Transcranial magnetic stimulation: a working reference for referring clinicians

Overview

TMS is a non-invasive cortical stimulation technique with clear FDA indications, real-world response and remission data, and a rapidly evolving protocol landscape. The useful questions for a referring clinician are usually practical: what protocols are available, what the evidence is for a given indication, and what the contraindications look like.

How we got here

TMS moved from a laboratory curiosity to an FDA-cleared treatment inside a single professional lifetime. Several of the major leaps came from circuit-level insights about brain networks rather than from chemistry, and several of the field’s most confident ideas have not survived randomized testing. Both threads are traced below.

• 1985Barker
  Anthony Barker and colleagues in Sheffield report non-invasive magnetic stimulation of the human motor cortex (Barker 1985, Lancet): a magnetic pulse over motor cortex produces a contralateral hand twitch. The essential ingredients for clinical translation are in place.
• 1990sDrevets, George
  PET imaging reveals metabolic abnormalities in the subgenual anterior cingulate cortex (Brodmann area 25) in depression (Drevets 1997). At the NIMH, Mark George reports the first open pilot of daily left prefrontal rTMS for depression (six patients; George 1995), and Pascual-Leone 1996 publishes the first sham-controlled crossover trial (17 patients with medication-resistant psychotic depression) — pointing to a circuit-based framework rather than a neurotransmitter-based one.
• 2005Mayberg
  Helen Mayberg's work reconceptualizes depression as dysfunction of a distributed network, with sgACC as a pathologic hub. Deep brain stimulation of sgACC produces sustained remission in four of six patients in an open-label series (Mayberg 2005). The network framing redirects attention from “chemical imbalance” toward circuit dysfunction — but the multisite sham-controlled BROADEN trial of sgACC DBS (n=90) had enrollment halted after a pre-planned futility analysis (response, defined as ≥40% improvement averaged over months 4–6, 20% vs 17%; Holtzheimer 2017), and sgACC DBS remains investigational.
• 2007–2010OPT-TMS, FDA
  The industry-sponsored pivotal trial (O’Reardon 2007, n=301) reaches its primary MADRS week-4 endpoint only after a post hoc correction for baseline imbalance; remission at week 6 is roughly twofold higher with active TMS, reaching significance on the MADRS and HAMD-24 but not the HAMD-17. In October 2008 the FDA authorizes NeuroStar for adults with MDD who have failed one adequate antidepressant trial in the current episode (de novo DEN070003). The NIMH-funded OPT-TMS trial (George 2010, n=190) then shows remission of 14.1% vs 5.1% with sham (NNT 12), with most remitters having low treatment resistance.
• 2012Fox
  Michael Fox and colleagues show, in a retrospective analysis of published stimulation sites and resting-state data from 98 healthy subjects, that DLPFC sites with better reported efficacy are more anticorrelated with the sgACC (Fox 2012). This became the conceptual basis for fMRI-guided personalized targeting. Prospective support has been mixed: small cohorts (Weigand 2018, n=25 and 16) supported it, the sgACC-connectivity measure explained only about 3% of outcome variance in THREE-D (Elbau 2023, n=295), and the largest randomized test of connectivity-guided targeting (BRIGhTMIND, n=255; Morriss 2024), which personalized the target on right anterior insula–DLPFC effective connectivity rather than sgACC anticorrelation and compared connectivity-guided iTBS with 10 Hz rTMS at F3, found no advantage over MRI-navigated F3 stimulation.
• 2018Blumberger
  The THREE-D randomized non-inferiority trial (n=414) shows that intermittent theta burst stimulation (iTBS, ~3 minutes) is non-inferior to standard 10 Hz rTMS (~37 minutes) in treatment-resistant depression (Blumberger 2018, Lancet; no sham arm; masked raters). Shorter sessions dramatically expand clinic throughput without compromising outcomes.
• 2022Cole
  Stanford Neuromodulation Therapy (SAINT/SNT) combines accelerated iTBS with fMRI-guided individualized targeting. In a sham-controlled trial stopped at its planned interim analysis (n=29; 14 active, 15 sham), 11 of 14 active participants (78.6%) met remission criteria at some point during the 4 weeks after treatment versus 2 of 15 (13.3%) on sham; remission at the 1-month visit itself was 46.2% (Cole 2022; FDA K220177 summary). FDA-cleared September 1, 2022 as the Magnus Neuromodulation System with SAINT Technology (510(k) K220177). SAINT’s senior investigators (Williams and Bentzley) trained at MUSC — continuing a regional research lineage. Durability and comparison with standard TMS are addressed in Cutting edge.
• 2024–2025Adolescent clearances
  NeuroStar (K231926, March 2024), Magstim (K243869, March 2025), MagVenture (K251125, August 2025), Mag&More Apollo (K243700, September 2025) and BrainsWay (K251391, November 2025) receive FDA clearance for adolescent MDD, ages 15–21, as an adjunct for the treatment of MDD (the labels do not name the primary treatment or require prior antidepressant failure). The NeuroStar clearance rests on retrospective TrakStar registry data (1,169 per-protocol patients aged 12–21, mean age 19.2; 77.8% meeting the FDA-accepted individual success criterion, which the public K231926 summary does not define; 30.0% remission, PHQ-9 <5); Magstim, MagVenture and Apollo were cleared on equivalence to NeuroStar without new adolescent data, and BrainsWay on its own registry data (80.9% meeting a ≥5-point PHQ-9 decrease; 19.3% remission at 6 weeks). None rests on a new sham-controlled trial. The only large sham-controlled adolescent RCT (Croarkin 2021; 13 sites; NeuroStar monotherapy; n=103) found no separation from sham: HAM-D-24 change −11.1 vs −10.6 (P=0.8), response 41.7% vs 36.4%, remission 29.2% vs 29.0%.

Protocols

Protocols differ in frequency, burst pattern, laterality, session duration, and therapeutic intent. Most share the same underlying logic; they differ in how stimulation is packaged and delivered.

Coil types

Coil geometry determines the field’s focality and depth — two properties that trade off against each other. Deng, Lisanby and Peterchev modeled 50 coil designs in a spherical head model and found that every design lies on a depth–focality curve: coils that reach deeper cannot be as focal (Deng 2013). No single coil is “better” — each is a deliberate choice in that tradeoff.

The rhythms, visualized

Protocol names proliferate; the underlying differences are mostly about how stimulation is packaged in time. The figures below show a few seconds of each protocol’s pulse structure at a consistent scale. They are schematic, not to clinical scale, but make the differences between protocols immediately visible.

Accelerated schedule: SAINT

Four protocols, one principle

The proliferation of names can obscure what’s actually varying. Across rTMS, iTBS, dTMS, and accelerated protocols, the underlying logic is the same: repeated, targeted stimulation of a cortical node in a dysfunctional network, summed over a course, to produce downstream circuit-level change. What changes between protocols is dose packaging — stimulation intensity (80–120% of motor threshold; 120% standard, 90% in SAINT), burst structure, session length, coil geometry, and schedule.

