an intellectually rigorous post. a thought-provoking great read

an intellectually rigorous post. a thought-provoking great read An SLP and PhD [researcher ](https://www.researchgate.net/publication/329280362_Stammering_and_Post-Traumatic_Stress_-Some_food_for_thought)stated: *"Freeze response may result in vasoconstriction (narrowing of bloodvessels), greatly reduced heart rate, cessation of breathing, and temporary full-body paralysis – all of which contribute tomaking the person appear dead – which may be especially useful in life-threatening situations where flight or fight responseswould be of no avail."* I re-read the paper and I noticed he mentioned freezing (the part about global/full-body freezing caught my attention) and wanted to share a few thoughts From what I understand, the amygdala can operate in (at least) two functionally distinct ways. 1. **Central amygdala (CeA)**: the canonical fast output that drives global defensive responses (PAG-mediated freezing/immobility). This looks like what this 2016 research study describes for full-body **freezing**. 2. **Basolateral amygdala (BLA)**: a more outcome-specific/value/associative node that can bias striatal gating and selectively suppress a particular motor program. Functionally this is conditioned suppression/action suppression rather than ethological “**freezing**. I think this distinction helps explain some reporting patterns in people who stutter (PWS). Many PWS interpret apparently “random”, "unpredictable" or context-independent stuttering as neurogenic — especially when it happens with comfortable listeners. My current view is that a large portion of developmental stuttering episodes could reflect BLA-driven, often nonconscious (subliminal) threat processing: the BLA can be triggered by cues or internal states the speaker isn’t consciously aware of, so the person doesn’t feel an obvious fear but the motor program is nonetheless suppressed. Human evidence indicates the basolateral/lateral amygdala (BLA) most often shows early, **nonconscious** sensitivity to threat-related cues, whereas the central nucleus (CeA/CeN) functions primarily as the downstream output node that generates defensive expressions. Put simply: BLA activation frequently occurs without conscious awareness and responds earlier to **subliminal/unseen** threat cues than CeA. ([source](https://docs.google.com/document/d/1Nu__nV8mXOkEjgQ5OzdqnfqYGK8IP7P_87W9KJeE9zk/edit?usp=sharing)) The amygdala reliably shows differential responses to threat-relevant stimuli even when those stimuli are not consciously perceived, so physiological/behavioral effects follow unseen stimuli. Many PWS seem to imply, “*I can sometimes stutter when I’m alone too, so it can’t be social fear — it must be neurogenic*.” I used to stutter alone as a child too. My explanation is simple: as a child I didn’t separate “alone” from “being watched.” I treated every speaking situation the same and developed an “all-presence” mindset — meaning that an internal expectation of social rejection was even present when I stuttered alone as a child. So that fear of social rejection could trigger the basolateral amygdala (BLA) without my ever feeling obvious fear, so the speech motor plan was suppressed even when I spoke alone. The researcher (PhD) stated: *"Neurogenic stuttering: Stuttering that appears to have been caused by a neurological injury of some sort. Usually, late-onset stuttering is presumed to be neurogenic, but there is no logical reason why early childhood stuttering cannot be neurogenic as well. Indeed, Alm and Risberg postulate that about 40% of all stuttering has a neurogenic component to it. It is quite possible that the percentage is much higher, including among young children."*  I'm still not totally sure what he or Per Alm mean by neurogenic stuttering: Are they referring to neurogenic stuttering as a "random" and "unpredictable" stuttering that appears not to be preceded by a cue (associated with fear of rejection) triggered by the BLA-amygdala? If this is the case, is it perhaps possible that they are confusing nonconscious / unseen (subliminal) threat processing–amygdala activation with neurogenic stuttering? My take: In my stutter experience, from what I understand now (my current understanding), I've never experienced truly random or unpredictable (neurogenic?) stuttering. So I'd say that, in my lifetime, almost all my stuttering (if not all) was actually triggered by the BLA-amygdala rather than from some kind of brain lesion/damage. Perhaps this could explain my many stuttering remissions and relapses (maybe). I have an extremely strong feeling that this applies to most individuals with developmental stuttering (coming from a family with 6 stutterers; 3 whom outgrew stuttering). In the research about post-traumatic stress and stammering, it was mentioned that some PWS reported a (psychological) traumatic event near stuttering onset. Additionally, other people report that they mostly stutter with anxiety while they almost do not stutter when there is no anxiety. In my current understanding, I believe that those PWS who stutter significantly more under strong obvious fear — I would simply label that "strong obvious fear" as a conditioned stimulus. Yet I would label