ECT and Brain Stimulation Therapies — Branching Viva

Stimulus

A 68-year-old man with a severe depressive episode believes he has bankrupted his family, is barely drinking and has become mute and posturing. He has chronic kidney disease, takes lithium and has a pacemaker. His partner says, “He cannot decide—just do ECT.”[4][7]

How to use this viva

Start at Node 1. The examiner chooses the next data release according to the candidate's answer. A candidate who recognises physiological compromise enters the urgent branch; one who notices fluctuation or atypical findings enters the organic branch; consent, high-risk medicine, seizure quality, cognition, nonresponse, pregnancy and modality selection each change the subsequent question. This is not a linear checklist.[1]

Node 1 — Frame the problem

Examiner: What is your working formulation, and why might ECT be considered now?[1]

Model answer: Severe major depression with psychotic guilt and probable catatonia, complicated by physiological risk from poor intake. ECT has strong acute efficacy and moves earlier when rapid response is needed. Catatonia needs a cause-directed work-up; urgent ECT assessment is justified by life-threatening compromise. I would reserve “malignant catatonia” for catatonia with pronounced autonomic abnormality, typically hyperthermia and autonomic dysfunction—not infer it from dehydration alone.[1][4][3]

Branch rule:[1]

• If the candidate treats “psychosis” or “suicidality” as an automatic ECT order, go to Node 2A.[1]
• If the candidate mentions delirium, late onset or organic cause, go to Node 2B.[4]
• If the candidate balances urgency and cause, go directly to Node 3.[4]

Node 2A — Correct the indication shortcut

Examiner: He says life is not worth living but has no current plan. Is suicidality alone enough?[1]

Model answer: No. Suicidal risk increases urgency, but the ECT decision integrates depressive severity, psychosis, catatonia, oral intake, prior treatments, patient preference and the expected speed of alternatives. Here, physiological compromise and catatonia—not a slogan about suicidality—make rapid treatment urgent.[1]

Next: go to Node 3.[1]

Node 2B — Organic data release

Examiner: His attention fluctuates, sodium is 126 mmol/L and his daughter reports a new anticonvulsant. What changes?[4]

Model answer: Stabilise and investigate in parallel. Review drugs and renal function, correct clinically significant electrolyte disturbance safely, assess delirium and consider neurological or medical causes of catatonia. A normal CT would not end that assessment. The anaesthetist decides readiness; I would not teach “do ECT before correcting sodium” as a universal rule.[4]

Examiner follow-up: Would you do a lorazepam challenge?[4]

Model answer: If it will not delay urgent definitive care: 1–2 mg IV or IM, or 2 mg orally, reassessing at about 5, 15 or 30 minutes respectively. About a 50% fall on a structured scale supports response but is not specific; a negative test does not exclude catatonia.[4]

Next: go to Node 3.[4]

Node 3 — Capacity, refusal and lawful authority

Examiner: His partner has consented. Can you proceed?[3]

Model answer: Not on that fact alone. Capacity is decision- and time-specific. I would support communication and assess whether he can understand, retain, use or weigh the relevant information and communicate a choice under the applicable jurisdiction. Diagnosis, detention, incapacity or family agreement does not itself authorise ECT. I must identify the exact local substitute-decision, tribunal, second-opinion or emergency pathway and document why delay is or is not dangerous.[3]

Branch rule:[3]

• If he has capacity and consents, go to Node 4.[3]
• If he has capacity and refuses, answer Node 3R.[3]
• If he lacks capacity, answer Node 3L.[3]

Node 3R — Capacitous refusal

Examiner: He understands and weighs the information but refuses because of memory risk.[3]

Model answer: His refusal is not erased by severity. Explore the reason, correct misconceptions, offer supported decision-making and alternatives, and reassess only if clinical state changes. Whether any emergency statutory override exists is jurisdiction-specific and exceptional; I would obtain senior legal/ethical advice rather than claim a universal mental-health-law power.[3]

Node 3L — Lacks capacity

Examiner: He cannot use or weigh information. What is your legal answer?[3]

