I mean this (my summary of the Libet experiments and their replications):
Brain activity detectable with EEG (Readiness Potential)begins between 350 and multiple seconds (depending on experiment and measurement resolution)before the person consciously feels the intention to act (voluntary motor movement).
Subjects report becoming aware of their intention to act (via clock tracking) about 200 ms before the action itself (e.g., pressing a button). 200ms seems relatively fixed, but cognitive load can delay.
To give a specific quote:
Matsuhashi and Hallet: Our result suggests that the perception of intention rises through multiple levels of awareness, starting just after the brain initiates movement.
[...]
1. The first detected event in most subjects was the onset of BP. They were not aware of the movement genesis at this time, even if they were alerted by tones. 2. As the movement genesis progressed, the awareness state rose higher and after the T time, if the subjects were alerted, they could consciously access awareness of their movement genesis as intention. The late BP began within this period. 3. The awareness state rose even higher as the process went on, and at the W time it reached the level of meta-awareness without being probed. In Libet et al’s clock task, subjects could memorize the clock position at this time. 4. Shortly after that, the movement genesis reached its final point, after which the subjects could not veto the movement any more (P time).
[...]
We studied the immediate intention directly preceding the action. We think it best to understand movement genesis and intention as separate phenomena, both measurable. Movement genesis begins at a level beyond awareness and over time gradually becomes accessible to consciousness as the perception of intention.
Now, I think you’d say that what they measured wasn’t S(A) but something else that is causally related, but then you are moving farther away from patterns we can observe in the brain. And your theory still has to explain the subclass of those S(A) that they did measure. The participants apparently thought these to be their decisions S(A) about their actions A.
I don’t think S(A) or any other thought bursts into consciousness from the void via an acausal act of free will—that was the point of §3.3.6. I also don’t think that people’s self-reports about what was going on in their heads in the immediate past should necessarily be taken at face value—that was the point of §2.3.
Every thought (including S(A)) begins its life as a little seed of activation pattern in some little part of the cortex, which gets gradually stronger and more widespread across the global workspace over the course of a fraction of a second. If that process gets cut off prematurely, then we don’t become aware of that thought at all, although sometimes we can notice its footprints via an appropriate attention-control query.
Does that help?
Maybe you’re thinking that, if I assert that a positive-valence S(A) caused A to happen, then I must believe that there’s nothing upstream that in turn caused S(A) to appear and to have positive valence? If so, that seems pretty silly to me. That would be basically the position that nothing can ever cause anything, right?
(“Your Honor, the victim’s death was not caused by my client shooting him! Rather, The Big Bang is the common cause of both the shooting and the death!” :-D )
I think your explanation in section 8.5.2 resolves our disagreement nicely. You refer to S(X) thoughts that “spawn up” successive thoughts that eventually lead to X (I’d say X’) actions shortly after (or much later). While I was referring to S(X) that cannot give rise to X immediately. I think the difference was that you are more lenient with what X can be, such that S(X) can be about an X that is happening much later, which wouldn’t work in my model of thoughts.
Intuitive model underlying that statement: There’s a frame (§2.2.3) “X wants Y” (§3.3.4). This frame is being invoked, with X as the homunculus, and Y as the concept of “inside” as a location / environment.
How I describe what’s happening using my framework: There’s a systematic pattern (in this particular context), call it P, where self-reflective thoughts concerning the inside, like “myself being inside” or “myself going inside”, tend to trigger positive valence. That positive valence is why such thoughts arise in the first place, and it’s also why those thoughts tend to lead to actual going-inside behavior.
In my framework, that’s really the whole story. There’s this pattern P. And we can talk about the upstream causes of P—something involving innate drives and learned heuristics in the brain. And we can likewise talk about the downstream effects of P—P tends to spawn behaviors like going inside, brainstorming how to get inside, etc. But “what’s really going on” (in the “territory” of my brain algorithm) is a story about the pattern P, not about the homunculus. The homunculus only arises secondarily, as the way that I perceive the pattern P (in the “map” of my intuitive self-model).
Thanks. It doesn’t help because we already agreed on these points.