Typical course and taper

A standard clinical course of conventional rTMS or iTBS runs 5 days per week for 6 weeks (30 sessions), followed by a 6-session taper spread over the following 3 weeks for a total of 36 sessions. The bulk of the treatment burden is in the first 6 weeks; the taper is intended to support consolidation of response, although a 2025 consensus statement notes that end-of-course tapering has little empirical support (Trapp 2025). Accelerated protocols deliver 2–10 sessions per day over 2–30 days; SAINT delivers 50 sessions (90,000 pulses, five times a standard iTBS course) in 5 days.

Devices

FDA has cleared multiple manufacturers' TMS systems for depression, with newer indications added over time. Devices differ in coil design, session length options, navigation capability, and business model. None is categorically “best” — the right choice depends on the protocols you plan to run and the indications you want to treat.

Some common TMS devices

Specialized / newer platforms

A handful of systems occupy specific niches beyond these:

• Magnus Medical (SAINT/SNT) — the Magnus Neuromodulation System with SAINT Technology (K220177, September 2022) pairs MagVenture stimulation hardware with neuronavigation and fMRI-derived targeting. Currently the only cleared system combining fMRI-guided individualized targeting with an accelerated schedule; BrainsWay (K251449, 2025) and MagVenture (K260189, 2026) have since cleared accelerated protocols without fMRI targeting (MagVenture’s May 22, 2026 labeling expansion covers accelerated rTMS and iTBS schedules). Separately, on June 3, 2026 the FDA cleared the Wave Neuroscience MeRT System (K260402) as an adjunct for adult PTSD, the first TMS clearance for that indication, on the basis of an unpublished 158-participant sham-controlled trial (PCL-5 primary endpoint, p<0.046). Medicare hospital-outpatient payment was established January 1, 2025 under New Technology APCs, per the manufacturer’s announcements (Category III CPT codes 0889T–0892T); commercial coverage remains limited and case-by-case.
• Nexstim NBT / NBS 6 — Finnish system originally designed for pre-surgical mapping, with SmartFocus MRI-based neuronavigation. FDA-cleared for MDD.
• Apollo (MAG & More) — German system using the HANS head-and-neck positioning approach. FDA-cleared for MDD, with adolescent MDD clearance added in 2025.
• Soterix — distributes the Brain Science Tools Neural Navigator (K191422; no line-of-sight requirement) and, since February 2026, its own SPRY TMS system (K251653).

Choosing a device: what actually matters

Disclosure

Our program currently uses NeuroStar, with Magstim and BrainsWay platforms being added, which broadens the protocol options available locally. This page is independent of any manufacturer and is not endorsed by or affiliated with any TMS device company; commercial figures are drawn from third-party sources (trade press, 2021 published vendor quotes, SEC filings) and are dated where given.

Targeting

Where the coil goes matters in principle: retrospective work links the stimulated site’s connectivity to outcome. Whether more precise targeting improves outcomes in practice is a separate question, and the randomized answer so far is mostly no.

Motor threshold (MT)

Stimulation intensity is individualized to each patient’s resting motor threshold — the minimum intensity over M1 that reliably produces a contralateral hand muscle response. Treatment doses (commonly 100–120% MT for prefrontal protocols; 90% in SAINT) are scaled from that reference.

Targeting methods, from least to most individualized

Brain networks

Understanding why L-DLPFC is the standard depression target requires stepping back from the coil and thinking about circuits. Depression is increasingly conceptualized as a disorder of large-scale brain networks rather than a single region or neurotransmitter — and TMS works by modulating a specific node within those networks.

Three canonical large-scale networks are implicated in depression, and their interaction is thought to be where the pathology lives:

The rhythms within the networks

Network anatomy is only half the story. The DMN, CEN, and salience networks don’t just have locations — they have rhythms, and those rhythms are how the networks communicate. On this model each network is associated with a characteristic dominant oscillatory frequency, and information moves between regions when their rhythms align in particular ways. In depression, both the rhythms themselves and the way they couple across networks are dysregulated. One hypothesis, not yet tested in a controlled trial, is that TMS works in part by retuning that rhythmic architecture.

The animation below shows what this looks like across three states — a healthy brain, a depressed brain, and a brain after a course of TMS. Each colored ring is a region; the pulsing represents the local oscillation; the lines between regions represent functional connectivity, with thickness proportional to coupling strength. The thought-text streaming from the DMN reflects what those network dynamics produce subjectively.

Click through the three tabs and watch what changes. In the healthy state, the regions oscillate at distinct frequencies with moderate amplitudes. The dashed line between DMN and CEN represents anticorrelation — when one ramps up, the other steps back, with the salience network arbitrating between them. The sgACC is present but not dominant, and thought content is mundane and outward-facing.

In the depressed state, three things change at once. The sgACC’s rhythm slows and amplifies — a finding consistent with the thalamocortical dysrhythmia framing of mood disorders, in which pathologically slow, monotonous oscillations replace flexible faster rhythms. The DMN–sgACC connection thickens and turns red, reflecting the abnormal hyperconnectivity Liston and colleagues documented (Liston 2014; Greicius 2007). Meanwhile the CEN ring shrinks — the dorsolateral prefrontal cortex is hypoactive (the cognitive symptoms of depression map directly onto this) — and its anticorrelation with the DMN breaks down. Cognitive control can no longer suppress the negative ruminative loop. Thoughts pour out of the sgACC-dominated DMN faster than the CEN can intercept them, and the content shifts to the cognitive distortions clinicians recognize: I’m a failure. Nothing will change. I ruin everything.

In the after TMS state, the 10 Hz coil over the dlPFC pulses at treatment frequency and the picture reorganizes. The CEN ring brightens and accelerates — a hypothesized entrainment that the available imaging did not show (Liston 2014 found no CEN connectivity change). The DMN–sgACC line thins back toward baseline, which is what Liston 2014 reported at group level after a 5-week open-label course (n=17; the authors could not rule out placebo), with related findings in a 20-patient crossover study (Baeken 2014); Taylor 2018 (n=32, sham-controlled) importantly observed that sgACC connectivity dropped with improvement in both active and sham arms, so the connectivity change tracks clinical improvement rather than active stimulation per se, though that trial found no active-versus-sham clinical difference and used a non-standard target, which the authors say limits negative conclusions. The CEN–sgACC line turns teal: restored top-down control, again a hypothesis. Rhythms re-synchronize, and the thought stream slows and shifts: I can try. This might pass.

The “feeling versus knowing” gap

Cognitive therapists have long described a clinical phenomenon that has resisted easy explanation: a patient can recite a perfectly sound rational reframe of their depressive cognition — I know I’m not actually a failure; I have evidence to the contrary; I’m loved by my family — and walk out of the session feeling exactly the same. They know the cognitive content. They cannot feel that they believe it. Stott (2007) named this rational-emotional dissociation (RED) — the “head versus heart” gap that limits how much pure cognitive intervention can accomplish in moderate-to-severe depression.

