TMS can reduce anxiety symptoms when the protocol targets the right brain region at the right frequency, but the standard depression protocol that most clinics use targets the wrong side. A growing body of US-based evidence supports low-frequency stimulation of the right dorsolateral prefrontal cortex for anxiety, with one meta-analysis finding a large clinical effect (SMD of -1.857). Here is what the research shows and why protocol design matters.
Anxiety disorders affect roughly 19% of American adults in any given year, according to the National Institute of Mental Health. That makes anxiety the most common category of mental health condition in the United States. Yet if you search for TMS (transcranial magnetic stimulation) clinics near you, almost every website focuses on depression. The anxiety page, if it exists at all, is an afterthought. (For background on how TMS works, see our guide to TMS therapy for depression.)
This gap between patient need and clinic marketing matters. A growing body of research suggests TMS can help with anxiety, but only when the protocol is designed for anxiety. The standard depression protocol targets a different brain region, at a different frequency, for a different neurological reason. Applying the wrong one can make anxiety worse.
Here is what the evidence actually shows, why protocol design matters so much, and what to ask before starting treatment.
Does TMS work for anxiety? What the research shows
TMS is not yet FDA-cleared for anxiety disorders. That is the honest starting point. It is FDA-cleared for major depressive disorder and obsessive-compulsive disorder (OCD), and its use for anxiety is considered off-label.
But “off-label” does not mean “unsupported.” The evidence base for TMS in generalized anxiety disorder (GAD) is growing and, in some studies, is quite strong.
A 2022 systematic review and meta-analysis published in the International Journal of Neuropsychopharmacology(Parikh et al.) analyzed six randomized controlled trials of repetitive TMS (rTMS) in adults with GAD. The pooled effect size was a standardized mean difference (SMD) of -1.857, which is considered a large clinical effect. For context, most psychiatric treatments aim for an SMD above 0.5 to be considered meaningful.
A 2025 meta-analysis and trial sequential analysis published in the Journal of Psychiatric Research expanded the evidence base, analyzing randomized controlled trials of rTMS for GAD. It found that rTMS combined with medication was more effective than medication alone for GAD symptoms, and that rTMS alone also outperformed sham stimulation. No serious adverse events were reported in the rTMS groups.
Researchers at US institutions, including NIH-funded multi-site studies and programs at the VA and academic medical centers, are identifying neurophysiological markers in the right dorsolateral prefrontal cortex (DLPFC) that may predict who responds well to TMS for anxiety. This kind of precision, using fMRI connectivity patterns and EEG biomarkers to guide patient selection, is where the field is heading.
The limitations are real. These studies are smaller than the large-scale randomized controlled trials that secured FDA clearance for TMS in depression. Protocols vary between studies. More controlled research is needed. But the direction of the evidence is consistent: TMS can reduce anxiety symptoms, and the effect sizes are clinically meaningful.
Why the brain target matters more than the device
This is where most TMS-for-anxiety conversations go wrong. TMS is not a single treatment. It is a delivery method. What matters is where the magnetic pulses are aimed and at what frequency. For more on how TMS targets specific brain circuits, see why TMS rewires pathways antidepressants cannot reach.
For depression, the standard protocol uses high-frequency stimulation (typically 10 Hz) on the left DLPFC. The left prefrontal cortex tends to be underactive in depression, so high-frequency TMS excites it, helping to restore normal activity. This is the protocol that earned FDA clearance, and it is what most clinics run by default.
Anxiety involves a different pattern. Research suggests that the right DLPFC is overactive in people with anxiety disorders. The worry circuits, the rumination loops, the physiological hyperarousal: these are associated with excessive right-hemisphere prefrontal activity. Low-frequency stimulation (1 Hz) on the right DLPFC can inhibit that overactivity, quieting the anxiety response.
