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312 The APA Publishing Textbook of Mood Disorders, Second Edition
https://t.me/med1917
Kleimann A, Kotsiari A, Sperling W, et al: BDNF serum levels and promoter methylation of
BDNF exon I, IV and VI in depressed patients receiving electroconvulsive therapy. J Neu
ral Transm (Vienna) 122(6):925–928, 2015 25387785 Knight F, Ridge D, McShane R, et al: Care, control, and the electroconvulsive therapy ritual:
making sense of polarized patient narratives. Qual Health Res 27(11):1675–1685, 2017
28799472 Kring IS, Bergholt MD, Midtgaard J: The perspectives of former recipients and experts on stig-
matization related to electroconvulsive therapy in Denmark: a focus group study. J Psychi-
atr Ment Health Nurs 25(5–6):358–367, 2018 29758121 Kruse JL, Congdon E, Olmstead R, et al: Inflammation and improvement of depression follow-
ing electroconvulsive therapy in treatment-resistant depression. J Clin Psychiatry
79(2):17m11597, 2018 29489077 Krystal AD, Weiner RD, Coffey CE: The ictal EEG as a marker of adequate stimulus intensity
with unilateral ECT. J Neuropsychiatry Clin Neurosci 7(3):295–303, 1995 7580187 Lambe S, Mogg A, Eranti S, et al: Trends in use of electroconvulsive therapy in South London
from 1949 to 2006. J ECT 30(4):309–314, 2014 24625707 Latey RH, Fahy TJ: Electroconvulsive therapy in the Republic of Ireland 1982: a summary of
findings. Br J Psychiatry 147:438–439, 1985 4075035 Leiknes KA, Cooke MJ, Jarosch-von Schweder L, et al: Electroconvulsive therapy during preg-
nancy: a systematic review of case studies. Arch Women Ment Health 18(1):1–39, 2015
24271084 Lesage A, Lemasson M, Medina K, et al: The prevalence of electroconvulsive therapy use since
1973: a meta-analysis. J ECT 32(4):236–242, 2016 27227401 Letemendia FJ, Delva NJ, Rodenburg M, et al: Therapeutic advantage of bifrontal electrode
placement in ECT. Psychol Med 23(2):349–360, 1993 8332652 Levy A, Taib S, Arbus C, et al: Neuroimaging biomarkers at baseline predict electroconvulsive
therapy overall clinical response in depression: a systematic review. J ECT 35(2):77–83,
2019 30628993 Lima NN, Nascimento VB, Peixoto JA, et al: Electroconvulsive therapy use in adolescents: a
systematic review. Ann Gen Psychiatry 12(1):17, 2013 23718899 Lisanby SH, McClintock SM, Alexopoulos G, et al: Neurocognitive effects of combined electro-
convulsive therapy (ECT) and venlafaxine in geriatric depression: phase 1 of the PRIDE
study. Am J Geriatr Psychiatry 28(3):304–316, 2020 31706638 Luchini F, Medda P, Mariani MG, et al: Electroconvulsive therapy in catatonic patients: efficacy
and predictors of response. World J Psychiatry 5(2):182–192, 2015 26110120 Matthews AM, Rosenquist PB, McCall WV: Representations of ECT in English-language film
and television in the new millennium. J ECT 32(3):187–191, 2016 27008331 McCall WV, Reboussin DM, Weiner RD, et al: Titrated moderately suprathreshold vs fixed
high-dose right unilateral electroconvulsive therapy: acute antidepressant and cognitive
effects (see comments). Arch Gen Psychiatry 57(5):438–444, 2000 10807483 McCall WV, Prudic J, Olfson M, et al: Health-related quality of life following ECT in a large
community sample. J Affect Disord 90(2–3):269–274, 2006 16412519 McDonald WM: Are modern neuromodulation therapies too precise? Pers Med Psychiatry
17:1–3, 2019 McDonald WM, van Rooij SJH: Targeting PTSD. Am J Psychiatry 176(11):894–896, 2019
31672041 McDonald WM, Phillips V, Figielo GS, et al: Cost-effective maintenance treatment of resistant
geriatric depression. Psychiatric Annals 28:47–52, 1998 McDonald WM, Meeks TW, Carpenter LL, et al: Electroconvulsive therapy and other neuro-
modulation therapies, in The American Psychiatric Publishing Textbook of Psychophar-
macology, 5th Edition. Edited by Schatzberg AF, Nemeroff CB. Washington, DC, American
Psychiatric Press, 2017, pp 861–899 Medda P, Perugi G, Zanello S, et al: Comparative response to electroconvulsive therapy in
medication-resistant bipolar I patients with depression and mixed state. J ECT 26(2):82–86,
2010 19710623
-
313 Electroconvulsive Therapy
https://t.me/med1917
Medda P, Mauri M, Toni C, et al: Predictors of remission in 208 drug-resistant depressive pa-
tients treated with electroconvulsive therapy. J ECT 30(4):292–297, 2014a 24625706
Medda P, Toni C, Perugi G, et al: The mood-stabilizing effects of electroconvulsive therapy.