We both understand that there is physical process in the brain—neurons firing etc. - as you describe in 3.3.6, that gives rise to a) S(A), b) A, and c) the precursors to both as measured by Libet and others.
We both know that people’s self-reports are unreliable and informed by their intuitive self-models. To illustrate that I understand 2.3 let me give an example: My son has figured out that people hear what they expect to hear and experimented with leaving out fragments of words or sentences, enjoying himself by how people never noticed anything was off (example: “ood morning”). Here, the missing part doesn’t make it into people’s awareness despite the whole sentence very well does.
I’m not asserting that there is nothing upstream of S(A) that is causing it. I’m asserting that an individual S(A) is not causing A. I’m asserting so because it can’t timing-wise and equivalently, that there is no neurological action path from S(A) to A. The only relation between S(A) and A is that S(A) and A co-occurring has been statistically positive valence in the past. And this co-occurrence is facilitated by a common precursor. But saying S(A) is causing A is as right or wrong as saying A is causing S(A).
I mean this (my summary of the Libet experiments and their replications):
Brain activity detectable with EEG (Readiness Potential) begins between 350 and multiple seconds (depending on experiment and measurement resolution) before the person consciously feels the intention to act (voluntary motor movement).
Subjects report becoming aware of their intention to act (via clock tracking) about 200 ms before the action itself (e.g., pressing a button). 200ms seems relatively fixed, but cognitive load can delay.
To give a specific quote:
Now, I think you’d say that what they measured wasn’t S(A) but something else that is causally related, but then you are moving farther away from patterns we can observe in the brain. And your theory still has to explain the subclass of those S(A) that they did measure. The participants apparently thought these to be their decisions S(A) about their actions A.
Thanks!
I don’t think S(A) or any other thought bursts into consciousness from the void via an acausal act of free will—that was the point of §3.3.6. I also don’t think that people’s self-reports about what was going on in their heads in the immediate past should necessarily be taken at face value—that was the point of §2.3.
Every thought (including S(A)) begins its life as a little seed of activation pattern in some little part of the cortex, which gets gradually stronger and more widespread across the global workspace over the course of a fraction of a second. If that process gets cut off prematurely, then we don’t become aware of that thought at all, although sometimes we can notice its footprints via an appropriate attention-control query.
Does that help?
Maybe you’re thinking that, if I assert that a positive-valence S(A) caused A to happen, then I must believe that there’s nothing upstream that in turn caused S(A) to appear and to have positive valence? If so, that seems pretty silly to me. That would be basically the position that nothing can ever cause anything, right?
(“Your Honor, the victim’s death was not caused by my client shooting him! Rather, The Big Bang is the common cause of both the shooting and the death!” :-D )
I think your explanation in section 8.5.2 resolves our disagreement nicely. You refer to S(X) thoughts that “spawn up” successive thoughts that eventually lead to X (I’d say X’) actions shortly after (or much later). While I was referring to S(X) that cannot give rise to X immediately. I think the difference was that you are more lenient with what X can be, such that S(X) can be about an X that is happening much later, which wouldn’t work in my model of thoughts.
Thanks. It doesn’t help because we already agreed on these points.
We both understand that there is physical process in the brain—neurons firing etc. - as you describe in 3.3.6, that gives rise to a) S(A), b) A, and c) the precursors to both as measured by Libet and others.
We both know that people’s self-reports are unreliable and informed by their intuitive self-models. To illustrate that I understand 2.3 let me give an example: My son has figured out that people hear what they expect to hear and experimented with leaving out fragments of words or sentences, enjoying himself by how people never noticed anything was off (example: “ood morning”). Here, the missing part doesn’t make it into people’s awareness despite the whole sentence very well does.
I’m not asserting that there is nothing upstream of S(A) that is causing it. I’m asserting that an individual S(A) is not causing A. I’m asserting so because it can’t timing-wise and equivalently, that there is no neurological action path from S(A) to A. The only relation between S(A) and A is that S(A) and A co-occurring has been statistically positive valence in the past. And this co-occurrence is facilitated by a common precursor. But saying S(A) is causing A is as right or wrong as saying A is causing S(A).