TMS Information for Patients

  • TMS stands for Transcranial Magnetic Stimulation. TMS is a non-invasive treatment that uses a magnetic field to stimulate nerves in the brain.

  • FDA indications for TMS include:

    • Major Depressive Disorder

    • OCD

    • Smoking cessation

    Most insurance carriers will cover TMS treatment for MDD and OCD.

    TMS can also be used to treat anxiety disorders like Generalized Anxiety Disorder.

  • Common side effects include:

    • Headache

    • Irritation near magnet placement

    • lightheadedness

    • Seizure

    • Mania

    • Hearing loss

  • TMS is typically conducted in an outpatient setting like an office. A typical course is 5 days a week for 36 treatments. (This may be different for an accelerated schedule which is explained below) An individual treatment can take anywhere between 3.5 to 40 minutes depending on the type of TMS machine being used, the indication and the individual settings of the machine.

    The TMS machine can be loud so it is recommended that patients wear ear plugs to minimize the risk of hearing loss. There are no driving restrictions so patients can drive themselves to and from treatment. Unlike ECT, TMS has no cognitive side effects and there is no anesthesia required.

  • Only a trained and experienced physician can tell you if you are a good candidate for TMS. Having said this, TMS may be appropriate for you if you are finding it difficult to control your depression symptoms with more traditional treatments like medications, psyhotherapy, lifestyle modifications etc.

  • Patients with the following should avoid TMS:

    • Seizure history

    • Implanted metal in head, neck or face

    • Cochlear implants

    • Cardiac pacemakers, vagal nerve stimulators or medication pumps

    • Patients actively abusing substances

  • The data indicate that TMS is not as effective as ECT but has a much more favorable side effects profile.

    • no anesthesia

    • no cognitive side effect

    • no driving restrictions

    • no systemic effects (GI upset, sexual side effects, etc. like some people can get from medicaions)

    • reduced time off from work for above mentioned reasons

  • TMS Society Patient and Family Information Page

    Dr. Nolan Williams Youtube interview

TMS Information for Clinicians

How does a TMS machine work?

  • A TMS machine works by sending an electrical current through a wire coil which produces a magnetic field. The coil (magnetic field) is placed next to the patient’s head in specific areas which has an induction effect on the neurons. This magnetic field causes the neurons in the brain to depolarize which can have a stimulatory or inhibitory effect based on the anatomic location and machine settings.

There are different targets that have different effects on the brain. One of the most common targets is the dorsal lateral prefrontal cortex on the left side of the brain. This area has been implicated in depression and is the target for many treatment protocols. Please see diagram below.

A common target for OCD utilizing deep TMS is the anterior cingulate cortex (aCC) and the medial prefrontal cortex (mPFC) as illustrated below. It takes a larger magnetic field to reach these areas as they are deeper in the brain.

What are the different types of coils?

  • Figure eight coil

  • H-Coil

  • Double Cone Coil

    There are other types but these are the most commonly used in FDA approved TMS treatment devices. One thing to consider is the trade off between increased magnetic field size like the H coil (able to penetrate deeper brain structures) and decreased target specificity. As your magnetic field gets bigger it is less focused and more broad.

For further technical information on coil types you may review Deng et al. 2016.

What are the different types of TMS?

  1. rTMS: This stands for “repetitive” TMS. It is the type of TMS that you are most likely to find in a clinical setting. This type of TMS can be used to treat depression and anxiety. This is typically delivered using a figure 8 coil magnet. rTMS involves giving a series of pulses, at a certain intensity, at a certain frequency for a certain duration of time. This set of pulses is often referred to as the “train.” The trains are followed by a rest period that can vary in duration.

rTMS can be delivered with:

  • High frequency: This is often referred to as “standard TMS.” (> 1 pulse per secnd) Typically delivered over Left Dorsal Lateral Prefrontal Cortex (lDLPC). This tends to have a stimulatory effect on the targeted area.

    • A typical treatment with high frequency left sided DLPC targeting will have 3000 pulses per session. This will typically involve 10 pulses per second (10 hz) at 100-120% MT (strength of magnetic field) with a pulse train lasting 4 seconds. A treatment session usually consists of 75 trains spaced approximately 10-50 seconds apart. This means the treatment will take approximately 17-54 minutes depending upon the machine settings.