J ECT 30(4):275–282, 2014b 25010031
Medda P, Toni C, Luchini F, et al: Catatonia in 26 patients with bipolar disorder: clinical fea-
tures and response to electroconvulsive therapy. Bipolar Disord 17(8):892–901, 2015 26643014
Minelli A, Congiu C, Ventriglia M, et al: Influence of GRIK4 genetic variants on the electrocon-
vulsive therapy response. Neurosci Lett 626:94–98, 2016 27222927
Moss L, Vaidya N: Does comorbid alcohol and substance abuse affect electroconvulsive ther-
apy outcome in the treatment of mood disorders? J ECT 30(1):22–25, 2014 23859979
Mukherjee S, Sackeim HA, Schnur DB: Electroconvulsive therapy of acute manic episodes: a
review of 50 years’ experience. Am J Psychiatry 151(2):169–176, 1994 8296883
Munk-Olsen T, Laursen TM, Videbech P, et al: Electroconvulsive therapy: predictors and
trends in utilization from 1976 to 2000. J ECT 22(2):127–132, 2006 16801829
Nahas Z, Short B, Burns C, et al: A feasibility study of a new method for electrically producing
seizures in man: focal electrically administered seizure therapy (FEAST). Brain Stimul 6(3):403–408, 2013 23518262
Nilsen SM, Willis KW, Pettinati HM: Initial impression of two new brief-pulse electroconvul-
sive therapy machines. Convuls Ther 2(1):43–54, 1986 11940844
Nivoli AM, Murru A, Goikolea JM, et al: New treatment guidelines for acute bipolar mania: a
critical review. J Affect Disord 140(2):125–141, 2012 22100133
Nobler MS, Luber B, Moeller JR, et al: Quantitative EEG during seizures induced by electrocon-
vulsive therapy: relations to treatment modality and clinical features, I: global analyses. J ECT 16(3):211–228, 2000 11005043
Nordenskjöld A, von Knorring L, Engström I: Predictors of the short-term responder rate of
electroconvulsive therapy in depressive disorders—a population based study. BMC Psy­chiatry 12:115, 2012 22900754
O’Connor MK, Knapp R, Husain M, et al: The influence of age on the response of major depres-
sion to electroconvulsive therapy: a C.O.R.E. report. Am J Geriatr Psychiatry 9(4):382–390, 2001 11739064
O’Reardon JP, Solvason HB, Janicak PG, et al: Efficacy and safety of transcranial magnetic stim-
ulation in the acute treatment of major depression: a multisite randomized controlled trial. Biol Psychiatry 62(11):1208–1216, 2007 17573044
Patel RS, Jain SB, Youssef NA: Electroconvulsive treatment utilization for the inpatient manage-
ment of severe manic episodes of bipolar disorder. J ECT 35(3):195–200, 2019 30870263
Perugi G, Medda P, Zanello S, et al: Episode length and mixed features as predictors of ECT
nonresponse in patients with medication-resistant major depression. Brain Stimul 5(1):18– 24, 2012 22037132
Perugi G, Medda P, Reis J, et al: Clinical subtypes of severe bipolar mixed states. J Affect Disord
151(3):1076–1082, 2013 24074482
Petrides G, Fink M, Husain MM, et al: ECT remission rates in psychotic versus nonpsychotic
depressed patients: a report from CORE. J ECT 17(4):244–253, 2001 11731725
