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Can you point me to a study showing these brain scans being different from those with diagnosed ADHD and not? The evidence would furthermore have to show that t

Can you point me to a study showing these brain scans being different from those with diagnosed ADHD and not? The evidence would furthermore have to show that this difference is apparent not just from adhd vs non adhd but adhd vs anxiety, depression etc. And lastly, are these changes perhaps an affect of taking stimulants? And how significant are these results? Are we talking about a few percent difference? Are 10% of diagnoses ADHD shown to have statistically significant differences, 20, 50, 90? Depending on the figure, my criticism of the diagnostic criteria remains. Because if it is a low figure like 10%, that means 90% of the diagnoses aren't supported by any scientific evidence. From what I've been told, including professionals this evidence does not exist. I've also seen studies which indicate that psychiatric evaluations are entirely inconsistent across physicians.

jaggederest 2y ago
> The morphometric findings predicted an ADHD diagnosis correctly up to 83% of all cases. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ It's not good enough for diagnosis - you want to hit 95+% accuracy for diagnostic. And MRIs are extremely expensive compared to 2-3 outpatient psychology appointments. But it's real.
- andoando 2y ago
  I admit the study looks pretty good, but Id still have to see if these changes are present in those with depression/anxiety, etc and 2. are not result of stimulant use to be convinced. I found this if youre interested which cites more studies https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11020281 https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2... >It's not good enough for diagnosis - you want to hit 95+% accuracy for diagnostic. This doesn't quite make sense to me, because you're comparing it to the current diagnostic criteria and assuming it to be 100% accurate. If we want to be totally scientific, we ought to just do these scans and diagnose people with low gray matter volume, etc and drop the DSM, ADHD etc.
  - pixl97 2y ago
    And if we start scanning tons of brains and finding out that X% of people with low gray matter volume do not exhibit any ADHD symptoms?
    - arcticbull 2y ago
      Bayes strikes again.
- Aurornis 2y ago
  > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ Two major problems with studies like this: 1. The number of brain sub-regions and associated variables they're looking at is huge. Perhaps more than the number of patients in the study, depending on how you look at the data. If you collect enough data points on two groups of about ~30 people each and you run enough regressions, eventually you'll find some model that works on your small data set. This would need to be tested against a much larger cohort. 2. They did not control for stimulant usage at all. In fact, they note that stimulant use was vastly higher in the ADHD group, because obviously you need an ADHD diagnosis to receive ongoing stimulant prescriptions. It's a delicate topic, but we know that stimulant use in some cases is associated with changes in brain structure and blood flow. It's a huge variable that is hard to control for in a study like this. Overall, I don't find a study with 31 ADHD patients that tested dozens and dozens of different variables to be all that conclusive. Perhaps useful for focusing future research, but a singular study like this isn't very conclusive.
  - andoando 2y ago
    According to this, stimulant use if anything normalizes the differences found. Without a proper understanding of the field, I have to admit its hard to criticize the specifics. https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11020281 https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2... That said, all these studies are done way after ADHD was established. That is, ADHD as a concept wasn't established by looking at neurological brain scans or any kind of physical evidence. Makes me wonder what the exact thought process was for establishing the DSM. I still feel like if I made up a disorder by coming up with 9 semi-normal behaviors as symptoms, enough people would just by chance meet most of the criteria, and imaging scans would find some difference. Wish I was rich so I could conduct that experiment myself.
  - somenameforme 2y ago
    I think there's also another critical issue that plagues every single observational study - the direction of causality. Our behaviors can and do physically change every single aspect of our body, including our brains. For instance chess masters not only activate different parts of their brain when playing chess than amateurs, but also have observable morphometric differences in their brains. [1] If the direction of causality there was not overtly obvious (as nobody starts out anything even close to a master), one could easily assume those differences caused one to be a master, rather than vice versa. It's the exact same issue here, except the direction of causality is unclear. You're seeing a shared morphometric difference among people of some trait (ADHD) and then just assuming that that difference causes ADHD, rather than that ADHD causes the difference! To even assume this is the case one would need to perform MRIs on random very young individuals prior to ADHD diagnoses, and then make a prediction, based solely on that MRI, on which ones would be diagnosed with ADHD with no input or information given to the participants before a follow study in a decade or so. That study would then help prove the direction of causality that's seemingly just simply being assumed in this one. [1] - https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2021.629478/full https://www.frontiersin.org/journals/neuroscience/articles/1...

