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by brockf
3418 days ago
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To your first point, I'm not sure how this helps the sufferers. What they have shown is that there is a different neural signature correlating with a different emotional response. There's no causal link here, meaning that I might still tell someone to just shrug it off. Maybe they can control their neural activity, just like I can control my neural activity related to thinking about elephants by not thinking about elephants. To your second point, I would offer two responses. First, while being able to measure something is a win in itself, we need to be clear about what they're measuring. They have shown that suffering ailment X increases the probability that they find neural signature X. They do not know the reverse, meaning this isn't going to unlock early diagnostics or anything. It is unclear how discriminating this response is. Second, it's not clear that this is the product/effect of the way their "brain is wired". Perhaps changes in neural activity caused the observations of different neural connectivity. Perhaps some other factor of their experience or biology caused this sensitivity and the visible differences in connectivity, neural activity, etc. We just don't know. (P.S. Listening to people eat drives me insane. I'm not going to self-diagnose, but I just want to be clear that I'm not criticizing the finding/report because of a lack of empathy for the sufferers.) (P.P.S. I'm a recovering cognitive scientist who had to hear about a lot of neuropsych findings that all boiled down to, "This part of the brain lights up when we hear/see/do this! Give me another $5mm grant!"). |
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It's not just the fact that they see a response in AIC that highlights the important aspect of this research, but rather the dissociation between sound evoked activity in controls vs misophonics. While control subjects found unpleasant sounds as annoying as the misophonics found trigger sounds, activity in AIC increased only in the misophonics, and only for the trigger sounds. Interesting to see also that for misophonics, AIC activation scales linearly with the degree of distress - I'm assuming this wasn't the case for unpleasant sounds (but I'm not positive and didn't read closely enough to tell).
You say it's not clear that it's a product of the way their brains are wired, but in the paper they highlight a potential for greater myelination in vmPFC in misophonics. They do this indirectly citing differences in magnetization transfer saturation. I don't know this technique, so I can't really comment on how legit it is, but it seems at least there's some effort to attribute this to structural rather than purely functional differences.
And yeah, of course it's always possible that it's some other factor that is underlying these effects, but I think this dissociation shows reasonably convincing evidence for pursuing more research on this condition (e.g., diffusion imaging to better understand potential structural differences)