Plakiotis C, George K, O’Connor DW: Has electroconvulsive therapy use remained stable over
time? A decade of electroconvulsive therapy service provision in Victoria, Australia. Aust N Z J Psychiatry 46(6):522–531, 2012 22375067
Pompili M, Dominici G, Giordano G, et al: Electroconvulsive treatment during pregnancy: a
systematic review. Expert Rev Neurother 14(12):1377–1390, 2014 25346216
Puffer CC, Wall CA, Huxsahl JE, et al: A 20 year practice review of electroconvulsive therapy
for adolescents. J Child Adolesc Psychopharmacol 26(7):632–636, 2016 26784386
Raffin M, Zugaj-Bensaou L, Bodeau N, et al: Treatment use in a prospective naturalistic cohort
of children and adolescents with catatonia. Eur Child Adolesc Psychiatry 24(4):441–449, 2015 25159089
Rapoport MJ, Mamdani M, Herrmann N: Electroconvulsive therapy in older adults: 13-year
trends. Can J Psychiatry 51(9):616–619, 2006 17007229
314 The APA Publishing Textbook of Mood Disorders, Second Edition
https://t.me/med1917
Rasmussen KG: Do patients with personality disorders respond differentially to electroconvul-
sive therapy? A review of the literature and consideration of conceptual issues. J ECT
31(1):6–12, 2015 25054362 Rasmussen KG, Mueller M, Rummans TA, et al: Is baseline medication resistance associated
with potential for relapse after successful remission of a depressive episode with ECT?
Data from the Consortium for Research on Electroconvulsive Therapy (CORE). J Clin Psy
chiatry 70(2):232–237, 2009 19192459 Redlich R, Opel N, Grotegerd D, et al: Prediction of individual response to electroconvulsive
therapy via machine learning on structural magnetic resonance imaging data. JAMA Psy
chiatry 73(6):557–564, 2016 27145449 Rootes-Murdy K, Carlucci M, Tibbs M, et al: Non-suicidal self-injury and electroconvulsive
therapy: outcomes in adolescent and young adult populations. J Affect Disord 250:94–98,
2019 30844603 Ross EL, Zivin K, Maixner DF: Cost-effectiveness of electroconvulsive therapy vs pharmaco-
therapy/psychotherapy for treatment-resistant depression in the United States. JAMA
Psychiatry 75(7):713–722, 2018 29800956 Rush AJ, Aaronson ST, Demyttenaere K: Difficult-to-treat depression: a clinical and research
roadmap for when remission is elusive. Aust N Z J Psychiatry 53(2):109–118, 2019 30378447 Saatcioglu O, Tomruk NB: The use of electroconvulsive therapy in pregnancy: a review. Isr J
Psychiatry Relat Sci 48(1):6–11, 2011 21572236 Sackeim HA: Central issues regarding the mechanisms of action of electroconvulsive therapy:
directions for future research. Psychopharmacol Bull 30(3):281–308, 1994 7878177 Sackeim HA, Prudic J, Devanand DP, et al: The impact of medication resistance and continua-
tion pharmacotherapy on relapse following response to electroconvulsive therapy in ma-
jor depression. J Clin Psychopharmacol 10(2):96–104, 1990 2341598 Sackeim HA, Prudic J, Devanand DP, et al: Effects of stimulus intensity and electrode place-
ment on the efficacy and cognitive effects of electroconvulsive therapy (see comments).
