Stuttering, Dopamine, and
Incentive Learning
Copyright © 2021 Paul H Brocklehurst
All rights reserved.
This Chapter was originally published in
May 2021 as an Appendix in my book “The Perfect Stutter”[1]
A PDF version is available here
In
this appendix, I discuss some recent developments in my understanding of the
role that dopamine plays in enabling us to respond appropriately to the various
stimuli we encounter in our lives, and I propose that phasic fluctuations in
synaptic dopamine may play a key role in the moment-to-moment regulation of the
availability of our speech plans for motor execution.
The relationship between
dopamine receptor density and stuttering
Back in 2006, Alm’s presentation at the British Stammering
Association’s annual conference in Telford had alerted me to how differences in
the prevalence of stuttering in different age groups closely mirrors
differences in the density of striatal dopamine receptors in those age
groups; the prevalence of stuttering being highest among the age group in which
the density of dopamine receptors is highest – which is between approximately
two and four years of age (see figure A1).
Now, fifteen years later, we
still do not know the reason for this correlation, nor do we know whether the
densities of dopamine receptors in stutterers’ brains differ from those of
non-stutterers of the same age.[2] All
that is currently known for sure is that striatal dopamine receptor density and
stuttering prevalence are closely correlated and that antipsychotic drugs which
de-activate D2 dopamine receptors cause a reduction in the severity of
stuttering symptoms – in a substantial proportion of adults who stutter.
Figure A1. Showing changes
in the density of D1 and D2 striatal dopamine receptors with age. Based on
post-mortem data published by Seeman et al (1987), from the brains of 247
humans between 0 and 104 years of age.
Until further research is
carried out, we can only speculate as to what may lie behind this correlation
between striatal dopamine receptor densities and stuttering prevalence, and as
there are so many details that we still don’t know, there is a risk that any
such speculations may ultimately turn out to be wrong. While remaining
conscious of this possibility, it seems to me that we can nevertheless glean
some useful insights into possible reasons for this correlation by considering
the following two questions: (1) “What function do striatal dopamine receptors
normally fulfil?” and (2) “Why do young children have such high densities of them?”
The most basic answer to the
first of these two questions is that our striatal dopamine receptors play a key
role in enabling us to respond to stimuli – by regulating the transmission of
nerve impulses from one neurone to the next. Moreover, all other things being
equal, the more functional striatal dopamine receptors a person has, the more
responsive to stimuli he or she is likely to be.
The two different types of
dopamine receptor facilitate two different sorts of response to stimuli: D2
receptors facilitate ‘diffuse’ responses; whereas D1 receptors facilitate
‘focussed’ responses. Diffuse responses are highly variable responses – which
are often referred to as ‘noise’ – reflecting the fact that the majority of
such responses are unhelpful. In contrast, the focussed responses facilitated
by D1 receptors are more stable and predictable – and, generally, desirable.[3] The
diffuse responses facilitated by D2 receptors do, nevertheless, fulfil a vital
function in enabling experimentation and learning, and it is useful to think of
diffuse responses as creative, alternative responses – rather than simply as
unwanted noise.
A possible clue to the answer
to the second question: “Why do young children have such high densities of
dopamine receptors?” can be gleaned from the finding that the density of D2
receptors peaks around two years of age whereas the density of D1 receptors
peaks about a year later – around three years of age (See Figure A1). This
suggests that, at two years of age, children are hard-wired to respond to
stimuli in a relatively variable, creative way, whereas at three years of age
they are hardwired to respond to stimuli in a more stable predictable way. This
shift between two and three years of age, from a tendency to produce many
variable responses to a tendency to produce a small number of stable responses,
is arguably exactly what children need to achieve in order to be able to
respond to stimuli in the most appropriate ways. Essentially, the initial high
density of D2 receptors may enable children to produce and experiment with
different responses – and thus discover which ones are most appropriate, and
then the subsequent high density of D1 receptors may enable them to consolidate
that learning so that they can then start to reliably respond to each stimulus
with the response that they have learned is the most appropriate.
The exceptionally high
densities of striatal dopamine receptors that are found in children between two
and four years of age thus quite likely play an important role in enabling
those children to quickly and efficiently adapt to their environment and learn
how to manipulate it. Similarly, these high densities of striatal dopamine
receptors are also likely to play an important role in enabling young children
to develop their language and conversational skills, and they could be seen as
providing a window of opportunity for intense learning, both of language
itself, as well as of the social and conversational skills that go along with
it.
Thus, the high densities of
D2 receptors in two-year-old children quite likely lead to a tendency for their
verbal responses to be highly variable and unpredictable. In contrast, around
three-years-of-age, the declining density of D2 receptors, together with the
high density of D1 receptors increasingly favours the execution of only the
most highly activated speech motor plans – the net result being that
three-year-old’s verbal responses are far less varied (less ‘creative’), more
predictable and more reliable. This gradual transition – from producing many
variable verbal responses to a stimulus to producing a single reliable response
– is exactly what is needed in order to maximise a young child’s ability first
of all to discover, and then to reliably select, the most appropriate speech plans
for the various speaking situations in which he finds himself in everyday life.
