Great observation! According to [this](https://www.researchgate.net/publication/352029918_STUTTERING_DOPAMINE_AND_INCENTIVE_LEARNING) new research (2021) about the dopaminergic system: * According to Alm, 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 * Alm (2004, p.343): “A negative emotional experience of stuttering could be described as an event that was less rewarding than predicted, thereby reducing dopamine release and weakening the motor program for the intended speech sequence that failed * Now, fifteen years later, researchers 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. 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 * How could **antipsychotic drugs** lead to an amelioration of stuttering symptoms? **Answer**: it may increase the ‘signal-to-noise ratio” of speech plans; and their effect of blocking D2 dopamine receptors causes a general reduction in responsivity. When the speaker realises that he is eliciting fewer negative responses from his listeners, the level at which his [release threshold](https://www.google.com/search?q=%22release+threshold%22+%22stuttering%22&tbm=isch&ved=2ahUKEwi4gLzF7vz_AhUQiP0HHWftCOgQ2-cCegQIABAA&oq=%22release+threshold%22+%22stuttering%22&gs_lcp=CgNpbWcQAzoHCAAQGBCABFDQDlirJWC-JmgAcAB4AIABfYgB2gWSAQQxMy4xmAEAoAEBqgELZ3dzLXdpei1pbWfAAQE) is set falls, and he finds that he can execute planned words more easily. As a result, the speaker will perceive the speech plan to be more appropriate and to contain fewer errors; it dampens our sensitivity so that the rises in synaptic dopamine are no longer so rewarding (pleasurable) and the falls are no longer so punishing. Additionally, PWS may misperceive the initial rise in dopamine which is really only signalling the detection of a novel stimulus as signalling a positive evaluation. It could lead us to perceiving people's responses more positive than they really are, but if some PWS start to realise this and start worrying, then it may result in more disfluencies * Surprisingly, the study by Langova and Moravek actually found that clutterers and ‘stutterer-clutterers’ symptoms actually improved on **antipsychotics**, whereas ‘pure stutterers’ (without cluttering) symptoms tended to improve on **stimulants** (like ritalin) * It highlights the possibility that stuttering symptoms may be ameliorated in the ‘attention deficit’ subgroup of stutterers by stimulants that increase dopamine metabolism (like Ritalin) - increasing the attentional control and reducing the hyperactivity * What function do striatal dopamine receptors normally fulfil? **Answer**: 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. The more functional striatal dopamine receptors a person has, the more responsive to stimuli he or she is likely to be. D2 receptors facilitate ‘diffuse’ responses vital in enabling learning (majority of such responses are unhelpful); whereas D1 receptors facilitate ‘focussed’ responses (which are more stable, predictable and, generally, desirable) * Why do young children have such high densities of them? **Answer**: it enables children to quickly and efficiently adapt to their environment and learn how to manipulate it * The development of our ability to **anticipate** when a primary reward is about to occur is thanks to the development of secondary rewarding stimuli in this way. The secondary rewarding stimulus triggers the **anticipation** of the primary rewarding stimulus that it is associated with * Phasic changes in the concentration of synaptic dopamine: * 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 increase – enabling further approach behaviour towards that stimulus * 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 * These phasic fluctuations in our synaptic dopamine levels relate to the Variable Release Threshold Hypothesis. We are hard-wired to find *food, sex and to experience successful communication* rewarding. So, successful communication constitutes a strong **primary reward** and communication failure constitutes a strong **primary punishment** * Any stimulus that causes us to **anticipate** that communication will be successful will constitute a powerful **secondary reward**; **anticipating** communication failure will constitute a powerful **secondary punishment**, such as evaluate negative listener responses, speech errors, and stuttering, 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 the striatum), and will inhibit the motor execution of the speech plan for those "**anticipated**" words (resulting in a speech block) * Such negative evaluations and anticipations then would start to trigger the phasic reductions in synaptic dopamine that cause them to produce stuttering blocks * The lower the dopamine levels, the greater the extent of the inhibition (aka the longer the speech block lasts). A drop in synaptic dopamine that occurs in this way may constitute the rise in the release threshold mechanism, and a resultant impairment of incentive learning * Some PWS don't have underlying neurological or physical impairments (that cause their speech to be error-prone), such as PWS whose problems stem primarily from unduly perfectionistic self-expectations * Stuttering remission may occur, if the novelty effect of a therapy lasts long enough to enable the development of faith in one’s ability to speak without stuttering. This may explain why some therapists with a convincing manner, succeed in eliciting better results, regardless of what type of therapeutic approach they adopt * PWS, similar to people with ADHD, as a consequence of the 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 * Stuttering occurs as a direct result of phasic reductions in synaptic dopamine, brought on by the perception (or anticipation) of communication failure * Clinical interventions: from the perspective of incentive- learning, one of the keys to successful speech therapy would be the ability to accurately identify the moments when the speaker is evaluating his performance. Then the speakers needs to find ways to ensure that the speaker’s synaptic dopamine levelsremain sufficiently high to cause appropriate positive evaluations to occur