Model answer: Name the jurisdiction before the power. Check advance preferences or directives, the authorised decision-maker or tribunal, best-interests or benefit test, independent review and any special ECT safeguards. Australian states and territories, New Zealand, England and Wales, Scotland and Northern Ireland differ. His partner's view informs the decision but is not automatically determinative.[3]

Next from either branch if authority is established: go to Node 4.[3]

Node 4 — High-risk medical branch

Examiner: What are the contraindications, and what do lithium and the pacemaker change?[7][3]

Model answer: There is no universally accepted absolute list. Raised intracranial pressure with mass effect, unstable cardiovascular or cerebrovascular disease, unstable aneurysm, phaeochromocytoma and severe pulmonary or anaesthetic risk need senior optimisation and a rescue-capable setting. Lithium may increase delirium or prolonged-seizure risk, especially with kidney disease and older age; review indication, level, renal function and exposure, then individualise rather than impose “hold the evening before.” Identify device, pacing dependence and interrogation needs; have external pacing/defibrillation rescue. Pacemaker asynchronous programming is dependence- and device-specific. For an ICD, disable anti-tachycardia detection/therapy before ECT, keep it disabled through the full treatment session including ictal/postictal sympathetic tachycardia, and restore it only afterward under the device plan.[7][3][12]

Examiner follow-up: He also takes apixaban. Must you stop or bridge it?[11]

Model answer: Not automatically. A 2025 review found few reported major bleeding or thromboembolic events with therapeutic warfarin or DOAC exposure during ECT, but evidence is observational and sparse. Confirm indication, adherence, renal function, interacting drugs/procedures and individual bleeding versus thrombosis risk. A fixed INR ceiling, routine interruption and bridging are not universal ECT rules.[11]

Branch rule:[7]

• If he is physiologically stable after optimisation, go to Node 5.[7]
• If imaging shows a mass with raised intracranial pressure, answer Node 4H.[7]

Node 4H — Raised intracranial pressure with mass effect

Examiner: MRI now shows a large lesion with oedema and mass effect. Do you proceed today?[7][3]

Model answer: Not as routine ECT. I would obtain urgent neurology/neurosurgery and anaesthetic input, treat the intracranial problem, quantify the consequence of psychiatric-treatment delay and consider alternatives. If ECT remains life-saving, it requires an exceptional multidisciplinary risk plan and a rescue-capable setting—not a rote claim that all brain lesions are absolute contraindications or all are manageable.[7][3]

Node 5 — Conduct one treatment

Examiner: Talk me through one modified ECT treatment.[3]

Model answer: Reconfirm indication, lawful authority, interval events, medication/fasting plan and anaesthetic readiness; apply general-anaesthesia monitoring and ECT EEG, establish IV access and preoxygenate. Give an individualised induction dose—the cited propofol range is 0.75–1 mg/kg IV; it can raise threshold and shorten seizure. After unconsciousness place the bite block, apply the isolated arm or leg cuff and inflate it above systolic pressure before neuromuscular blocker circulates, while retaining EEG. Then give individualised blockade—the cited succinylcholine range is 0.3–1 mg/kg IV—deliver the prescription, record EEG/motor expression and ventilate until recovery.[3]

Examiner challenge: Do RANZCP or ANZCA require routine atropine, beta-blocker and succinylcholine?[3]

Model answer: No. RANZCP provides ECT governance and practice guidance; ANZCA provides general anaesthesia standards. Anticholinergic, beta-blocker, hyperventilation strategy and neuromuscular blocker are selected for the patient and local service; neither body creates one ECT-specific anaesthetic recipe.[3]

Examiner challenge: When would you avoid succinylcholine?[3]

Model answer: Use an anaesthetist-planned non-depolarising alternative for pseudocholinesterase deficiency/prolonged apnoea risk, malignant-hyperthermia susceptibility, major burns or denervation, severe neuromuscular disease, hyperkalaemia or another hyperkalaemia-prone state. Plan reversal where relevant and never stop assisted ventilation before adequate neuromuscular and respiratory recovery.[3]

Branch rule:[3]

• If the EEG seizure is brief or poor quality, go to Node 6A.[3]
• If EEG seizure activity continues, go to Node 6B.[3]
• If treatment is uncomplicated, go to Node 7.[3]

