ECT: A Clinical Reference

Overview

Modern ECT bears little resemblance to its early-20th-century origins. It is performed under general anesthesia with muscle relaxation, titrated to individual seizure threshold, delivered with brief or ultrabrief-pulse square-wave stimulation, and monitored continuously with EEG and EMG. Despite 85+ years of clinical use, it remains the most effective treatment available for severe or treatment-resistant depression.

This page is organized to serve as a day-to-day working reference. The first half covers the practical aspects of delivering ECT: schedule, placement, dosing, medications, procedure, physics, and calculations. The second half covers background and context: history, mechanism of action, efficacy evidence, cognitive side effects, and special populations. The page ends with referral information for the Prisma Health Neuromodulation Program.

ECT schedule

A standard ECT course is divided into three phases: index, continuation, and maintenance. The specific cadence is individualized based on response trajectory, side effect burden, and relapse risk.

Index course

Index ECT is typically given 3 times per week, conventionally Monday / Wednesday / Friday. An average index course runs 9–12 treatments, though this varies considerably. Some patients respond after 6 sessions; others may require 15 or more to reach maximal benefit. The clinical plateau (two or more consecutive treatments without additional gain) is a reasonable indicator to transition out of the index phase.

Some centers use twice-weekly index scheduling, which produces comparable end-point efficacy with somewhat reduced cognitive burden at the cost of slower time-to-response. The choice depends on urgency, patient tolerance, and logistics.

Continuation

The continuation phase follows the index course and lasts approximately 6 months. Its purpose is to prevent early relapse during the high-risk post-index window. A typical taper:

• Week 1 post-index: 1 treatment
• Weeks 2–4: every 1–2 weeks
• Months 2–3: every 2–3 weeks
• Months 4–6: every 3–4 weeks

Maintenance

Maintenance ECT refers to treatments delivered more than 6 months after the index course, aimed at preventing recurrence. Frequency is individualized: monthly is common, but intervals of 6–8 weeks are also well-tolerated for stable patients. Indications favoring long-term maintenance ECT:

• Multiple prior episodes with rapid relapse off ECT
• Intolerance or inadequate response to continuation pharmacotherapy
• History of psychotic depression (higher recurrence risk)
• Strong prior response to ECT relative to other modalities

Maintenance ECT and continuation pharmacotherapy are not mutually exclusive; many patients do best on a combined strategy, particularly during the first year after an index course.

Lead placement

The three commonly used electrode configurations are bitemporal (bilateral), right unilateral (RUL), and bifrontal. Each has a distinct efficacy-to-cognitive-side-effect profile.

Common ECT electrode placements: bilateral (bitemporal), right unilateral (RUL), and bifrontal.

Dosing

ECT dose is properly expressed as electrical charge (millicoulombs), a function of amplitude, frequency, pulse width, and duration. Higher doses produce more reliable seizures and may work faster — but at the cost of increased cognitive burden. Individualized titration balances these tradeoffs.

Why titrate?

Seizure threshold varies across patients by a factor of 40 or more. Fixed-dose approaches risk either under-dosing (subthreshold, inefficacious) or over-dosing (supratherapeutic, unnecessarily cognitively burdensome). Titration determines the individual seizure threshold at the first treatment, then dose subsequent treatments as a defined multiple of that threshold.

• Bitemporal / bifrontal: 1.5–2× seizure threshold is adequate for efficacy. Higher doses add cognitive burden without improving outcomes.
• Right unilateral: 5–6× seizure threshold is standard. Doses below 2.5× ST have minimal efficacy — this is the most common error in RUL ECT.

Dosing schedules

The dosing tables below reflect a standard titration approach used in clinical practice — originally developed and refined at the University of Michigan ECT program and broadly representative of current best practice.

Bilateral (bitemporal / bifrontal) titration schedule. Starting dose is determined empirically at the first treatment; subsequent treatments dose at approximately 1.5× seizure threshold.

Right unilateral titration schedule. Because RUL requires markedly suprathreshold dosing for efficacy, the titration curve is steeper and the maintenance dose is approximately 5–6× seizure threshold.

Practical notes and interpretation tips for the RUL titration schedule.