The neural mechanism is becoming clearer, and it lives in the cross-frequency structure of the rhythms above. In simplified form: theta is a slow carrier wave (4–8 Hz) and gamma is the activity that carries specific content (30–100 Hz). For cortical content generated in the dlPFC to integrate with limbic representations of self-worth, threat, or felt safety, the gamma packets must arrive on a particular phase of the theta cycle (in the two causal studies below, both using transcranial alternating-current stimulation in healthy volunteers, the theta peak rather than the trough). This is theta-gamma phase-amplitude coupling (PAC), and phase-dependence has been shown causally for specific cognitive functions: Bramson and colleagues (2020) demonstrated that targeting long-range theta-gamma PAC between anterior PFC and sensorimotor cortex causally improved emotional-action control in 41 healthy men, with the benefit confined to the peak-locked (in-phase) condition and to participants in whom stimulation measurably strengthened prefrontal–sensorimotor inhibition, that is, dependent on both relative phase and effective dose. Alekseichuk (2016) showed in a parallel paradigm that working memory only improved when gamma bursts were phase-locked to theta peaks — phase-mismatched stimulation didn’t work.

The speculative step is the next one. Frontal-midline theta — the midfrontal rhythm Cavanagh and Frank (2014) identified as a signature of the need for cognitive control — is one candidate carrier. Whether theta–gamma coupling is reduced in depression, and whether sgACC low-frequency activity is decoupled from prefrontal gamma, has not been established; the thalamocortical-dysrhythmia literature the idea draws on actually reported increased low–high frequency coherence in a mixed-diagnosis MEG series (Llinás 1999). One speculative synthesis is that rational-emotional dissociation reflects cognitive content produced as gamma activity without a properly entrained theta carrier to deliver it into limbic representation, so the affective system never receives the update. No study has tested this.

The animation below makes this visible. The dlPFC at the top continuously generates gamma packets carrying CBT-style cognitive content. The slow purple wave between cortex and limbic is the theta carrier, with a glowing window that follows a particular phase of each cycle — this is when the door is open. Watch what happens to the packets in each state.

In the depressed state, the theta wave is shallow and irregular; the lock-window glow flickers in and out. Most packets miss the window entirely and scatter when they hit the wave — visible as red rings dissipating without ever reaching the limbic receiver. The integration meter (an animation setting, not a measured quantity) sits around 12%. The limbic region’s caption stays still feels like a failure. This is RED at the rhythm level: the cognitive content is being generated faithfully, but the bridge to felt belief is broken.

In the CBT alone state, the theta carrier strengthens somewhat — the rhythmic stabilization that comes from sustained cognitive engagement — and a portion of packets begin to phase-lock with the rising window. You’ll see occasional teal landings: moments where a reframe actually integrates as felt belief. The limbic caption shifts to glimpses of belief. The integration meter rises to roughly 32% (again an animation setting). The clinical analogy is the partial and variable response to CBT in moderate-to-severe depression; “integration” is not a measured construct.

In the TMS-restored state, the theta carrier becomes robust and stable — the rhythmic substrate has been retuned. Packets now consistently catch the window, ride the wave down, and land as integrating bursts in the limbic region. The nearest measured correlate is Noda (2017): in 31 depressed patients treated open-label with high-frequency left dlPFC rTMS, resting gamma power increased at frontal electrodes (F3/F4) and theta–gamma coupling increased at central and temporal electrodes (C3/T3); the gamma change correlated with depression scores, while the coupling change correlated with a cognitive measure (Wisconsin Card Sorting errors), not with mood. Consistent with the model; not a demonstration of it. The limbic receiver in the animation transforms from coral to teal as the integration setting crosses 50%, and the caption shifts to and now I feel it. In our clinical impression, some patients describe this transition with phrases like “I knew it before, but now I feel it.”

This framework offers one rationale for the iTBS pattern, which delivers gamma-frequency bursts (3 pulses at 50 Hz) on a theta-frequency carrier (5 Hz); the protocol was originally adapted from hippocampal long-term-potentiation paradigms (Huang 2005), not designed from this model. Closed-loop timing has now had a first randomized test: EEG alpha-phase-synchronized rTMS (George 2023, 28 patients treated) produced no overall clinical difference versus unsynchronized stimulation (intention-to-treat remission 2 of 15, 13%, synchronized vs 6 of 13, 46%, unsynchronized, not significantly different, with responders running the other way, 5 vs 1); only a secondary analysis linked consistency of entrainment to response. A completed 17-person basic-science crossover study in Tübingen (NCT02920840) also tested phase-synchronized pulses. Whether timing pulses to ongoing oscillations improves outcomes remains untested at scale.

What this means clinically

The rhythm-level framing reframes some familiar clinical observations. Patients who tell you they “know all the right things to think but cannot feel them” are not failing at CBT — they are describing a network state in which the cognitive content is being generated but not delivered. Patients who report sudden moments of felt insight during a TMS course (“something shifted yesterday and I can’t describe it, but the same thoughts feel different now”) may be describing the moment when carrier-wave integration was restored. And an anecdotal observation from our practice, that TMS responders often describe their pre-treatment cognitions as more accurate than their post-treatment cognitions — without remembering having “decided” that — would make sense if the mechanism were rhythm restoration rather than belief replacement. It is an impression, not a finding. The cortical content didn’t change. The brain’s ability to feel what it already knew did.

Can CBT during or right after TMS make the gamma packets land?

The mechanistic picture above predicts something specific and clinically actionable: if TMS works partly by restoring the theta carrier and the integration window, then cognitive content delivered during or immediately after a session should integrate more efficiently than the same content delivered weeks later in a clean therapy office. The packets aren’t just being generated — they’re being delivered into a transiently more plastic, better-coupled receiver. There is now a small but real literature testing this prediction.

The plasticity-window basis. Kozyrev and colleagues (2018, PNAS) showed in anesthetized cat visual cortex (seven 10 Hz experiments) that 30 minutes of 10 Hz TMS produces a transient cortical state of increased excitability and response variability — a permissive period during which directed input gets preferentially imprinted onto the local map. In their paradigm, 30 minutes of passive visual exposure to a single orientation, applied during this post-TMS window, produced a stable shift in cortical orientation preference toward the trained input that was not seen without the TMS priming. The general principle is well-established in spike-timing-dependent plasticity: when TMS modulates a circuit and behaviorally relevant input arrives within a defined post-stimulation window, the synaptic changes that get consolidated reflect the input. This is the bench-science basis for the idea that what you do during and right after a TMS session may shape what gets retuned.

The clinical signal in depression. Donse and colleagues (2018, Brain Stimulation) reported on 196 patients with non-psychotic MDD or dysthymia (most, 115 of 196, received 1 Hz right-sided stimulation, 74 received 10 Hz left and 7 both; outcomes were self-rated on the BDI) receiving simultaneous rTMS and CBT in a large naturalistic cohort — therapy delivered during the stimulation session itself, with the cognitive content delivered during the session (the authors’ rationale was shared neurobiological mechanisms; the plasticity-window framing is ours). 66% of patients responded and 56% remitted at end of treatment; among the 73 patients (37%) with 6-month data, 60% had sustained remission. The authors noted these rates are relatively high compared to previous findings in RCTs, though the design was open-label and naturalistic rather than randomized. Xu and colleagues (2023, Brain Sciences) meta-analyzed 27 RCTs of rTMS combined with psychological interventions across multiple conditions and found that active rTMS plus psychological intervention significantly outperformed sham rTMS plus the same psychological intervention on overall clinical symptoms (k=16, SMD 0.31, p<0.01). For the CBT-specific subgroup with 10 or more sessions, the effect was smaller but still significant (k=3, SMD 0.21, 95% CI 0.05–0.36).