  • Low frequency: (1 pulse per second or less) Typically delivered over right Dosal Lateral Prefrontal Cortex (rDLPC). This tends to have an inhibitory effect on the targeted area.

    • A typical treatment with low frequency right sided DLPC targeting will have a frequency of 1 hz (1 pulse per second) or less for 15-20 minutes for a total of 900 -1200 pulses per treatment session.

2. Deep TMS: Not all TMS machines can do “deep” TMS. This involves an “H” coil which is different than a figure eight coil. This creates a slightly larger magnetic field that is able to penetrate deeper into the brain. The pulse parameters tend to be similar to rTMS as noted above. The benefits are that it can effect deeper structures but the area affected is much larger and thus (less targeted) compared to TMS using a figure 8 coil. An H coil can be used for MDD, OCD and even smoking cessation treatment. There is some evidence that it is less tolerated compared to other types of TMS. There was however a study by Filipcic et al. 2019 that compared regular “cortical” rTMS to “deep” TMS. The remission rates in the two groups were comparable but the response rates were higher in the deep TMS group (67%) vs. (44%) in the rTMS group.

3. iTBS: This stands for intermittent theta burst. Intermittent Theta burst TMS is a specific frequency of stimulation which is comprised of 50 hz frequency triplet bursts firing at a frequency of 5 hz for 2 seconds. This equals 30 pulses in a 2 second period. This is typically followed by an 8 second pause before the next train. (hence the term intermittent) The goal is to get 600 pulses per treatment. Obviously this cuts down the treatment time. A typical treatment duration is around 3.5 minutes.

Theta is a brain wave frequency between 4-7 hz. It is thought to be the frequency at which different parts of the brain communicate with each other. It is thought that treating at this frequency may help tune into the brains natural frequencies.

Theta burst TMS is a specific rhythm characterized by 3 pulse bursts at a rate of 50 hz. Those triplet pulses at 50 hz occur at a frequency of 5 hz. This occurs for 2 seconds in duration with an 8 second pause before the next train. This is referred to as intermittent theta pulse. There is also continuous theta burst which would continue without pause.

  • Intermittent theta burst or iTBS is safe and just as effective as rTMS but it requires only 600 pulses which can be completed in around 3.5 minutes where as rTMS requires 3000 pulses per treatment and typically takes anywhere between 17 and 40 minutes to complete.

  • Bulteau et al. 2022 compared iTBS with rTMS. Response rates were 36.7% and 33.3%, and remission rates were 18.5% and 14.8%, in the iTBS and 10 Hz rTMS groups respectively. This paper concludes that iTBS is just as effective as rTMS and is probably more cost effective.

4. aTMS: aTMS stands for accelerated TMS. Accelerated TMS is any TMS protocol that involves more than one treatment session per day. A study by Caufield et al. 2022 reviewed 63 different studies with 43,837 different aTMS sessions with 1543 participants. This review looked at safety, side effects and efficacy. With accelerated programs the seizure rate was 0.0023% vs. 0.0075% with once daily TMS. The most common side effects listed with aTMS were headaches, fatigue and scalp discomfort. The efficacy was reviewed of aTMS in 23 depression studies which showed a response rate of 42.4% and a remission rate of 28.4%. The treatment protocols ranged from 2-10 sessions per day with 2-30 treatment days, 10-640 minutes between sessions for a total of 9-104 total sessions per patient. This paper stated, “qualitatively response rate tends to be higher with an increasing number of sessions per day, total sessions, and total pulses.”

5. SAINT or SNT: SAINT stands for Stanford accelerated intelligent Neuromodulation therapy. SNT stands for Stanford Neuromodulation Therapy. They are the same protocol just renamed for branding purposes.

