Transcranial magnetic stimulation (TMS) is an established, evidence-based treatment for depression, but people do not all respond in the same way. For post-traumatic stress disorder (PTSD), the evidence is less mature and more inconsistent.
One possible explanation is that the brain networks involved in symptoms vary between individuals. Researchers are therefore testing whether functional magnetic resonance imaging (fMRI) can help identify a more personalised stimulation target.
How personalised TMS works
TMS uses magnetic pulses from a coil placed on the scalp to influence brain activity. Clinicians commonly choose the stimulation site using scalp measurements or standard brain coordinates.
An imaging-guided approach uses a person’s resting-state brain scan to locate an accessible area that is connected to deeper regions thought to be involved in their symptoms. The aim is not simply to stimulate the same location in everyone, but to account for individual differences in brain connectivity.
That approach remains under investigation. Prospective trials are needed to establish whether selecting targets in this way leads to better clinical outcomes.
What the depression trial found
Taylor and colleagues randomised 40 adults with treatment-resistant depression to an accelerated TMS protocol in a triple-blind trial. Participants received ten sessions daily for five days.
One group had its target selected using each participant’s resting-state scan. The other used the Beam F3 scalp-measurement method. Both groups received neuronavigated stimulation, and the main outcome was clinician-rated depression severity one month after treatment.
Depression improved substantially in both groups. The median reduction on the Montgomery–Åsberg Depression Rating Scale was 24 points with connectivity-based targeting, compared with 18 points with scalp-based targeting. This difference was statistically significant.
Sixteen of 20 people in the imaging-guided group met the study’s definition of clinical response—a reduction in symptoms of at least 50%—compared with 12 of 20 in the scalp-targeted group.
However, the apparent advantage was not seen immediately after treatment, one week later or on a self-rated depression measure. The study was also small, and its sample size reflected feasibility rather than a formal power calculation. The researchers’ estimate that five people would need to be scanned for one additional response was described as hypothesis-generating, not as a robust basis for clinical decisions.
What the PTSD trial found
A separate trial randomised 50 adults with PTSD symptoms to active or sham low-frequency stimulation, delivered twice daily for ten days. Imaging was used to identify a point in the right dorsolateral prefrontal cortex most strongly connected to the right amygdala.
The study’s primary outcomes focused on amygdala responses to threat and sweating during trauma recall. Symptom measures were secondary outcomes.
Active stimulation reduced right-amygdala responses to threat more than sham treatment. However, that result did not remain statistically significant after correction for multiple comparisons, although it did in a women-only subgroup analysis. The groups did not differ significantly in sweating responses during trauma recall.
Both groups showed immediate improvements in hyperarousal and overall PTSD symptoms, without a significant difference between them. At the three-to-six-month follow-up, active stimulation was associated with greater reductions in hyperarousal and total symptoms. These longer-term findings are harder to interpret because only 34 of 47 participants provided follow-up data, and 17 had received open-label active stimulation beforehand.
The PTSD study also did not include a standard-target active-treatment group. As a result, it could not clearly separate the effect of active stimulation from any additional benefit provided by personalised imaging.
Promising findings, practical limits
In the depression trial, targets calculated from separate halves of the same participant’s scan were closer together than targets calculated between different participants. This is consistent with the idea that target locations may be more similar within an individual than across people.
But the depression study’s functional scan took 41 minutes. Personalised targeting also requires MRI access, a sufficiently long and high-quality scan, validated data analysis, quality control, specialist staff and neuronavigation. The PTSD trial used a scan lasting under ten minutes, but shorter or simpler methods still need further evaluation.
These requirements could increase costs and waiting times, and might limit access if personalised treatment depends on specialist academic centres. Centralised analysis could potentially reduce some of these barriers, but its practical value has not yet been established.
What the evidence means now
Together, the trials support further research into circuit-guided TMS, rather than routine imaging-guided treatment. The depression result came from a specific high-dose accelerated protocol and cannot automatically be extended to standard once-daily treatment.
Larger, multicentre studies are needed to test whether the depression finding can be reproduced and whether benefits last beyond one month. For PTSD, future trials should compare personalised active treatment, standard-target active treatment and sham treatment so researchers can identify the added value of imaging.
Researchers also need to clarify which people are most likely to benefit, how consistently targets can be reproduced, whether benefits endure, how acceptable the process is, and whether the approach is cost-effective and accessible.
AI tools were used to assist with the preparation of this article.
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