In your own words, why are we not aware of the amygdala activation during a stuttering block?

In your own words, why are we not aware of the amygdala activation during a stuttering block? Some answers I came up with: * Many **people who stutter (PWS)** are so focused on controlled fluency (i.e., compensatory or error responses) that they are not conscious of what is going on in the amygdala **stutter cycle.** So **PWS** might focus too much on error-avoidance—for example, avoiding fear and other stimuli—preventing the subconscious brain from allowing execution of the speech plan (to say the words/sounds). * Culturally and therapeutically (etc.), we are taught not to consider the approach–avoidance conflict during moments when we are not consciously aware of any fear. Often we have been raised to ignore or dismiss an error-avoidance mechanism, especially in moments when we do not consciously experience a trigger, even though the error-avoidance mechanism has still been activated. * Culturally speaking, we may have been raised to believe that only negative emotions like fear can trigger an approach–avoidance conflict—completely overlooking how the underlying conflict or error-avoidance mechanism actually works… because that is simply not how it works. * Culturally, we have been taught that: if we fear a word/situation which results in (more) stuttering, then it must mean it's a fear-based response. However, I argue that when we label it as fear-based, we overlook the more relevant perspective/side of the coin, which is: it's probably a much better label to say that it's protection-based rather than fear-based. Yes indeed, a protection mechanism (that protects us from anticipatory fear) means that fear is present, but on a primary or relevant note/side, it's better to imply it's protection-mechanism–based. Because otherwise we overlook the stuttering where we are not consciously aware of fear, yet the approach–avoidance conflict was still triggered. * We often confuse a fear response with a protection mechanism response. Take this example: the older the child, the more emphasis there is on polite, measured, or appropriate *speech execution–regulation*. Listeners begin cultivating criticism for talking back. Conclusion: if we do not stutter when speaking alone, but switch to a social situation, we might start stuttering even if we are completely comfortable with the listener. Yes indeed, the approach–avoidance conflict is triggered, but more in the sense of a protection or regulatory mechanism (rather than a fear-of-a-lion survival response). Does that make sense? The difference between speaking alone and speaking with another person is, of course, a fear of judgment (often very subconscious and a low amount of fear that we are not even aware of), but not the intense, survival-level fear-of-a-lion emotion. So, rather than considering the approach–avoidance conflict as this lion-survival kind of fear, it might be better to consider that it's less about a lion-fear-survival response and more about a response in which we regulate the execution of the speech plan based on a protection-mechanism to guide and streamline our speech execution (in a maladaptively learned way); this mechanism avoids errors based on fear of judgments — but error-avoidance here is more relevant than the lion-fear-survival response. * SLPs might prefer less-precise terminology (e.g., they avoid adopting the term "subconscious suppression of speech plan execution") and instead use layman's terms like "holding back speech," because it’s descriptive and avoids psychoanalytic baggage. Even though this leads most people who stutter to unnecessary confusion and wrong assumptions, in real life it mostly makes us unaware of the approach–avoidance conflict whenever we stutter. **Conclusion**: *And because most of us are not aware of this, we are not able to consciously notice when our approach–avoidance conflict is triggered whenever we stutter.* **Below are science-based answers to the main question of the post:** The amygdala reliably shows differential responses to threat-relevant stimuli even when those stimuli are not consciously perceived (masked/subliminal, blindsight, CFS, etc.). 1. **Physiological/behavioral effects can follow unseen stimuli.** Skin conductance responses (SCR), startle potentiation, and expectancies can be conditioned to masked fear-relevant stimuli (snakes, spiders, fearful faces). That is, autonomic learning and responses occur without subjective awareness. 2. **A rapid, likely subcortical route can drive early amygdala responses.** Research point to a pathway through superior colliculus → pulvinar → amygdala that can transmit low-spatial-frequency threat signals rapidly and without the cortex’s conscious identification. Many studies (and influential reviews) interpret this as a mechanism for “unseen” fear processing. 3. **Low-spatial-frequency (LSF) information:** many studies find the early/nonconscious amygdala sensitivity is strongest for LSF versions of faces — consistent with magnocellular inputs that feed fast subcortical channels. 4. **Right vs left amygdala differences:** some imaging analyses report stronger subcortically driven effects in the right amygdala (Morris et al.). **Many studies report that the** ***right*** **amygdala is preferentially engaged by rapid, automatic or nonconscious threat signals** (masked faces, blindsight, CFS, etc.), most likely because a fast subcortical route (superior colliculus → pulvinar → amygdala) feeds right-sided responses, while the left amygdala is more involved in conscious, sustained or elaborative processing --> **In my opinion**: this is interesting because in stuttering the right hemisphere is more dominant during a stuttering event (due to compensatory/error strategies and inhibition). 5. **Behavioral potency:** nonconscious amygdala activation can bias subsequent judgments, learning rates, and autonomic responses even when participants deny any awareness of the trigger. 6. Amygdala ≠ full emotion experience: amygdala activation alone is not the same as conscious feeling of fear; it can be sufficient to trigger autonomic/behavioral bias. 7. Research supports multiple routes by which amygdala activation (often via its central and basolateral nuclei) can bias basal-ganglia motor-gating circuits and brainstem motor centers so that a prepared motor program is suppressed, delayed, or not executed. CeA → basal ganglia / brainstem → immobility or conditioned suppression (action suppression) 8. **Amygdala → striatum (ventral and dorsal) → pallidum/SNr → thalamus → cortex:** the amygdala (especially basolateral complex, BLA) projects heavily to the ventral striatum (nucleus accumbens) and also influences dorsal striatal circuits. These inputs bias the basal-ganglia “action-selection” gates: enhancing indirect/hyperdirect activity or modulating SNr output can suppress initiation/execution of motor programs. BLA→NAcc interactions are central in Pavlovian→instrumental interactions (see PIT/conditioned suppression). 9. the amygdala can influence midbrain dopamine neurons, changing striatal excitability and direct/indirect pathway balance — a powerful way to bias whether an action is facilitated or suppressed. 10. Lesions or inactivation of amygdala subnuclei alter conditioned suppression. 11. Freezing is a canonical example of a motor program that is actively inhibited or held.