  • Cole et al. 2020 (SAINT) was an open label, accelerated, fMRI targeted TMS study looking at efficacy and safety in patients with Major Depressive Disorder with an N of 22. All patients received baseline fMRI to target the region of the left DLPFC most anticorrelated with sgACC. All patients then received 10 minutes of iTBS with 50 minute breaks for a total of 10 treatments per day for a total of 5 days. (180 pulses per minutes with iTBS x 10 = 1800 pulses per 10 minute session x 10 sessions = 18,000 pulses per day x 5 days = 90,000 pulses for total treatment course) The study found 86.4% - 90.5% of patients achieved remission by end of day 5. Neuropsychological testing demonstrated no negative cognitive side effects

  • Cole et al. 2022 (SNT) was a randomized, double blind, comparison of the SAINT TMS protocol with sham TMS. The primary outcome measure was change in MADRS score from baseline to week 4 post treatment. With an n of 29, the mean percent reduction from baseline in MADRS score 4 weeks after treatment was 52.5% in the active treatment group and 11.1% in the sham treatment group. Secondary measures included remission and response rates. In the treatment group 86.7% met response criteria (a reduction ≥50% in MADRS score) vs. 26.7% in the sham group in atleast one of the 5 posttreament assessments. In the treatment group, 78.6% met remission criteria (a MADRS score ≤10) vs. 13.3% in the sham group in the 4 week follow up period.

What are the methods used to correctly target the correct brain region?

  • 5.5 cm method: This method involves stimulating the motor strip causing isolated movement in the contralateral abductor policies bravis muscle. (Thumb) We then move the magnet 5.5 cm anterior from that point.

  • Beam method: This method involves taking three different measurements and calculating the DLPC location from those measurements. The measurements include ear tragus to tragus, nasion to inion, and head circumference. These measurements are put into a formula which gives two numbers. The first number is the distance from the centerline that should be marked. (on a patient cap) Then the second number is the distance from the vertex of the head to the first marked point. Beam method formula can be found here.

  • 10-20 method: Involved EEG leads which can be time and labor intensive. This is usually reserved for research settings.

  • Anatomic MRI: This method involves a patient undergoing a brain MRI with a special stereotactic headgear that can be used as a reference point. The patient then wears this head gear in a treatment room where a special camera can determine the exact location of the DLPC based on the MRI data. This is a costly method that does not necessarily lead to better outcomes. Li et al. 2020 concluded, “Left prefrontal piTBS monotherapy is effective for the treatment of recurrent depression, and the MRI-guided method of coil targeting is not better than the standard method.”

  • Functional MRI: It is hypothesized that depression arises from aberrantly functioning brain networks. Hadas et al. 2019 found “The findings of this study further implicate left DLPFC-SGC effective connectivity and SGC excitability in the pathophysiology of MDD and treatment with rTMS. These findings suggest that DLPFC-SGC connectivity may be a marker of rTMS treatment responsiveness.” This is the method utilized in the saint protocol.

For further reading on the various methods please refer to Zhang et al. 2021.

TMS Evidence:

  • For Major Depressive Disorder:

  • Schutter et al. 2010: This study was a meta analysis of studies that compared double blinded sham-controls to TMS for treatment of depression symptoms. This study showed “a significant overall weighted mean effect size, d=0.39 [95% confidence interval (CI) 0.25-0.54], for active treatment was observed (z=6.52, p<0.0001)".” The paper concluded that high frequency rTMS over the left DLPFC was better than sham TMS. They commented that the effect size was compared to antidepressant medications.

  • Dunner et al. 2014: This study was a multisite, naturalistic, observational study looking at effectiveness of TMS in patients with Major Depressive Disorder who did not benefit from medication management. 257 patients completed a course of acute TMS treatment and consented to follow-up over 52 weeks. Assessments were obtained at 3, 6, 9, and 12 months with Clinical Global Impressions- Severity of illness scale, Inventory of Depression Symptoms- Self Report, 9-Item Patient Health Questioniare. 53% of all patients met remission or response criteria after the acute series. Among 120 patients who met IDS-SR response or remission criteria at the end of acute treatment, 75 (62.5%) continued to meet response criteria throughout long-term follow-up.(1 year) After the first month, when the majority of acute TMS tapering was completed, 93 patients (36.2%) received reintroduction of TMS. In this group, the mean (SD) number of TMS treatment days was 16.2. The conclusions of this study were that TMS demonstrated a statistically and clinically meaningful durability of acute benefit over 12 months of follow-up.