jaggederest 2y ago

> The morphometric findings predicted an ADHD diagnosis correctly up to 83% of all cases. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ It's not good enough for diagnosis - you want to hit 95+% accuracy for diagnostic. And MRIs are extremely expensive compared to 2-3 outpatient psychology appointments. But it's real.

andoando 2y ago
I admit the study looks pretty good, but Id still have to see if these changes are present in those with depression/anxiety, etc and 2. are not result of stimulant use to be convinced. I found this if youre interested which cites more studies https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11020281 https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2... >It's not good enough for diagnosis - you want to hit 95+% accuracy for diagnostic. This doesn't quite make sense to me, because you're comparing it to the current diagnostic criteria and assuming it to be 100% accurate. If we want to be totally scientific, we ought to just do these scans and diagnose people with low gray matter volume, etc and drop the DSM, ADHD etc.
- pixl97 2y ago
  And if we start scanning tons of brains and finding out that X% of people with low gray matter volume do not exhibit any ADHD symptoms?
  - arcticbull 2y ago
    Bayes strikes again.
Aurornis 2y ago
> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5391018/ Two major problems with studies like this: 1. The number of brain sub-regions and associated variables they're looking at is huge. Perhaps more than the number of patients in the study, depending on how you look at the data. If you collect enough data points on two groups of about ~30 people each and you run enough regressions, eventually you'll find some model that works on your small data set. This would need to be tested against a much larger cohort. 2. They did not control for stimulant usage at all. In fact, they note that stimulant use was vastly higher in the ADHD group, because obviously you need an ADHD diagnosis to receive ongoing stimulant prescriptions. It's a delicate topic, but we know that stimulant use in some cases is associated with changes in brain structure and blood flow. It's a huge variable that is hard to control for in a study like this. Overall, I don't find a study with 31 ADHD patients that tested dozens and dozens of different variables to be all that conclusive. Perhaps useful for focusing future research, but a singular study like this isn't very conclusive.
- andoando 2y ago
  According to this, stimulant use if anything normalizes the differences found. Without a proper understanding of the field, I have to admit its hard to criticize the specifics. https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2011.11020281 https://ajp.psychiatryonline.org/doi/full/10.1176/appi.ajp.2... That said, all these studies are done way after ADHD was established. That is, ADHD as a concept wasn't established by looking at neurological brain scans or any kind of physical evidence. Makes me wonder what the exact thought process was for establishing the DSM. I still feel like if I made up a disorder by coming up with 9 semi-normal behaviors as symptoms, enough people would just by chance meet most of the criteria, and imaging scans would find some difference. Wish I was rich so I could conduct that experiment myself.
- somenameforme 2y ago
  I think there's also another critical issue that plagues every single observational study - the direction of causality. Our behaviors can and do physically change every single aspect of our body, including our brains. For instance chess masters not only activate different parts of their brain when playing chess than amateurs, but also have observable morphometric differences in their brains. [1] If the direction of causality there was not overtly obvious (as nobody starts out anything even close to a master), one could easily assume those differences caused one to be a master, rather than vice versa. It's the exact same issue here, except the direction of causality is unclear. You're seeing a shared morphometric difference among people of some trait (ADHD) and then just assuming that that difference causes ADHD, rather than that ADHD causes the difference! To even assume this is the case one would need to perform MRIs on random very young individuals prior to ADHD diagnoses, and then make a prediction, based solely on that MRI, on which ones would be diagnosed with ADHD with no input or information given to the participants before a follow study in a decade or so. That study would then help prove the direction of causality that's seemingly just simply being assumed in this one. [1] - https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2021.629478/full https://www.frontiersin.org/journals/neuroscience/articles/1...