the unconditioned stimulus (fear of social rejection) as a low or even unseen/nonconscious amount of fear (i.e., fear that, by default, is too subtle to notice during real-life stuttering events in daily life; low subtle fear primarily used for guiding speech motor movements — i.e., BLA-amygdala — rather than a lion-in-the-room survival alarm kind of fear — i.e., CeA-amygdala). So the model would then look like: **Model:** (**very relevant for research labs**) Subset 1: PWS who stutter significantly more with anxiety: obvious fear (CS) --> nonconscious/unseen fear of social rejection (US) Subset 2: PWS who usually stutter the same in all situations: not-obvious fear (CS) --> nonconscious/unseen fear of social rejection (US) \~\~ When people want to speak “appropriately,” formally, or make a good impression, they tend to tighten and more strictly regulate speech-plan execution — a drive that is ultimately rooted in fear of social rejection. Often, if we stutter in that moment we don’t consciously notice the fear, but it’s still present non-consciously and the BLA-amygdala responds, triggering selective suppression of (a segment of) the speech motor plan. Importantly: PWS can be happy and excited (i.e., experiencing a positive emotion) while wanting to speak more appropriately/formally. So positive emotions do not necessarily result in loosening the regulation of speech plan execution. **(Very relevant for research labs.)** In my current understanding, even though conditioned stimuli are ultimately linked to FEAR of social rejection, I think **it's not a fear problem** but rather an associative problem where PWS fail to extinguish the conditioned stimulus (CS) from the conditioned response (CR). (i.e., ultimately it's about properly fine-tuning the release threshold rather than speaking without fear). Put simply: the problem is a **NEED** for excessive error-avoidance and a **NEED** to excessively regulate speech-plan execution in which even very subtle stimuli start triggering the approach–avoidance "cognitive" conflict and selective suppression of the motor program. (*Importantly: There are also* ***reasons*** *why we rely on those needs but I'll explain that later in the stutter image below*) So, in another viewpoint, the problem is the subconscious brain "**needing**" to avoid those errors excessively - specifically to properly regulate the execution of the speech plan. PWS simply fail to unlearn reliance on those needs to avoid errors to execute the speech plan (extremely relevant for **research labs**). Another reason why it's not a fear problem: During a stuttering block in which there is obvious fear, the subconscious brain eventually allows the execution of the speech plan — eventually (e.g., after 2 s) — without having reduced any anticipatory fear. What I mean is that the classic model "**fear -> triggers stuttering**" is incomplete (this model, based on the approach–avoidance conflict, misses pieces). Another reason why it's not a fear problem: Earlier I mentioned that speaking more formal/appropriately tends to increase regulation of speech-plan execution — because it's ultimately linked to fear of rejection. In the same way, non-stutterers interact with stimuli associated with fear of rejection throughout the whole day, yet they do not stutter. So fear of rejection is not the problem (*here I'm pointing to the many SLPs that misunderstood this*); rather, the poor fine-tuning of the release threshold is the main problem toward stuttering remission and subconscious fluency. In a subset of PWS, authority stress or fear of stuttering can actually lead to more fluency (e.g., from my own stutter experience). In this case, fear leads to loosening the regulation of speech execution. (Extremely relevant for **research labs**.) My hypothesis is that this happens because of the reasons (why I rely on those needs) which gives a low salience/positive valence tag to the basal ganglia *(see the stutter image below — which I created)*. Additionally, acceptance approaches (from SLPs) can result in a subset of PWS believing (mostly subconsciously): "I don't need to resolve the approach–avoidance conflict during a stutter" (after all, I accept my stutter as it is; stuttering is my way of talking). (Extremely relevant for research labs.) My point is: adopting random SLP techniques with a desensitization component is not necessarily effective to resolve the approach–avoidance conflict during a stutter. In fact, random desensitization techniques can sometimes maintain/reinforce the approach–avoidance conflict (stimulus generalization). Also, the classic statement by most SLPs: "*Fear exacerbates stuttering*." This email counters that statement by saying that fear doesn't trigger stuttering, rather the poor fine-tuning of the release threshold does. Many SLP techniques that include desensitization mainly target the “fear of stuttering” and therefore may miss the many other conditioned stimuli that trigger approach–avoidance conflict and excessive regulation of speech-plan execution. If SLPs broadened the target to include those additional conditioned stimuli, I think therapy could help a wider range of people and lead to more stuttering remissions and subconscious fluency (over controlled fluency). \~\~ **Many SLPs see the approach-avoidance as: desire to speak vs fear to stutter/speak.