  • Senova et al 2019: This study was a systematic review and meta analysis of depression outcomes 3 months (732 patients), 6 months ( 695 patients) and 12 months (247 patients) after a course of TMS. Among initial responders, 66.5% sustained response at 3 months following treatment (95% CI = 57.1-74.8%, I2 = 27.6%), 52.9% at 6 months following TMS (95% CI = 40.3-65%, I2 = 0%), and 46.3% at 12 months (95% CI = 32.6-60.7%, I2 = 0%) The study concluded that “rTMS is a durable treatment for depression, with sustained responder rates of 50% up to 1 year after a successful induction course of treatment. Maintenance treatment may enhance the durability of the antidepressant effects of rTMS, and should be considered in clinical practice, as well as systematically explored in future clinical trials.”

  • Sackeim et al. 2020: This study was an evaluation on the registry data of 7759 patients in 103 practice sites who had a diagnosis of MDD and received a course of TMS. 5010 patients were included in an intent-to-treat (ITT) analysis. Response (58-83%) and remission (28-62%) rates were notably high across self-report and clinician-administered assessments. The paper concluded, “Strong efficacy and the low side effect and medical risk profile suggest that TMS be evaluated as a first-line treatment for MDD. The findings derive from the largest registry of clinical outcomes in MDD for any treatment.”

  • Via et al. 2023: This study looked at, “19 randomized double-blinded sham-controlled studies were included for quantitative analysis for response (n = 854 patients) and 9 studies for remission (n = 551 patients). The risk ratio (RR) for response and remission are 2.25 and 2.78, respectively for patients after two treatment failures using rTMS as add-on treatment compared to standard pharmacotherapy. Cochrane’s Q test showed no significant heterogeneity. No publication bias was detected.” 9 of the studies had remissions rates which were 35.71% in the active rTMS group and 8.37% in the sham rTMS group.

  • For Anxiety:

  • Cox et al. 2022: This paper is a systematic review and meta-analysis of patients with either Generalized Anxiety Disorder or Panic Disorder receiving rTMS and what effect the rTMS had on their symptom rating scales. The paper looked at 13 different studies with 677 patients total, 404 of which were in the treatment group and 273 did not receive rTMS) Per Cox et al, “In GAD patients with or without any comorbidities, rTMS therapy demonstrated significant improvements in anxiety (SMD = 1.45; P < .001) and depression (SMD = 1.65; P < .001) scores regardless of rTMS parameters. Overall anxiety (SMD = 0.24; P = .48) and panic severity (SMD = 1.19; P = .054) scores did not significantly improve after rTMS therapy in patients with PD.” Therefor, the study concludes that rTMS can be a safe and effective treatment for improving anxiety scores in GAD.

  • For Obsessive Compulsive Disorder:

  • Carmi et al. 2019: This study was a multi-center, randomized, double-blind, sham controlled trial comparing deep TMS with sham TMS for the treatment of OCD. Both treatment and sham groups had 29 treatment sessions with 5 treatment days per week for 5 weeks then 4 treatment days the 6th week with one day for assessments. The primary outcome measure was change in YBOC score 6 weeks after treatment initiation. The active treatment group received 20 hz frequency dTMS at 100% MT with 2 second pulse trains and 20 second intervals between trains. This totaled 50 trains or 2000 pulses per treatment session. The primary outcome measure was change in YBOC which was -6 points for treatment group (95% CI 4.0-8.1) and -3.3 points for the sham group (95% CI 1.2, 5.3). Effect size was 0.69. Secondary measures included response rate which was 45.2% in the treatment group and 17.8% in the sham group.

  • Gersner et al. 2019: This paper looked at two different studies, one of a multicenter study where patients received active dTMS (n=42) and an open label sample (n = 26). All patients received YBOC assessments weekly. The YBOC scores reduced by 8.6 + or - 0.8 or a 30.1% reduction from baseline through week 6 of treatments. (P < 0.001) 60.3% had a partial response as defined by atleast 20 percent decrease in YBOCS. 47.1% of patients met response criteria which is atleast a 30 % reduction in YBOCS.

How long does TMS last?

  • Like any other psychiatric treatment, TMS is not a cure for depression. Individual results can vary from patient to patient. There is no good way to predict whether or not someone will respond to TMS let alone how long the improvement will last. Some the data below may be helpful in answering some of these questions.

    • Per the Dunner et al. 2014 study, 53% of patients met criteria for response/remission. 36.2% of those patients received some sort of taper after their acute series of 36 treatments. At 1 year follow up 62.5% of those that responded or remitted still met criteria fo response. In other words 12 months after starting TMS, 33% of all patients in this study continued to meet response criteria. It is confounded by some of the patients receiving more than a standard course of 36 treatments.