The honest limitation. A more recent scoping review and meta-analysis (Giron 2025) made the more rigorous comparison — active rTMS plus an active psychological intervention versus active rTMS plus sham intervention — and found no significant added benefit across the four controlled trials that enabled this contrast (p = 0.96). The Adu 2023 randomized pilot of rTMS plus internet-delivered CBT in treatment-resistant depression also showed no advantage over rTMS alone. The directionally positive Donse data and the Xu meta-analytic signal are real, but the cleaner controlled question — does adding therapy to TMS outperform TMS by itself? — remains genuinely open. Possible reasons: unguided digital CBT may be insufficient; the optimal timing window may be tighter than current trials have tested; therapy modality and patient-therapist alignment matter; and existing trials have been small.

The PTSD case is instructive. Isserles and colleagues (2013) ran a pilot in PTSD pairing brief script-driven trauma exposure with deep TMS over the medial PFC and showed reductions in intrusive symptoms not seen in either control arm. The follow-up multisite RCT (Isserles 2021, Biological Psychiatry, n=125) tested the same combination more rigorously and found that both groups improved substantially, with the sham-TMS-plus-exposure arm doing significantly better than active-TMS-plus-exposure (CAPS-5 improvement 20.5 vs 16.3 points at 5 weeks, p=.027; 24.4 vs 19.0 at 9 weeks, p=.024). The authors’ interpretation: brief script-driven exposure may itself be a viable PTSD treatment, and mPFC stimulation may have interfered with the trauma memory–mediated extinction the exposure was driving. The lesson isn’t that combination doesn’t work — it’s that combinations are sensitive to mechanism. Pairing stimulation with cognitive content that engages the same circuit isn’t automatically additive; the timing, frequency, and target need to match the kind of learning the therapy is trying to produce.

What this means for practice. The mechanism-level argument for offering CBT alongside a TMS course is plausible but untested: the brain is in a transiently more plastic state during and after sessions, the cognitive content that drives clinical change in CBT may depend on the integration architecture TMS is hypothesized to restore (no study has tested this), and the largest naturalistic cohort with concurrent treatment reports better-than-typical outcomes. The randomized data on incremental benefit over TMS alone is mixed and the best-controlled comparisons are still small. A reasonable clinical posture: where patients are already engaged in CBT or interested in starting it, scheduling sessions during or shortly after the TMS course is biologically sensible and, in depression, unlikely to be harmful in our judgement (the PTSD exposure-pairing result above is a reminder that pairing is not always neutral), and may help. Whether it adds enough over TMS alone to justify recommending it for patients who are not otherwise interested is not yet settled.

This framework generates several testable clinical hypotheses: that precision matters (in a small retrospective series the clinically applied site lay on average about 30 mm from each person’s fMRI-derived optimum, and closer proximity tracked better response; Cash 2021), that individualized fMRI-guided targeting might improve outcomes (the sgACC-anticorrelated DLPFC locus varies between individuals; the largest randomized test of personalized targeting, BRIGhTMIND, n=255, used an insula-based target and found no advantage over F3-targeted rTMS, while three smaller 2026 trials of sgACC-based personalization were mixed: better early outcomes in Li 2026, n=123, not sustained at 12 weeks, and in Taylor 2026, n=40, but no benefit over sham in Appelbaum 2026, n=51), and that response prediction may become possible (a patient’s own baseline sgACC connectivity predicted improvement in Liston 2014, n=17; the sgACC anticorrelation of the stimulated site, estimated from a normative connectome, predicted response in Weigand 2018, n=25, replicated in a 16-patient cohort; the measure explained about 3% of variance in THREE-D; and it did not replicate in the primary analysis of a 66-patient 2026 routine-care cohort using normative connectivity, Khosravani 2026, where only a post hoc model with clinical covariates recovered a weak association).

Evidence by indication

Evidence strength varies substantially by indication and does not always track FDA clearance. This section separates sham-controlled trial results from open-label and registry results, and it includes the negative trials.

Major depressive disorder

Sham-controlled versus open-label: why the numbers differ

The rates quoted for TMS depend almost entirely on study design. Blinded, sham-controlled trials isolate the effect of stimulation; open-label and registry data add expectancy, daily clinical contact, and time. Both are real; they answer different questions.

Other protocol comparisons

• Effect size: Schutter 2009 (30 sham-controlled studies, 1,164 patients) found a weighted mean d=0.39 (95% CI 0.25–0.54) for high-frequency left rTMS, which the author described as comparable to at least a subset of antidepressant drugs.
• Low-frequency right-sided rTMS: Berlim 2013 (8 RCTs, n=263): response 38.2% vs 15.1% sham (OR 3.35), remission 34.6% vs 9.7% (OR 4.76). Chen 2013: no efficacy difference between high-frequency left and low-frequency right stimulation (OR 1.15, 95% CI 0.65–2.03); the tolerability comparison was inconclusive.
• iTBS versus 10 Hz: non-inferior in THREE-D (n=414, Blumberger 2018); a single-centre trial found similar outcomes (Bulteau 2022, n=60: response 36.7% vs 33.3%, remission 18.5% vs 14.8%). Prolonged iTBS (triple the standard dose) as 2-week monotherapy was superior to sham in a 105-patient three-arm trial that also included a 10 Hz rTMS arm; it did not test standard iTBS (Li 2020).
• Bilateral versus unilateral: no advantage for sequential bilateral stimulation over right-sided unilateral priming rTMS in a 179-patient RCT (Fitzgerald 2013) or in a 2025 meta-analysis (bilateral vs unilateral response RR 1.20, 95% CI 0.83–1.72, not significant; Cai 2025). In older adults, bilateral theta-burst was non-inferior to bilateral standard rTMS (FOUR-D, Blumberger 2022).

Durability and maintenance

Response is often temporary. Among initial responders across 18 studies, 66.5% (95% CI 57.1–74.8) still met response criteria at 3 months, 52.9% (40.3–65) at 6 months and 46.3% (32.6–60.7) at 12 months, but 11 of the 18 studies provided maintenance rTMS during follow-up (Senova 2019). In the NeuroStar 12-month study, 120 of 257 patients (46.7%) met IDS-SR response or remission criteria at the end of the acute course (62.2% by CGI-S, 61.5% by PHQ-9); of those 120, 62.5% still met response criteria throughout the year under a regimen that allowed continuation medication and re-treatment, and 36.2% received re-treatment after the first month (mean 16.2 treatment days, SD 21.1) (Dunner 2014). Without maintenance, sham-controlled follow-up effects are small and decay (Kedzior 2015), event-free remission fell to 22.6% at 6 months in one 204-remitter cohort (Cohen 2009), remission in routine US practice fell from 19.1% at end of course to 9.0% about three months later (Bastiaens 2024), only 20% of BRIGhTMIND participants were sustained responders at 16 and 26 weeks (Morriss 2024), and about half of remitters relapse within a year (Miljevic 2019).

