What causes stuttering? - According to Mark onslow (PhD researcher)

What causes stuttering? - According to Mark onslow (PhD researcher) The curious PWS (person who stutters) in me read [this](https://www.researchgate.net/publication/223508249_On_the_cause_of_stuttering_Integrating_theory_with_brain_and_behavioral_research) research. After finishing the 12 pages, I summed up the key points. **Intro:** * A recent meta-analysis concluded that the aberrant neural activations are a consequence of stuttering rather than a cause, and that stuttering is a disorder of the initiation of speech motor plans (aka the initiation of syllables). This is underpinned by a disturbance of neural function in SMA * Our syllable initiation (SI) theory has evolved from our working model, the variability or Vmodel. SI theory draws not only on brain research in stuttering but also on research into speech production deficits after brain damage. SI theory locates stuttering at the interface of speech and language and we suggest that it provides a plausible and parsimonious explanation of the cause and critical phenomena of stuttering * Most children recover naturally from stuttering mostly within two years of stuttering onset * Girls recover from stuttering more often than boys * Recovery in adulthood is also reported to occur occasionally * Adopting strategies to conceal stuttering, or superfluous behaviors (like grimacing/grunting) is associated with chronic stuttering * The proximal (aka final link in the causal chain) cause of stuttering is difficulty initiating syllables (Onslow) * Variability model, or Vmodel (Onslow & Packman) * We provide evidence to support the idea that this difficulty initiating syllables is underpinned by disrupted function of the supplementary motor area (SMA) * We suggest that the focus on the syllable and syllable initiation (SI) in our theory provides the missing link between language and speech production that is fundamental to understanding the nature and cause of stuttering **The search for cause: brain imaging** * Unusual brain activity in PWS: * Recent meta-analysis indicates increased right hemisphere activation, decreased temporal lobe activity, and unusual cerebellar activation * Structural brain anomalies: increased size and symmetry of planum temporale and an increase in the number of gyri and in gyral variability; increased size of right planum temporale has been shown to be associated with more severe stuttering * Signal transmission in the Rolandic operculum is less than optimal * It may be that site of anomaly is more important than type * Future research * Future research should develop a model that unifies the observed actions and interactions of the neural systems involved * Efference copy: feed-forward of motor plans * Brown (PhD) concluded that the under and over activations observed during the speech of adults who stutter are a consequence of stuttering, rather than a cause * They concluded that stuttering is a problem with the initiation of motor programs. (SI theory is based on this idea) * SI theory: the core feature of the mechanism underlying stuttering is a difficulty initiating speech motor programs for syllables * It is tempting to attribute this initiation problem to the structural anomalies. However, assuming causal relationship from co-occurrence is hazardous. The primary question still remains: Do structural anomalies have a causal role in stuttering? Is it the years of struggling to speak and the use of motoric strategies for dealing with stuttering the cause for structural anomalies? Are structural anomalies present in young children prior to the onset of stuttering? More research is needed **The importance of the syllable** * Levelt: learned syllable-sized articulatory programs—are stored in a mental syllabary. Access to stored syllable gestures reduces the computational load during speech production * Linguistic meaning is given to syllables relative changes in pitch, duration and/or loudness (aka contrastive stress is achieved motorically) * Babbling represents syllable frames without content and content typically starts to be inserted into frames during the second year of life, to form the child’s first words **Our working model** * We found that adults reduced the variability of linguistic stress when using prolonged speech to control their stuttering * Reducing syllabic stress contrasts reduces the need to vary motoric effort * Vmodel: stuttering is triggered by the motoric demands of linguistic stress; namely, the variation in effort required to vary emphasis from syllable to syllable. Hence, reducing that variability, as occurs with prolonged speech and rhythmic speech, results in reduction of stuttering * The Vmodel proposed a trigger mechanism * PWS have an unstable speech motor control system that is more susceptible to perturbation by high task demands. One such demand is the varying of linguistic stress * The Vmodel explains the two best-known features of the onset of stuttering: * Onset coincides with children putting words into short utterances andthe repetition of syllables is the predominant sign of stuttering at onset * The fact that children do not stutter when they babble or on their first words, but only when they are putting words together, indicates that something triggers stuttering at this stage of speech and language development. Syllables are fairly equally stressed in children’s babbling and early utterances and children must learn to de-stress in order to achieve the variationrequired by the adult model * stuttering manifests when the motoric demands of varying linguistic stress start to overwhelm the child’s compromised speech system * At points when those demands cannot be met the child is unable to move forward in speech * communicative context and its