Thus, by the time this window
of opportunity comes to an end and their dopamine receptor densities start to
fall, most children have successfully undergone vocabulary and grammar spurts,
and will have learned how to modulate their speech production in social
settings to elicit rewards and avoid punishments.
As I noted in Chapter 33,
during this period of intense activity and learning, most children pass through
a phase – between two-and-a-half and four years of age – during which they
produce an increased number of stuttering-like dysfluencies. The fact that
large-scale epidemiological studies have revealed an early-childhood incidence
of stuttering in young children as high as 11% (Reilly et al., 2013) and 18% (Mĺnsson, 2007) suggests that this period of increased
dysfluency is likely to be a normal and largely benign phenomenon that occurs
as their speech and language capacities are rapidly developing. And, as I
argued in chapter 27, it is possible that this transient increase in the
production of stuttering-like dysfluencies in young children is a side-effect
of the fine-tuning of their release threshold mechanisms to the characteristics
of the physical and social environments in which they habitually communicate.
When the fine-tuning is complete and the release threshold mechanism is
functioning appropriately, it should enable them to say words and phrases that
are likely to elicit positive (rewarding) responses from listeners and prevent
them from saying words and phrases that are likely to elicit negative
(punishing) responses from listeners.
In the vast majority of
children, this period of increased dysfluency lasts only a few weeks or months
and then their speech once again becomes more fluent; the return of relatively
fluent speech perhaps reflecting the fact that the fine-tuning of the release
threshold has been successfully accomplished. However, if, for one reason or
another, a child misses this window of opportunity, he or she may find it
substantially more difficult to attain these communication skills after the
density of their dopamine receptors has died back
to the much lower levels that are typically found in older children and adults.
Children who miss this window of opportunity may thus remain less skilled at
adjusting their speech to suit the requirements of the speaking environment and
may therefore tend to continue to elicit more punishments and fewer rewards
compared to children who have developed these skills. As a consequence, such
children are likely to be at risk of developing persistent stuttering.
Phasic fluctuations in
dopamine release – a cause of moments of stuttering?
The early peaks in dopamine
receptor densities that Alm highlighted in his thesis and associated
publications (Alm, 2004; 2005) may well play an important role in providing a
window of opportunity for rapid language learning and for the fine-tuning of
the variable release threshold mechanism[4] to be
accomplished. However, because changes in receptor density happen slowly, over
a period of months, they cannot explain the fluctuations in fluency that occur
from moment to moment while speaking. These moment-to-moment fluctuations may,
however, potentially be successfully explained as resulting from
moment-to-moment ‘phasic’ fluctuations in the quantity of dopamine released
from dopaminergic neurones (the cells in which dopamine is synthesised and
stored) in response to the various punishing and rewarding listener-responses
that speech elicits.[5]
To clarify how such
fluctuations in dopamine release may impact upon the variable release-threshold
mechanism and thus also on our ability to initiate the motor execution of the
words we want to say, I need, first of all, to briefly outline some findings
from research that has investigated the role that dopamine plays in regulating
our responses to rewards and punishments.
The role of dopamine in
reward based learning
In common with all
neurotransmitters, Dopamine enables nerve impulses to travel from one nerve
cell to another. In particular, it facilitates the transmission of the nerve
impulses that enable us to move our muscles, to speak, and also to think.
In the early 1970s, thanks to
advances in electrophysiology, researchers found a way to insert
micro-electrodes into dopaminergic neurones. From that time onwards, it has
been possible to record the exact moments when these neurones fire and release
some of the dopamine they store. Over the decades that followed, a large number
of studies have been carried out on a variety of different animals (including,
rats, monkeys, and more recently, human beings)
that have made it possible to start
to pinpoint exactly what kinds of stimuli cause these dopaminergic neurones to
fire and what effect they have when they fire.[6]
As a result of these studies,
the following coherent picture has gradually emerged…
In the absence of any
stimuli, dopaminergic neurones will fire periodically at a low rate, releasing
small amounts of dopamine and thus maintaining a background ‘tonic’ level of
dopamine in the synaptic spaces that connect them to neurones further
downstream. This tonic release of dopamine is responsible, amongst other
things, for maintaining the background muscle tone that our muscles exhibit
when in a resting state.
If an animal is then
presented with a stimulus that is intrinsically rewarding (a ‘primary rewarding
stimulus’), such as food or access to a sexual partner, its dopaminergic
neurones suddenly start to fire at a much faster rate, releasing, within
milliseconds, much more dopamine into the synaptic spaces.
This resulting increase in
synaptic dopamine then stimulates dopamine receptors on downstream
(post-synaptic) neurones, some of which facilitate the execution of motor plans
for ‘approach behaviours’ – i.e., for muscle movements and physiological
responses that enable the animal to approach (and potentially benefit from) the
rewarding stimulus. In human beings, these phasic spikes in synaptic dopamine
may also facilitate the execution of speech plans for the muscle movements that
result in the production of words and phrases that help the person attain that
rewarding stimulus or goal.