Seizure quality assessment

Duration alone is an incomplete measure of adequate ECT. Beyond the 25–60 second target window, seizure quality is assessed by:

• Ictal EEG morphology — high-amplitude polyspike activity, clear postictal suppression
• Postictal suppression index — higher isoelectric percentage post-ictally correlates with stronger seizure
• Heart rate response — adequate tachycardic response indicates adequate seizure generalization
• Midictal EEG amplitude — higher amplitudes correlate with greater clinical benefit

Adequate duration with poor quality (low amplitude, minimal postictal suppression, blunted HR response) warrants technical adjustment rather than simply continuing the course.

ECT medications

Most patients receive several medications at each ECT treatment, administered via IV. A typical regimen includes an anesthetic, a paralytic, an analgesic, an antiemetic, and an antimuscarinic. Doses are individualized to body mass, anesthetic response, and specific requirements.

The procedure itself

A typical ECT treatment visit runs 90–120 minutes door-to-door. The procedure itself — from anesthesia induction through wake-up — takes about 10–15 minutes.

1. Arrival and check-in (15–20 min): NPO status confirmed, vital signs, brief clinical assessment covering interval symptom changes and any side effects from the prior session, informed consent reviewed.
2. IV and monitoring setup (10–15 min): IV access, EKG, pulse oximetry, BP cuff, bilateral frontomastoid EEG electrodes, stimulation electrodes per planned placement, tourniquet on one limb for cuff-isolated motor seizure observation.
3. Pre-oxygenation and induction (3–5 min): 100% O2 via mask, anesthetic administered IV, followed by paralytic. Bite block placed before stimulation.
4. Stimulus delivery and seizure (1–2 min): Once the patient is adequately paralyzed and fasciculations have subsided, stimulus delivered. Seizure duration monitored on EEG and on the cuffed limb. Ideal seizure duration 25–60 seconds.
5. Immediate recovery (5–10 min): Mask ventilation until spontaneous respiration resumes, then supplemental O2. Continuous vital sign monitoring.
6. PACU-equivalent recovery (45–90 min): Extended observation until the patient is fully oriented, ambulating safely, tolerating PO, and meeting standard discharge criteria.

Common intra-procedure events and management

• Hypertensive surge: Expected and usually transient. Pre-treat with labetalol or esmolol in patients with cardiovascular disease or unusually large HR/BP responses.
• Bradycardia or asystole: Brief post-stimulation vagal response. Glycopyrrolate often given prophylactically, particularly for subthreshold stimulations and with propofol anesthesia.
• Prolonged seizure (>2 min): Terminate with midazolam or additional methohexital; ensure adequate ventilation throughout.
• Missed or inadequate seizure: Reassess anesthetic dose, consider hyperventilation before restimulation, check stimulus parameters and electrode contact; caffeine can be added for subsequent treatments if the pattern persists.
• Postictal agitation or confusion: More common in older patients. Ensure oxygenation, minimize sensory input, low-dose benzodiazepine if severe.

Physics of ECT

ECT dose is fundamentally a question of delivered electrical charge. Understanding the physics clarifies why modern parameter choices (square wave, brief/ultrabrief pulse, biphasic delivery) improve efficacy-to-side-effect ratios.

Waveform

Early ECT devices delivered a sine wave — the natural waveform of alternating household current. This waveform is highly inefficient for neuronal depolarization: much of the delivered charge is "wasted" on subthreshold portions of the wave that don't contribute to depolarization but do contribute to cognitive side effects. Modern devices deliver a square wave, which is approximately equal in efficacy to sine-wave stimulation while requiring substantially less total charge.

Sine wave (top, older ECT devices) vs. square wave (bottom, modern ECT devices). Square-wave stimulation produces equivalent efficacy with substantially reduced charge and cognitive burden.

Most modern devices deliver a biphasic (bidirectional) square wave, effectively doubling the frequency — this must be accounted for in charge calculations.

Waveform parameters

Four parameters together determine the delivered dose:

• Amplitude (mA) — peak current, typically 800–900 mA in modern devices
• Frequency (Hz) — pulses per second (doubled for biphasic waveforms)
• Pulse width (ms) — duration of each individual pulse
• Train duration (s) — total duration of the stimulus

The four parameters that together determine delivered charge: amplitude, frequency, pulse width, and train duration.

Pulse width: brief vs. ultrabrief

Pulse width matters because neuronal chronaxie — the minimum time needed to produce depolarization at twice rheobase — is approximately 0.1–0.2 ms (Geddes 1987). Pulses longer than this are "wasted" charge from a depolarization standpoint.

