Stuttering: incidence
Annotation
and causes
Neil Gordon MD FRCP HonFRCPCH, Huntlywood, 3 Styal
Road, Wilmslow SK9 4AE, UK.
Correspondence to author at above address.
E-mail: neil-gordon@doctors.org.uk
Definition
Stuttering, or stammering as it is also referred to, is a devel-
opmental speech disorder, which usually appears in chil-
dren between the ages of 3 and 8 years. More often than not
it remits before puberty, but it can persist into adult life.1
Stuttering is characterized by involuntary syllable repeti-
tions, syllable prolongations, or interruptions (blocks) in the
smooth flow of speech. There may sometimes be difficulty in
differentiating infants who definitely stutter from those who
show the dysfluency often seen in infancy as a normal stage
of speech development. However, the two are distinct.2 The
overall frequency of dysfluency, the proportion and duration
of dysfluency types, and the associated behaviours not
directly related to speech such as eye, head, and body move-
ments, can help to distinguish between the two.3 There has
certainly been controversy over the exact definition of stut-
tering when selecting participants for research studies.4
Wingate5 criticized Yairi and coworkers6–8 for not being
strict enough in their selection of affected children and for
including those who were classified as having stutter-like
dysfluencies, especially whole-word repetitions. However,
Yairi and colleagues9 refuted these claims, stating that
although syllable repetitions are the most common compo-
nent of stuttering, whole-word repetitions do occur in stut-
tering and therefore this is not a criteria for exclusion. In fact,
whole-word repetitions seem to be more common when the
onset of stuttering is early in life.10
Incidence of stuttering
It is usually accepted that the overall incidence of stuttering is
about 1%, but in the preschool and school populations it is
around 4%, and at all ages seems to be more common among
males than females. About 80% of those who stutter will out-
grow their disability, but there is no way of guaranteeing that
this will happen.11 Young12 concluded that the 80% recovery
rate is an overestimate as retrospective studies are not likely
to yield verifiable data.
According to recent American reports, stuttering affects
more than 15% of children in the age range of 4 to 6 years,
dropping to 1 to 2% among adults.14 A study of stuttering in a
university population in Boston, USA, found prevalence to be
2.1%. 11 Also, 3.4% of those questioned had previously experi-
enced a problem with stuttering. More males than females
stuttered and right-handed females who stuttered were less
278 Developmental Medicine & Child Neurology 2002, 44: 278–282
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likely to have lost their stutter than were right-handed males.
All had a family history of stuttering and, at that time, there
was no evidence of a decline of the disorder over the previous
few decades in spite of an increased number of speech clinics
in the area. In 1984 no decreasing trend was reported.13
In a survey of children in junior and senior schools in
Alabama, USA, twice as many black students had speech disor-
ders, such as stuttering and articulatory problems, as white
students,15 and among 793 adults in the UK with significant
learning disorders, 6.3% were dysfluent for no definite rea-
son. These included examples of stuttering, cluttering, and
atypical dysfluencies – the first group being the largest.16
Another study involved 9930 pupils from 150 schools for
children with hearing impairments. Only 12 of these children
were said to stutter: three in the oral mode only, six in manual
communication only with effortless repetition using sign lan-
guage, and three in both modes. Of those dysfluent in the
manual mode, only one child was reported to repeat the first
syllable and show perseverations and incoordinate manipula-
tions. There was also blocking on some signs with difficulty in
continuing through the block. One child had weakness in
motor skills, which caused signs to be jerky and hesitant, and
another child was described as beginning a sign and then
stopping and repeating it. The findings, although intriguing,
are open to criticism: those on manual dysfluency were not
based on any particular standard and the language level of the
children was not given so that some of the results may have
been within the normal limits of a child in the early stages of
language learning, or be due to other neuromotor deficits.17
Possible causes of stuttering
The exact cause of stuttering remains unproven but it is, no
doubt, multifactorial. Some of the possible reasons for the
condition will be considered with particular reference to the
results of neuroradiological studies. It has long been held
that people who stutter have a greater right cerebral hemi-
sphere involvement in speech than do fluent speakers, but
the two conditions cannot be clearly contrasted as stuttering
is an intermittent condition and fluent speech occurs in both
groups.1 The advent of neuroimaging has meant that more
detailed investigations of this condition can now be carried
out.18 It may well be that the causes are organic, psychologi-
cal, and social, but PET studies favour an organic cause with
 involvement of both the motor and perceptual elements of
speech. However, psychosomatic aspects of the condition
must also be considered as they will influence how the patient
copes with the disability.19 Understandably, the anxiety of
people who stutter is mainly restricted to their attitude
towards communication situations, for example, having to
