JWCSC Montreal day 2

The day 2 keynote was shared between Soo-Eun Chang, Edward Conture and Pascal van Lieshout. Chang told the conference how she had received many emails from the public describing stuttering onset following infection by SARS-CoV-2, and asking if she could explain what was happening. She suggested that overactive glial cells could prune back nerve cell connections. The effect would be a reduction in the strength of electrical signals travelling between different parts of the brain, compared to the situation prior to COVID-19. If parts of the brain affected are also those identified in brain studies of stuttering, then stuttering behaviour might be expected to follow. Chang further pointed out that several of the reports she had received were from parents whose children had begun stuttering following COVID-19. In such cases, it is difficult to disambiguate stuttering induced by COVID-19 from a more typical developmental stuttering. Thus, in some cases it may merely be coincidence that stuttering began following COVID-19.

Conture discussed stuttering in children aged between about 3 and 6 years old, with a focus on variability. Understanding variability is crucial, since if we cannot do so we do not really understand stuttering. Conture suggested that if a predisposition to stuttering (e.g. through genetics) is accompanied either by less emotional regulation, or by more variable emotional regulation, more stuttering might be expected. The assertion was supported with a variety of child studies. Closer tracking of emotional regulation during onset of stuttering (age 3 to 6) may help us to track the variability of stuttering more accurately than perspectives which focus on causality alone.

Van Lieshout highlighted that brain research on stuttering does not clearly identify stuttering as a speech-motor disorder. This is because no research has established brain differences between stutter and non-stutter groups which can be considered necessary to induce stuttering. Rather, the group differences in neural measures are subtle. Difficulty follows in disambiguating prospective symptoms of a disorder from a compensatory neural development. Despite these classification difficulties, stuttering remains an essential topic for speech-motor research. This is because of the way that stuttering is so prominently expressed in the speech-motor system. Van Lieshout compared skill at control of the speech-motor system to skill at control of the body whilst playing golf. So, a few people are very good or very poor golf players, but most of us will be average at golf and have the prospect of improving somewhat with practice. The same may apply to speech-motor control. Sometimes, as with a speaker such as Barack Obama, speech-motor control may naturally be near to perfect. Other times, as with a speaker such as Joe Biden, speech-motor control may not appear so perfect. Note that this comment applies just to fine-grained control of articulatory musculature – not to the content or effectiveness of what is said! Nevertheless, just as we cannot all play golf like Jack Nicklaus or Tiger Woods, so we won’t all speak as fluidly as Barack Obama. Most speakers will have speech-motor control skill somewhere between that of Obama and Biden.

Thus, for van Lieshout, people who stutter are in a group who find it difficult to obtain a high degree of speech-motor control even with extensive practice. Van Lieshout went on to describe speech-motor control using a dynamic systems model. Greater understanding of the different oscillators which comprise such a model may enable us to devise more appropriate speech learning for those of us who would prefer to stutter on fewer occasions, and/or for shorter periods of time.

The three-part keynote covered a huge amount of stuttering research. It explains why, for example, we can categorically state that stuttering is not caused primarily by a nervous disposition. It used to be the case (and still is, in some countries) that stutterers could be told to “snap out of it”. The expectation is that just a bit more effort on the part of the speaker would remove stuttering behaviour. Thanks to work such as that presented in Saturday’s keynote, it is now apparent that such demands are unreasonable.

As on Friday, it was sadly impossible to attend all the parallel sessions. But we did get to many of them. Katrina Ntouru described an eye tracking study which presented children with pictures having emotional valence. Her presentation covered similar themes to those described by Conture, but with an additional consideration of how attentional bias could contribute to the development of social anxiety following a history of stuttering. Marine Pendeliau showed videos demonstrating how a highly exaggerated form of speech motor learning might be effective for speakers wishing to gain greater control of stuttering and cluttering behaviours. This followed directly from the considerations described by van Lieshout.

Gareth Walkom exhibited his withVR virtual reality system throughout the weekend. It enables stutterers to practice speaking situations with 3D avatars, thus providing a mechanism through which feared situations can be practiced with no fear of a genuine social consequence. We tried the system, and can confirm that the avatar performance is sufficiently realistic that it could be programmed to elicit stuttering. The technology has clinical applications, several of which were presented by Walkom to an audience of speech and language pathologists in the main auditorium.