• Brief pulse (0.5–1.5 ms): Standard modern waveform. Efficient relative to sine wave; produces adequate seizures with modest charge.
• Ultrabrief pulse (<0.5 ms, typically 0.25–0.37 ms): More closely matches cortical neuron chronaxie. Requires less total charge to produce seizures and is associated with significantly reduced cognitive side effects (Sackeim 2008). When paired with suprathreshold RUL stimulation, efficacy is preserved; with subtherapeutic RUL dosing, ultrabrief pulse can underperform.

Brief pulse vs. ultrabrief pulse. Ultrabrief pulse (<0.5 ms) more closely matches cortical neuron chronaxie and reduces cognitive burden when paired with adequate RUL dosing.

Calculations

The math behind ECT dosing, at a level sufficient for parameter adjustments and ballpark understanding of device settings.

Charge (dose)

ECT dose is measured in millicoulombs (mC). One coulomb equals approximately 6.24 × 10¹⁸ electrons. Since charge equals current times time:

Energy delivered

Energy depends on the impedance between the electrodes (typically 100–300 Ω in adequately prepped patients):

Voltage

Voltage follows from energy and charge:

For most clinical purposes, the important number is charge in millicoulombs. Device interfaces express dose either as a percentage of maximum output, directly in mC, or as individual parameter settings. What's happening mechanically is the same: a specified amount of electrical charge, delivered over a specified duration, at a specified amplitude.

A brief history of ECT

Modern practice looks almost nothing like its origins. Knowing the history clarifies both the current technique decisions and the persistent stigma surrounding the treatment.

Mechanism of action

We understand ECT's clinical effects far better than its mechanisms. The field has converged on a multi-system model rather than any single pathway.

Monoamine system

Similar to pharmacologic antidepressants, ECT modulates synaptic serotonin, norepinephrine, and dopamine. Receptor sensitivity changes follow, leading to adaptive changes in the function of mood-relevant circuits. The monoamine framework alone, however, cannot explain ECT's speed or its efficacy in medication-refractory cases.

Neurotrophic factors

ECT robustly upregulates BDNF (Brunoni 2014) and VEGF (Minelli 2011). Animal models show upregulation of c-Fos, Egr1, Neuritin 1, BDNF, SNAP-29, synaptotagmin III, synapsin I, and PSD-95 (Dyrvig 2014). The clinical correlation between BDNF changes and symptom improvement has not been consistently established, but the pattern of neurotrophic upregulation is reproducible.

HPA axis

Elevated cortisol is a common finding in severe depression. ECT appears to normalize HPA-axis dysregulation (Haskett 2014). Whether this is a direct therapeutic mechanism or a downstream effect of clinical improvement remains debated.

Functional connectivity

Resting-state fMRI studies show ECT alters connectivity in depression-relevant networks. Beall 2012 demonstrated increased connectivity from the anterior cingulate cortex to the right dorsolateral prefrontal cortex and posterior cingulate cortex, with correlation to clinical improvement. Other studies (Abbott 2013, Li 2013, Posner 2013) have found less consistent connectivity-outcome correlations. More recent work has focused on subgenual cingulate and default-mode network changes.

GABA and glutamate

ECT increases cortical GABA (Esel 2008), contributing to anticonvulsant effects observed over the course. Glutamatergic modulation — acute increases in glutamate release followed by NMDA and AMPA receptor downregulation — is also well-described.

Neuroplasticity at the network level

Hippocampal volume increases after a course of ECT are a reliable MRI finding; the clinical significance remains debated. The volume change correlates with both antidepressant response and with cognitive side effects in different studies. Hippocampal enlargement may be a marker of a broader plasticity response rather than a specific therapeutic mechanism.

Evidence & outcomes

ECT has one of the largest evidence bases in psychiatry, including multiple RCTs against sham and head-to-head trials against pharmacotherapy and other neuromodulation.

ECT vs. sham ECT

The UK ECT Review Group (2003) summarized 6 RCTs (n=256) of real vs. sham ECT, with a pooled effect size of −0.91 (95% CI −1.27 to −0.54) in favor of real ECT. The review also concluded that ECT was significantly more effective than pharmacotherapy (18 trials, n=1144, SES −0.80).

Anderson 2021 reviewed 11 sham-controlled RCTs and 5 meta-analyses, concluding that "despite their methodological differences, there is a consistent direction in the findings of the RCTs of at least a numerical benefit for ECT over sham ECT... and all meta-analyses report a significant pooled result in favor of ECT."