speak in public.20
Genetic factors
Hereditary factors also appear to contribute to stuttering. To
investigate this, Drayna and coworkers14 assembled more
than 100 families with multiple cases of persistent stuttering
and compared them with families with cases of sporadic stut-
tering. Males predominated among this latter group, but
among families where persistent stuttering occurred, males
and females were affected more equally. It has been noted
that among monozygotic twins there is a 90% chance that if
one twin stutters the other sibling will stutter, whereas there
is only a 20% chance of stuttering in dizygotic twins; and there
is frequently a family history of the disorder.11
To try and analyze the genetic contribution to stuttering,
Ambrose and colleagues21 studied the immediate and extend-
ed families of 66 children who stuttered. It was found that
females had a better prognosis. Also, persistence and recov-
ery were both familial, with families tending to express either
persistent or recovered stuttering. There was statistical evi-
dence for the multifactorial nature of the disorder contribut-
ing to both types, which were unlikely to be genetically
independent. The type of stuttering which recovers does not
appear to be a milder form of that which persists, and the lat-
ter appears to be due, in part, to other transmitted genetic fac-
tors, in addition to underlying abnormalities which may make
a child more at risk of stuttering.
Developmental stuttering
The complex nature of speech production with the participa-
tion of auditory, motor, and linguistic systems makes it difficult
to distinguish between causes and consequences, and devel-
opmental stuttering present since childhood may result from
disturbances in any one of these systems. In a study by
Salmelin and coworkers,22 it was shown that in some affected
individuals, the functional organization of the auditory cortex
differed from that in normally developing control individuals.
They recorded neuromagnetic responses to monoaural tones
in nine participants who stuttered and 10 fluent speakers
while the participants read silently with mouth movements
only, aloud, or in chorus with another person. In the group
which stuttered there was an altered interhemispheric bal-
ance affected by speech production as a result of changes in
the left auditory cortical representation. This was more severe
in self-paced than accompanied speech. This could lead to
transient non-optimal interpretation of the auditory input and
affect speech fluency. It did not occur in fluent speakers.
Brown and colleagues23 examined the effects of reduced
auditory feedback on stuttering. No differences in hearing
thresholds were found between those who stuttered and
those who did not, but those who stuttered had a lower
threshold for auditory discomfort. The study also showed
that fluency is inversely related to auditory feedback. Masking
the auditory feedback of the affected individuals’ own voice
by a sound transmitted through earphones had a dramatic
effect in improving stuttering.23 This suggests that the trans-
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ference of stimuli from peripheral sense neurons to the cen-
tral analyzing systems, or the very analysis, synthesis, and
selection on filtration, are impaired in those who stutter.
Executive dysfluency occurs due to the fact that the signals are
abnormal and masking reduces such malfunction either by
providing additional encoding activity or by altering the dura-
tion, frequency, and intensity of the physical qualities of the
perceived stimuli. These findings obviously have consider-
able implications when prescribing treatment. Likewise,
delayed auditory feedback, in which affected individuals hear
what they are saying several milliseconds after it has been pro-
nounced, often prevents stuttering, as does singing. However,
delayed auditory feedback causes non-stutterers to become
dysfluent. Zanini and coworkers,24 compared the effect of
delayed auditory feedback in one group of 12 students with
the effect of normal auditory feedback in 12 control individu-
als. Results showed that, in the group with delayed auditory
feedback, there was disruption when speaking at a normal
rate. However, as the rate of speaking increased, the number
of errors decreased in this group but increased in the control
group with normal auditory feedback. This difference was
more marked when the auditory input was applied to the
right ear. This may be explained by the left hemisphere being
less resistant to the disruptive effect of the feedback because
of its extensive involvement with language function, while
the better performance of the right hemisphere, with its many
connections with the reticular activating system, may be due
to its critical role in attention. These findings stress the role of
sensory contribution to the causation of stuttering.11
In their research, Peters and coworkers25 found no sup-
port for the claim that those who stutter differed from those
who do not in assembling motor plans for speech, although
physiological data suggest that those who stutter may have
different ways of initiating and controlling speech. It may be
that the disability results from a deficiency of speech motor
skills, so that they reach the maximum movement rate (i.e.
the rate at which dysfluencies begin) at a lower speech rate
than those who do not stutter. In choral reading and singing,
which markedly reduce stuttering, movement rate is usually
slower, less accurate articulation is required, and external
timing may provide a signal that enhances coordination.