When animals and children are
very young, most of the stimuli they encounter are neutral – i.e., neither
rewarding nor punishing. Over time,
however, neutral stimuli that consistently occur together with (or immediately
prior to) a primary rewarding stimulus start to become associated with that
stimulus and start to elicit similar phasic spikes in dopamine release. In this
way, stimuli that were originally neutral become ‘secondary rewarding stimuli’.[7]
The transformation of neutral
stimuli into secondary rewarding stimuli in this way has been confirmed in many
animals, and experimental research suggests that virtually any neutral stimulus
can become a secondary rewarding stimulus if it is repeatedly presented at the
same time as or immediately before a primary rewarding stimulus.[8] The
development of our ability to consciously or unconsciously anticipate when
a primary reward is about to occur is thanks to the development of secondary
rewarding stimuli in this way. Essentially, the secondary rewarding stimulus triggers
the anticipation of the primary rewarding stimulus that it is associated
with. Thus, for example, for Pavlov’s dogs, the sound of the bell started to
trigger the (conscious or unconscious) anticipation of the food they were about
to receive.
Conversely, any neutral
stimulus that becomes associated with a primary punishing stimulus or with a
reduction in an animal’s access to a primary rewarding stimulus will acquire
the status of a secondary punishing stimulus. Secondary punishing stimuli
trigger the anticipation that a primary punishment is about to occur.
Both primary and secondary
rewarding stimuli have been shown to cause phasic spikes in dopamine release
and to trigger approach behaviours. One
might therefore expect that primary and secondary punishing stimuli would do
the opposite, i.e., they would cause phasic troughs in dopamine release – which
would inhibit approach behaviours. So, researchers in the 1980s were surprised
to discover that, although some punishing stimuli do indeed cause phasic
decreases in dopamine release, many punishing stimuli in fact seem to cause
phasic increases in dopamine release, just like rewards do! For several
years this unexpected finding cast doubt on the theory that the phasic release
of dopamine by dopaminergic neurones plays a key role in enabling animals to
respond appropriately to rewards and punishments.
In more recent years, the
improved ability of researchers to track changes in the concentration of
synaptic dopamine over very small time-periods led the Cambridge-based
researcher, Wolfram Schultz, to
propose a plausible explanation for this unexpected finding: Schultz (2016) proposed that all novel and unexpected stimuli
(both rewards and punishments) lead to an initial phasic increase in
synaptic dopamine which occurs before the animal has had time to identify and
evaluate them. Thus, initially, all such stimuli cause approach
behaviours. Then, if the animal subsequently evaluates the stimulus as
‘punishing’, the initial phasic increase in synaptic dopamine is reversed, and
the animal’s synaptic dopamine levels do indeed fall – causing a phasic trough
in synaptic dopamine and inhibiting approach behaviour from that moment
onwards. The reason for researchers’ confusion about this back in the 1980s was
because sometimes it takes a while for an animal to evaluate a stimulus as
punishing, so the fall in dopamine that those researchers had expected to see
in response to a punishing stimulus did not always occur straight away.[9]
Schultz (2016) proposed that
the initial spike in synaptic dopamine that all novel or unexpected stimuli
cause probably serves the purpose of attracting animals’ attention to those
stimuli – to facilitate their ability to evaluate them. This tendency of novel
or unexpected stimuli to attract an animal’s attention in this way has been
well documented over many years and is known as the ‘orienting response’. Thus
it seems that the initial phasic spikes in synaptic dopamine that occur in
response to novel stimuli enable this orienting response to occur.
To summarise, phasic changes
in the concentration of synaptic dopamine occur as follows…
· Novel or unexpected stimuli cause an initial phasic
spike in synaptic dopamine levels – enabling the animal to orientate his
attention towards those stimuli in order to identify and evaluate them.
· If a novel stimulus is then evaluated as rewarding,
this spike in synaptic dopamine will be prolonged and its magnitude may further
increase – enabling further approach behaviour towards that stimulus.[10]
· In contrast, if a novel stimulus is evaluated as
punishing, the initial spike in synaptic dopamine will be reversed and a trough
in synaptic dopamine levels will ensue – which inhibits approach behaviours
toward that stimulus.
· Any stimulus that leads to the anticipation of
a primary reward will also cause a phasic spike in synaptic dopamine,
facilitating approach behaviour towards that anticipated reward.
· Any stimulus that leads to the anticipation of
a primary punishment will cause a phasic trough in synaptic dopamine,
inhibiting approach behaviour towards that anticipated punishment.[11]
So, how might these phasic
fluctuations in our synaptic dopamine levels relate to the Variable Release
Threshold Hypothesis of
stuttering?
