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322 The APA Publishing Textbook of Mood Disorders, Second Edition
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The optimal number of TMS sessions or weeks of treatment was not known at the
time each regulatory trial commenced, so several studies planned phases to evaluate
whether additional TMS treatments (after the fixed number delivered in a blinded
acute phase) would bring more patients to the point of response or remission. An
open-label extension trial enrolled 77 participants who had not responded to 6 weeks
of active TMS in the blinded trial and continued to provide daily (five per week) ses
sions for up to 6 additional weeks (Avery et al. 2008). Of these patients who had their
acute course extended beyond 30 sessions, 32% went on to achieve response and 15%
remission with the additional treatments.
An open-label follow-up phase after completion of 3–6 weeks in the blinded phase
in the NIMH-funded trial allowed patients to receive additional 10-Hz sessions (over
the same left DLPFC target) or several weeks of additional 1-Hz treatments above the
right DLPFC (McDonald et al. 2011). The final remission rate climbed to 30% after that
open phase, again suggesting that optimal outcomes for many patients will require
extension of an acute course beyond 3–6 weeks. Data from the continuation phase of
the BrainsWay pivotal trial also underscored this point: 61% of nonresponders follow
ing 4 weeks (20 sessions) of active TMS were “converted” to responders with 4 more
weeks of active treatment delivered on a schedule of two sessions per week (Yip et al.
2017). The “take-home message” from these studies encourages patients and providers to continue with an extension of the acute TMS course when a trajectory of improvement is seen but remission is not achieved at the end of 4–6 weeks.
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Maintenance and Retreatment
Although the durability of the positive effect following an acute course of TMS therapy is considered quite good overall, outcomes do vary, and no treatment modality
to date offers a permanent cure for MDD. A prospective study followed 99 patients
who had significant clinical benefit from their acute course of TMS and were maintained on one antidepressant medication after stopping stimulation (Janicak et al.
2010). Although 38% met criteria for some symptom worsening during the 6-month
follow-up period, most improved when TMS was reintroduced, and only 10% of patients relapsed into a new major depressive episode. Naturalistic data from 257 TMS
patients followed for 1 year showed that 63% of those who initially responded to TMS
maintained their clinically improved state, but 36% of the group had received addi
tional TMS sessions to maintain that status (Dunner et al. 2014). Several studies have
shown that those who respond to or remit with their initial course of TMS are likely
to respond or remit again when they undergo another acute treatment series initiated
at the time of depression relapse (Fitzgerald et al. 2006a; Fukuda et al. 2019; Kelly et
al. 2017).
Several approaches to maintenance TMS treatment have been prospectively investigated to prolong the time until subsequent depressive symptom relapse or episode
recurrence (Fitzgerald et al. 2016; Haesebaert et al. 2018; Philip et al. 2016a; Wang et
al. 2017), including regular or taper treatment schedules, intermittent “clusters” of
maintenance TMS treatments, and symptom-triggered thresholds for repeat treatment series. No consensus has yet been found as to the best schedule or strategy for
using TMS after finishing an initial acute series; it may be that individually custom-
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ized scheduling is needed for each patient because some will remain well for a relatively long period of time and others will experience symptom relapse within days or
weeks after their final acute-phase treatment series. Emerging evidence suggests that
several different maintenance TMS practices are useful for preventing relapse, but
more prospective controlled studies are needed to shape formal guidelines for the
field.
Safety and Clinical Considerations
A meta-analysis of 29 RCTs of TMS (Berlim et al. 2014) reported dropout rates ranging
from 0% to 17.6%, with the exception of one study in which a 45.5% discontinuation
rate was seen in a group assigned to unilateral TMS (Blumberger et al. 2012); the
events reported for that group were not judged to be side effects from stim ulation, per
se, or safety issues directly related to TMS. No difference was found between the
overall dropout rates for high-frequency TMS treatment (7.5%) and sham treatment
(7.6%), suggesting good overall tolerability of treatment with figure-eight coil de
vices. A meta-analysis of 19 studies comparing antidepressant effects between TMS
delivered with H-coils and that with figure-eight coils found comparable treatment
outcomes, although dropout rates were somewhat higher in H-coil trials (Gellersen
and Kedzior 2019). Theta-burst stimulation (TBS), described in detail later, has shown
a comparable safety profile to conventional TMS pattern protocols (Blumberger et al.
