1. Eye-freezing, i.e. loss of potential mobility co-occurring with the block. I deem it so vital I wouldn't even classify it as a secondary behavior, and perhaps go as far as to say that we could address eye-freezing and stuttering through an equivalence model of causal inference, or how an overall effect (the eye-freezing) relates to the occurrence of the outcome. And by potentially addressing the effect you would cancel out the occurrence of a block before it can even materialize. I hypothesize visual feedback has shown to be effective in reducing stuttering (together with DAF) because it has a disruptive effect on the freezing phenomenon, meaning it conditions the anticipatory systems to update at a rate other than the habituative patterns of stuttered speech. If there's a way to hack this without mirrors or other external mechanisms, that's the way to go. And to draw an inference, the laryngeal muscles are the fastest firing muscles in the body. The laryngeal muscles have a unique ability to express a wide range of myosin heavy chains (MyHCs), including here extraocular (EO or 2L) myosin heavy chains which control eye movements and are adapted for rapid and precise movements. Counter-intuitively enough, extraocular muscles are highly resistant to fatigue despite the rapid contraction rates. Saccades, tracking, and more require such movements, and the vocal folds do too. Further, the substantia nigra, part of the basal ganglia, is positively correlated with stuttering severity, pointing to a modulatory effect. And the SN pars reticulata is related to eye movement together with ability to learn and think, while the SN pars compacta contains the dopamine. The eyes freeze in an instance of stuttering, i.e. lose potential mobility. Might the issue be localized here, especially given that the neurotransmitter GABA in the SN pars reticulata inhibits activity of brain cells to redirect and/or stop signals from reaching the muscles? There is a connection between speech and vision. I have intuited this for a while now, and some pieces are coming together nicely. 2. The most widely hypothesized underlying mechanism to saying the desired utterance is the basal ganglia I mentioned for a bit just above. A desired utterance would be neurologically represented as a single motor command with an accompanying dopaminergic signal. It is hypothesized that stutterers have excess dopamine production in the basal ganglia as a result of competing dopaminergic signals where the signal containing the desired utterance is not the clear winner. The mechanism that underlies and predisposes triggers would have to be the anticipatory mechanisms, but there are too many circuits and areas involved to expand here. 3. I am not sure what you mean by learning. 4. The answer to the first question might be one, so visual and auditory cortices. Beyond that, I don't know. I am not equipped to answer. 5. I do not know what you mean by elements exactly. If you mean secondary behaviors for example, I don't think it's necessary to tackle each and every one. Linear sequence is perhaps a better way to put it than hierarchical structure. Tackle the first element in the chain that leads to stuttering and other elements fall with it much like dominoes, at least to my assumptions. Clarify if you meant other than this. 6. Highly excitable and hyper-sensitive predisposition, especially in earlier years. Then I'd say it's also societal factors. Parents make it a big deal, it becomes a big deal. Society makes it a big deal, it becomes a big deal. These would be factors occurring at the onset. From then on, compounding effect and formation of corresponding functional connectivity patterns as I stated in a previous comment. To add an interesting sociological observation, but to be taken with a grain of salt because it's anecdotal - I come from a war-torn developing country. When I was a kid, speech therapists did not exist here. People might tease and joke, but no one used to give a shit about it. In a way perhaps, didn't pay much attention to it as serious condition to be treated. I have only met 2 or 3 stutterers in my 28 years of life here. 1% of the population, never. They aren't conditioned to think about it and eventually overcome it. 7. It is not incentive nor learning because stuttering is not the objective or desirable outcome. Maladaptation is a better way to put it. And I don't know, perhaps the answer to the question or perhaps its validity. I don't know that I would treat fluency goals as the causal link. 8. You mean not notice and so bypass the anticipatory effect resulting in spontaneous fluency, correct? I don't know that I can say. If I say don't think of an apple, you think of an apple. And so you couldn't condition yourself into not thinking of apples by consciously reiterating it to yourself again and again.