Response and remission rates

Parameter-specific comparative data

• Sackeim 1987 (n=52): Low-dose bilateral ECT (70% response) vs. low-dose RUL (28%). Early demonstration that RUL requires suprathreshold dosing.
• Sackeim 1993 (n=96): Threshold vs. 2.5×threshold, bilateral vs. RUL. Response rates: 2.5×ST bilateral 63%, threshold bilateral 65%, 2.5×ST RUL 43%, threshold RUL 17%.
• Sackeim 2000 (n=80): High-dose bilateral (150% above ST) and high-dose RUL (500% above ST) both 65% response; low-dose RUL substantially worse (30–35%).
• McCall 2000: Fixed-dose 403 mC RUL 67% response vs. 2.25×ST RUL 39%. Higher RUL doses produce better outcomes.
• Sackeim 2008: Ultrabrief RUL non-inferior to brief-pulse RUL for efficacy, with markedly reduced cognitive burden.
• Kolshus 2017 (meta-analysis): High-dose RUL comparable to bitemporal for efficacy; RUL superior for reorientation time and retrograde memory.

ECT vs. other treatments

Continuation treatment: the Sackeim 2001 CUC trial

Continuation treatment is not optional. Sackeim 2001 (the Columbia University Consortium trial) randomized 84 ECT-remitted patients to three continuation regimens:

The CORE continuation trial (Kellner 2006) found continuation ECT non-inferior to combination pharmacotherapy for relapse prevention. For patients who cannot tolerate lithium or tricyclics, modern regimens substitute SSRIs/SNRIs + lithium or lamotrigine, with somewhat less robust supporting evidence.

Cognitive side effects

Cognitive effects are the most-discussed, most-feared, and most-important side effect of ECT. Their management is central to modern practice.

Domains of effect

• Acute postictal confusion: Universal; resolves spontaneously within minutes to hours.
• Anterograde memory impairment: Difficulty forming new memories during the course. Detectable on neuropsychological testing; typically resolves within weeks of course completion.
• Retrograde amnesia: Loss of memories from the period around treatment. Recent events are more affected than remote events (Ribot's law).
• Autobiographical memory gaps: The most persistent and patient-relevant effect. A minority of patients report long-lasting difficulty recalling specific life events from before or during treatment. Severity and duration are variable.
• Global cognitive slowing: Word-finding difficulty, reduced processing speed. Typically resolves within weeks to months.

The Semkovska 2010 meta-analysis

Semkovska and McLoughlin (2010) meta-analyzed cognitive outcomes across ECT studies, finding that most cognitive abnormalities are limited to the first 3 days post-treatment, and that pre-treatment functioning is subsequently recovered. Beyond day 15, processing speed, working memory, anterograde memory, and some aspects of executive function actually improve beyond baseline — almost certainly reflecting the lifting of depression-related cognitive impairment.

Technique choices that reduce cognitive burden

• RUL placement over bitemporal
• Ultrabrief pulse width over brief pulse (when paired with adequate suprathreshold dosing)
• Twice-weekly scheduling over thrice-weekly, when urgency permits
• Minimum effective stimulus dose rather than ceiling dosing
• Methohexital or etomidate over propofol when seizure threshold elevation is a concern
• Discontinuation of benzodiazepines and anticholinergics during the course when clinically feasible

Special populations

Older adults

ECT is more effective in older adults than younger adults, with higher remission rates and faster response. Older patients experience more cognitive side effects but these are typically transient, and medication side effects are often substantially more problematic than ECT in this population. For severe depression in elderly patients — particularly with cardiovascular comorbidity that limits pharmacologic options — ECT is often the safest effective treatment available.

Pregnancy

ECT is safe throughout pregnancy and is sometimes preferred over pharmacologic treatment to avoid fetal medication exposure. Practical considerations: obstetric consultation per gestational age, left lateral uterine displacement during procedure in the second and third trimesters, anesthetic selection with fetal considerations in mind. No trimester is specifically contraindicated.

Psychotic depression

Remission rates in psychotic depression approach 80%, substantially higher than with pharmacotherapy combinations. ECT should be considered early (often first-line) rather than after multiple medication failures.

Bipolar disorder

Effective for both bipolar depression and mania. Unlike pharmacologic antidepressants, ECT does not typically precipitate mood switching. Monitor lithium levels carefully around the ECT course — the combination of high lithium levels with ECT may increase cognitive burden.