N Engl J Med 328(12):839–846, 1993 8441428 Sackeim HA, Devanand DP, Nobler M: Electroconvulsive therapy, in Psychopharmacology:
The Fourth Generation of Progress. Edited by Bllom FE, Kupfer DJ. New York, Raven,
1995, pp 1123–1142 Sackeim HA, Prudic J, Devanand DP, et al: A prospective, randomized, double-blind compar-
ison of bilateral and right unilateral electroconvulsive therapy at different stimulus inten-
sities (see comments). Arch Gen Psychiatry 57(5):425–434, 2000 10807482 Sackeim HA, Haskett RF, Mulsant BH, et al: Continuation pharmacotherapy in the prevention
of relapse following electroconvulsive therapy: a randomized controlled trial (see com-
ments). JAMA 285(10):1299–1307, 2001 11255384 Sackeim HA, Prudic J, Fuller R, et al: The cognitive effects of electroconvulsive therapy in com-
munity settings. Neuropsychopharmacology 32(1):244–254, 2007 16936712 Sackeim HA, Prudic J, Nobler MS, et al: Effects of pulse width and electrode placement on the
efficacy and cognitive effects of electroconvulsive therapy. Brain Stimul 1(2):71–83, 2008
19756236 Sahlem GL, Short EB, Kerns S, et al: Expanded safety and efficacy data for a new method of per-
forming electroconvulsive therapy: focal electrically administered seizure therapy. J ECT
32(3):197–203, 2016 27379790 Scangos KW, Weiner RD, Coffey EC, et al: An electrophysiological biomarker that may predict
treatment response to ECT. J ECT 35(2):95–102, 2019 30531398 Shoirah H, Hamoda HM: Electroconvulsive therapy in children and adolescents. Expert Rev
Neurother 11(1):127–137, 2011 21158560 Sienaert P: Based on a true story? The portrayal of ECT in international movies and television
programs. Brain Stimul 9(6):882–891, 2016 27522170 Spellman T, Peterchev AV, Lisanby SH: Focal electrically administered seizure therapy: a novel
form of ECT illustrates the roles of current directionality, polarity, and electrode configu-
ration in seizure induction. Neuropsychopharmacolo
gy 34(8):2002–2010, 2009 19225453
-
-
315 Electroconvulsive Therapy
https://t.me/med1917
Spodniaková B, Halmo M, Nosáľová P: Electroconvulsive therapy in pregnancy—a review.
J Obstet Gynaecol 35(7):659–662, 2015 25526509
Steffens DC, Krystal AD, Sibert TE, et al: Cost effectiveness of maintenance ECT. Convuls Ther
11(4):283–284, 1995 8919583
Sun Y, Farzan F, Mulsant BH, et al: Indicators for remission of suicidal ideation following mag-
netic seizure therapy in patients with treatment-resistant depression. JAMA Psychiatry 73(4):337–345, 2016 26981889
Taylor MA, Fink M: Catatonia in psychiatric classification: a home of its own. Am J Psychiatry
160(7):1233–1241, 2003 12832234
Tew JD Jr, Mulsant BH, Haskett RF, et al: Relapse during continuation pharmacotherapy after
acute response to ECT: a comparison of usual care versus protocolized treatment. Ann Clin Psychiatry 19(1):1–4, 2007 17453654
Thase ME, Rush AJ: When at first you don’t succeed: sequential strategies for antidepressant
nonresponders. J Clin Psychiatry 58 (suppl 13):23–29, 1997 9402916
Tørring N, Sanghani SN, Petrides G, et al: The mortality rate of electroconvulsive therapy: a sys-
tematic review and pooled analysis. Acta Psychiatr Scand 135(5):388–397, 2017 28332236
Trenton A, Pelchat R: Medical students’ perceptions of electroconvulsive therapy: the impact
of direct exposure. J ECT 32(1):20–22, 2016 26075694
Unal A, Altindag A, Demir B, Aksoy I: The use of lorazepam and electroconvulsive therapy in
the treatment of catatonia: treatment characteristics and outcomes in 60 patients. J ECT 33(4):290–293, 2017 28640169
Valentí M, Benabarre A, García-Amador M, et al: Electroconvulsive therapy in the treatment of
mixed states in bipolar disorder. Eur Psychiatry 23(1):53–56, 2008 18191551
van Diermen L, van den Ameele S, Kamperman AM, et al: Prediction of electroconvulsive ther-
apy response and remission in major depression: meta-analysis. Br J Psychiatry 212(2):71– 80, 2018 29436330