• Maintenance TMS: the evidence is low quality (Wilson 2022). A single scheduled monthly session was no better than observation in a 49-patient randomized pilot, though 63–78% of those who relapsed re-responded to reintroduction (Philip 2016). Weekly 1 Hz maintenance was comparable to lithium with fewer adverse effects in the 75-patient MAINT-R trial, which had no untreated arm (Noda 2025). Clustered monthly rTMS reduced relapse versus antidepressants alone in antidepressant remitters, without a sham arm (Wang 2017). A 2025 consensus statement notes that end-of-course tapering has little empirical support (Trapp 2025).
• Re-treatment works for most prior responders in open-label series: 84.2% re-achieved benefit in the NeuroStar durability study (Janicak 2010); 78.6% response and 57.1% remission in a naturalistic re-treatment series (Fukuda 2019); 82.5% response and 54.2% remission among 177 prior responders across 20 centres (Lyndon 2026).

TMS compared with other treatments

• ECT: meta-analyses favour ECT for acute efficacy, particularly in severe and psychotic depression (Ren 2014; Mutz 2019, bitemporal ECT OR 8.91 vs sham). In a 2026 comparison of non-psychotic treatment-resistant patients, ECT worked faster while rTMS avoided anesthesia and subjective memory complaints (Lin 2026). See the ECT page.
• Ketamine and esketamine: no adequately powered randomized head-to-head trial against TMS has been published; comparisons rest on indirect estimates; an individual-participant-data comparison of THREE-D and TRANSFORM-2 found no significant difference (HDRS-17 −2.46, 95% CI −5.82 to 0.89, favouring rTMS; Kaster 2025). See the ketamine page.
• Medication: TMS is added to medication in most trials; there is no evidence that stopping medication helps, and the added-versus-switched question has not been settled (Rakesh 2024).

Obsessive–compulsive disorder

FDA-cleared in 2018 for deep TMS with the H7 coil targeting medial prefrontal cortex and anterior cingulate (De Novo DEN170078), as an adjunct; later cleared for MagVenture (2020), NeuroStar (2022), Magstim (2023) and Apollo (2025). Labeling notes that safety and effectiveness have not been established under age 22 or over 68.

• Carmi 2019 — multicentre, double-blind, sham-controlled, 29 sessions over 6 weeks (20 Hz at 100% MT, 2,000 pulses per session, with symptom provocation). In the modified intent-to-treat set (n=94 of 99 randomized) the primary Y-BOCS change was −6.0 vs −3.3 points; response (secondary endpoint, ≥30% Y-BOCS reduction) 38.1% vs 11.1% at 6 weeks and 45.2% vs 17.8% at 1-month follow-up. In the full intent-to-treat set the primary endpoint was not significant (−6.0 vs −4.1 points, p=0.099); response was 37.2% vs 18.4% and remission (Y-BOCS <10) 4.7% vs 8.2%, while in the modified ITT set remission was 4.8% vs 4.4% (FDA De Novo summary DEN170078). Separation was driven by more severe patients (Storch 2021).
• Post-marketing data — 219 patients at 22 sites, 167 analysable: first response 72.6%, sustained one-month response 52.4%, end-of-course (29-session) response 57.9%; uncontrolled and manufacturer-affiliated (Roth 2021).
• Syntheses — Steuber 2023 meta-analysis: g=0.65, response RR 3.15; Figueiredo 2026: pooled Y-BOCS difference −3.30 points (below the usual 4.9-point minimal clinically important difference), NNT 6; Reddy 2026 found no evidence of benefit for remission; the 2020 international guidelines rated OCD evidence below Level B (Lefaucheur 2020).

Smoking cessation

FDA-cleared in 2020 (BrainsWay H4 coil, K200957) as an aid to short-term smoking cessation. In the pivotal trial (Zangen 2021, 262 adults with prior failed quit attempts randomized, 234 in the intent-to-treat efficacy set), the 4-week continuous quit rate through week 18 was 19.4% vs 8.7% with sham (intent-to-treat, p=0.017; 28.0% vs 11.7% in completers). Whether symptom provocation before stimulation adds benefit is unproven: in a 2025 meta-analysis of OCD and nicotine trials the estimated added effect was not significant (SMD −0.22 and −0.21), although the authors concluded it “may enhance” response (Bello 2025), and a 2024 medial-prefrontal iTBS trial for tobacco use was null (Addicott 2024).

Comorbid anxiety in MDD

The FDA wording is “decreasing anxiety symptoms” in adults with MDD who “may exhibit comorbid anxiety symptoms” (BrainsWay K210201, 2021; NeuroStar K220127, 2022; Magstim K223154, 2023; MagVenture K251119, 2025), not a DSM “anxious distress” specifier and not a standalone anxiety indication. The clearances rested on retrospective analyses of anxiety-factor scores in depression trials and registry data. In the NeuroStar registry (n=1,820) anxious patients improved on anxiety measures but had significantly lower categorical response and remission than non-anxious patients (Hutton 2023).

Generalized anxiety and panic: Cox 2022 pooled 13 interventional studies (677 patients), not only sham-controlled RCTs, and reported SMD 1.45 for anxiety in GAD with no significant effect in panic disorder; Parikh 2022 pooled 6 studies (152 patients; SMD −1.86) and called for rigorous RCTs. Neither reports response or remission rates.

Off-label and emerging indications

For most conditions beyond the cleared indications the literature consists of small trials, heterogeneous protocols and meta-analyses with important limitations. The table summarizes the strongest evidence and the negative trials a referring clinician should know about.

How to read this table. Effect sizes come from published meta-analyses, not individual trials, and are not directly comparable to the response and remission rates quoted for MDD. For off-label use, “there is a signal, with negative trials” is a more accurate characterization than a response-rate number.

FDA clearance history

Decision dates and 510(k)/De Novo numbers from the FDA device databases (openFDA, September 2026). TMS devices are cleared, not approved.

All adolescent clearances are adjunctive to medication and rest on retrospective registry data; the largest sham-controlled adolescent RCT (n=103) was negative (Croarkin 2021). SAINT’s cleared indication is MDD in adults who have failed prior antidepressant medication in the current episode; the protocol parameters (1,800 pulses per session, 10 sessions per day for 5 days, 90% motor threshold, fMRI-derived target) are described in the K220177 summary.