To answer this question, it
is necessary to bear in mind that humans are essentially social animals, and
throughout their evolutionary past, the ability to be accepted in a social
group has been vital for their survival. And, to a large extent, our success in
being accepted into a social group has depended on our ability to communicate
successfully with other people in that social group. So, just as we are
hard-wired to find food and sex rewarding, we are almost certainly also
hard-wired to experience successful communication as rewarding. In other words,
for human beings, successful communication constitutes a strong primary reward
– just like food and sex, whereas communication failure constitutes a strong
primary punishment. Similarly, any stimulus that we have learned to associate
with successful communication or that causes us to anticipate that
communication will be successful will constitute a powerful secondary reward;
whereas any stimulus we have learned to associate with communication failure or
any stimulus that leads to the anticipation of communication failure
will constitute a powerful secondary punishment. Thus our brains are likely not
only to compute communication failure as punishing, but they are also likely to
evaluate negative listener responses, speech errors, and of course stuttering
itself as punishing. Indeed, any stimulus that causes us to anticipate
communication failure will be computed as a punishing stimulus – which will
result in an immediate phasic decrease in the amount of dopamine released from
the dopaminergic neurones in parts of the brain that regulate muscle movements
for speech (including, most notably, the striatum).
As soon as a speaker
perceives or anticipates that his words will result in communication failure,
the resultant phasic decrease in synaptic dopamine inhibits the motor execution
of the speech plan for those words. The greater the decrease, the greater the
extent of the inhibition. It would appear likely that this drop in synaptic
dopamine that occurs in this way may constitute the mechanism behind the rise
in the release threshold that is hypothesised to take place at such times
(Brocklehurst, Lickley, & Corley, 2013). Both the drop in synaptic dopamine
and the resultant rise in the release threshold will last as long as the
experience of communication failure (or the anticipation of communication
failure) lasts.
Because such phasic reductions
in synaptic dopamine delay or prevent the motor execution of speech plans, they
reduce the likelihood that a speaker will say things that will elicit negative
responses from his listeners. They also reduce the likelihood that the speaker
will make speech errors – because plans for words or syllables that are
erroneous tend not to become so highly activated, and their execution is thus
inhibited by a rise in the release threshold. However, a side-effect of such
phasic reductions in synaptic dopamine is dysfluent speech. And, if a speaker’s
past experiences have caused him to evaluate dysfluent speech negatively, those
dysfluencies will themselves act as secondary punishing stimuli and will lead
to a prolongation of the drop in synaptic dopamine, thus sustaining or even
prolonging the inability of the speaker to execute the problem syllables or
words. [12]
The speaker may then only
regain the ability to initiate execution of a problem syllable or word after
the concentration of synaptic dopamine finally rises back up to a more normal
level (with the consequence that the release threshold falls back down to a
lower level).
How could antipsychotic drugs lead to an amelioration of stuttering
symptoms?
One possible explanation is
that their effect of blocking D2 dopamine receptors causes a
general reduction in responsivity. And if a speaker is less responsive, he is
less likely to do things or say things that elicit negative responses from his
listeners. When the speaker realises that he is eliciting fewer negative
responses from his listeners, the level at which his release threshold is set
falls, and he finds that he can execute planned words more easily.
A related possibility, as
proposed by Alm in his thesis (which I discussed in Chapter 27), is that thanks
to their effect of blocking D2 receptors, antipsychotic drugs may increase the
‘signal-to-noise ratio” of speech plans. As a result, the speech plans that the
speaker tries to execute will tend to be more appropriate and to contain fewer
errors. The net result, once again, is speech that is more likely to be
received positively by listeners, thus prompting a fall in the release
threshold and a corresponding increase in fluency. Because both of these
explanations involve a learning process (whereby repeated experiences of
speaking impress upon the speaker the fact that his speech is no longer
eliciting so many negative responses from people and is no longer so
error-prone) one would expect that the speaker would have to take
antipsychotics for a few weeks
before he would start to experience a related improvement in his fluency –
which is indeed exactly what studies of the effects of antipsychotic drugs on
stuttering have tended to find.
A further alternative
explanation for the ameliorative effect of antipsychotics is that, by
blocking dopamine receptors, antipsychotics dampen our sensitivity to phasic rises
and falls in synaptic dopamine. So, essentially the rises in synaptic dopamine
are no longer so rewarding (pleasurable) and the falls are no longer so
punishing. So, although the speaker may continue to make speech errors and may
continue to elicit negative responses from his listeners, these errors and
negative listener responses may no longer result in such a great rise in the
level at which the release threshold is set.
It occurs to me that these
three explanations are not mutually exclusive and all three could contribute to
an amelioration of stuttering symptoms in a person who stutters.
Salience and evaluation: Two-components of the dopamine
response
In addition to providing a
parsimonious explanation for why stutterers tend to stutter most when they
anticipate or experience communication failure, the theoretical article by
Schultz (2016), which I discussed in the sub-section on reward based
learning, also provides a potential explanation for why the experience of novelty frequently
results in a reduction in stuttering.