van Waarde JA, Scholte HS, van Oudheusden LJ, et al: A functional MRI marker may predict
the outcome of electroconvulsive therapy in severe and treatment-resistant depression. Mol Psychiatry 20(5):609–614, 2015 25092248
Vieta E: Bipolar mixed states and their treatment. Expert Rev Neurother 5(1):63–68, 2005
15853475
Vukadin M, Birkenhäger TK, Wierdsma AI, et al: Post-dexamethasone cortisol as a predictor for
the efficacy of electroconvulsive therapy in depressed inpatients. J Psychiatr Res 45(9):1165–1169, 2011 21481419
Wachtel LE, Dhossche DM, Kellner CH: When is electroconvulsive therapy appropriate for
children and adolescents? Med Hypotheses 76(3):395–399, 2011 21129852
Ward HB, Fromson JA, Cooper JJ, et al: Recommendations for the use of ECT in pregnancy: lit-
erature review and proposed clinical protocol. Arch Women Ment Health 21(6):715–722, 2018 29796968
Watts BV, Groft A: Retrospective evaluation of the dexamethasone suppression test as a predic-
tor of response to electroconvulsive therapy in patients with comorbid major depressive disorder and posttraumatic stress disorder. J ECT 26(3):213–217, 2010 20386115
Watts BV, Groft A, Bagian JP, et al: An examination of mortality and other adverse events re-
lated to electroconvulsive therapy using a national adverse event report system. J ECT 27(2):105–108, 2011 20966769
Yao Z, McCall WV, Essali N, et al: Precision ECT for major depressive disorder: a review of clin-
ical factors, laboratory, and physiologic biomarkers as predictors of response and remis­sion. Pers Med Psychiatry 17:23–31, 2019
Youssef NA, McCall WV: Relapse prevention after index electroconvulsive therapy in treat-
ment-resistant depression. Ann Clin Psychiatry 26(4):288–296, 2014 25401716
Yrondi A, Sporer M, Péran P, et al: Electroconvulsive therapy, depression, the immune system
and inflammation: a systematic review. Brain Stimul 11(1):29–51, 2018 29111078
Zhand N, Courtney DB, Flament MF: Use of ele
treatment-resistant depressive disorders: a case series. J ECT 31(4):238–245, 2015 25830809
ctroconvulsive therapy in adolescents with
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CHAPTER 19
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Transcranial Magnetic
Stimulation
Andrew M. Fukuda, M.D., Ph.D.
Brian C. Kavanaugh, Psy.D.
Shiwen Yuan, M.D.
Linda L. Carpenter, M.D.
As is evident throughout this textbook, major depressive disorder (MDD) is a
debilitating and widespread illness, with 19.4 million adults (18 years or older) in 2019 having at least one major depressive episode in the United States alone, accord­ing to the National Institute of Mental Health (NIMH; Substance Abuse and Mental Health Services Administration 2020). Although pharmacotherapy is successfully able to treat many, a substantial portion of those with MDD have limited responses to medications or develop intolerable side effects, so alternative treatment options are necessary.
Transcranial magnetic stimulation (TMS) is a noninvasive method for therapeutic modulation of brain activity. Although it has been increasingly used since 1985 (Barker and Cain 1985; Barker et al. 1985) as a research tool to elucidate certain aspects of brain function, TMS has been further developed and clinically utilized for treating pa­tients with pharmacoresistant forms of MDD. Since the FDA cleared the first TMS de­vice (Neuronetics, Malvern, Pennsylvania; 510[k] number: K083538) to treat MDD in 2008, multiple other devices have received regulatory approval for that same thera­peutic indication. In 2018, a TMS device received the first FDA clearance for treatment of patients with obsessive-compulsive disorder (OCD), and a portable TMS device was FDA-cleared for treatment of migraine in 2013. Clinical research continues to ex­plore the potential for TMS to treat a broad array of neuropsychiatric disorders and symptoms related to behavioral health, addiction, and overall wellness. However, the focus of this chapter is the use of TMS for MDD.