How TMS works — mechanism

The mechanism by which TMS alleviates depression remains incompletely understood. Current evidence suggests modulation of prefrontal–limbic circuits rather than a single-pathway pharmacologic effect. The human evidence is small and mostly uncontrolled:

• Subgenual cingulate connectivity — the stimulated site’s anticorrelation with the sgACC related to outcome retrospectively (Fox 2012) and in two small prospective cohorts (n=25 and 16; Weigand 2018), but explained about 3% of outcome variance in THREE-D (Elbau 2023, n=295) and did not predict response in a 2026 routine-care cohort (Khosravani 2026, n=66).
• Network change with treatment — an open-label course normalized sgACC–default-mode hyperconnectivity at group level without altering central-executive connectivity (Liston 2014, n=17); in a sham-controlled study the connectivity changes were not specific to active stimulation (Taylor 2018, n=32).
• Structural change — a near-significant increase in left amygdala volume in responders in a 29-patient MRI study; preliminary and unreplicated (Furtado 2013).
• Circuit context — cortico-striatal-thalamic loops of the salience network are a plausible substrate for stimulation effects across disorders (Peters 2016, review).

Cutting edge & prediction

Three trends define where the field is moving: precision targeting (fMRI-guided individualization), accelerated protocols (days, not weeks), and prediction (biomarkers and machine learning). Each has real data behind it, and each has randomized results that cut the other way. Both are summarized here, followed by a candid look at non-response.

fMRI-guided targeting

The rationale is sound (Fox 2012; Weigand 2018) and personalized targets are reproducible to a few millimetres (Cash 2021, Hum Brain Mapp). The randomized record is mixed and mostly null: BRIGhTMIND (n=255) found no advantage of connectivity-guided iTBS over MRI-navigated F3 rTMS (Morriss 2024); Appelbaum 2026 found fMRI-individualized accelerated iTBS no better than sham (n=51); Terao 2025 pooled ten active-controlled trials (personalized vs fixed targeting SMD 0.15, 95% CI −0.23 to 0.54). Two 2026 single-site trials were positive in the short term (Taylor 2026, n=40; Li 2026, n=119 of 123 randomized, where tractography-guided targeting beat the 5-cm rule at week 2 and both connectivity-guided arms beat it at week 6, with no difference by week 12). The much-cited community comparison is a retrospective, propensity-matched series from one subspecialty clinic (DeSouza 2025, medRxiv preprint; 71 matched pairs; CGI-I response 77.5% vs 62.2%, OR 2.30), not peer-reviewed. Full details are in the Targeting section.

SAINT / SNT

Stanford Neuromodulation Therapy: 5-day accelerated iTBS (10 sessions per day, 1,800 pulses each, 90% motor threshold) with fMRI-guided individualized targeting. Open-label n=21: 90.5% remission (Cole 2020). Sham-controlled RCT stopped at the planned interim analysis, n=29 (14 active, 15 sham): MADRS reduction 52.5% vs 11.1% at 4 weeks; 11 of 14 active participants (78.6%) met remission criteria at some point during the 4 weeks after treatment versus 2 of 15 (13.3%) on sham, with 46.2% in remission at the 1-month visit itself (Cole 2022; FDA K220177 summary). Replication RCT (Kratter 2026, n=48; planned 100): remission at 1 month 50.0% vs 20.8% (p=0.035), response 54.2% vs 25.0%. FDA-cleared September 2022 (K220177). Durability: in an open-label series of 46 patients, 70% were in remission the week after SNT but only 15 of 46 (33%) remained in remission at 12 weeks, 47% of those who had remitted (Geoly 2025). The same dose without fMRI targeting produced 1-month remission in 1 of 8 patients and, after an optional 4-week tDCS course, none in remission at 6 months in a small open-label series (Chen 2026). Open-label data from seven US private clinics in a Magnus Medical-run study (six authors are Magnus employees with equity; Feyder 2026, n=101 per protocol) report CGI-I of 2 or better in 68.3% at day 5, without remission rates; a single-centre prospective cohort of 46 patients given 30 iTBS sessions over 5 days reported 28.3% response and 26.1% remission after treatment (Khanna 2026). No trial has compared SNT with standard once-daily TMS.

Accelerated protocols more broadly

Accelerated iTBS beats sham: Ramos 2025 (JAMA Psychiatry, n=100, three sessions per day for 15 days, non-navigated) reported response 52% vs 22% and remission 34% vs 16%; a 2026 meta-analysis of 15 sham-controlled trials (n=704) found SMD 0.69, response NNT 5 and remission NNT 10 (Santos 2026). Head-to-head against once-daily schedules, accelerated schedules have shown no efficacy advantage and, apart from secondary speed-of-response outcomes in the BrainsWay non-inferiority trial (Hanlon 2026; Tendler 2026), no speed advantage: twice-daily vs once-daily iTBS (CARTBIND, n=208; Blumberger 2021), accelerated bilateral theta burst (two sessions a day over 10 days) vs once-daily left 10 Hz rTMS (Chen 2021, n=300, single-blind), accelerated vs standard rTMS (Fitzgerald 2018, n=115), and different inter-session intervals (Goodman 2024, n=182). Accelerated TMS has not outperformed sham for suicidality in two 2026 syntheses (Joseph 2026; Traynor 2026); a third 2026 meta-analysis of six iTBS trials, not restricted to accelerated schedules, reported a reduction in suicidal ideation versus sham with high heterogeneity (Bilal 2026).

SWIFT

BrainsWay’s accelerated H1 protocol (5 sessions per day for 6 treatment days over 2 weeks, then 2 sessions weekly for 4 weeks). Multisite randomized non-inferiority trial against standard once-daily H1 deep TMS, no sham arm (Hanlon 2026; n=104 randomized, 89 per protocol): HDRS-21 change −19.0 vs −19.8; week-6 response 87.8% vs 87.5%; remission 78.0% vs 87.5% (numerically lower with the accelerated arm); time to remission 21 vs 28 days; patient-rated remission 57.5% vs 58.5% (Tendler 2026). Headache 41% vs 15%; one hypomania; two participants stopped for adverse events. FDA-cleared September 13, 2025 (K251449). A 12-month figure circulating from a 2026 conference poster is not peer-reviewed.

ONE-D

A single-day regimen: 20 iTBS sessions (600 pulses, 120% MT, scalp targeting) every 30 minutes over 9.5 hours, combined with single-dose off-label d-cycloserine and lisdexamfetamine. Published in November 2025 as an open-label retrospective case series (Vaughn 2025, n=32; 13 were prior TMS responders); no comparator in the published series, although a January 2026 propensity-matched retrospective comparison with once-daily TMS has been posted as a non-peer-reviewed preprint; by week 26 half had relapsed or been re-treated. Percentages differ between the preprint and the journal abstract and are not quoted here.

Why some patients don't respond

In sham-controlled trials roughly 30% respond and 20% remit (versus 10% and 5% with sham; Berlim 2014); pooled across clinical trials about 46% respond and 31% remit (Fitzgerald 2016); in open-label practice, clinician-rated response is roughly 58% and remission 37% (Carpenter 2012), and 58–83% response and 28–62% remission depending on sample and instrument in the NeuroStar registry (Sackeim 2020). Either way, a large minority do not get better. The clinically useful question is why. Non-response is not a single phenomenon, and it is not a moral failing of the treatment or the patient. The three-part taxonomy below is a clinical heuristic, not a validated classification, but the distinctions matter because the right next step differs across them.

Clinically, this framework shifts the first question after a limited response from “was the TMS protocol adequate?” to “which of these three factors is most likely in play, and what’s the next reasonable move?”

