The Stanford accelerated protocol, replicated: remission in 50% versus 21% on sham at one month, in 48 people
The second randomised trial of Stanford neuromodulation therapy enrolled 53 people with treatment-resistant depression and randomised 48; at one month, 50.0% on active treatment were in remission versus 20.8% on sham.
Reasonable evidence with real limitations. how we score evidence
Caveat on this rating: A 48-person trial with a one-month primary endpoint, from the developers, following a 29-person trial from the same group. The FDA clearance record in this wave notes that effectiveness of the device "has not been established beyond the timepoints evaluated" and that the trials behind it were single-site. Early, promising, and not yet independently replicated.
Significant findings
Stanford neuromodulation therapy (SNT) is a rapid, high-dose intermittent theta burst protocol: in the companion mechanism paper it is described as ten sessions a day over five consecutive days, about 90,000 pulses, aimed at the left dorsolateral prefrontal cortex. An earlier randomised trial had found it effective; the authors write that "replication in a larger sample is needed". This is that replication. Fifty-three people with treatment-resistant depression were enrolled and 48 who still met entry criteria were randomised to active or sham, 24 each.
At one month the primary outcome, remission, was reached by 50.0% of the active group and 20.8% of the sham group (chi-squared 4.5, p = 0.035). Response was 54.2% versus 25.0% (p = 0.039). On EEG, frontal beta power fell after active but not sham treatment, in both this trial and the earlier one, which the authors propose as a possible marker of who will respond.
Both halves belong together. The numbers are striking. They also come from 48 people, at one month, in a trial run by the group that developed the protocol, and the companion paper discloses that the protocol's inventor "holds patents for the SNT protocol and has equity in Magnus Medical, which has licensed the SNT technology". That disclosure is in print, which is how it should work; it is context for how much weight two small positive trials from the inventors can carry until someone else runs a larger one.
Worth asking
Is the clinic's protocol the same dose and schedule as the trials, or a shorter version with the same name? And what happens after the one-month mark, which is where the trial's evidence ends?
Source
Stanford neuromodulation therapy for treatment-resistant depression: a randomized controlled trial confirming efficacy, and an EEG study providing insight into mechanism of action and a potentially predictive biomarker of efficacy — Kratter IH, Austelle CW, Lissemore JI, Wada M, Geoly A, Chaiken A (2026)
Top-tier peer-reviewed journal
Read the source: https://doi.org/10.1002/wps.70032
DOI: 10.1002/wps.70032
How this was scored
- Study design
- Randomised controlled trial
- Funding
- Funding not disclosed
- Published in
- Top-tier peer-reviewed journal
- Sample size
- 48
- Preregistered
- not recorded
- Conflicts disclosed
- not recorded
- Independent of proponent
- No
- Retracted
- No
Read the full scoring rubric, including what it can't tell you.
Published September 15, 2026.
Questions
How strong is the evidence behind this?
veisund rates this source "moderate evidence". Reasonable evidence with real limitations. It scores 55 out of 100 on our published rubric. One caveat travels with that badge: A 48-person trial with a one-month primary endpoint, from the developers, following a 29-person trial from the same group. The FDA clearance record in this wave notes that effectiveness of the device "has not been established beyond the timepoints evaluated" and that the trials behind it were single-site. Early, promising, and not yet independently replicated. The score is calculated from recorded facts about the source — study design, funding, publication venue, sample size, preregistration — not typed in by an editor.
What is the source for this?
Stanford neuromodulation therapy for treatment-resistant depression: a randomized controlled trial confirming efficacy, and an EEG study providing insight into mechanism of action and a potentially predictive biomarker of efficacy — Kratter IH, Austelle CW, Lissemore JI, Wada M, Geoly A, Chaiken A (2026). Published in: Top-tier peer-reviewed journal. DOI: 10.1002/wps.70032. The full source is linked on this page so you can read it yourself.
Who paid for this research, and does that matter?
Study design: Randomised controlled trial. Funding: Funding not disclosed. The researchers were not independent of whoever benefits from the result. Industry sponsorship is one of the most reliably measured biases in medicine, which is why funding carries real weight in the score rather than sitting in a footnote.
Is this medical advice?
This is information to bring to your prescriber, not medical advice and not a reason to change anything on your own. Nothing here is an instruction to stop or reduce a medication. If you are in crisis, call or text 988.
This is information to bring to your prescriber, not medical advice and not a reason to change anything on your own. Nothing here is an instruction to stop or reduce a medication. If you are in crisis, call or text 988.