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What Is Transcranial Magnetic Stimulation Therapy?
Application of TMS requires the delivery of a pulsed magnetic field from a TMS “coil” placed on the patient’s head. The coil contains multiple windings of copper wire (or other material that conducts electricity) covered by a hard case and a cooling mecha nism of some sort; electricity traveling through the coil in a fluctuating manner gener­ates an electromagnetic field that is emitted from the coil and passes through skin, bone, and other cranial tissues without impedance, subsequently exerting its effects on the targeted regions of superficial cortex several centimeters below the surface. Con sistent with Faraday’s law of electromagnetic induction, pulsed magnetic fields from the TMS coil induce an electrical current in a perpendicular plane in the underlying tis sues, which translates to the firing of neuronal action potentials when the intensity is at a certain threshold.
TMS coils can be constructed with internal windings in various shapes and sizes; most TMS therapy devices use a simple figure-eight-shaped coil, but one manufac turer has a system that uses larger and more complex coil geometries (known as He­sed or H-coils). Figure-eight coils deliver a stimulation that is fairly focal, whereas H­coils activate a broader area of cortex. In stationary TMS device systems such as those approved for MDD, one or more components provide electricity to the coil from a standard power source, and an integrated computer allows the clinician to select pa­rameters for the desired protocol. Some systems include, or are capable of integration with, additional components to enhance their functionality, such as a robotic arm to hold the coil on the patient’s head, gauges marking coordinates in multiple planes for frameless stereotaxis, or tracking tools and software to guide placement of the coil to a specific area on the patient’s scalp (or MRI-guided navigation to stimulate a specific target in the patient’s brain).
Standard commercial TMS devices emit magnetic pulses with a strength similar to that of a standard MRI scanner to patients who are awake and in a seated or reclined position. With each pulse, the person receiving TMS experiences a mild percussive sensation on the head underneath the coil, but this is generally well tolerated, and pa­tients accommodate to it after several sessions (Borckardt et al. 2013). No anesthesia or sedation is required, and patients drive themselves to and from their daily outpa tient treatment sessions. Immediate physiological after-effects of a single TMS appli­cation last about 30 minutes, but a series of repeated sessions (typically 20–30 over 4– 6 weeks) is needed to produce enduring resolution of MDD symptoms.
Clinicians may choose from several parameters for delivering TMS therapy. Some of these parameters relate to the targeted brain region; for MDD, the target is most often the left dorsolateral prefrontal cortex (DLPFC), but evidence also exists for treatment over the right DLPFC or midline areas of the prefrontal cortex (PFC). Other parameters describe the characteristics of the magnetic energy itself—that is, relative intensity (strength of the magnetic field), frequency (number of magnetic pulses delivered per second [Hz]), pulse pattern (e.g., standard “trains” of pulses at 10 Hz vs. very rapid “bursts” or pulses delivered at a 5-Hz “carrier frequency”), and duration of the “rest” times between the strings of TMS pulses. Additional clinically relevant treatment pa­rameters relate to how many total pulses a patient is given in a single session, how often the treatment sessions occur (typically once daily, 5 days per week), and how
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many treatment weeks compose a standard course of acute therapy for the disorder (typically 4–6 weeks, followed by additional treatments in a taper schedule).
Motor Threshold Procedure
One of the personalized-medicine features of TMS therapy relates to the fact that the intensity of stimulation is individually customized and calibrated against each pa tient’s unique level of cortical excitability. A standard procedure done on the first day of a course of treatment involves finding the exact location on the patient’s scalp that corresponds with the underlying spot in that patient’s primary motor cortex where stimulation with a single TMS pulse generates the most robust response. With the cor­rect placement, neurons connect, via corticospinal tracts and peripheral nerves, to produce a motor-evoked potential (identified as a visible “twitch” or alternatively by the peak amplitude of an evoked potential as measured by electromyogram) in the muscles of the fingers on the contralateral hand. This location on the scalp, along with the minimum intensity of magnetic energy required to elicit the contralateral muscle response, together define the “motor threshold” (MT).