What the data say about non-response

• Early non-improvement predicts non-response. Less than 20% improvement by session 10 predicted eventual non-response with a negative predictive value of about 88% in a retrospective series of 101 patients treated with dorsomedial (not DLPFC) rTMS (Feffer 2018); similar results hold for 10 Hz and accelerated theta-burst courses (Nguyen 2025). Response trajectories in THREE-D were heterogeneous: 11% non-response, 19% rapid response and 70% gradual linear improvement (Kaster 2019).
• Clinical predictors are modest. In THREE-D, higher baseline depression and anxiety severity and more prior treatment failures lowered the odds of remission, and current employment raised them; the combined model had a c-index of only 0.687 (Trevizol 2020). Remission was 17.3% with three or more prior failures versus 29.4% with fewer (Hsu 2019). Greater resistance predicted poorer outcome in the pivotal-trial cohort as well (Lisanby 2009).
• Benzodiazepines may blunt response in naturalistic data (18% vs 38% response with concomitant lorazepam; Deppe 2021).
• What to do next is largely untested. The one randomized switching study found that moving non-responders to 1 Hz right-sided or sequential bilateral stimulation was no better than continuing left 10 Hz (Fitzgerald 2018, n=59). Naturalistic extension data show a meaningful fraction of late responders (Yip 2017: 61% of deep-TMS non-responders responded with four further weeks; Razafsha 2023: 53.6% response and 32.1% remission with a mean of about 70 total sessions; Tendler 2023; Lew 2025). Changing mechanism (ECT, ketamine or esketamine) is reasonable on clinical grounds but has not been tested head-to-head after TMS failure.

Can we predict response before the first session?

Prediction research has moved substantially in the past five years. Three signal classes are emerging — imaging-based, EEG-based, and multimodal machine learning — that may let us stratify patients to likely-responder and likely-non-responder groups before a course begins. Each has real data behind it and real limitations worth naming.

AI in TMS today

AI is already used in TMS research and, in a few settings, in treatment planning; whether it changes outcomes is not yet shown. The thread running through all of it: TMS is heterogeneous (patients, brains, responses), and AI is how we're finally engaging that complexity at scale. Three places it lives in current practice:

What this means for practice today

None of these prediction tools are yet standard of care, and none should be used to deny a reasonable TMS trial to a patient who would otherwise qualify. But the framing has shifted. The sequence — treat first, then learn retrospectively who responded — is beginning to flip toward stratify first, then treat.

For the referring clinician today, the practical implications are modest but real:

• A pre-TMS workup that screens for — and treats — medical contributors (thyroid, sleep, B12, pain, substance use) is good practice; whether it changes TMS outcomes has not been studied.
• A social and environmental assessment matters. If the life circumstance is actively driving the pathology, a stimulation-only plan is likely to disappoint regardless of targeting precision.
• When a patient has not responded to one TMS protocol, the evidence on what to do next is thin: the one randomized switching study found no advantage for changing laterality (Fitzgerald 2018), while naturalistic data show late responders with extension (Yip 2017; Razafsha 2023). Changing mechanism (ECT, ketamine or esketamine) is reasonable clinically but untested head-to-head after TMS failure.
• Biomarker-guided stratification — particularly EEG-based measures like iAF that are cheap and repeatable — is the most plausible near-term clinical entry point. Worth tracking. Not yet ready to deploy, and the field’s record on replication (Drysdale 2017 / Dinga 2019; Bailey 2021 / 2025) argues for independent-cohort validation before any biomarker is used to select patients.

Contraindications & safety

The most common reason a referral is declined or delayed. Worth screening for before sending the patient. The lists distinguish what device labeling forbids from what our program treats conservatively.

Absolute contraindications (device labeling)

• Ferromagnetic or conductive metal in or near the head — aneurysm clips or coils, intracranial stents, metallic fragments or shrapnel, and other non-removable metal hardware within roughly 30 cm of the coil (a distance stated in device labeling, not in the professional guidelines). Standard dental amalgam fillings are explicitly acceptable in device labeling and Medicare policy (BrainsWay labeling; LCD L34869); titanium plates, rods and clips are non-ferromagnetic and, per the 2021 IFCN guidelines, “do not appear to experience significant forces” or heating (Rossi 2021). Confirm the implant material before treating.
• Implanted stimulators and electrodes in the field — cochlear implants, deep brain stimulators, intracranial electrodes. Vagus nerve stimulators are contraindicated by NeuroStar labeling; the 2021 IFCN guidelines treat them as a relative contraindication because the components lie outside the field, so treating a VNS patient is off-label and should be documented as such.

Relative contraindications / caution

• Cardiac pacemakers, ICDs and other physiologically controlled implants — labeling says “use with caution” even when the device is more than 30 cm from the coil; the 2021 IFCN guidelines consider figure-8 TMS acceptable if the coil is never discharged within 10 cm of electronic components such as the pulse generator in the neck or torso, with lead loops kept out of the field; Medicare policies treat them as contraindicated only within 30 cm. Cardiology input and device interrogation are prudent.
• Seizure history or lowered seizure threshold — personal seizure history, epilepsy, recent CNS lesions or stroke, brain tumour, recent significant head trauma, withdrawal states, sleep deprivation, or seizure-threshold-lowering medication. The 2021 IFCN guidelines no longer advise special caution for medications that lower the seizure threshold (bupropion included by implication) while recommending that such drugs be documented; device labeling still lists them as risk factors. See the numbers below.
• Bipolar spectrum, active mania or rapid cycling — risk of treatment-emergent mood elevation. Pooled across 10 sham-controlled depression trials, treatment-emergent mania occurred in 0.84% of active and 0.73% of sham patients, not significantly different (Xia 2008; 13 published cases, mostly in bipolar patients); OR 1.3 (95% CI 0.7–2.4) across bipolar-depression RCTs (Ventura 2026).
• Psychosis, catatonia, dementia, raised intracranial pressure — listed in device labeling and in Medicare policy as reasons for caution or exclusion; ECT is usually the better-supported option for psychotic depression.
• Active substance use — complicates seizure-risk assessment, adherence, and interpretation of response.
• Pregnancy — cumulative published exposure is small (a 2026 systematic review counted roughly 230 pregnancies across trials, pilot studies and case series; Khalesi 2026); short-term safety data are reassuring, but the review rates the certainty as low and notes that absence of observed harm is not evidence of safety; the only sham-controlled trial (Kim 2019, 22 women, 1 Hz right-sided) showed a depression benefit but three late-preterm births, all in the active arm (the authors note a possible association and that a larger sample would be needed to test it). Labeling states TMS has not been studied in pregnancy. Case-by-case review with obstetrics; document the discussion.
• Hearing — coil clicks can exceed 130 dB peak at close range; rated earplugs for patient and operator are standard, and hearing was unchanged in trials that used them.
• Unstable medical or psychiatric comorbidity — acute suicidality, unstable cardiac disease, or uncontrolled medical illness may warrant stabilization or a different treatment (ECT, ketamine) first.
• Age — adult labeling; adolescents 15–21 only as an adjunct to medication, on registry rather than sham-controlled evidence (Croarkin 2021 was negative); BrainsWay labeling extends to age 86.