Here is the comparison at a glance:
| Condition | Brain Target | Frequency | Goal |
|---|---|---|---|
| Depression | Left DLPFC | High (10 Hz) | Excite underactive circuits |
| Anxiety | Right DLPFC | Low (1 Hz) | Inhibit overactive circuits |
The critical problem: if a clinic applies the standard depression protocol (high-frequency, left-side) to someone whose primary issue is anxiety, it can actually increase anxiety. Exciting the left DLPFC without addressing right-sided overactivity may further destabilize the interhemispheric balance that is already off in anxious individuals. Research published in Translational Psychiatry has shown that high-frequency stimulation to the right DLPFC tends to enhance anxiety expression, while low-frequency right DLPFC stimulation produces the opposite, anxiolytic effect.
This is why “going to any TMS clinic” for anxiety carries risk. The device on the shelf is the same. The protocol running through it determines whether anxiety improves or worsens.
When depression and anxiety overlap: the 60% problem
Depression and anxiety rarely travel alone. According to a review published in Psychiatric Times, the prevalence of comorbid anxiety disorder and major depressive disorder (MDD) may be as high as 60%, citing data from Kessler et al. in Archives of General Psychiatry (2005) and Kaufman & Charney in Depression and Anxiety (2000). The National Comorbidity Survey Replication found that 59.2% of people with lifetime MDD also met criteria for an anxiety disorder.
For these individuals, unilateral TMS (targeting only one hemisphere) may leave half the problem untreated. If a clinic runs the standard left-side depression protocol without addressing right-sided anxiety circuits, depressive symptoms may improve while anxiety symptoms persist or worsen. For another approach to comorbid depression and anxiety, see our guide to ketamine infusion for dual-diagnosis depression and anxiety.
Bilateral TMS protocols address both. The approach is sequential: high-frequency stimulation (10 Hz) to the left DLPFC targets depression first, followed by low-frequency stimulation (1 Hz) to the right DLPFC for anxiety, all in the same session.
A review in Clinical Psychopharmacology and Neuroscience described a preliminary pilot study of 13 adults with comorbid MDD and GAD who received sequential bilateral rTMS. After 24 to 36 sessions, 76.9% achieved remission of depression (HAMD-21 score below 8) and 84.6% achieved remission of anxiety (GAD-7 score below 5). Depression scores dropped 65% and anxiety scores dropped 75%. These are early results from a small, uncontrolled study, and larger controlled trials are needed, but the direction aligns with the broader bilateral TMS evidence.
A 2024 consensus update from the Clinical TMS Society, National Network of Depression Centers, and International Federation of Clinical Neurophysiology supports bilateral DLPFC stimulation (left high-frequency, right low-frequency in one session) as an evidence-based approach, with multiple randomized controlled trials showing superiority over sham stimulation.
Most TMS clinics run unilateral, left-only protocols. For the roughly 60% of depression patients who also have anxiety symptoms, that leaves a considerable gap.
The off-label conversation: what patients should understand
TMS for anxiety is off-label. Some people hear “off-label” and assume it means experimental or unproven. In psychiatry, off-label use is routine.
A 2006 study by Radley, Finkelstein, and Stafford published in Archives of Internal Medicine found that 21% of prescriptions for 160 commonly prescribed drugs were written for off-label purposes. The rate is higher for psychiatric medications specifically: anticonvulsants were prescribed off-label 74% of the time, and antipsychotics 60%. More recent research suggests the overall off-label rate may be even higher, with one econometric model estimating up to 38% of prescriptions as off-label.
Common psychiatric examples that most people do not realize are off-label:
- Gabapentin for anxiety (FDA-approved for seizures and nerve pain)
- Trazodone for insomnia (FDA-approved for depression)
- Quetiapine for depression augmentation (FDA-approved for schizophrenia and bipolar disorder)
Each of these is considered standard of care despite lacking FDA approval for the indication most commonly prescribed. TMS for anxiety sits in the same category: strong and growing evidence, not yet FDA-cleared, used by informed clinicians who understand the protocol requirements. TMS itself is already FDA-cleared for OCD through deep TMS protocols, demonstrating the technology’s expanding clinical applications. (For another example of how off-label treatments work in mental health care, see our guide to ketamine’s FDA approval status and off-label use.)
What to ask your clinician before starting TMS for anxiety
Not every TMS provider has experience tailoring protocols for anxiety. Before beginning treatment, consider asking:
- Are you using right DLPFC targeting for my anxiety symptoms, or the standard left-side depression protocol?
