[instagraham]

I might be oversimplifying, but isn't a lot of our neurological understanding about ADHD based on "fMRI shows decreased activity in the frontal cortex"? Or for that matter, our neurological understanding of a lot of mental health conditions.

I know the actual diagnosis is several times more layered than this attempt at an explanation, but I always felt that trying to explain the brain by peering at it from outwards is like trying to debug code by looking at a motherboard through a bad microscope.

[D-Machine]

I do not think there is much neurological understanding about ADHD at all from current fMRI research, there are far too many quality and reliability issues here, not just on the fMRI end or limited amount of data overall, but in the measurement and diagnosis of ADHD itself (i.e. ADHD subtypes, and of course ADHD is a complicated diagnosis with many components manifesting to different degrees in different individuals, which makes it very hard to cleanly link to messy fMRI signals).

Or, as I have commented elsewhere here, the idea that statements like "fMRI shows decreased activity" are ever valid is just fundamentally suspect (lower BOLD response could mean less inhibition or less excitation, and this is a rather crucial difference that fMRI simply can't distinguish). EDIT: Or to be more precise: it may well be that fMRI research suggests less metabolic activity in certain regions, but this could mean the region is actually firing more than normal, less than normal, is more efficient than normal, etc., and interpreting anything about what is functioning differently in ADHD, given this uncertainty, is what is going to be suspect.

Your analogy is largely correct IMO.

[instagraham]

Thanks for the excellent explanation, I didn't know it couldn't distinguish inhibition and excitation.

It seems then that while oxygenation itself may be a good proxy for brain health, the way we measure it is unreliable

[supersour]

Yes this is true, but we actually have a lot more data to back this on than exclusively fMRI analysis - for example the ADHD medication guanfacine works only because the alpha 2 receptors happen to be wired differently in the prefrontal cortex than it is in other areas of the brain (a2 is inhibitory for most brain regions, but in the PFC they're positioned to amplify connections between neurons) , so by stimulating alpha 2 we allow for a more “top down” control from the prefrontal cortex than we do without, which improves executive function.

So that is one extremely robust way to understand neurological conditions like ADHD or Parkinson’s

[instagraham]

With such medications, besides behavioural changes, how are they able to measure outcomes without fMRIs? Like knowing whether neuron connections are amplified or not?