2018; Rachid 2017) when delivered with figure-eight coils; serious adverse effects, including seizures, were rare when TBS was delivered over the DLPFC.
Published reports (e.g., Ontario Health [Quality] 2021) and clinical experience
have identified adverse effects attributable to TMS; these are typically mild to mod
erate in severity and transient. Headache (4.5%–60%) can be common, both during
and after TMS application, in the early weeks of a course of treatment. A higher MT
level (and hence, a greater magnetic pulse intensity and a stronger sensation of percussion on the scalp) is related to a more intense headache. Headache associated with
TMS typically resolves with habituation or from the direct analgesic effect of the stim
ulation (Taylor et al. 2012). Notably, TMS does not increase the risk of migraine in a
healthy population or in patients with a history of migraine; on the contrary, singlepulse TMS has been proven to be effective in treating acute migraine (Lipton et al.
2010). Scalp discomfort (4.5%–33% in most clinical trials, 78.9% in one particular trial
[Loo et al. 2007]) is also common and may incorporate twitching or superficial muscle
movements at or near the location of the TMS delivery site, occasionally extending to
facial areas including the ipsilateral eye, ear, nose, or jaw. Nausea and other types of
gastrointestinal discomfort have been reported in conjunction with rTMS (5%–22%),
although in these studies, a similar rate of nausea and gastrointestinal discomfort was
reported in conjunction with sham treatment as well (0%–22%) (Ontario Health [Quality] 2021); however, it is unclear whether events reported in this category are secondary to head pain, anxiety, presyncope, or concurrent medications.
Induction of hypomania has occurred during delivery of high-frequency protocols
and is often preceded by treatment-emergent irritability or agitation (Dolberg et al.
2001). Damage to auditory acuity is a risk associated with some coil models when the
intensity is set to relatively high settings and the delivery of pulse trains from the coil
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emits a loud clicking sound; however, this risk is avoided when ear protection (at least
30 dB noise reduction) is worn (U.S. Food and Drug Administration 2011). Skin burn
from overheating of TMS coils is a theoretical risk; this is now prevented by FDA reg
ulations that require all coils to have sensors that interrupt stimulation when the coil
reaches a preset temperature limit. No evidence has been found of pathological
changes in brain tissue resulting from TMS delivered within the established safety
ranges (Mutz et al. 2019; Rossi et al. 2009; Wassermann 1998), but unknown risks remain for protocols that utilize stimulation parameters outside evidence-based data.
A vasovagal response associated with anxiety, pain, hypoglycemia, or dehydration
may occur in the form of syncope during or after TMS (Wassermann 1998) and should
be differentiated from a TMS-induced seizure. Often similar in appearance to seizure,
syncope can happen during or after TMS applications and mimics seizure on the basis
of diminished consciousness and limb movements (Rossi et al. 2009). Syncope is typ
ically preceded by pallor, dizziness, weakness, visual field changes, and autonomic
changes, and it usually resolves rapidly without the classic postictal confusion that
occurs following seizures. Induction of seizure during TMS is a rare side effect estimated in 2012 to have a risk of 0.003% per treatment for figure-eight coils (Carpenter
et al. 2012); since then, millions of treatments have been delivered safely, and the cur
rent seizure risk is likely much lower. A 2018 seizure estimate for TMS delivered by
H-coils (which might be expected to carry greater seizure risk based on their large
windings and relatively greater volume of current induction in the cortex) was less
than 0.001% (Tendler et al. 2018). To date, TMS-associated seizure almost exclusively
has occurred in patients with preexisting risks, including heavy alcohol use or with
drawal or concurrent use of seizure threshold–lowering medications (Rossi et al.
2009). The seizure tends to be tonic-clonic when it does occur, due to the direct stim
ulation of the motor cortex or adjacent areas spreading neuronal excitation. Constant
observation of patients during TMS application allows for monitoring of signs (e.g.,
movement of contralateral hands or limbs during stimulation trains) that might herald the onset of a TMS-induced seizure.