concomitant level of arousal affecting this threshold influences the threshold for the appearance of individual stuttering moments, and their severity * However, while unable to move on to the next syllable, the child can still repeat thesyllable just uttered. This repetition of syllables can be seen as an ontogenic retreat to an earlier stage of speech development—to babbling—where variation in linguistic stress across syllables is minimal * Thus, these syllable repetitions serve a purpose to enable the child to accommodate the underlying perturbation in speech motor control. Over time, this default position is reinforced through instrumental learning **Stuttering and SMA** * This difficulty in initiating syllables might arise in the SMA which is involved in the preparation and control of complex sequential movements, including the initiation of propositional speech (cf. non-propositional = expressions/utterances without conveying meaning) - that are internally initiated (rather than a response to an external stimulus). SMA has a role in speech motor performance rather than assignment of content * The role for the anterior pre-SMA is to represent syllable or word-sized frames and to coordinate serial position/timing signals with the motor apparatus via the SMA * SMA is involved in the difficulty in initiating and sequencing syllables * Structures in the inferior frontal lobe, such Broca’s area provide syllabic content * Adults who stutter have been shown to have slower speech, phonation and manual reaction times than controls. Compared to controls, these reaction times do not appear to decrease with practice * A study showed that adults who stutter have increased thresholds for motor evoked potentials in the dominant hand * Speech and hand (co-speech) gestures are functionally and evolutionarily related * Stutterers don't have a lesion (damage) of SMA **Discussion:** * Stuttering variability, severity, frequency and the amount of struggle behavior might be determined by the amount of arousal stimulated by the communicative context and by the strategies adopted by the speaker to conceal stuttering. It might be effective because it prompts children to learn to adjust for the underlying neural processing deficit * CWS usually start stuttering when they start to use contrastive linguistic stress at age 3-4 * A simple operant behavioral treatment involving parental comments for stuttered and stutter-free speech is efficacious with young children but adults show only a modest response to similar operant procedures * Alm proposed that stuttering is a disorder of timing that is underpinned by dysfunction (i.e., inactivity) of the basal ganglia * We cannot say that stuttering is underpinned by neuropathology, suggesting that it is premature to assert that stuttering is caused by structural or functional abnormalities in the nervous system/brain **Tips**: (that I extracted from the research) * Don't blame aberrant neural activations for not being able to execute speech motor programs, because they are the consequence of stuttering rather than a cause * Address the initiation of speech motor plans (aka the initiation of syllables which is the final link in the causal chain) - disturbed by the neural function in SMA. Don't give up on addressing this SI problem, because (1) stuttering recovery in adulthood is also reported to occur occasionally, and (2) stutterers don't have a lesion (damage) of SMA * Don't adopt strategies to conceal stuttering, or superfluous behaviors (like grimacing/grunting) which reinforces chronic stuttering. Years of struggling to speak and the use of motoric strategies for dealing with stuttering causes structural anomalies * Address the linguistic meaning given to syllables (such as, changes in pitch, duration, loudness and other contrastive stress achieved motorically) * Address the represented syllable content * Reduce the variability of linguistic stress to initiate syllables * Reduce syllabic stress contrasts - to reduce the need to vary motoric effort * Reduce motoric demands of linguistic stress, such as, the variation in effort required to vary emphasis from syllable to syllable * Address the trigger mechanism - to stabilize the speech motor control system that is susceptible to perturbation by high task demands (e.g., varying of linguistic stress). The fact that young children do not stutter when they babble or on their first words, but only when they are putting words together, indicates that something triggers stuttering * De-stress syllables - to resemble syllables that are fairly equally stressed in children’s babbling and early utterances * Address the motoric demands of varying linguistic stress * Address the threshold of communicative context and its concomitant level of arousal * Don't serve a purpose by applying repetitions to enable ourselves to accommodate the underlying perturbation in speech motor control, as it will be reinforced through instrumental learning * Address how we perceive and respond to propositional speech (expressions/utterances with conveying meaning) that are internally initiated (rather than a response to an external stimulus) * Don't link triggers, propositional speech, heightened demands/threshold, etc, to limit SMA's speech motor performance, or to limit the anterior pre-SMA's **timing** signals, or inactivate the basal ganglia's **timing** processes * Address the heightened monitoring-response mechanism - to address the slower speech, phonation and manual reaction times than controls * Address the amount of arousal stimulated by the communicative context - to reduce stuttering variability, severity, frequency and the amount of struggle behavior * Learn to adjust for the underlying neural processing deficit - to reduce stuttering * Address the contrastive linguistic stress