How TMS Works

An electromagnetic coil rests against your scalp and generates brief magnetic pulses. Those pulses pass through the skull and induce a small electrical current in the brain tissue directly beneath the coil, causing neurons in that region to fire.

Two things follow from this.

It's targeted, not systemic

A medication travels through your bloodstream and reaches every organ — which is why antidepressants cause side effects unrelated to mood. A magnetic pulse affects tissue within a few centimeters of the coil. That's why TMS doesn't cause weight gain, sexual side effects, or emotional blunting.

It builds over time

One session doesn't treat depression. The change comes from repeated stimulation over weeks, working through the brain's capacity to strengthen connections based on patterns of use. That's why a course is measured in weeks rather than doses.

TMS is delivered to the front of the head, which can seem like an odd place to treat mood or obsessive-compulsive symptoms. The explanation is about circuits rather than locations — and the specific target differs depending on what's being treated.

The depression target

At Houston Mind & Brain, depression is treated with BrainsWay Deep TMS, which uses an H-coil to reach a broader field than the figure-8 coils used in older TMS protocols. For depression, the standard target is the left dorsolateral prefrontal cortex, behind the upper left forehead.

This region helps regulate attention and emotional response, and it's connected to deeper structures involved in depression — including the subgenual cingulate, a region far too deep to reach with a coil. Research has found that the prefrontal sites producing the best clinical outcomes are those most strongly anticorrelated with that deeper region: stimulating the accessible surface target is associated with quieting the one underneath.¹

This is the leading model of how TMS treats depression, and researchers are still refining it.

The OCD target

For OCD, Deep TMS uses a different coil configuration entirely, targeting the medial prefrontal and anterior cingulate cortices rather than the site used for depression.



Obsessive-compulsive symptoms are associated with overactivity in a loop connecting the cortex, the striatum, and the thalamus — the circuitry underlying the sense that something is wrong and must be corrected, running unchecked. The relevant cortical entry points to that loop are the medial prefrontal cortex and the anterior cingulate cortex, which sit deeper and more centrally than the depression target.

Reaching them requires a different coil. Deep TMS uses an H-coil that produces a broader, deeper field than the figure-8 coils used for standard depression protocols. This is why TMS for OCD is not simply the depression protocol pointed at a different spot — it is a different device configuration reaching a different circuit.⁹

OCD protocols also include brief symptom provocation immediately before stimulation, so the circuits being targeted are actively engaged rather than at rest. That step was part of the trial supporting FDA clearance, and it's a component some providers omit.

What repeated stimulation changes

Hitting the right target explains where the coil goes. It doesn't explain why the effect outlasts the session — or why a course takes weeks rather than a single visit.

The working answer is neuroplasticity: repeated stimulation appears to change how readily circuits activate, in a way that persists after stimulation stops. Much of the research attention here has focused on brain-derived neurotrophic factor, or BDNF — a protein involved in forming and strengthening neural connections, and one known to be reduced in depression.

The evidence is genuinely mixed. Some studies have found BDNF levels rise over a course of TMS; a pooled analysis across studies did not find a reliable increase, and analyses that did find one could not link the change to whether patients actually improved.¹⁰ ¹¹ It's also possible that blood levels are simply a poor window into what's happening in the brain itself.

We mention it because it's the most discussed theory of why TMS works over time, not because it's settled. What is well established is the clinical observation underneath it: the benefit builds across a course of treatment and persists after treatment ends, which is not how a drug taken daily behaves.

TMS is FDA-cleared for depression and OCD on the basis of randomized controlled trials, and it is generally well tolerated. That does not make it risk-free. Here is what the research actually shows.

The common side effects

The most frequent are mild scalp discomfort and temporary headache during early sessions. Both typically fade as treatment continues and can usually be managed with adjustments to coil position or intensity, or with over-the-counter pain relief.

These effects rarely cause people to stop treatment. In a nationwide study of 497 patients with treatment-resistant depression, 4.2% discontinued because of adverse effects.²

Does TMS cause brain damage?