In his 2016 article, Schultz discussed the
problematic finding from dopamine research that punishing stimuli
often cause an initial phasic rise in synaptic dopamine levels. As I
mentioned earlier, this finding eventually led to the suggestion that, rather
than being associated with the perception of a rewarding stimulus, phasic rises
in synaptic dopamine may occur in response to the detection of any new
stimulus – positive or negative; the rise essentially signalling the
detection of something novel rather than something rewarding.
To account for these
findings, Schultz proposed that
the dopamine response to novel stimuli may in fact be made up of two
components: an initial ‘detection’ component and a later ‘evaluation’
component. Thus the initial rise in synaptic dopamine that occurs in response
to all sorts of new stimuli probably fulfils the function of attracting
attention to the new stimulus (the orienting response). Then, that rise is
either sustained or discontinued depending on how the new stimulus is
evaluated. Schultz pointed out that this initial rise makes perfect sense
because, although many novel stimuli or experiences have the potential to be
rewarding, the only way we can find out whether or not they really are
rewarding is by first of all paying attention to them. So, it makes sense that
humans (and other animals) have evolved to be attracted towards novelty and to find it
(initially) attractive and even pleasurable. This is especially true of new
experiences that are salient, either due to their occurring in close proximity
to other rewarding stimuli, or due to their unusualness, or simply due to their
intensity. (See Schultz, 2016 pp.185-187)
Thus, initially, novel
experiences are generally attractive and elicit approach behaviour – when we
first begin processing them. Then, once we have had time to evaluate them, they
may continue to elicit approach behaviour, or they may become neutral, or they
may inhibit approach behaviour.
It seems likely that the same
principle must apply in novel speaking situations. And this may explain why, for people who
stutter, novel speaking situations or novel ways of speaking (such as speaking
with an unusual accent, with unusual speed, unusual pitch, or unusual loudness)
often lead to an initial increase in fluency. Presumably, novel speaking
situations and novel ways of speaking lead to an initial phasic rise in
synaptic dopamine and an associated lowering of the release threshold. However,
this initial fluency-enhancing effect of novelty is often short
lived and may die away as soon as the speaker starts to evaluate the feedback
he receives – including the responses of his audience. This initial rise in dopamine
may also account for the placebo effect that often occurs when a stutterer
begins a novel course of therapy for his stutter, or when he first starts
taking a particular type of medication. Similarly, it could explain the
transient improvement in my fluency that I experienced from hypnotherapy.
The role of dopamine in
drug-induced psychosis.
Schultz dedicated a
short section of his 2016 paper to a potential explanation for the phenomenon
of drug-induced psychosis. In it, he explained that any drugs that cause a
prolonged rise in synaptic dopamine levels may cause an abnormal prolongation
of the initial ‘detection component’ of the dopamine response. This
prolongation of the detection component causes it to impinge upon the
‘evaluation component’. As a consequence, a person on a stimulant drug is
likely to misperceive the initial rise in dopamine which is really only
signalling the detection of a novel stimulus as signalling a positive
evaluation of that stimulus. Hence he is likely to make positive
evaluations that are inappropriate – and which may sometimes ultimately get him
into trouble. Often, only when the effects of the drug start to wear off is he
likely to realise that his positive evaluations were a side-effect of the drug.
After reading Schultz’ account of this two-component response to novel
stimuli, I realised that it provided a neat explanation for the initial
improvement and then subsequent deterioration in my speech that I experienced
as a teenager when I first started experimenting with cannabis with my friends
from school…
Initially cannabis made me very
talkative, and very fluent. Indeed, I don’t remember stuttering at all when I
first tried it. In addition to being fluent, the pleasant feeling that the drug
induced in me probably played a role in causing me to perceive that the people
I chatted to while under its influence were responding positively to me. It was not until some of my friends pointed
out to me that my excessive talkativeness was annoying that I realised that the
drug had the capacity to make me misevaluate people’s responses and to perceive
them as more positive than they really were. As soon as I realised that I was
misevaluating the responses of the people I was talking to, I started worrying
that I was rambling and talking too much, and my speech deteriorated – to the
point where I found it almost impossible to say anything at all. Then, on
subsequent occasions when I took the drug, it no longer had any beneficial
effect at all on my fluency. Indeed, quite the opposite.
Of
course, one’s drug-induced positive misevaluations of a situation may also
elicit positive responses from other people. So it is always possible that, for
some individuals who stutter, cannabis and other
stimulants may continue to effect a reduction in their stuttering long after
the identification component of the dopamine response has ended. This may be
especially likely to occur in stutterers who do not have any underlying
neurological or physical impairments that cause their speech to be error-prone,
such as stutterers whose problems stem primarily from unduly perfectionistic
self-expectations. It may also explain why some experimental studies –
including the ones by Fish & Bowling (1965), and Langova
& Moravek (1964) that I discussed in Chapter 27 –
have found that temporary use of stimulants elicited a lasting reduction in
stuttering symptoms in a proportion of their stuttering participants.