A 2018 consensus report recommended elements of pre-TMS evaluation and informed consent that are crucial to ensure safe treatment (McClintock et al. 2018). A
comprehensive review of the patient’s medical, surgical, and psychiatric history de
termines indications for and potential risks and benefits of TMS therapy. Such an
evaluation should particularly assess seizure risks and employ screening tools such
as the TMS Adult Safety Screen (Keel et al. 2001) to facilitate quantification of risk fac
tors. Accurate localization of the MT site optimizes stimulation amplitude, thus
avoiding falsely high pulse intensity for treatment and minimizing side effects. Contraindications to TMS include ferromagnetic metal objects (e.g., medical implants,
pacemakers, fragments, nonremovable piercings) in the head and neck areas close to
the coil due to risk of heating or to movement of those objects causing damage to the
surrounding tissues. Metal objects below the head and neck regions are generally
considered safe due to rapid dissipation of the magnetic strength with distance (Deng
et al. 2013).
Patients should be hemodynamically stable and comfortably seated in the TMS
treatment chair, with sufficient support of their spine and adequate ear protection.
Once the treatment session begins, they should be closely monitored. Providers should
inspect the patient’s contralateral hand for twitching or involuntary movements
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during a TMS session as a sign of excitation spread to the motor area, to determine the
need to abort a treatment session or to make parameter adjustments to decrease risk of
possible seizure. Evaluation of changes in sleep and mood, including emergence of
irritability or agitation, should be conducted prior to each TMS application. For headaches or scalp discomfort, over-the-counter analgesics can be taken orally or used topically before or after a TMS session to effectively control the symptoms (Trevino et al.
2011). Reducing the intensity of TMS pulses also enhances tolerability, although evi
dence is limited for antidepressant effects when stimulation intensity is consistently
delivered below 110% MT.
Outside of the indicated populations, the safe therapeutic use and clinical benefit
of TMS have been suggested in preliminary studies of adolescents with depression
(Donaldson et al. 2014; Wall et al. 2011), women with perinatal depression (Kim et al.
2011), and patients with geriatric depression (Sabesan et al. 2015), bipolar disorder
depression (Yatham et al. 2018), or PTSD comorbid with MDD (Philip et al. 2016b).
Cost-Effectiveness
The cost of a standard outpatient acute TMS series (20–40 sessions) to treat MDD
ranges from about $8,000 to $20,000 and remains less costly than a standard course of
electroconvulsive therapy. Analyses have shown that TMS is cost-effective for TRD
(Nguyen and Gordon 2015; Simpson et al. 2009) and non-treatment-resistant depression (Voigt et al. 2017).
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Alternative Protocols for Major Depressive
Disorder
When designing the first therapeutic TMS protocols for MDD, researchers selected
ously published imagining results showing that depressed patients showed decreased
activity in that region, hyperactivity of the right DLPFC (George et al. 1994), and lat
eralized cognitive function abnormalities (Grimm et al. 2008) relative to healthy control subjects. Early TMS experiments identified opposite neuromodulatory effects of
high- versus low-frequency TMS on excitability of cortical neurons in the motor cortex
(Pascual-Leone et al. 1994), and high-frequency stimulation to the left DLPFC was hypothesized to reduce MDD symptoms by addressing a regional deficit in that hemisphere (George et al. 1995). Other parameters and cortical TMS targets have also been
investigated for MDD; notable among them are protocols that deliver low-frequency
(1 Hz) TMS to the right DLPFC (Berlim et al. 2013a), which was hypothesized to
dampen excessive activity in the right hemisphere and was found to be better tolerated than high-frequency stimulation (Feinsod et al. 1998). Subsequent studies evaluated the potential utility of combining both high-frequency TMS on the left side and
low-frequency on the right side with sequential-bilateral stimulation protocols (Berlim et al. 2013b; Fitzgerald et al. 2006b). Efficacy of all three protocols (high-frequency
on left, low-frequency on right, and sequential bilateral) is superior to sham stimula-
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tion, and they appear to produce similar response rates (Berlim et al. 2013a; Chen et
al. 2013, 2014).
“Accelerated” TMS protocols have applied multiple sessions per day to hasten the
antidepressant effect (Sonmez et al. 2019); pilot studies have shown rates of success
comparable with those of standard, once-daily session approaches, but prospective
data showing superiority of accelerated TMS schedules are currently lacking. TMS
treatments on a once-daily schedule (typically five per week on weekdays) define the
standard of care at present.