Seizure risk in numbers

TMS-related seizures occur during stimulation; the 2021 IFCN guidelines regard them as provoked events with “minimal risk of recurrent seizures in the absence of such a provocation” (Rossi 2021). The surveyed clinical rate is low but not zero, and it differs by coil.

• Taylor 2021 (Clinical TMS Society survey; 134 responses, 125 analysed): 18 seizures in 586,656 sessions and 25,526 patients; 0.31 per 10,000 sessions and 0.71 per 1,000 patients; BrainsWay H-coil 5.56 per 1,000 patients versus 0.14 per 1,000 for the three most widely used figure-8 devices combined (p < 0.001).
• Lerner 2019 (2012–2016 survey): within published guidelines in people without risk factors, fewer than 1 seizure per 60,000 sessions (4 in 242,067); over 62% of seizures occurred at first exposure and 75% within the first three; syncope or presyncope was the most common adverse event, reported by 17% of sites, and must be distinguished from seizure.
• NeuroStar labeling: estimated risk under ordinary use less than 1 in 30,000 treatments and less than 1 in 1,000 patients. Accelerated TMS: 1 seizure in 43,873 sessions across published accelerated protocols (Caulfield 2022). H-coil surveillance: 46 seizures or convulsive syncope events in 48,252 patients (Zibman 2019, as reported in Rossi 2021).

Common side effects (not contraindications)

Headache (reported by about two-thirds of patients in THREE-D with systematic ascertainment, at similar rates in both arms; roughly 28% vs 16% with sham in the sham-controlled trials pooled in the 2009 IFCN guidelines), scalp pain or discomfort at the stimulation site (about 39% vs 15% with sham in the same pooled data; Rossi 2009), transient lightheadedness, and fatigue after sessions. These usually diminish over the first one to three weeks. Discontinuation for adverse effects in pooled sham-controlled trials was about 2.5% with active and 2.7% with sham treatment across 93 TMS trials in all indications (Zis 2020), with no excess of serious adverse events.

Referral tools

Practical guidance for referring clinicians.

What to include in the referral note

The items below are the clinical documentation that supports a good TMS evaluation — and, independent of any specific program's intake process, they are the elements payers typically require for prior authorization.

• Current PHQ-9or equivalent severity score.
• Antidepressant trials in the current episodefor each, include class, dose, duration, and reason for stopping or insufficient response. South Carolina Medicare requires two trials from at least two classes (or intolerance of two agents, prior rTMS response, or current ECT); many commercial plans (Aetna, for example) require two antidepressants from different classes plus an augmentation trial; some Medicare contractors elsewhere require only one.
• Psychotherapy trialCBT or equivalent, with duration and outcome. Required by the South Carolina Medicare policy (“of an adequate frequency and duration”) and by some commercial plans.
• ECT statusconsidered, offered, or reason not appropriate.
• Contraindication screendocumented, including implants and seizure risk.
• Diagnosis and severitydocumented in the current note, not just the problem list. Medicare in South Carolina requires an order from a psychiatrist (MD or DO) who has examined the patient.

Coverage in South Carolina

When to refer

What we can say confidently

Seven statements that hold up across the current evidence base. Useful when talking to patients, families, and skeptical colleagues.

References

Full reference list for material cited above, in AMA format with DOIs and PMIDs where available. Every PubMed entry was checked against the NCBI record in September and again in October 2026; preprints, conference material and industry documents are labeled as such.

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187. U.S. Food and Drug Administration. De Novo classification DEN070003 / 510(k) K061053: NeuroStar TMS System, indicated for major depressive disorder in adults who have failed to achieve satisfactory improvement from one prior antidepressant medication at or above the minimal effective dose and duration in the current episode. Decision October 7, 2008. FDA De Novo database.
188. U.S. Food and Drug Administration. 510(k) summary K173620: MagVita TMS Therapy System with Theta Burst Stimulation (standard 10 Hz session 19–37.5 min; iTBS 3 min). Decision August 14, 2018. PDF.
189. U.S. Food and Drug Administration. De Novo DEN170078: BrainsWay Deep TMS System, adjunct treatment of adult patients with obsessive-compulsive disorder. Decision August 17, 2018 (decision summary includes the intent-to-treat analysis of the pivotal trial). FDA De Novo database.
190. U.S. Food and Drug Administration. 510(k) summary K220177: Magnus Neuromodulation System with SAINT Technology, Model 1001K. Decision September 1, 2022. PDF.
191. U.S. Food and Drug Administration. 510(k) summary K231926: NeuroStar Advanced Therapy System, adjunct for adolescents aged 15–21 with MDD (based on retrospective TrakStar registry data, 1,169 per-protocol patients). Decision March 22, 2024. PDF.
192. U.S. Food and Drug Administration. 510(k) summary K251449: BrainsWay Deep TMS System, accelerated iTBS protocol (multisite randomized non-inferiority trial vs standard H1 protocol). Decision September 13, 2025. PDF.
193. U.S. Food and Drug Administration. Device clearance records for product code OBP and related codes (K122288, K143531, K150641, K160703, K171902, K180313, K182853, K183376, K193006, K200957, K201158, K203735, K210201, K212289, K220127, K221544, K222171, K222196, K223154, K243539, K243700, K243869, K251119, K251125, K251391, K251653, K252358, K260189, K260560), queried September 2026 via openFDA.
194. Palmetto GBA. Local Coverage Determination L34869: Repetitive Transcranial Magnetic Stimulation (rTMS) in Adults (Jurisdictions J and M, including South Carolina; original effective date 10/01/2015; OCD coverage effective 03/13/2022; revision R13 effective 01/16/2025, hyperlink update only). CMS Medicare Coverage Database.
195. Neuronetics, Inc. NeuroStar Advanced Therapy System Instructions for Use (contraindications, warnings for implanted devices, and seizure-risk estimate of fewer than 1 in 30,000 treatments and fewer than 1 in 1,000 patients). Current labeling available from the manufacturer.
196. Magnus Medical. Press release, November 11, 2024: CMS establishes hospital outpatient payment for SAINT (CPT III codes 0889T–0892T) effective January 1, 2025. Company communication; payment amounts should be verified against the current OPPS addenda.
197. Carlat Psychiatry Report. TMS device comparison chart (vendor-quoted pricing for NeuroStar, BrainsWay, MagVenture and Magstim systems). February/March 2021. Trade publication; figures are dated vendor quotes.

Entries 1–61 are the original v4 list (two unverifiable entries removed: a 2019 conference abstract and a manufacturer press release, both replaced by peer-reviewed sources); the entries that follow were added in v5 and cover the sham-controlled and comparative trials, durability and maintenance, targeting and accelerated-protocol RCTs, prediction, safety, special populations, and the FDA and Medicare documents cited in the text. Preprints (DeSouza 2025) and industry communications are labeled.

Last updated: October 2026 · This page is educational and does not constitute individual clinical advice.