It occurs to me that a similar mechanism – whereby the
detection phase of the dopamine response is prolonged into the evaluation
phase, thus leading to a falsely positive evaluation of one’s performance – may
explain why, occasionally, novel and unusual forms of therapy bring about
lasting reductions in stuttering: If the novelty effect of a
therapy lasts long enough to enable the development of faith in one’s ability
to speak without stuttering, its results may then indeed be sustained over the
long-term. This may explain why faith healers and similar sorts of
practitioners occasionally succeed in bringing on lasting remissions. It may
also explain why some therapists, especially those with an impressive or
convincing manner, apparently succeed in eliciting better results than those
with a less convincing or impressive manner, regardless of what type of therapeutic
approach they adopt.
It is noteworthy that even when stutterers don’t take
any form of medication and don’t undergo any therapy, the severity of their
stuttering nevertheless has a tendency to fluctuate, and many stutterers
(myself included) have experienced how they seem to progress in their lives
through repeated cycles of remission and relapse; the periods of remission and
relapse often lasting for weeks, months, or even years. It is possible that
some of these fluctuations may arise as a result of long-term fluctuations in
the density of dopamine receptors in stutterers’
brains. Alternatively, they may reflect long-term fluctuations in the amount of
dopamine synthesised in the brain or long-term fluctuations in the ability of
dopaminergic neurones to release and reabsorb the dopamine they store.
Stuttering and ADHD
In his thesis, Alm (2004,2005) presented evidence
strongly suggestive of the existence of a subgroup of stutterers whose
stuttering began following brain damage caused by an injury or infection in
early childhood. Unlike stutterers with a family history of stuttering, these
individuals frequently have a history of delayed speech and language
development, poor control over their attention, and some also have a history of
hyperactivity. Alm noted that the behaviour of these individuals is often
similar to that of people with Attention Deficit Hyperactive Disorder (ADHD) or
Attention Deficit Disorder (ADD), although their symptoms are generally not
severe enough to warrant formal diagnoses of these disorders. Alm noted that
stutterers showing these symptoms would generally tend to have been classified
by Van Riper as having a ‘Track 2’ onset of stuttering.
Because the symptoms these individuals produce overlap
to some extent with those of ADD and ADHD, I was particularly interested to
discover that a hypothesis exists that attributes ADHD and ADD to an
under-production of dopamine and a resultant impairment of incentive learning.
Specifically, in his (2018) book, Life's
rewards: Linking dopamine, incentive learning, schizophrenia and the mind, Beninger (pp. 236-244) proposed that children with
ADHD have hypoactive dopamine metabolisms that are just active enough to enable
them to orient towards novel stimuli but are not active enough to enable them
then subsequently evaluate those novel stimuli as rewarding or non-rewarding.
As a consequence of this evaluation failure, a far greater proportion of the
stimuli they encounter in their everyday lives continue to be perceived as
‘novel’ and continue to attract their attention. Thus, their capacity to ignore unimportant
stimuli is much reduced and their attention continues to be orientated towards
every little stimulus they encounter in their environment.
Beninger also pointed out that the hyperactivity
component of ADHD is only highly prominent in very young children with the
disorder; it generally diminishes as they grow older, and often disappears
entirely – resulting in the lesser diagnosis of Attention Deficit Disorder (ADD).
This gradual reduction in hyperactivity may reflect that fact that, as young
children with ADHD grow older, they do eventually learn to recognise which
stimuli are likely to be unrewarding or punishing, but because they still take
longer to recognise and evaluate stimuli compared to normal children or adults
of the same age, many more stimuli continue to attract their attention.
With regard to speech, Alm (2004) clarified that the
subgroup of stutterers who have a history of brain injury not only tend to show
signs of attention-deficits and hyperactivity, but often also produce symptoms
of cluttering – including a tendency to rush ahead and leave many words
incomplete. In light of Beninger’s hypothesis of ADHD, it seems likely that
cluttering symptoms may occur in these children because their attention is
continually being attracted towards different stimuli while they talk. The
classical stuttering symptoms – of being unable to initiate speech or to move
forward – may only start to occur in such children somewhat later, after
repeated experiences of communication failure and eliciting negative responses
from listeners.[13] Whatever the
case, there is no doubt that children with ADHD do elicit a lot of negative
responses from listeners, as their behaviour is often perceived as annoying –
leading to the frequent perception that they are ‘naughty children’. And, even
though children with ADHD may be slow to evaluate such listener feedback as
negative, repeated exposure to it, together with repeated experiences of
communication failure are nevertheless likely to eventually lead them to
evaluate their speech as ‘not good enough’, and to anticipate that their
attempts to speak will result in communication failure and negative listener
responses.[14] Such negative
evaluations and anticipations then would start to trigger the phasic reductions
in synaptic dopamine that cause them to produce stuttering blocks in addition
to their cluttering and other speech-related symptoms.
If these attention deficit disorders do indeed stem
from an under-production of dopamine and/or an underactive dopamine metabolism,
this would go some way to explaining why the stimulant drug Ritalin – which
increases dopamine metabolism – has been found to ameliorate their symptoms –
increasing the attentional control and reducing the hyperactivity of people
suffering from these conditions. It also highlights the possibility that
stuttering symptoms may be ameliorated in the ‘attention deficit’ subgroup of
stutterers by stimulants that increase dopamine metabolism.