No. TMS does not damage brain tissue. The magnetic pulses induce a small electrical current in the cortex directly beneath the coil — the same physical principle used in diagnostic neurology for decades.

TMS is frequently confused with ECT, which is a different treatment entirely. ECT induces a controlled seizure under general anesthesia and can cause memory effects. TMS induces no seizure, requires no anesthesia, and is not associated with memory loss.

Seizure risk

The significant risk with TMS is an unintended seizure. It is rare, but it is real, and you should understand it before starting.

In a survey of 714 TMS labs and clinics covering roughly 318,560 sessions, 24 seizures were reported — about 8 per 100,000 sessions. When TMS was delivered within published safety guidelines to people without risk factors, that dropped to 4 seizures across 242,067 sessions, or fewer than 1 in 60,000.³ In placebo-controlled trials, seizure rates have been comparable between active TMS and sham.⁴



Screening is what manages this risk. Because stimulation increases cortical excitability, we review seizure history, neurological conditions, and medications that lower seizure threshold. We also screen for implanted metal and medical devices in or near the head. Seizures, when they occur, are most likely during the first few exposures to TMS — which is one reason early sessions are closely supervised.³

Can TMS make anxiety worse?

Some patients notice increased anxiety, restlessness, or difficulty sleeping in the first week or two of treatment. For most, this settles as the course continues. If it doesn't, tell your treatment team — adjustments to timing, intensity, or protocol are often enough to resolve it.

When TMS doesn't work

TMS does not work for everyone, and no honest provider will tell you otherwise.

In a meta-analysis of 29 randomized controlled trials covering 1,371 patients, 29.3% of people receiving active TMS responded and 18.6% reached remission after about 13 sessions — compared with 10.4% and 5% on sham.⁵ With a full course of 20 to 30 sessions, the numbers are substantially better: one large trial reported 49% response and 32% remission for theta burst stimulation, and 47% and 27% for standard 10 Hz stimulation.⁶

Two things are worth taking from those figures. Completing a full course matters — the difference between the two sets of numbers is largely session count. And roughly half of people will not respond, which is worth knowing before you start rather than after.

Why do clinics report better numbers than these studies?

You will see response rates quoted by TMS clinics — including ours — that run higher than the trial figures above. That gap is worth explaining rather than glossing over.

Part of it is how the numbers are built. Clinical trials count every enrolled patient, including those who stop early, and they measure a fixed protocol: a set number of sessions, one treatment, strict diagnostic criteria, no adjustments along the way. Clinics generally report on patients who completed treatment. Those are different denominators, and they produce different percentages.

The other part, in our case, is that we don't treat TMS as a fixed protocol. We track symptom scores throughout treatment. If someone isn't responding by around session 20, we often consider adding Spravato, intranasal ketamine, or psychotherapy alongside TMS to improve the chance of a meaningful response.

We think that's better care. But it also means that when those patients improve, the improvement reflects a combination of treatments rather than TMS alone. Our outcomes are real — they're simply not measuring the same thing a controlled trial measures, and you should know that when comparing numbers between clinics.

Can TMS make things worse?

A minority of patients feel worse during or after treatment. This is a real part of the picture and it deserves a straight answer.

One specific concern is a shift into mania or hypomania. The data here is reassuring: across randomized trials that tracked it specifically, this occurred in 0.84% of patients on active TMS and 0.73% on sham — no meaningful difference.⁷ In unipolar depression specifically, the rate was 0.34%.⁷ A 2025 meta-analysis of 1,709 patients with bipolar depression found the same pattern.⁸

Symptoms can also worsen for reasons unrelated to stimulation: an underlying diagnosis that TMS isn't the right tool for, depression lifting unevenly, or a protocol that isn't the right match.

If something isn't working, the goal is to catch it early and change course — not to finish a course because it was scheduled.