PET and other studies
Neuroimaging research data and the effectiveness of
dopamine receptor antagonists in the treatment of develop-
mental stuttering, has raised the possibility of a hyper-
dopaminergic origin for the condition, with an overactive
presynaptic dopamine system in regions of the brain that
modulate verbalization.26
To distinguish the neural systems of normal speech from
those of stuttering, Fox and colleagues27 used PET combined
with choral reading to induce fluency in order to investigate a
group with stuttering of varying severity. It was found that
stuttering induced widespread overactivation of the motor
system in both the cerebrum and cerebellum, with right cere-
bral dominance. Stuttered reading lacked left-lateralized acti-
vations of the auditory system which was thought to support
the self-monitoring of speech. There was also selective deacti-
vation of a fronto-temporal system implicated in speech
production. Induced fluency decreased or eliminated overac-
tivity in most motor areas and largely reversed the auditory
system underactivations and the deactivation of the speech
Annotation 279
 production system. It was concluded that stuttering was a dis-
order affecting the multiple neural systems used for speaking.
Fox and colleagues carried out a further study28 using PET
images of brain blood flow. Two groups were studied: 10 right-
handed males who stuttered and 10 right-handed, age- and
sex-matched control individuals who did not. Ninety PET
blood-flow images were obtained in each group and striking
differences were found in studies of stutter rate and syllable
rate. Their findings supported the theories that implicate the
speech-motor regions of the non-dominant cerebral hemi-
sphere, usually on the right, in those who stutter, and also
added evidence that the non-dominant cerebellar hemisphere,
usually the left, is also affected. The cerebellum seems to have a
specific role in the fluent utterances of those who stutter and
who also have auditory processing problems.
Using PET during new and practice performances of a sim-
ple verbal response selection task, such as saying an appro-
priate verb for a visually presented noun, Raichle and
coworkers 18,29 found that different brain circuits were recruit-
ed for learned and automatic language processing tasks.
Activation of Broca’s area occurred during learned language
processing, but diminished as the task became more auto-
matic; and this occurred rapidly even after short periods of
practice. Therefore, two distinct circuits can be used for ver-
bal response selection, and a critical factor in determining the
circuitry used seems to be the degree to which a task is
learned or automatic. It is reasonable to assume that the dif-
ference between those who stutter and those who do not is
that in the former, the circuitry normally activated during
learned language tasks does not function properly, and that
the disability will be improved by the use of tasks which mini-
mize learned speech production.
Braun and coworkers,30 using regional cerebral blood
flow measured with H2150 PET, confirmed that during the
production of stuttered speech the anterior forebrain
regions, which play a role in the regulation of motor function,
are disproportionately active. In contrast, the post-rolandic
regions, which are involved in perception and decoding of
sensory information, are relatively silent. Comparison with
control individuals in the same situations suggests mecha-
nisms by which fluency-evoking manoeuvres may affect the
anterior and posterior cerebral areas in different ways and
may facilitate speech production in those who stutter.
Activation of the left cerebral hemisphere seems to be related
to the production of stuttered speech, while activation of the
right may represent compensatory processes linked to the
reduction of the disability. The normal pattern of left-hemi-
sphere dominance for language is not seen in affected indi-
viduals who do not activate the relevant areas or activate them
bilaterally. Also, the posterior regions may fail to provide the
sensory feedback on which the anterior regions depend for
coordination of speech output. Then, activities which
improve stuttering, such as singing, may reduce demands on
the frontal areas of the brain and may enhance the sensory
processing in the posterior areas.
