Reactive Inhibitory Control Precedes Overt Stuttering Events

Abstract

Research points to neurofunctional differences underlying fluent speech between stutterers and non-stutterers. Considerably less work has focused on processes that underlie stuttered vs. fluent speech. Additionally, most of this research has focused on speech motor processes despite contributions from cognitive processes prior to the onset of stuttered speech. We used MEG to test the hypothesis that reactive inhibitory control is triggered prior to stuttered speech. Twenty-nine stutterers completed a delayed-response task that featured a cue (prior to a go cue) signaling the imminent requirement to produce a word that was either stuttered or fluent. Consistent with our hypothesis, we observed increased beta power likely emanating from the R-preSMA—an area implicated in reactive inhibitory control—in response to the cue preceding stuttered vs. fluent productions. Beta power differences between stuttered and fluent trials correlated with stuttering severity and participants' percentage of trials stuttered increased exponentially with beta power in the R-preSMA. Trial-by-trial beta power modulations in the R-preSMA following the cue predicted whether a trial would be stuttered or fluent. Stuttered trials were also associated with delayed speech onset suggesting an overall slowing or freezing of the speech motor system that may be a consequence of inhibitory control. Post-hoc analyses revealed that independently-generated anticipated words were associated with greater beta power and more stuttering than researcher-assisted anticipated words, pointing to a relationship between self-perceived likelihood of stuttering (i.e., anticipation) and inhibitory control. This work offers a neurocognitive account of stuttering by characterizing cognitive processes that precede overt stuttering events.

Psychedelics in developmental stuttering to modulate brain functioning: a new therapeutic perspective?

“…As in a vicious circle, this anxiety is reinforced by the anticipation of stuttering which increases in extent and complexity throughout development ( Jackson et al, 2015 , 2018 , 2019 ; Rodgers and Jackson, 2021 ), thus possibly resulting in further repetitive and negative thinking or rumination ( Tichenor and Yaruss, 2020 ). Interestingly, Orpella et al (2024) suggest that this may result in a further abnormal involvement of control on processes during speech production, especially prior to anticipated and stuttered (vs. fluent) speech ( Jackson et al, 2022 ). In this regard, it has been suggested that internally-(vs. externally -)directed focus may contribute to disrupt simple/automatic movements ( Wulf et al, 2001 ; McNevin et al, 2003 ; Kal et al, 2013 ), also in DS (e.g., Eichorn et al, 2016 , 2019 ; Jackson et al, 2016 ).…”

“…In this regard, stuttering events seem to correlate with the presence of higher inhibitory activity in sensorimotor networks ( Korzeczek et al, 2022 ; Orpella et al, 2024 ). In this case, evidence suggests that “maladaptive” processes, also involving the above-described patterns and, possibly, abnormal modulation of action-stopping networks ( Neef et al, 2018a , 2022 , 2023 ; Busan et al, 2020 ; Korzeczek et al, 2022 ), may have a role in interaction with circuits involved in emotion regulation ( Neef et al, 2018b , 2022 , 2023 ; Montag et al, 2019 ; Chow et al, 2023 ).…”

“…There are several pre-clinical and clinical indications that psychedelics (e.g., LSD) may have a therapeutic role in alleviating anxiety (see, for a recent review, Inserra et al, 2023 ). Thus, by reducing anxiety in DS, psychedelics may modulate activity in overactivated (or underactivated) systems, thereby reducing difficulties and allowing “easier” control (i.e., with limited interferences) of speech-motor systems ( Alm, 2014 ; Jackson et al, 2022 ; Orpella et al, 2024 ). The mechanisms could be through effects on brain metabolism and their capacity to promote plasticity, also in networks such as the SCN/DMN and emotional regulatory systems (compare with Ly et al, 2018 ).…”

“…The previous sections described the neuropathological mechanisms of DS, as well as the likely mechanisms for psychedelic drugs to act on brain networks. Considering that (frontal) brain metabolism may be aberrant in PWS, and that the “maladaptive” intervention of networks such as the SCN and the DMN could add further “neural noise” to the system (thus worsening the functionality of “goal-directed” networks and behaviors; compare with Alm, 2014 ; Jackson et al, 2022 ; Orpella et al, 2024 ), we propose that controlled treatment with psychedelics should be investigated to help in disrupting maladaptive neural functions in DS, thus restoring a more “adaptive” plasticity in the neural networks involved. More specifically, this should be done in the attempt to reduce social anxiety interacting with speech-motor networks, both precipitating and maintaining stuttering [always keeping in mind that serotonergic drugs may also modulate the functioning of motor excitability in humans ( Thorstensen et al, 2024 ), as well as speech-motor circuits in DS (see Busan et al, 2009 )].…”

“…Recent work is clarifying the brain dynamics of DS using neuroimaging and neurophysiological methods: indeed, stuttering is thought to be a speech-motor issue related to basal ganglia dysfunction and impairments of speech/motor cortical areas, also resulting in atypical neural connectivity ( Etchell et al, 2018 ). Thus, while there are many unanswered questions regarding the underlying neural basis of DS, a common perspective is that stuttering is associated with altered brain regulation of motor sequencing and timing of volitional control of speech ( Craig-McQuaide et al, 2014 ; Etchell et al, 2014 , 2015 , 2018 ; Busan et al, 2019 , 2020 ; Busan, 2020 ; Chang and Guenther, 2020 ; Tendera et al, 2020 ; Alm, 2021b ; Gastaldon et al, 2023 ; Orpella et al, 2024 ). Nevertheless, stuttering remains difficult to treat and no resolutive treatment is available, especially when it persists in adulthood.…”