Evan Usler described his research on speech rhythmicity. He works on the basis that cognitive conflict (e.g. motivational conflict) may result in hesitations and/or perseverations in speech. Thus, stuttering is the physical manifestation of an inner conflict over whether or not to continue speaking. This line of research is consistent with work by Joe Sheehan on approach-avoidance conflict. A simplified version of Sheehan’s approach-avoidance conflict is known to many who stutter via the “iceberg model” of stuttering, in which thoughts and feelings about stuttering cannot be seen by listeners, and only the overt stuttering behaviours (jaw jerks, tremors and so on) are visible. Usler’s research suggests that greater variation in speech rhythm for those who stutter may be associated with an underlying cognitive conflict over whether to continue a particular speech act.

Bert Bast introduced a clinical model of stuttering, combining several strands of current thinking. Onset of stuttering is tied to either a genetic predisposition, or to random factors. A typical path to secondary stuttering behaviour follows when a child becomes aware that their speech is more difficult than they would expect (i.e. difficult compared to their level of motor control for non-speech tasks, or difficult compared to the apparent ease with which other children speak). Thus, early intervention is crucial to avoid adverse psychological consequence. The model of Bast and colleagues is biopsychosocial. It thus has scope to incorporate some of the themes identified through application of a social model of disability to stuttering, although the authors did not do so in this presentation.

Emily LeRose examined the co-occurrence of several types of psychological diagnosis with stuttering. Analysis was of data not specifically designed for stuttering research – the consensual use of discarded blood samples following routing medical testing. The data are not ideal. For example, there is a reliance on self-report, and instances of stuttering are identified via a complex keyword search having a high rate of false negatives (thus, sampling may be biased). Despite this, the data set has a major advantage that genetic sequencing is available, enabling a genome-wide association study. Several presentations at the conference were based around these data, but this is the only one we were able to attend. Co-occurence of psychological diagnosis was identified at rates many times higher than chance. These notably included anxiety and trauma disorders, with post-traumatic stress disorder the most prominent. Trauma-informed stuttering therapy had also been addressed by Chaya Goldstein on Friday, but unfortunately we were unable to attend due to our own presentation being scheduled at the same time. Conference scheduling is so frustrating!

A concern which arises from presentations at the conference is that the identification of anxiety and trauma disorders related to stuttering has implication not just for treatment of stuttering, but also for advocacy. Thus, there is a risk that campaigns which draw attention to stigma around stuttering, or which deliberately promote stuttering-related stigma, could re-traumatise people who stutter. Care and consideration may be required over the appropriateness or otherwise of such campaigning.

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    • #336
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      JWCSC day two featured a three-way keynote from Soo-Eun Chang, Edward Conture and Pascal van Lieshout.

      [See the full post at: JWCSC Montreal day 2]

    • #347
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      A few thoughts on the COVID-stuttering connection. Neural effects following COVID-19 were identified early on in the pandemic. They are now colloquially described as brain fog. This is one of the many deleterious effects of a syndrome referred to as long covid.

      Current indication is that COVID-19 particles are not overabundant in the brain, but rather that the issue is a prolonged immune system response leading to neuroinflammation.

      Long covid is at present under-reported in the media, however the pandemic remains ongoing, with continued evolution of the virus in variants such as the Omicron cluster. Thus, stuttering following COVID-19 is unfortunately likely to be an area to watch. Stuttering acquired following COVID-19 may have different characteristics to the stuttering which develops following a more typical childhood onset.

      COVID-19 in connection with childhood stuttering adverts to a broader point: acquired stuttering is just as possible in children as in adults. We know from twin studies that only about 70% of childhood stuttering is hereditary. Subtyping childhood stuttering, and developing appropriate treatment plans, may require a greater appreciation of the role disease can play in the onset of stuttering. One example of a candidate disease which may have historically contributed to stuttering is streptocoppal infection, described in this recent article by Per Alm: https://www.frontiersin.org/articles/10.3389/fnhum.2020.569519/full.

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