Catatonia

First-line for catatonia is high-dose lorazepam. ECT is indicated for:

• Benzodiazepine-refractory catatonia (typically after 2–5 days of adequate trial)
• Malignant catatonia with autonomic instability or hyperthermia
• Neuroleptic malignant syndrome unresponsive to supportive management

Response is often dramatic, with substantial improvement possible within 1–3 treatments.

Medical comorbidities

• Cardiovascular disease: Not an absolute contraindication. Most patients can be safely treated with appropriate anesthetic management and pre-treatment (beta-blockade where indicated). Recent MI (typically <3 months) is the highest concern.
• Parkinson's disease: ECT improves both mood and motor symptoms in PD; motor effects are transient but often meaningful.
• Epilepsy: Not a contraindication. Anticonvulsant-related elevated seizure threshold may require higher stimulus dose or brief medication holds.
• Dementia: Not a contraindication, but requires baseline neuropsychological assessment and conservative dosing choices.
• Intracranial lesions: Small, stable lesions without mass effect are typically not contraindications. Unstable aneurysms, recent hemorrhage, or lesions with meaningful mass effect warrant deferral and neurosurgical consultation.

Referring a patient

How ECT referrals flow through the Prisma Health Neuromodulation Program.

Referral pathway

1. Initial referral call or faxed referral form to the Neuromodulation Program at the Behavioral Health and Wellness Pavilion
2. Records review by the coordination team; additional records requested as needed
3. Outpatient ECT consultation scheduled (typically 1–3 weeks out for non-urgent; expedited for urgent/inpatient referrals)
4. Medical clearance and anesthesia evaluation scheduled
5. Treatment course scheduled at the appropriate facility — inpatient at Greenville Memorial Hospital; outpatient at Baptist Hospital Columbia or Baptist Easley Hospital depending on geography and clinical factors

What to include in a referral

• Demographics and contact information
• Primary diagnosis and target symptoms for ECT
• Medication history with doses, durations, and responses (a summary list is fine)
• Psychotherapy history
• Prior neuromodulation (TMS, ketamine, prior ECT) with response
• Medical comorbidities and current medications
• Recent psychiatric evaluation or hospitalization records
• Cognitive concerns or baseline neuropsychological assessment, if available
• Urgency level (active suicidality, inpatient status, catatonia)

Urgent referrals

Flag as urgent:

• Active suicidality with severe depression unresponsive to medications
• Severe inanition or catatonia
• Severe psychotic depression
• Currently inpatient requiring rapid definitive treatment
• Pregnancy with severe psychiatric illness where medications are contraindicated
• Neuroleptic malignant syndrome unresponsive to supportive care

References

Key sources cited throughout this page. Organized thematically rather than in order of appearance.

Efficacy and outcomes

1. UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet 2003;361(9360):799–808. PMID: 12642045
2. Anderson IM. Electroconvulsive therapy (ECT) versus sham ECT for depression: do study limitations invalidate the evidence (and mean we should stop using ECT)? BJPsych Advances 2021;27(5):285–291.
3. Meechan CF, Laws KR, Young AH, McLoughlin DM, Jauhar S. A critique of narrative reviews of the evidence-base for ECT in depression. Epidemiol Psychiatr Sci 2022;31:e10.
4. Espinoza RT, Kellner CH. Electroconvulsive Therapy. N Engl J Med 2022;386(7):667–672. PMID: 35172057
5. Belge JB, van Eijndhoven P, Mulders PCR. Mechanism of action of ECT in depression. Curr Top Behav Neurosci 2024;66:279–295.
6. Semple DM, Suveges S, Steele JD. Electroconvulsive therapy response and remission in moderate to severe depressive illness: a decade of national Scottish data. Br J Psychiatry 2024;225(6):547–555.

Electrode placement and dosing

1. Sackeim HA, Decina P, Kanzler M, Kerr B, Malitz S. Effects of electrode placement on the efficacy of titrated, low-dose ECT. Am J Psychiatry 1987;144(11):1449–1455. PMID: 3314538
2. Sackeim HA, Prudic J, Devanand DP, et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med 1993;328(12):839–846. PMID: 8441428
3. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;57(5):425–434. PMID: 10807482
4. McCall WV, Reboussin DM, Weiner RD, Sackeim HA. Titrated moderately suprathreshold vs fixed high-dose right unilateral electroconvulsive therapy. Arch Gen Psychiatry 2000;57(5):438–444. PMID: 10807483
5. 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 2008;1(2):71–83. PMID: 19756236
6. Kolshus E, Jelovac A, McLoughlin DM. Bitemporal v. high-dose right unilateral electroconvulsive therapy for depression: a systematic review and meta-analysis of randomized controlled trials. Psychol Med 2017;47(3):518–530. PMID: 27780482
7. Pisvejc J, Hyrman V, Sikora J, et al. A comparison of brief and ultrabrief pulse stimuli in unilateral ECT. J ECT 1998;14(2):68–75.
8. Kho KH, van Vreeswijk MF, Simpson S, Zwinderman AH. A meta-analysis of electroconvulsive therapy efficacy in depression. J ECT 2003;19(3):139–147.