Node 6A — “Inadequate” seizure branch

Examiner: The motor seizure is 18 seconds. Must you immediately restimulate?[2]

Model answer: No binary duration rule. Confirm stimulus delivery and cuff technique, assess EEG generalisation, evolution and post-ictal suppression, review threshold-raising medicines and anaesthetic agent, and consider the course's clinical trajectory. A short motor seizure can accompany adequate EEG expression. Restimulation, dose change or later re-titration follows the unit protocol and whole assessment—not an automatic 25-second cut-off.[2]

Examiner follow-up: Give defensible stimulus ranges.[3]

Model answer: In the 2023 guideline, conventional brief pulse is 0.5–2 ms and ultrabrief 0.2–0.4 ms. Typical teaching ranges are about 1.5× threshold for bilateral brief pulse, 4–6× for right-unilateral brief pulse and about 6× for right-unilateral ultrabrief. These are attributed ranges, not manufacturer-independent prescriptions; ultrabrief bilateral ECT lacks evidence.[3]

Examiner follow-up: What is ECT's mechanism?[10]

Model answer: The brief electrical stimulus produces a generalised cerebral seizure; that seizure initiates interacting neurochemical, neuroplastic and network effects. Human imaging supports network change, but no single BDNF, neurogenesis or default-mode story is proved as the causal clinical mechanism.[10] Seizure duration alone does not establish treatment adequacy.[3]

Next: go to Node 7.[2]

Node 6B — Prolonged-seizure branch

Examiner: EEG seizure activity continues. What do you do?[3]

Model answer: Separate efficacy from emergency timing. Do not use a rigid minimum-duration rule, but attempt ictal termination when EEG activity continues beyond 120 seconds; more than 180 seconds is prolonged in the cited guideline. Maintain airway, oxygenation and ventilation, confirm EEG, call the anaesthetist/ECT lead and follow the rehearsed protocol with a benzodiazepine, induction anaesthetic or barbiturate, or protocol-selected phenytoin/valproate. Continue EEG to resolution; check glucose/electrolytes and causal medicines, observe for non-convulsive activity and revise the next treatment. A tardive seizure after recovery requires emergency assessment.[3]

Next: go to Node 7.[3]

Node 7 — Cognition versus speed

Examiner: After four treatments his depression is improving, but he reports losing memories of his daughter's wedding. What now?[2][5]

Model answer: Take the report seriously; assess subjective and objective cognition, orientation, delirium and functional impact. Revisit consent. Options include reducing frequency, lowering dose where efficacy allows, changing from bitemporal to right unilateral, or using ultrabrief right unilateral—with an explicit possible trade-off in speed or efficacy. Group-average objective cognition often recovers after the acute period, but an individual's autobiographical loss may persist.[2][5][3]

Branch rule:[5]

• If the patient is improving and accepts the trade-off, continue with review and go to Node 9.[5]
• If no clinical response after an adequate initial course, go to Node 8A.[2]
• If a non-urgent patient asks for a non-convulsive option, go to Node 8B.[6]

Node 8A — Nonresponse branch

Examiner: There is no rating-scale or clinical change after six right-unilateral treatments.[2]

Model answer: Recheck diagnosis, comorbidity, substance and medical causes, medications that raise threshold, EEG quality, dose relative to threshold and whether six treatments are enough for this trajectory. Then consider higher dose, changing pulse width or moving to bilateral placement, balancing urgency against cognition and re-consenting. I would not stop automatically at six or promise that 12 is always required.[2]

Next: go to Node 9.[2]

Node 8B — rTMS and device-status branch

Examiner: A medically stable outpatient with nonpsychotic treatment-resistant depression wants to avoid anaesthesia. Compare rTMS.[6]

Model answer: rTMS or TBS offers focal, non-convulsive outpatient treatment with no consistent cognitive-impairment signal; headache and scalp discomfort are common and seizure is rare but protocol- and risk-dependent. It is generally less compelling than ECT when severe psychosis, catatonia, physiological compromise or maximal speed dominates. THREE-D supports 3-minute iTBS as non-inferior to a 37.5-minute 10 Hz protocol in its trial population, not every device or diagnosis.[6]