    • Per the Senova et al 2019 study, among initial responders, 66.5% sustained response at 3 months following treatment, 52.9% at 6 months and 46.3% at 12 months. The study concluded that “rTMS is a durable treatment for depression, with sustained responder rates of 50% up to 1 year after a successful induction course of treatment. Maintenance treatment may enhance the durability of the antidepressant effects of rTMS, and should be considered in clinical practice, as well as systematically explored in future clinical trials.”

How does low frequency rTMS compared to traditional left-sided high frequency TMS?

The data suggest right sided, low-frequency, rTMS is just as effective as traditional left sided, high frequency TMS. It may have less side effects and have a lower risk of seizure.

  • Berlim et al 2013: This was a meta-anaylsis of randomized, double-blind, sham controlled trials investigating the effectiveness of low frequency right sided r TMS. This study included 8 RCT studies with an n of 263. This study showed 34.6% of those receiving low frequency, right sided rTMS met criteria for remission. 9.7% in the sham group met remission criteria.(OR=3.35; 95% CI=1.4–8.02; p=0.007) This study also demonstrated 38.2% of the active group met response criteria vs. 15.1% in the sham group. (OR=4.76; 95% CI=2.13–10.64; p<0.0001). The study concluded, “LF-rTMS is a promising treatment for MD, as it provides clinically meaningful benefits that are comparable to those of standard antidepressants and high-frequency rTMS. Furthermore, LF-rTMS seems to be an acceptable intervention for depressed subjects.”

  • Chen et al 2013: This was a systematic review and meta-analysis of 8 randomized studies comparing high frequency (HF) left sided r TMS with low frequency (LF) right sided r TMS. There was an N of 249. The two treatments were comparable. (odds ratio (OR) = 1.15; 95% confidence interval = 0.65-2.03).The study concluded, “The pooled examination demonstrated that both rTMS methods were equally effective therapies for MDD. However, considering that LF right-sided rTMS produces fewer side effects and is more protective against seizures, its clinical applicability shows greater promise and should be explored further.”

How effective is TMS compared to ECT?

  • Berlim et al. 2014: This study was a review and meta analysis comparing the effectiveness of TMS vs. ECT. Data included 7 randomized trials (n = 294) with all subjects having Major Depressive Disorder. After an average of 15.2 HF-rTMS sessions 33.6% of subjects met remission criteria and after an average of 8.2 ECT sessions, 52% of subjects met remission criteria (OR = 0.46; p = 0.04). This study concluded that ECT was more effective than HF-rTMS for treating MDD.

How does TMS work for depression?

The exact mechanism by which TMS alleviates symptoms of depression remains elusive. There is some evidence that it possibly restores aberrantly functioning neurocircuits that are implicated in depression. There is evidence that certain networks (in depressed patients) are not functioning the same as healthy controls .

Think of TMS as exercising the DLPC so that it can be strong enough to do its normal role and function properly.

Weigand et al 2018 showed “functional connectivity between an individual's rTMS cortical target (DLPC) and the subgenual cingulate predicts antidepressant response.”

Per Furtado et al. 2013, neuroimaging showed increased in left amygdala volume in those patients with symptom improvement and non-responders showed a decline in left hippocampus volumes. The study stated, “rTMS may promote neurogenesis or other effects that favor neuronal plasticity.”

Peters et al. 2016: This paper is nothing but a powerhouse in terms of its descriptions of the neurological underpinnings of depression. It goes into vivid detail about the CSTS (cortico-striatal-thalamic-cortical) loop. It also describes some key functional networks.

Background Information: The term Salience Network or SN. The salience network is per Peters et al. 2016, “ proposed to play a key role in cognitive control (Ham et al. 2013), i.e., switching brain activity between introspective, ruminative functions of the default-mode network and externally focused, task-based functions of the central executive network (Menon and Uddin, 2010).” The SN has connections to dorsal anterior cingulate cortex (dACC), the anterior insula(AI) the dorsal lateral prefrontal cortex (dlPFC) and the inferior partial lobule. It also connects to the caudate nucleus, the mediodorsal nucleus of the thalamus (MDN) and dopanergic nuclei in the brain stem. The Peters paper states,”Together, these structures complete a discrete cortico-striatal-thalamic-cortical (CSTC) loop that can be discerned using structural or functional neuroimaging.”