Mechanism of action

1. Brunoni AR, Baeken C, Machado-Vieira R, et al. BDNF blood levels after electroconvulsive therapy in patients with mood disorders: a systematic review and meta-analysis. World J Biol Psychiatry 2014;15(5):411–418.
2. Haskett RF. Electroconvulsive therapy's mechanism of action: neuroendocrine hypotheses. J ECT 2014;30(2):107–110.
3. Beall EB, Malone DA, Dale RM, et al. Effects of electroconvulsive therapy on brain functional activation and connectivity in depression. J ECT 2012;28(4):234–241.
4. Esel E, Kose K, Hacimusalar Y, et al. The effects of electroconvulsive therapy on GABAergic function in major depressive patients. J ECT 2008;24(3):224–228.
5. Singh A, Kar SK. How Electroconvulsive Therapy Works?: Understanding the Neurobiological Mechanisms. Clin Psychopharmacol Neurosci 2017;15(3):210–221.

Cognitive effects and safety

1. Semkovska M, McLoughlin DM. Objective cognitive performance associated with electroconvulsive therapy for depression: a systematic review and meta-analysis. Biol Psychiatry 2010;68(6):568–577. PMID: 20673880
2. Watts BV, Groft A, Bagian JP, Mills PD. An examination of mortality and other adverse events related to electroconvulsive therapy using a national adverse event report system. J ECT 2011;27(2):105–108. PMID: 20966769

Continuation treatment

1. Sackeim HA, Haskett RF, Mulsant BH, et al. Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA 2001;285(10):1299–1307.
2. Kellner CH, Knapp RG, Petrides G, et al. Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study from CORE. Arch Gen Psychiatry 2006;63(12):1337–1344.

ECT vs. alternatives

1. Berlim MT, Van den Eynde F, Daskalakis ZJ. Efficacy and acceptability of high frequency repetitive transcranial magnetic stimulation (rTMS) versus electroconvulsive therapy (ECT) for major depression: a systematic review and meta-analysis of randomized trials. Depress Anxiety 2013;30(7):614–623.
2. Ren J, Li H, Palaniyappan L, et al. Repetitive transcranial magnetic stimulation versus electroconvulsive therapy for major depression: a systematic review and meta-analysis. Prog Neuropsychopharmacol Biol Psychiatry 2014;51:181–189.
3. Anand A, Mathew SJ, Sanacora G, et al. Ketamine versus ECT for Nonpsychotic Treatment-Resistant Major Depression. N Engl J Med 2023;388(25):2315–2325.
4. Rhee TG, Shim SR, Forester BP, et al. Efficacy and Safety of Ketamine vs Electroconvulsive Therapy Among Patients With Major Depressive Episode: A Systematic Review and Meta-analysis. JAMA Psychiatry 2022;79(12):1162–1172.
5. Ekstrand J, Fattah C, Persson M, et al. Racemic Ketamine as an Alternative to Electroconvulsive Therapy for Unipolar Depression: A Randomized, Open-Label, Non-Inferiority Trial (KetECT). Int J Neuropsychopharmacol 2022;25(4):339–349.
6. Deng ZD, Luber B, McClintock SM, et al. Clinical outcomes of magnetic seizure therapy vs electroconvulsive therapy for major depressive episode: a randomized clinical trial (CREST-MST). JAMA Psychiatry 2024;81(3):240–249.

Physics and neurophysiology

1. Geddes LA. Electrical stimulation of the central nervous system. Physiologist 1987;30(4 Suppl):S66–S68.
2. Ranck JB Jr. Which elements are excited in electrical stimulation of mammalian central nervous system: a review. Brain Res 1975;98(3):417–440.
3. Weiner RD, Rogers HJ, Davidson JR, Squire LR. Effects of stimulus parameters on cognitive side effects. Ann N Y Acad Sci 1986;462:315–325.