rather
poor, his articulation was sometimes slurred, and his writing was disinte-
grated. All of these are patterns that are considered suggestive of cluttering
(Daly, 1993). In addition, the observation that a limited number of therapy
sessions resulted in a significant improvement of G.’s speech, at least tempo-
rarily, could indicate cluttering. It is a well-known fact that clutterers can, for
a period of time, control their speech. Insofar as the speech pattern displayed
by our subject is similar to that of other patients with TS, the present study
raises the question whether the disfluency associated with TS is not a manifes-
tation of cluttering rather than stuttering. A counter-argument for cluttering is
the fact that G. showed a negative speech-associated attitude that was signifi-
cantly elevated. A mal-attitude toward speech is not typically seen among
clutterers. It is, however, common among stutterers.
Whether the finding that the pattern of fluency failures found in this subject
is more reminiscent of cluttering than of stuttering implies that the underlying
236 VAN BORSEL and VANRYCKEGHEM
mechanism of the disfluent behavior is different from that of developmental
stuttering is hard to tell. It seems reasonable to assume that the fluency fail-
ures in individuals with TS are somehow related to the central neurotransmit-
ter systems dysfunction that is assumed to be at the base of TS. Several sites
of pathogenesis have been postulated, including the basal ganglia, the limbic
system, the (pre)frontal cortex and the thalamus (Singer, 1997; Singer &
Walkup, 1991; Van Woerkom, Van de Wetering, & Buitelaar, 1996). How-
ever, recent neuroimaging studies have mentioned all of these brain areas as
being involved in developmental stuttering (Logan, 1999). Moreover, Ab-
wender and colleagues (Abwender, Trinidad, Jones, Como, Hymes, & Kurlan,
1998) examined twenty-two stutterers for neuropsychiatric features com-
monly seen in TS, including tics, obsessive-compulsive behaviors, and atten-
tion deficit disorders. These authors found that eleven subjects displayed mo-
tor tics, and symptoms of obsessive-compulsive behavior were observed at
rates similar to those seen in persons with Tourette syndrome. According to
Abwender and colleagues (Abwender, Trinidad, Jones, Como, Hymes, &
Kurlan, 1998) their findings are consistent with models suggesting extrapyra-
midal involvement in developmental stutterers and raise the possibility that
developmental stuttering and TS are pathogenetically related.
It is clear that more research is needed in order to clarify issues that relate
to type of disfluency and accompanying features of the fluency failures in TS.
Studies, with a larger number of participants, investigating not only the behav-
ioral but also the affective and cognitive components of the disorder will shed
light on the constituent elements of fluency problems in this population and
improve differential diagnostic determinations.
Abwender, D.A., Trinidad, K.S., Jones, K.R., Como, P.G., Hymes, E., &
Kurlan, R. (1998). Features resembling Tourette’s syndrome in develop-
Brain and Language, 62
American Psychiatric Association (1994).
Diagnostic and statistical manual
of mental disorders.
ed.) Washington, D.C.
Aronson, A. (1980).
Clinical voice disorders — an interdisciplinary ap-
New York: Brian Decker Division of Thieme Stratton.
Brain, R. (1961).
Speech disorders: aphasia, apraxia and agnosia.
ton, D.C.: Butterworth.
Breakfield, X.O., & Bressman, S. (1987). Molecular genetics of movement
disorders. In S. Fahn & E.D. Marsden (Eds.),
Movement disorders II.
DYSFLUENCY IN TOURETTE SYNDROME 237
Bruun, R.D., Cohen, D.J., & Leckman, J.F. (1997). Guide to the diagnosis and
treatment of Tourette syndrome. http://www.mentalhealth.com/book/p40-
Cardoso, F., Veado, C., & Teotonio de Oliveira, J., (1996). A Brazilian cohort
of patients with Tourette’s syndrome.
Journal of Neurology, 60
Colligan, N. (1989). Recognizing Tourette syndrome in the classroom.
Comings, D., & Comings, B. (1993). Comorbid behavioral disorders. In R.
Handbook of Tourette’s syndrome and related tic and behav-
New York: Marcel Dekker, Inc.
Daly, D.A. (1993). Cluttering. Another fluency syndrome. In R.F. Curlee
Stuttering and related disorders of fluency
(pp. 179–204). New York:
Thieme Medical Publishers.
Deelman, W.B.G., Koning-Haanstra, M., Liebrand, K., & Van De Burg, W.
S.A.N. Test. Een afasietest voor auditief taalbegrip en mondeling
Lisse: Swets & Zeitlinger.
Duffy, J.R., (1995).
Motor speech disorders
(pp. 210–211). New York:
Erickson, R.L. (1969). Assessing communication attitudes among stutterers.
Journal of Speech and Hearing Research, 12
Gilles de la Tourette, G. (1885). Etude sur une affection nerveuse caractérisée
par de l’incoordination motrice accompagnée d’écholalie et de coprolalie
Archives de Neurologie, 9
, 19–42, 158–200.
Graetz, P., De Bleser, R., & Willmes, K. (1992).
De Akense afasie test. Ned-
. Lisse: Swets & Zeitlinger.
International Phonetic Association (1974).
The principles of the International
London: International Phonetic Association.
Itard, J. (1825). Mémoire sur quelques fonctions involontaires des appareils
de la locomotion, de la préhension et de la voix.