TBS is a type of TMS pulse pattern originally inspired by observations of neuronal
firing during rodent exploration behaviors in preclinical studies. Complex spike pat
terns were modeled by “bursts” of TMS pulses applied at a high frequency (50 Hz, or
within the gamma frequency band of 30–60 Hz) and repeated approximately every
20 ms (5 Hz, mimicking the endogenous theta band rhythm). Theta-burst-patterned
transcranial stimulation was adapted to human protocols, where it was found to pro
mote superior brain plasticity compared with conventional TMS pulses (Suppa et al.
2016).
Experiments using intermittent TBS delivered at subthreshold intensity (i.e., 80%
MT) were successful for inducing an excitatory effect on neurons when delivered in
protocols containing short (2-second) trains of bursts following 10 seconds of rest
(Huang et al. 2005). Continuous TBS protocols with an 80% MT intensity were likewise found to induce an inhibitory effect on the motor cortex when administered as a
single, uninterrupted train of magnetic bursts (Di Lazzaro et al. 2011). Superior neu
ronal plasticity effects produced by TBS, compared with conventional TMS, eventually
led to clinical investigations wherein TBS protocols were investigated as an alternative
to conventional TMS therapy for the treatment of MDD. Several pilot studies investi
gating intermittent TBS over the left DLPFC for MDD demonstrated efficacy that was
superior to sham (see the meta-analysis by Berlim et al. 2017), raising the exciting pos
sibility that efficacy equivalent to that of the 37-minute standard session could be
achieved with a TMS protocol duration of less than 4 minutes.
Ultimately, a large, randomized noninferiority trial was conducted at three Canadian sites in an open-label study comparing the outcomes of 4–6 weeks of standard
10-Hz stimulation with an intermittent TBS protocol using the Magventure figureeight coil device. This study enrolled and randomly assigned 414 patients with MDD
who were on stable concurrent antidepressants and other psychotropic medications
(Blumberger et al. 2018). Unlike prior studies, the intermittent TBS was delivered at
120% MT in this trial, resulting in patient-rated pain ratings that were significantly
higher than those for the 10-Hz stimulation condition. However, antidepressant efficacy was equivalent between intermittent TBS (which provided a therapeutic dose in
3 minutes) and 10-Hz stimulation (in which each session lasts 37.5 minutes), and the
dropout rate did not differ between the two protocols. These results supported FDA
clearance of intermittent TBS parameters for the Magventure device and several other
devices that have established technical equivalence since then.
Several TMS devices now have FDA clearance for MDD treatment, and all are capable of delivering multiple different stimulation protocols. Although the original
high-frequency left-sided protocols are currently the most commonly utilized as a result of strong evidence from multiple published RCTs, ongoing research into alternatives will continue to advance the field and define future standards.
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Potential Mechanisms of Therapeutic Action
Multiple lines of research inform our understanding of how TMS works to relieve depression. Application of TMS transiently entrains cortical oscillatory rhythms (Brignani et al. 2008; Johnson et al. 2010) and subsequently modulates oscillatory rhythms
(Ding et al. 2014; Fuggetta and Noh 2003) as measured by electroencephalogram. In
terleaved imaging with TMS applied to the PFC shows it immediately induces activation in subcortical limbic regions directly beneath the coil (Li et al. 2004). Other
studies have demonstrated the TMS-associated production of brain-derived neuro
trophic factor (BDNF) and cellular proliferation in the hippocampus (Wang et al.
2014), as well as posttreatment increases in gray matter volume (Lan et al. 2016). This
aligns with a study by Oliveira-Maia et al. (2017) suggesting that a pretreatment mea
sure of brain plasticity in the motor cortex can predict who will respond clinically to
TMS over the left DLPFC.
