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What you’ll learn (and what you won’t)
- Useful: default-mode vs central-executive vs salience network balance; whether your DLPFC is anti-correlated with sgACC enough to inform TMS targeting; basic structural exclusions.
- Not magic: it won’t tell you if your mitochondria are lazy. It’s network plumbing, not a metabolic assay.
If you want it to drive treatment, not just vibes
- Pair the scan with a clinic that can target TMS from rs-fMRI. That’s how SAINT-style targeting picks the most anti-correlated DLPFC spot for your sgACC, which is the grown-up way to stop your DMN from running the place. Evidence says it helps, even if it’s not a silver bullet.
As with everything - data is everything, you can use AI to interpret
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Short version: yes. If you’re doing accelerated TMS in the SAINT/SNT style, resting-state fMRI gives you something QEEG simply can’t: a map of the exact left-DLPFC sub-region that’s most anti-correlated with your subgenual cingulate (sgACC). That network fingerprint is the whole point of the protocol and is what the targeting algorithm needs. QEEG can’t see deep structures like sgACC or quantify that anti-correlation.
Here’s the clean split:
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What fMRI buys you (and QEEG doesn’t):
- Individualized network target for coil placement. Outcomes track how strongly your chosen DLPFC spot is anti-correlated with sgACC; stronger anti-correlation generally predicts better antidepressant response. That’s measured with resting-state fMRI, not scalp EEG.
- Neuronavigation on your actual anatomy. Even without fancy connectivity, structural MRI lets the clinic place the coil precisely on your cortex instead of using scalp rules. Useful for any high-dose/accelerated schedule where precision matters.
- Compatibility with SAINT/SNT workflows. The FDA-cleared SAINT system was built around structural + resting-state fMRI to compute that target; clinics offering it will ask for those scans.
- What QEEG does well (but doesn’t replace fMRI here):• Captures cortical rhythms/state (alpha, theta, etc.), which can be useful for researchy personalization, response prediction, or closed-loop TMS-EEG experiments. Promising, but still maturing for routine clinical decision-making. Think “state meter,” not “GPS.”
- **About accelerated TMS specifically:**The whole “accelerated” idea stacks many iTBS sessions per day over a few days. The flagship SAINT/SNT studies that drove adoption used fcMRI-guided targeting and reported strong effects; newer work keeps showing that target-to-sgACC connectivity matters. If you skip the fMRI, you lose the very feature tied to those results.
Tiny metaphor so we don’t die of boredom: QEEG hears the surface chatter at the party; fMRI shows you the group chats and who’s subtweeting sgACC. Accelerated TMS needs the group-chat map.
Bottom line: if you’re pursuing a SAINT-style accelerated course, get the MRI package (T1 + ~8–12 min resting-state fMRI). Keep QEEG if you want additional state tracking or experimental biomarkers, but it won’t substitute for the connectivity-based target that accelerated protocols rely on.