So far, there is little evidence of gross structural abnormali-
ties of the brain among individuals who stutter, or of consistent
differences in cerebral blood flow in the resting state between
adults who stutter and those who do not. PET has shown that
during tasks which invoke dysfluent speech, those who stutter
show hypoactivity in cortical areas associated with language
processing but hyperactivity in areas associated with motor
280 Developmental Medicine & Child Neurology 2002, 44: 278–282
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function, compared with control individuals. Also, those who
stutter lack the strong left cerebral dominance for speech gen-
erally seen among those who do not,18 although the role of
cerebral dominance in causing this disability is certainly not as
strongly supported as it used to be.31 An important study by
Foundas and colleagues32 using volumetric MRI has shown evi-
dence that cerebral processes regulating the speech-motor
control system are disrupted and although emotional stress
will aggravate a stutter, it is not the cause. Their investigations
on adults showed that many of those who stutter have an
enlarged planum temporale and less asymmetry of this region,
which is a component of Wernicke’s area, and abnormal gyral
patterns in the cortex involved with language function, such as
the frontal opercular diagonal sulcus and superior bank of the
sylvian fossa. However, there is no specific disruption common
to all who stutter. It is suggested that developmental stuttering
may result from an instability between an outer linguistic loop
and an inner phonatory loop served by these structures.33
Perkins and coworkers34 discuss a number of theories,
which have been put forward to explain the dysfluency. They
theorize that two variables, speech disruption and time pres-
sure, are necessary and together are sufficient to account for
stuttered and non-stuttered dysfluency, if stuttering is defined
as a disruption of speech that is experienced by the speaker as
loss of control under time pressure, and, when relatively
unaware of the cause of the dysfluency. For example, when in
command of the situation, stuttering is unlikely to occur, and
this fits in with the old adage that children who stutter are
speaking faster than they can think. Time pressure to continue
an utterance when it is already disrupted is of obvious causal
importance.
Acquired stuttering among people over the age of 18 years is
most frequently due to neurogenic causes: e.g. vascular lesions
and trauma affecting areas of the brain, such as the internal and
external capsules, the thalamus, and the basal ganglia; or the
causes are drug related. Such stuttering seems to appear
throughout the utterance, and not just at the start, and fails to
respond to typical fluency-evoking manoeuvres. Those affect-
ed are seldom disturbed by their disordered speech33and most
of these patients improve, although few make a complete
recovery.35
Conclusions
Although it is not entirely clear to what extent the incidence of
stuttering has changed over the years, there is, today, a better
understanding of the condition. Incomplete lateralization of
speech, and other motor functions, is no longer accepted as
the definite cause of stuttering.28 The investigations by Braun
and coworkers 30 and the comparable studies by Fox and col-
leagues 28 suggest that the right and left cerebral hemispheres
seem to play distinct and opposing roles in the generation of
stuttering. They indicate that the symptoms are associated with
activation of anterior forebrain regions almost exclusively in
the left hemisphere, while both anterior and posterior perisyl-
vian areas of the right hemisphere are activated as speech
became more fluent. This suggests that this improvement may
possibly be due to coupling of motor and sensory areas within
the right hemisphere. This model can integrate a number of
previous theories of stuttering such as hemisphere asymmetry,
disorders of language processing, motor planning or sequenc-
ing, and defective auditory feedback.
Investigations have been carried out on the prognosis for
 children who stutter. Yairi and coworkers35 found on a conser-
vative estimate that about two-thirds of those who stutter
recover. The risk of chronic stuttering seems to be related to a
number of genetic and environmental factors, such as age at
onset, duration of the disorder, family history of persistent
and recovered stuttering, and scores on language and non-
verbal measures. Also, females seem to have a better chance
of recovery. Research has also shown that linguistic skills do
not differ between children who stutter and those who do
not,36 and that a persistent stutter is linked to a child’s articu-
latory skills and the mother’s communicative style and lan-
guage complexity.37 When carrying out such research it must
always be noted that especially rapid recovery can occur dur-
ing the 6 months after the onset of stuttering, and this must be
accounted for when selecting study participants.38
Further prospective studies on the incidence of stuttering
would surely be of interest, and of help in planning services,
and be of assistance in defining more accurately how urgent it
is to start a particular child on treatment. It is not known if the
neurophysiological patterns in adults who stutter are always
present in children when they start to stutter. Also, there may
be other questions about how patterns in children who spon-
taneously recover from stuttering differ from those who do
not.18 It is possible that these two developmental paths are
influenced by genetic factors, especially an association with
other deficits, which may complicate stuttering and prevent or
slow down the recovery process. In addition, phonological
and language skills may have a role in the recovery and persis-
tence of stuttering,7 as may environmental factors, such as par-
ents’ responses to the disability.8 These and other questions
may be answered with the use of investigations such as PET.
Accepted for publication 26th September 2001.
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Annotation 281
 The Royal Society of Medicine
Feeding pre-term and term babies
Feeding pre-term and term babies
The Royal Society of Medicine
FRIDAY 17 MAY 2002
1 WIMPOLE STREET, LONDON, W1G OAE

9.00 am Registration and coffee

Meetings

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9.25 am Introduction: feeding in babies. Martin Bax, Imperial College, London

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Keith

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Mac

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