The
role of reward-based learning in the onset of stuttering
Schultz’ two-component explanation of the initial rise in
dopamine levels brought on by novel experiences also provides some potential
further insights into the onset of stuttering.
Initially, young children’s experiences can be divided
into three sorts – (1) those which are intrinsically pleasurable or rewarding –
i.e., the primary rewards like milk and interaction with their mother; (2)
experiences that are intrinsically unpleasant or punishing, like pain, isolation, and sudden loud noises; and (3) neutral
experiences that are neither intrinsically rewarding nor punishing.
When very young, a large proportion of children’s
experiences are neutral inasmuch as they have not yet become associated with
positive or negative evaluations. As time passes, these neutral experiences
then gradually become associated with such evaluations, but before these
associations develop, if Schultz’ two-component theory is accurate, young children’s
novel neutral experiences will initially elicit phasic rises in their synaptic
dopamine levels and thus will tend to elicit orienting and approach behaviour
and will tend to be perceived as pleasurable. Similarly, children’s early
vocalisations are likely to elicit phasic rises in synaptic dopamine, which may
partially explain why young children spend so much time vocalising and engaging
in vocal play, even when there is nobody there listening to them. Essentially,
they enjoy the rise in synaptic dopamine that such novel behaviour (and indeed
any novel behaviour) elicits. It seems likely that the rise in synaptic
dopamine that accompanies their early vocalisations keeps their release
thresholds at a constantly low level, rendering it easy for them to execute
whatever speech plans arise in their brains.
It is only somewhat later in their development, and
after the novelty value of vocal
play and other early vocalisations has worn off, that children become aware
that their words can elicit both positive and negative responses from other
people. And, when they do realise this, their ability to vocalise and to speak
then becomes subject to the second component of the dopamine response: the
evaluation component.
Once the evaluation component of the dopamine response
comes into play, whenever the child anticipates that a word or phrase is likely
to elicit negative listener responses his synaptic dopamine levels fall. This
fall triggers a rise in the release threshold which renders it difficult or
impossible for him to speak that word or phrase out loud.
Thus, Schultz’ two component dopamine response predicts that
children’s initial vocalisations and first words will always be executed with
ease, and that their stuttering-like dysfluencies should only start to appear
at the point of time in their development when their vocalisations are no
longer ‘novel’, and they start to notice that some of those vocalisations
elicit negative responses from listeners.
This prediction fits well with many of the
observations that speech and language researchers have made in relation to the
initial onset of stuttering symptoms in young children, that I discussed in
Chapter 33.
Looking towards the future –
The importance of stuttering subtype awareness
There is already a consensus
among stuttering researchers that there are at least two major stuttering
subtypes, and a recognised priority for ongoing research is to clearly identify
the characteristics of these subtypes. Historically, researchers have
distinguished between ‘developmental stuttering’ and ‘neurogenic stuttering’,
and they have understandably tended to consider early-onset stuttering as
‘developmental’ and late (adult) onset stuttering as ‘neurogenic’. In categorising stuttering in this way, they
have, however, consistently overlooked the fact that young children are at
least as prone to suffering neurological damage from accidents, infections,
etc., as are adults. Consequently, they have consistently overlooked the fact
that much of the stuttering that occurs in young children is almost certainly
neurogenic in origin, even though its early onset means that it does have a
strong developmental dimension to it.
On the basis of the research
Alm reviewed in his thesis, it is possible to identify two major subgroups of
stutterers: One in which there is a family history of stuttering, and one in
which stuttering starts following an event, such as an infection or injury,
that results in neuronal damage (see Alm & Risberg, 2007).
As discussed in Chapter 27,
stutterers in the first group tend to be highly social, with ‘easy
temperaments’ and tend, if anything, to have somewhat above-average
intelligence and precocious language skills; whereas those in the other group
tend towards hyperactivity, have a poor level of control over their attention,
and often show signs of ADHD and cluttering. They frequently also have a
history of delayed or impaired language or speech development.
The characteristics displayed
by the first group of stutterers (the high-performing group) are all
characteristics that have been found to be associated with a high density of D2
dopamine receptors (Alm and Risberg, 2007, p.32). And it seems likely that
their high density of D2 dopamine receptors enables them, as children, to learn
quickly and to adapt easily to their physical and social environments. Alm
(2004) proposed that stutterers whose onsets belonged to Van Riper’s tracks 1 and 3 could both fit into this
high-performing category.[15]
In contrast, Alm’s second
group (in whom stuttering began following a brain injury of some kind) probably
contains many individuals who would have been classified by Van Riper as having
Track 2 onsets. Depending on how early in their lives the brain injury
occurred, many in this group may never have experienced a period of ‘normal’
speech. In this group, difficulty paying or maintaining appropriate attention,
poor articulation skills, reactive temperaments, and hyperactivity may all
contribute to their communication attempts frequently resulting in failure and
eliciting negative responses from listeners.