Schimmelpfenning: Another powerhouse for understanding brain networks and how they may be implicated in certain behaviors, actions or certain psychiatric phenomenon like depression.

The SN may play a ket role in being a switch between the DMN (Default mode network) (autobiographical memory, introspection, mental time travel, thinking of others intentions) and the FP (Frontoparietal Network) (task selection and executive functioning according to Schimmelpfenning et al. 2023 . The paper goes on to say the DMN is comprised of posterior cingulate cortex (PCC), precuneus, and ventromedial prefrontal cortex (VMPFC). The frontal parietal network has notes in the Lateral posterior parietal cortex (PPC) and the dorsal lateral prefrontal cortex (DLPC)

The paper states “The SN functions as a dynamic switch between concentration on self and the inner world, mediated by the DMN, and task-related and directed attention on outside stimuli maintained by the FPN”

  • “A central role of the SN is filled by the insula, acting as a gatekeeper of executive control. Thanks to a widespread connectivity fingerprint, its posterior part integrates signals from within the body with external stimuli. Then, the interaction of the anterior and posterior parts of the insula moderates autonomic reactions and generates a signal sent to the anterior cingulate cortex (ACC), selectively intensifying salient stimuli that require further cortical analysis. The right dAIC is considered to be a unique brain region, functioning as a hub that influences both the FPN and DMN (Uddin, 2015). A strong negative correlation between the DMN and FPN relates to the higher efficiency of executive functions (Posner et al., 2016; see Figure 2)”

  • “All of the above results seem consistent with the SN model and suggest that AI overactivation leads to excessive sensitivity and anxiety arousal, and maybe a joint transdiagnostic characteristic in numerous conditions. This is likely related to the low excitability threshold of the structures that make up the SN (particularly the right AI) and the classification of excessive stimuli as important. This leads to the generalization and over-mobilization of stress reactions in non-threatening situations (Menon and Uddin, 2010; Hermans et al., 2014).”

McTeague et al. 2017 investigated common neural circuits that are disrupted in a variety of psychiatric conditions. The study compared 5,728 healthy controls with 5,493 patients with different psychiatric diagnosis including Major Depressive Disordfer, Bipolar DIsorder, Schizophrenia, Anxiety disorders and Substance use disorders. The study showed, “abnormal activation was evident in the left prefrontal cortex as well as the anterior insula, the right ventrolateral prefrontal cortex, the right intraparietal sulcus, and the midcingulate/presupplementary motor area. Disruption was also observed in a more anterior cluster in the dorsal cingulate cortex, which overlapped with a network of structural perturbation that the authors previously reported in a transdiagnostic meta-analysis of gray matter volume.” The paper then concluded, “the anterior-cingulo-insular or "salience network" demonstrated to be transdiagnostically vulnerable to gray matter reduction. Thus, networks intrinsic to adaptive, flexible cognition are vulnerable to broad-spectrum psychopathology.”

Salience Network (SN):

Nodes in

  • dorsal anterior cingulate cortex (dACC)

  • bilateral insula

Default Mode Network (DMN):

  • posterior cingulate (PCC)

  • Precuneus

  • Ventromedial Prefrontal cortex (VMPFC)

FP:

connects the lateral posterior parietal cortex (PPC) and the dorsolateral prefrontal cortex (DLPFC)

TMS appears to have a connection to the vagus nerve which can affect the heart. TMS stimulation of the DLPC will cause the heart rate to decrease.

According to Iseger et al. 2019, iTBS applied to the DLPF can affect decrease heart rate. This study also showed showed a correlation between the degree to which HR changes from baseline and clinical response. The study concluded, “Active iTBS applied to the DLPFC is able to transsynaptically modulate the autonomic ner- vous system, in particular the parasympathetic branch, similar to what has been found for conventional rTMS methods. Furthermore, data suggest that the larger the autonomic changes induced at baseline, the better the clinical response after 30 sessions of iTBS.”

DLPC- sgacc- Insula- amgydala- Nucleus tractus solitarius - vague nerve

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