Examiner challenge: Is “TMS FDA-approved for depression and OCD” precise?[6]

Model answer: No. Say a specific device is FDA-cleared for a specific indication and protocol. ECT device classification is also indication- and population-specific: US Class II status under 21 CFR 882.5940 is limited to catatonia or severe MDE in patients aged 13 or older who are treatment-resistant or require rapid response; other intended uses remain Class III.[6]

Branch rule: if the patient wants a weak-current non-convulsive option, answer Node 8C; if the examiner asks about a convulsive experimental option, answer Node 8D; if implantation or esketamine is proposed, answer Node 8E; otherwise go to Node 9.[13][14][16][17][18]

Node 8C — tES / tDCS branch

Examiner: Is home tDCS simply a safer ECT?[14][15]

Model answer: No. tDCS is an awake, repeated-session, weak direct-current tES research protocol—usually targeting prefrontal regions—not a seizure therapy. The cited individual-patient meta-analyses support a modest protocol-dependent acute depression signal and no consistent cognitive-harm signal. They do not quantify individual adverse-effect frequencies, define contraindications, establish home-use equivalence or prove a current regulatory boundary. For clinical use, check the exact device instructions and current local safety/regulatory authority rather than inventing universal implant, epilepsy, pregnancy or supervision rules.[14][15]

Next: go to Node 9.[14]

Node 8D — magnetic seizure therapy branch

Examiner: Could magnetic seizure therapy give ECT efficacy without cognition or anaesthesia?[13]

Model answer: MST is still a convulsive treatment: high-output magnetic stimulation intentionally induces a seizure under general anaesthesia and neuromuscular blockade. Small trials and meta-analysis suggest possible cognitive advantages, but comparative antidepressant efficacy remains uncertain. Anaesthetic, seizure, cardiovascular and equipment burdens remain; it belongs in specialist research, not routine substitution or ordinary FDA-approved care.[13]

Next: go to Node 9.[13]

Node 8E — implant and drug-comparator branch

Examiner: Compare VNS, DBS and esketamine for refractory depression.[16][17][18]

Model answer: VNS uses a surgically implanted pulse generator and cervical vagal lead for chronic adjunctive stimulation; response can be delayed, and surgery, infection, hardware failure, voice change, cough and dyspnoea matter. Evidence supports an adjunctive signal, but US depression approval is the narrow adult long-term P970003/S050 supplement, not the epilepsy indication recycled. DBS uses implanted intracranial electrodes and programmable stimulation, adding haemorrhage, infection, hardware and neuropsychiatric risk; depression remains investigational, while OCD H050003 is an HDE. Esketamine is a supervised intranasal drug, not stimulation; dissociation, sedation, blood-pressure rise and misuse risk require monitored delivery. Current Spravato PI and REMS govern US monotherapy and acute-suicidality labels; TRANSFORM-1 did not meet its prespecified primary endpoint and cannot establish today's label alone. None replaces urgent ECT automatically.[16][17][18]

Next: go to Node 9.[18]

Node 9 — Pregnancy data release

Examiner: The same syndrome occurs at 28 weeks' gestation. Is ECT “safe in pregnancy”?[8]

Model answer: I would say it can be used when benefits outweigh risks, not promise universal safety. Evidence is mainly observational. Coordinate psychiatry, obstetrics, anaesthesia and neonatology as required; address aspiration and aortocaval physiology, position later gestation appropriately and individualise fetal assessment. Discuss transient fetal bradycardia, uterine contractions and preterm labour alongside the harm of untreated severe illness.[8]

Next: go to Node 10.[8]

Node 10 — Ending the course without losing the gain

Examiner: He remits after nine treatments. What is your discharge and relapse plan?[9]

Model answer: Confirm functional recovery, suicide risk, nutrition, cognition and decision-making; document driving and activity advice from the local service. Optimise illness-specific pharmacotherapy and discuss continuation ECT if relapse history, medication resistance, preference and tolerability support it. “Continuation” commonly covers roughly the first six months and “maintenance” thereafter, but frequency is response- and burden-led—not a mandatory weekly–fortnightly–monthly ladder.[9]