If you're researching TMS because you've read accounts from people who had a bad experience, those accounts are worth taking seriously. Outcomes vary, informed consent should include the downside, and any provider who tells you there's no risk isn't giving you the full picture.

The differences are about the pattern of stimulation, not its strength.

Standard TMS

Pulses delivered at a steady rate over about 20 minutes.

Theta burst stimulation

Pulses delivered in short rapid bursts patterned after a natural brain rhythm, which appears to engage the brain's plasticity mechanisms more efficiently — the same dose in about three minutes. In a multicentre randomised trial in treatment-resistant depression, three-minute sessions were non-inferior to standard 37-minute sessions.⁶

Deep TMS for OCD

Uses a different coil to reach a different target — the medial prefrontal and anterior cingulate cortices rather than the prefrontal site used for depression. OCD protocols also include brief symptom provocation before stimulation, so the relevant circuits are active while being stimulated. That step was part of the trial supporting FDA clearance.⁹

1. Fox MD, Buckner RL, White MP, Greicius MD, Pascual-Leone A. Efficacy of transcranial magnetic stimulation targets for depression is related to intrinsic functional connectivity with the subgenual cingulate. Biological Psychiatry. 2012;72(7):595-603.
2. Matsuda et al. Nationwide observational study of 497 patients with treatment-resistant depression across 21 institutes, 2019–2023. Psychiatry and Clinical Neurosciences Reports. 2026.
3. Lerner AJ, Wassermann EM, Tamir DI. Seizures from transcranial magnetic stimulation 2012–2016: Results of a survey of active laboratories and clinics. Clinical Neurophysiology. 2019.
4. Systematic review of 93 placebo-controlled clinical trials of rTMS (n=2,290 active, n=1,854 placebo).
5. Berlim MT, van den Eynde F, Tovar-Perdomo S, Daskalakis ZJ. Response, remission and drop-out rates following high-frequency repetitive transcranial magnetic stimulation for treating major depression: a systematic review and meta-analysis. Psychological Medicine. 2014.
6. Blumberger DM, Vila-Rodriguez F, Thorpe KE, et al. Effectiveness of theta burst versus high-frequency repetitive transcranial magnetic stimulation in patients with depression (THREE-D): a randomised non-inferiority trial. Lancet. 2018;391(10131):1683-1692.
7. Review of 53 randomized controlled trials of rTMS for depression; 10 specifically assessed treatment-emergent affective switch.
8. Systematic review and meta-analysis of 56 articles covering 1,709 patients with bipolar depression, 1995–2025. Biological Psychiatry: Global Open Science. 2025.
9. Carmi L, Tendler A, Bystritsky A, et al. Efficacy and safety of deep transcranial magnetic stimulation for obsessive-compulsive disorder: a prospective multicenter randomized double-blind placebo-controlled trial. American Journal of Psychiatry. 2019;176(11):931-938.
10. Meshkat S, Alnefeesi Y, Jawad MY, et al. Brain-Derived Neurotrophic Factor (BDNF) as a biomarker of treatment response in patients with Treatment Resistant Depression (TRD): A systematic review & meta-analysis. Psychiatry Research. 2022. 36 articles, 1,198 patients. Peripheral BDNF increased overall across TRD treatments (Hedges' g = 0.336, p < 0.05); no association found with depressive symptom change.
11. Meta-analysis of clinical trials of rTMS and serum BDNF: pooled effect size −0.12 (95% CI −0.30 to 0.06, p = 0.193) — rTMS did not reliably increase serum BDNF. Neurophysiologie Clinique. 2019.

References

We accept most major plans for FDA-cleared treatments (including standard TMS and Spravato). We verify benefits, manage prior authorization, and provide a written estimate before treatment so there are no surprises.

Research-informed care that integrates medication management, psychotherapy, TMS, and Spravato/ketamine into a coordinated treatment plan. Treatments are thoughtfully sequenced and monitored within a structured clinical model to support safety, consistency, and meaningful outcomes.

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