** I opt that SLPs should stop viewing “approach” (in approach–avoidance) as a desire to speak, because a feeling (or thought) of desire is simply a conditioned stimulus, which can lead to more stuttering and stricter regulation of speech-plan execution. I opt that SLPs should stop considering the “avoidance” part (of approach–avoidance) as primarily fear of stuttering (or fear of speaking), because, as I explained earlier, fear of stuttering can lead to less stuttering and to loosening of regulation of speech-plan execution. My point is: most SLPs misunderstand the approach–avoidance conflict entirely. **Recommended solution:** Instead, I recommend SLPs adopt: * Avoidance = excessive avoidance of errors (i.e., conditioned stimuli) to execute the speech plan. (Source: [VRT hypothesis #1 ](https://drive.google.com/file/d/1URZwb2e7KNBnKr4PdfhaaOKXJ4r3GqkZ/view?usp=sharing)and [\#2](https://drive.google.com/file/d/1wlQUzx-fzXh4KGxNKSq4g3e974YcYhkA/view?usp=sharing) and [\#3](https://drive.google.com/file/d/17ATnNnubJICGbTaeYRqmfkUjnApf5SLn/view?usp=sharing))  * Approach = the Intention to speak. (Source: Levelt (1989) and Usler (2022)) Here “intention” is treated as an explicit, cognitive stage of speech production (conceptualizer → formulation → phonological encoding → motor program). In neuroscience it’s operationalized as the time window when the brain prepares the utterance (preparatory neural activity / readiness potentials) — i.e., the mental decision to speak before motor execution. This is more technical than the phenomenological “desire” and maps onto cognitive/brain processes. Personally, I have been using the terminology: Approach is where ALL HUMANS send an instruction to the subconscious brain of WHEN it should start executing the speech plan. Approach is, simply put, letting your subconscious mind know that it should start speaking (in exactly the same way as — how every human instructs their brain to start moving their hands or their feet, for that matter). **Importantly**: this 'instructing' is a fluency law (required in all people), explained in the stutter image below (which I created). (**Extremely relevant for research labs** — because without letting your brain know the ready-signal or go-signal, humans are not able to speak.) My point is: we should replace “relying on needs (such as error/compensatory responses) to execute the speech plan” with this fluency law, in a natural non-controlled manner (toward stuttering remission and subconscious fluency), because this is exactly what non-stutterers are doing. Below stutter diagram (that I created) supports everything that I mentioned in this post. https://preview.redd.it/s4blvamglorf1.png?width=3028&format=png&auto=webp&s=1b968608173b8f8d130938be5242998dc8f33a07 *Stutter diagram (image):* [*https://drive.google.com/file/d/1pDE-rm3hpleQz-Yex8KwKVTVdLNb79cP/view?usp=sharing*](https://drive.google.com/file/d/1pDE-rm3hpleQz-Yex8KwKVTVdLNb79cP/view?usp=sharing) *Stutter diagram (PDF version):* [*https://drive.google.com/file/d/1P2EPM-8kt2Vtpb0ZqVBSJ1R-XLCH9zaA/view?usp=sharing*](https://drive.google.com/file/d/1P2EPM-8kt2Vtpb0ZqVBSJ1R-XLCH9zaA/view?usp=sharing) \~\~ Everything in this post is just my own personal take on it. I want to thank the SLP and PhD researcher for his work. The VRT hypothesis is an essential piece of work for PWS and SLPs. My hope is that **research labs** around the world will in a short timeframe read the VRT hypothesis. Because it will likely lead to significant progress in research development. If only I had the network connections and the skills to write a simple VRT format that researchers in  **research labs** can actually understand, process, and use in statistically empirical future research. My take on what  **research labs** SHOULD do with the VRT hypothesis: * Analyze if most stuttering events (in developmental stuttering) are triggered by BLA-amygdala. * Analyze the ratio between neurogenic stuttering (in developmental stuttering) vs. BLA-amygdala stuttering. * Analyze stuttering derived from nonconscious/unseen (subliminal) fear processing / amygdala activation (that is likely mostly confused with neurogenic stuttering). * Analyze BLA-amygdala activation — between when PWS stutter alone vs. speak fluently alone. There’s a large (robust) body of research on nonconscious/subliminal fear processing that reports amygdala activation — broadly speaking dozens of human neuroimaging/iEEG studies (and several meta-analyses/reviews), and hundreds of related papers if you include the animal BLA fear-learning literature. However, stutter researchers have not yet started with this. Therefore, perhaps once  **research labs** get to read the VRT hypothesis (but in a more synthesized format hopefully?), stutter research will likely make strong progress in this area too. This could be revolutionary and change the SLP field upside down — i.e., both in stutter theory and intervention. So perhaps the real question is: What do you need, to accomplish this? Who is able to properly synthesize a format of the VRT hypothesis for  **research labs**? Then finally: Who will contact  **research labs** (and do the interviews)?