Finding the MT location and determining the MT level are the first steps in deliv­ery of TMS; application of TMS therapy sessions without this step could adversely impact both safety and efficacy because other treatment parameters are calibrated rel ative to a patient’s MT. Data suggest no significant difference exists between MT lev­els determined by electromyogram and those determined by visual observation of a muscle twitch (Badran et al. 2019), so most clinical TMS devices rely on the latter method. MT level is the basis for knowing what intensity of stimulation is likely to modulate the activity of cortical neurons in a patient’s brain. The FDA-cleared MDD treatment protocols involve delivery of TMS at 120% intensity relative to the MT level. This means that the intensity of all magnetic pulses targeting the PFC during a treatment session is 20% higher than the minimal (threshold) intensity needed for a single pulse to activate specific neurons in the patient’s motor cortex as determined during the MT procedure on the first day.
The functional MT location on a patient’s scalp is also a parameter that may subse­quently guide placement of the coil on another area of the scalp for treatment of depres­sion. The MT location (defined as the motor cortex location that optimally activated the contralateral thumb muscle or proximal hand muscles) is used by many to navi­gate the TMS coil to a scalp location (5–6 cm anteriorly in a parasagittal line) over the DLPFC for therapeutic stimulation. Although this method for finding the scalp target for delivery of stimulation to the left DLPFC was employed in all MDD regulatory tri als, research has subsequently shown that fixed measurements from the MT location are not consistently reliable for targeting that brain region (Herwig et al. 2001).
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Use in Pharmacoresistant Major Depressive Disorder
At present, FDA-cleared TMS devices for MDD are specifically indicated for use in patients whose illness has failed to respond to at least one antidepressant medication
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trial during the current depressive episode (hereafter referred to as treatment-resistant depression, or TRD). The first FDA clearance (in 2008) for a TMS device (with figure­eight coil) followed a series of regulatory trials by Neuronetics. Results of a large reg ulatory trial using an H-coil TMS device by BrainsWay (Jerusalem, Israel) generated the second FDA clearance for MDD in 2013. Since then, other device manufacturers have sought and achieved FDA clearance to market their TMS devices in the United States without conducting any new regulatory clinical trials; these approvals have been based on demonstration of technical equivalence to the Neuronetics device—that is, having similar figure-eight coils and stimulation features.
The TMS parameters and protocols for TRD used in the two major industry-spon­sored sham-controlled regulatory trials (Neuronetics and BrainsWay) consisted of high-frequency (10 Hz and 18 Hz, respectively) pulses administered in short trains (4 and 2 seconds, respectively) at an intensity that was 120% of the patient’s MT, inter spersed with rest periods without any stimulation (20 and 26 seconds, respectively). The targeted area of the brain was the left DLPFC, although the broad area covered by the H-coils also delivered some stimulation to the right DLPFC. Treatment ses­sions were given 5 days per week for 4–6 weeks. Because large samples were used to demonstrate efficacy and safety in randomized, sham-controlled trials that employed rigorous and standardized methods across multiple study sites, these parameters de­fine the “doses” of TMS that are considered to have the strongest evidence base for clinical care.
Numerous other TMS clinical trials investigating different parameters or ap­proaches to TMS therapy have also been published, both before and after the two seminal FDA approvals. Several studies employing alternate designs (e.g., prospec tive open-label trials, randomized noninferiority trials, naturalistic treatment studies, and meta-analyses of pooled data from multiple smaller studies) provide varying de grees of compelling evidence that it is also safe and efficacious to administer TMS us­ing various different stimulation parameters. Some of these have resulted in revision or extension of the original FDA-approved “labels” and now appear in the official “indication for use” documents associated with individual TMS devices. Results from several key investigations shaping the current evidence base for TMS to treat MDD are summarized in the discussion that follows.