Although these two stuttering
subtypes may result from substantially different aetiologies, it seems likely
that both share the same ‘final common pathway’ – inasmuch as the moments of
stuttering that occur in both subtypes occur as a direct result of phasic
reductions in synaptic dopamine, brought on by the perception (or anticipation)
of communication failure.
Despite being theoretically
possible, it may well never be practical to measure dopamine metabolism in
stutterers attending speech therapy. Nevertheless, now that the role of
dopamine in incentive learning is well established and understood, and now that
we have a clearer awareness of the important role that dopamine plays in both
the identification and evaluation stages of learning, this knowledge
can potentially be used to develop speech therapy approaches uniquely suited to
the different learning styles that likely characterise the two main stuttering
subtypes. From the perspective of incentive- learning, one of the keys to
successful speech therapy for stuttering would be the therapist’s ability to
accurately identify the moments when the speaker is evaluating his performance.
Having identified when those moments occur, the therapist then needs to find
ways to ensure that, during those moments, the speaker’s synaptic dopamine
levels remain sufficiently high to cause appropriate positive evaluations to
occur. It is also possible that the temporary use of stimulants like Ritalin
may be found to help young children with co-occurring stuttering and attention
deficits.
It is my hope that, as time
passes, systematic research into the details of the relationship between
stuttering and dopamine will be carried out, and as a result, a clearer
understanding of the roles that dopamine plays in the stuttering subtypes will
emerge. My feeling is that, of all the avenues of research into stuttering that
could be pursued, studies of dopamine metabolism and dopamine-mediated
incentive learning in people who stutter have the potential to bear much fruit.
References
Alm, P. A. (2004). Stuttering and the basal ganglia circuits:
a critical review of possible relations. Journal of communication disorders,
37(4), 325-369.
Alm, P. A.
(2005). On the Causal Mechanisms of Stuttering. Lund University.
Alm, P.
A., & Risberg, J. (2007). Stuttering in adults: The acoustic startle
response, temperamental traits, and biological factors. Journal of
Communication Disorders, 40(1), 1-41.
Barona-Lleo,
L., & Fernandez, S. (2016). Hyperfunctional voice disorder in children with
Attention Deficit Hyperactivity Disorder (ADHD). A phenotypic characteristic? Journal
of Voice, 30(1), 114-119.
Beninger,
R. J. (2018). Life's rewards: Linking dopamine, incentive learning,
schizophrenia and the mind. Oxford UK: Oxford University Press.
Brocklehurst,
P.H. (2021). The Perfect Stutter. Google Play Books.
Brocklehurst,
P. H., Lickley, R. J., & Corley, M. (2013). Revisiting Bloodstein's
Anticipatory Struggle Hypothesis from a psycholinguistic perspective: A
Variable Release Threshold Hypothesis of stuttering. Journal of
communication disorders, 46(3), 217-237.
Fish, C.
H., & Bowling, E. (1965). Stuttering—The Effect of Treatment with
D-Amphetamine and a Tranquilizing Agent, Trifluoperazine; A Preliminary Report
on an Uncontrolled Study. California medicine, 103(5), 337.
Langova,
J., & Moravek, M. (1964). Some results of experimental examinations among
stutterers and clutterers. Folia Phoniatrica et Logopaedica, 16(4),
290-296.
Maguire, G. A., Riley, G. D., Franklin, D. L., Maguire, M.
E., Nguyen, C. T., & Brojeni, P. H. (2004). Olanzapine in the treatment of developmental
stuttering: a double-blind, placebo-controlled trial. Annals of Clinical
Psychiatry, 16(2), 63-67.
Maguire,
G. A., Yeh, C. Y., & Ito, B. S. (2012). Overview of the diagnosis and
treatment of stuttering. Journal of Experimental & Clinical Medicine, 4(2),
92-97.
Mĺnsson,
H. (2007). Complexity and diversity in early childhood stuttering. Paper
presented at the Fifth World Congress of Fluency Disorders, Dublin.
Reilly,
S., Onslow, M., Packman, A., Cini, E., Conway, L., Ukoumunne, O., et al.
(2013). Natural history of stuttering to 4 years of age: A prospective
community-based study. Pediatrics, 132(3), 460-467.
Schultz, W. (2016). Dopamine reward
prediction error signalling: a two-component response. Nature Reviews
Neuroscience, 17(3), 183-195.
Seeman,
P., Bzowej, N. H., Guan, H. C., Bergeron, C., Becker, L. E., Reynolds, G. P.,
et al. (1987). Human brain dopamine receptors in children and aging adults. Synapse,
1(5), 399-404.
Wu, J. C.,
Maguire, G., Riley, G., Lee, A., Keator, D., Tang, C., et al. (1997). Increased
dopamine activity associated with stuttering. Neuroreport, 8(3),
767-770.
Yairi, E.,
& Ambrose, N. (2005). Early Childhood Stuttering. Austin, TX:
PRO-ED, Inc.