Archives Générales de Mé-
Jankovic, J. (1997). Phenomenology and classification of tics.
Clinics of North America, 15
Johnson, W., & Associates (1959).
The onset of stuttering.
versity of Minnesota Press.
Kurlan, R., Behr, J., Medved, L., Shoulson, I., Pauls, D., Kidd, J., & Kidd, K.
238 VAN BORSEL and VANRYCKEGHEM
(1986). Familial Tourette syndrome: report of a large pedigree and potential
for linkage analysis.
Kurlan, R., Behr, J., Medved, L., Shoulson, I., Pauls, D., & Kidd, K. (1987).
Severity of Tourette’s syndrome in one large kindred: implication for deter-
mination of disease prevalence rate.
Archives of Neurology, 44
Lebrun, Y. (1993). Repetitive phenomena in aphasia. In G. Blanken, J. Dittmann,
H. Grimm, J.C. Marshall, & C.W. Wallesch (Eds.),
Linguistic disorders and
pathologies. An international handbook.
Berlin/New York: Walter de Gruyter.
Logan, R. (1999).
The three dimensions of stuttering: Neurology, behaviour
London: Whurr Publishers.
Ludlow, C.L., Polinsky, R.J., Caine, E.D., Bassich, C.J., & Ebert, M.H.
(1982). Language and speech abnormalities in Tourette syndrome.
vances in Neurology, 35
Malison, R., McDougle, C., Van Dyck, C., Scahill, L. Baldwin, R., Seibyl, J.,
Price, L., Leckman, J., & Iniis, R. (1995). CIT Spect imaging of striatal
dopamine transporter binding in Tourette’s disorder.
American Journal of
O’Quinn, A., & Thompson, R. (1980). Tourette’s Syndrome: An expanded
Pauls, D., & Leckman, J. (1986). The inheritance of Gilles de la Tourette’s
syndrome and associated behaviors: evidence for autosomal dominant
New England Journal of Medicine, 315
Pauls, D., Leckman, J., & Cohen, D. (1993). Familial relationship between
Gilles de la Tourette syndrome, attention deficit disorder, learning disabili-
ties, speech disorders, and stuttering.
Journal of the American Academy
Child Adolescent Psychiatry, 32
Rassas Cohn, E.R., Shames, G.H., McWilliams, B.J., & Ferketic, M. (1983).
Dysfluency as the predominant speech symptom in a patient with Gilles de
la Tourette syndrome.
World Congress of the International Association
of Logopedics and Phoniatrics,, 591–596.
Singer, H.S. (1992). Neurochemical analysis of postmortem cortical and stri-
atal brain tissue in patients with Tourette syndrome.
Advances in Neurol-
Singer, H.S. (1997). Coprolalia and other coprophenomena.
ics of North America, 15 (2)
Singer, H., Pepple, J. Ramage, A., & Butler, I. (1978). Gilles de la Tourette
Syndrome. Further studies and thoughts.
Annals of Neurology, 4
DYSFLUENCY IN TOURETTE SYNDROME 239
Singer, H.S., & Walkup, J.T. (1991). Tourette Syndrome and other tic disor-
ders: diagnosis, pathophysiology, and treatment.
Van de Wetering, B., Cath, D., & Buitelaar, J. (1996). Klinische presentatie,
epidemiologie en comorbiditeit. In J. Buitelaar & B. van de Wetering (Eds),
Syndroom van Gilles de la Tourette. Een leidraad voor diagnostiek en be-
Assen: Van Gorcum.
Van de Wetering, B., & Pauls, D. (1996). Genetisch onderzoek. In J. Buitelaar
& B. van de Wetering (Eds),
Syndroom van Gilles de la Tourette. Een
leidraad voor diagnostiek en behandeling.
Assen: Van Gorcum.
Van Woerkom, T., Van de Wetering, B., & Buitelaar, J. (1996). Neurolo-
gische aspecten. In J. Buitelaar & B. van de Wetering (Eds),
Gilles de la Tourette. Een leidraad voor diagnostiek en behandeling.
Woods, D., & Miltenberger, R. (1995). Habit reversal: A review of applica-
tions and variations.
Journal of Behavior Therapy and Experimental Psy-
Disfluency in Tourette Syndrome: A Case Report
1. Tourette syndrome has its onset:
a. At birth
b. In the third decade of life
c. In the fourth decade of life
d. Before the age of 18 years
e. After the age of 18 years
2. Tourette syndrome is:
a. Twice more likely among males than females
b. Twice more likely among females than males
c. Three to four times more likely among males than females
d. Three to four times more likely among females than males
e. As likely among males as females
3. The exact neuroanatomic localization of the dysfunction in Tourette syn-
a. The limbic system
b. Presently unknown
c. The thalamus
d. The frontal cortex
240 VAN BORSEL and VANRYCKEGHEM
e. The prefrontal cortex
4. Tourette syndrome was first described:
a. By J.M. Itard
b. By George Gilles de la Tourette
c. By Marquise de Dampierre
d. In the eighties
e. In 1885
5. Coprolalia is:
a. The involuntary repetition of all or part of the speech partner’s utterance
b. The compulsive reiteration of a phrase or word which the patient often
reiterates with increasing rapidity and with decrescendo of voice vol-
c. A simple phonic tic
d. A complex phonic tic
e. A simple motor tic