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Acute Efficacy
Three double-blinded randomized controlled trials (RCTs) comparing outcomes in groups receiving either active or sham treatments played pivotal roles in the establish­ment of TMS as an effective acute therapy for MDD. O’Reardon et al. (2007) reported acute-phase results of the Neuronetics-sponsored RCT that took place at 23 interna tional sites (in the United States, Canada, and Australia) and included 301 medication­free patients. Both response and remission rates were significantly higher in the active group (24% response and 17% remission, respectively) compared with the sham-treat­ment group (15% response and 8% remission, respectively) after 6 weeks of treatment (30 sessions).
Results of a subsequent RCT funded by NIMH and without industry sponsorship was published in 2010 by George et al. (2010). Neuronetics’ TMS devices (which have
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figure-eight-shaped coils) were donated to four university study sites where treat­ments were delivered using the same stimulation parameters reported by O’Reardon et al. (2007) during the blinded acute phase (n=190). Unique features of this study in cluded a variable-length blinded phase (continuation beyond 3 weeks was contingent on threshold clinical improvement) and brain MRI evaluation to determine whether the position of the coil should be advanced anteriorly by another 1 cm (beyond the spot found, 5 cm anterior to the MT location) to target the left DLPFC. Activation of face and scalp muscles with small electrodes during stimulation trains was a method used to make the sham TMS feel more like active TMS and thus optimize the blinding. The response rate was 15% and remission rate 14% for the group treated with active TMS, whereas only 5% of sham-treated patient outcomes achieved both response and remission. The odds for remitting with active stimulation were 4.2 times greater than for remitting with sham (George et al. 2010).
A third clinical trial of marked importance in establishing TMS clinical efficacy for MDD was the pivotal RCT sponsored by BrainsWay (Levkovitz et al. 2015) using H­coil devices targeting the bilateral (predominantly left, but also right) DLPFCs in 212 patients with TRD at 20 different study sites across four countries. After 4 weeks (20 sessions), all participants transitioned to a schedule of two sessions per week for an­other 12 weeks, during which they received the same (blinded) active or sham stim­ulation. Acute-phase response and remission rates at week 5 (after 22 sessions) were significantly higher in the active group (37% and 30%, respectively) than for sham­treated subjects (28% and 16%, respectively). These results supported FDA clearance of the BrainsWay H-coil TMS device for TRD.
Following FDA clearance of the Neuronetics device and its early uptake by clinical practices, a large multisite naturalistic treatment study confirmed similar efficacy for patients with MDD who were treated outside of research protocols with the device (Carpenter et al. 2012). This study reflected “real-life” TMS clinical practice, where most patients are taking one or more antidepressant or other psychotropic medica tions at the time of referral and remain on concurrent medication during the TMS treatment course. Outcomes for 307 patients (whose treatment costs were supported by their health insurance or through self-pay) across 42 clinics demonstrated that about half (42%–58%, depending on which scale is used) of patients were responders (defined by at least 50% improvement from baseline) and approximately one-third reached the threshold scores for remission (27%–37% across three measures). These findings were largely consistent with other open-label data, such as the crossover phase in the Neuronetics regulatory trial (Avery et al. 2008).
Despite the apparent consistency of positive results across regulatory RCTs and naturalistic and open trials, a recent RCT investigating TMS in 164 U.S. veterans with TRD failed to demonstrate statistical superiority of active stimulation over sham TMS. Following 20–30 sessions (4–6 weeks) of blinded 10-Hz TMS sessions delivered by a figure-eight coil device, remission was achieved by 41% of those randomized to the active group and 37% randomized to the sham group (Yesavage et al. 2018). Co­morbid PTSD emerged as a slight moderator of inferior outcomes, but the authors speculated that a high sham response rate in this study was likely attributable to the frequent contact veteran participants had with study personnel and other clinicians who not only monitored their participation in the trial’s procedures but also enforced adherence to concurrent psychiatric medications.
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