- What frequency will you use, and why?
- If I have both depression and anxiety, will you use a bilateral protocol?
- Am I taking any medications (particularly benzodiazepines) that could affect TMS outcomes?
- What outcome measures will you track, and how often?
That last question matters. Research on benzodiazepine use during TMS has produced mixed findings. Kaster et al. found that benzodiazepine use was associated with a lower rapid response rate (OR=0.40) and higher nonresponse (OR=2.25) among 388 patients receiving rTMS. Hunter et al., published in the American Journal of Psychiatry, similarly found lower response to left DLPFC rTMS with concurrent benzodiazepine use. More recent data has been less definitive, with some studies finding no significant effect on outcomes, but the potential interaction is important enough that your clinician should account for it. Research by Ferrarelli et al. at the University of Wisconsin, published in the Journal of Neuroscience (2014), used TMS-EEG to document how benzodiazepines, as positive modulators of GABA-A receptors, alter cortical excitability patterns, which may influence how effectively TMS can engage target circuits. This is one reason why having a prescribing psychiatrist involved in protocol design, not just treatment delivery, can make a meaningful difference in outcomes. For people exploring non-medication alternatives, ketamine-assisted therapy for anxiety is another option Nushama offers.
How Nushama approaches TMS for anxiety
At Nushama, our psychiatric team designs each TMS protocol individually. For anxiety, that means right DLPFC targeting at the correct frequency, not a default depression protocol applied to every person who walks in.
For members with comorbid depression and anxiety, we use bilateral protocols: sequential stimulation that addresses both hemispheres in the same session. We also coordinate medication management, including careful benzodiazepine tapering where appropriate, to support TMS efficacy.
Structured outcome tracking is part of the process. We use validated measures like the GAD-7 at defined intervals so you can see, in numbers, whether the treatment is working.
If you are exploring TMS for anxiety and want to understand whether it could help, our care team can walk you through the evidence, the protocol options, and what to expect. You can also explore our guides on accelerated TMS protocols, alternative treatments for depression, or non-medication treatment options in Manhattan.
Book an evaluation to discuss whether TMS may help your anxiety symptoms
FAQs
Is TMS FDA-approved for anxiety?
TMS is not currently FDA-cleared for anxiety disorders. It is FDA-cleared for depression and OCD. Its use for anxiety is off-label, meaning clinicians prescribe it based on clinical evidence outside its formal approval. Off-label prescribing is common in psychiatry and accounts for roughly 21% of all prescriptions, according to Radley et al. in Archives of Internal Medicine (2006).
What is the difference between TMS for depression and TMS for anxiety?
The key difference is brain target and frequency. Depression protocols typically use high-frequency (10 Hz) stimulation on the left DLPFC to excite underactive circuits. Anxiety protocols use low-frequency (1 Hz) stimulation on the right DLPFC to calm overactive circuits. Applying the depression protocol to someone with primarily anxiety symptoms can paradoxically increase anxiety.
Can TMS treat both depression and anxiety at the same time?
Yes, through bilateral TMS protocols. Sequential bilateral stimulation targets the left DLPFC (for depression) and then the right DLPFC (for anxiety) in the same session. A preliminary pilot study of comorbid populations showed remission rates of 76.9% for depression and 84.6% for anxiety using this approach, as reviewed in Clinical Psychopharmacology and Neuroscience. Larger trials are needed to confirm these results. A 2024 consensus update from the Clinical TMS Society supports bilateral stimulation as an evidence-based approach.
Does TMS for anxiety have side effects?
The most common side effects of TMS are mild and temporary: scalp discomfort at the stimulation site and occasional headache. Serious side effects are rare. The 2025 meta-analysis of rTMS for GAD reported no serious adverse events compared to medication therapy alone.
How many TMS sessions are needed for anxiety?
Most anxiety-focused TMS protocols involve 20 to 36 sessions, typically delivered over four to six weeks. The bilateral protocol studied in comorbid depression and anxiety populations used 24 to 36 sessions. Your clinician will adjust the treatment course based on your response, tracked through standardized outcome measures.