Neural network dysfunction has been hypothesized to be associated with MDD. A
meta-analysis of resting-state functional MRI (fMRI) data showed specific abnormal
ities in brain connectivity in MDD (Kaiser et al. 2015), particularly hypoconnectivity
with the frontoparietal network (FPN), whose key function is cognitive control or
“top-down” regulation. Hypoconnectivity between the FPN and dorsal attention network (involved in externally oriented attention) is another prominent finding, along
with hyperconnectivity within the default mode network (DMN; involved in inter
nally oriented attention) and hyperconnectivity between the FPN and DMN. Similar
regional deficits have been identified in structural imaging studies, such as increased
cortical thickness in DMN structures and decreased cortical thickness in frontal and
temporal regions (Li et al. 2020).
In recent years, a number of studies have obtained functional MRI or electroencephalographic data before and after a clinical course of TMS for MDD to identify neurobiological markers or mechanisms of its antidepressant effects. A universal mechanism
for the therapeutic action in MDD has yet to be identified, perhaps in part due to the
significant methodological variability of published studies, including various statisti
cal/data analyses (e.g., regions vs. networks; positive vs. negative or anticorrelations),
various modalities of brain assessment, a range of TMS parameters, and diverse stim
ulation targets. An emerging pattern of neuroimaging findings has been described in
published reviews (Anderson et al. 2016; Philip et al. 2018; Taib et al. 2018).
With regard to regional changes observed following a standard course of TMS
therapy, a review by Taib et al. (2018) identified alterations in a range of frontotempo
roparietal and subcortical brain regions: the subgenual anterior cingulate cortex, perigenual anterior cingulate cortex, superior medial frontal gyrus, DLPFC, dorsomedial
PFC, bilateral middle frontal gyri, left precuneus, hippocampus, thalami, putamen,
parietal lobes, insula, right orbitofrontal cortex, and middle temporal cortex. With regard to network-specific findings, changes in the DMN, including activity increases
and its connectivity to other networks, have been one of the most consistent findings;
alterations in the FPN and salience network have also been noted (Anderson et al.
2016; Philip et al. 2018). Researchers have at times noted a surprising lack of findings
in the FPN, given that the left DLPFC is a common site of TMS application and is also
a hub of that network (Philip et al. 2018).
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Additional work has sought to identify specific neurobiological predictors of clinical response to TMS, particularly within the context of the significant clinical heterogeneity found in MDD. One large-scale functional MRI study identified four neurophysiological “biotypes” of depression based on distinct patterns of dysfunctional
connectivity (Drysdale et al. 2017). Although 82.5% of patients with “biotype 1” ex
perienced (>25%) symptom improvement after TMS, only 61% with biotype 2 improved, and less than 30% of patients characterized by biotype 3 or 4 improved.
Clinical symptoms did not predict treatment response, but the authors found that
patterns of connectivity between the dorsomedial PFC (stimulation site) and the left
amygdala, left DLPFC, bilateral orbitofrontal cortex, and posterior cingulate cortex
did predict outcome with 78.3% accuracy.
Of particular relevance to TMS, Padmanabhan et al. (2019) investigated whether
the location of the brain lesion in patients who had had a stroke was associated with
the presence of poststroke depression. Although no single region uniformly led to depression, all lesions that did lead to depression mapped onto the left DLPFC–related
brain circuit, highlighting the potential importance of the left DLPFC as a target for
TMS administration and its relevance to subsequent clinical response. In a related
study by Weigand et al. (2018), connectivity from the stimulation target (location un
der the TMS coil) to the subgenual cingulate region was examined as a function of
clinical TMS outcome. Stimulation sites that were more anterolateral and those that
were negatively correlated with the subgenual cingulate were both associated with a
better TMS treatment response, but only the subgenual cingulate correlation persisted as a significant predictor in a replication cohort. Notably, the subgenual cingulate correlation predicted improvement in cognitive and affective symptoms of MDD
but not somatic symptoms.
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Conclusion
TMS therapy was first introduced into psychiatric practice following the 2008 FDA
clearance of the first device to treat MDD. Since then, it has become a standard of care
for TRD, with numerous clinical studies confirming its efficacy and safety. The field
has evolved with regard to our understanding of TMS’s effects and mechanisms, and
recent exciting work suggests further potential for optimizing TMS outcomes with
the discovery of new biomarkers and application of a personalized medicine approach. TMS therapy has not replaced electroconvulsive therapy but, rather, offers
another option for adult outpatients with MDD who are not benefiting from standard
antidepressant interventions such as pharmacotherapy and psychotherapy.
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