I think schizophrenia is generally recognized as involving more deficiencies in local than long-distance cortex-to-cortex communication. I don’t have any particular knockdown studies for this and your Google Scholar judo seems on a level with mine. But as far as I understand it, autism is the disorder associated with deficits in longer white matter tracts; I believe this is because axons grow too densely and mesh too tightly during fetal development, while in schizophrenia the opposite happens and you end up with fewer axons [also probably fewer neurons because fewer neural progenitor divisions but this wouldn’t a priori affect the shape of the connectome].
I figure, when a neurotypical person is subvocalizing, there’s communication between the motor cortex parts that are issuing the subvocalization commands (assuming that that’s how subvocalization works, I dunno), and the sensory cortex parts that are detecting the subvocalization which is now happening. Basically, the sensory cortex has ample warning that the subvocalization is coming. It’s not surprised when it arrives.
But in schizophrenia, different parts of the cortex can’t reliably talk to each other. So maybe sometimes the sensory cortex detects that a subvocalization is now happening, but hadn’t gotten any signal in advance that this subvocalization was about to be produced endogenously, by a different part of the same cortex. So when it arrives, it’s a surprise, and thus is interpreted as exogenous, i.e. it feels like it’s coming from the outside.
I don’t see how your theory would make this prediction. To me it seems like your theory predicts, if anything, weaker subvocalization in schizophrenics—not subvocalization that’s more perceptible. The “it inhibits the warning shot but not the actual data packet” thing frankly feels like an epicycle.
I don’t see how Dehaene clarifies anything or how your theory here relies on him.
I don’t see how your theory would make this prediction.
Those two paragraphs you quoted are a first draft of something that I later described much better in Model of psychosis, take 2. Does your complaint / confusion apply to that post too?
I don’t see how Dehaene clarifies anything or how your theory here relies on him.
I thought the Dehaene excerpt (“Diffusion tensor imaging reveals…”) was straightforwardly supporting my headline claim, right?
Oh, or are you saying that Dehaene doesn’t clarify and support my discussion of positive symptoms in particular?
OK, now let’s look at the sentences in the above excerpt one-by-one:
For the first sentence (on genes): Consider a gene that says “Hey neurons! When in doubt, make more synapses! Grow more axons! Make bigger dendritic trees!” This gene would probably be protective against schizophrenia and a risk factor for autism, for reasons discussed just above. And vice-versa for the opposite kind of gene. Nice!
Why would your theory [which says that schizophrenia is about deficient connections] predict that a gene that predisposed toward a more fully-connected connectome, would protect against schizophrenia?
I’m confused about the fact that you’re confused … If schizophrenia involves too few connections, then more connections means less schizophrenia, right?
Great post!
I think schizophrenia is generally recognized as involving more deficiencies in local than long-distance cortex-to-cortex communication. I don’t have any particular knockdown studies for this and your Google Scholar judo seems on a level with mine. But as far as I understand it, autism is the disorder associated with deficits in longer white matter tracts; I believe this is because axons grow too densely and mesh too tightly during fetal development, while in schizophrenia the opposite happens and you end up with fewer axons [also probably fewer neurons because fewer neural progenitor divisions but this wouldn’t a priori affect the shape of the connectome].
I don’t see how your theory would make this prediction. To me it seems like your theory predicts, if anything, weaker subvocalization in schizophrenics—not subvocalization that’s more perceptible. The “it inhibits the warning shot but not the actual data packet” thing frankly feels like an epicycle.
I don’t see how Dehaene clarifies anything or how your theory here relies on him.
Those two paragraphs you quoted are a first draft of something that I later described much better in Model of psychosis, take 2. Does your complaint / confusion apply to that post too?
I thought the Dehaene excerpt (“Diffusion tensor imaging reveals…”) was straightforwardly supporting my headline claim, right?
Oh, or are you saying that Dehaene doesn’t clarify and support my discussion of positive symptoms in particular?
Something else I later noticed should confuse me:
Why would your theory [which says that schizophrenia is about deficient connections] predict that a gene that predisposed toward a more fully-connected connectome, would protect against schizophrenia?
I’m confused about the fact that you’re confused … If schizophrenia involves too few connections, then more connections means less schizophrenia, right?