References

1. [1]UK ECT Review Group Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis Lancet, 2003.PMID 12642045
2. [2]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 Archives of General Psychiatry, 2000.PMID 10807482
3. [3]Thirthalli J, Sinha P, Sreeraj VS Clinical Practice Guidelines for the Use of Electroconvulsive Therapy Indian Journal of Psychiatry, 2023.PMID 37063631
4. [4]Rogers JP, Oldham MA, Fricchione G, et al. Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology Journal of Psychopharmacology, 2023.PMID 37039129
5. [5]Semkovska M, McLoughlin DM Objective cognitive performance associated with electroconvulsive therapy for depression: a systematic review and meta-analysis Biological Psychiatry, 2010.PMID 20673880
6. [6]Blumberger DM, Vila-Rodriguez F, Thorpe KE, et al. Effectiveness of theta burst versus high-frequency repetitive transcranial magnetic stimulation in patients with depression (THREE-D): a randomised non-inferiority trial Lancet, 2018.PMID 29726344
7. [7]Blumberger DM, Seitz DP, Herrmann N, et al. Low medical morbidity and mortality after acute courses of electroconvulsive therapy in a population-based sample Acta Psychiatrica Scandinavica, 2017.PMID 28922451
8. [8]Bobo WV, Moore O, Hurley CB, et al. Modified electroconvulsive therapy for perinatal depression: scoping review Frontiers in Psychiatry, 2025.PMID 40901266
9. [9]McCall WV, Lisanby SH, Rosenquist PB, et al. Effects of continuation electroconvulsive therapy on quality of life in elderly depressed patients: A randomized clinical trial Journal of Psychiatric Research, 2018.PMID 29195125
10. [10]Leaver AM, Espinoza R, Wade B, Narr KL Parsing the Network Mechanisms of Electroconvulsive Therapy Biological Psychiatry, 2022.PMID 35120710
11. [11]Khalid A, Khalid A, Waite S, Plevin D Exploring the use of electroconvulsive therapy in the anticoagulated population: A systematic review Australian and New Zealand Journal of Psychiatry, 2025.PMID 39252452
12. [12]Purohith AN, Vaidyanathan S, Udupa ST, et al. Electroconvulsive Therapy in Patients With Cardiac Implantable Electronic Devices: A Case Report and Systematic Review of Published Cases Journal of ECT, 2023.PMID 35482902
13. [13]Chen M, Yang X, Liu C, et al. Comparative efficacy and cognitive function of magnetic seizure therapy vs. electroconvulsive therapy for major depressive disorder: a systematic review and meta-analysis Translational Psychiatry, 2021.PMID 34420033
14. [14]Brunoni AR, Moffa AH, Fregni F, et al. Transcranial direct current stimulation for acute major depressive episodes: meta-analysis of individual patient data British Journal of Psychiatry, 2016.PMID 27056623
15. [15]Martin DM, Moffa A, Nikolin S, et al. Cognitive effects of transcranial direct current stimulation treatment in patients with major depressive disorder: An individual patient data meta-analysis of randomised, sham-controlled trials Neuroscience and Biobehavioral Reviews, 2018.PMID 29660416
16. [16]Bottomley JM, LeReun C, Diamantopoulos A, et al. Vagus nerve stimulation (VNS) therapy in patients with treatment resistant depression: A systematic review and meta-analysis Comprehensive Psychiatry, 2019.PMID 31978785
17. [17]Wu Y, Mo J, Sui L, et al. Deep Brain Stimulation in Treatment-Resistant Depression: A Systematic Review and Meta-Analysis on Efficacy and Safety Frontiers in Neuroscience, 2021.PMID 33867929
18. [18]Fedgchin M, Trivedi M, Daly EJ, et al. Efficacy and Safety of Fixed-Dose Esketamine Nasal Spray Combined With a New Oral Antidepressant in Treatment-Resistant Depression: Results of a Randomized, Double-Blind, Active-Controlled Study (TRANSFORM-1) International Journal of Neuropsychopharmacology, 2019.PMID 31290965