Electroconvulsive therapy and neuromodulation

• Electroconvulsive therapy (ECT) is the deliberate induction of a generalised seizure by a brief electrical stimulus passed across the brain through scalp electrodes, given under general anaesthesia with muscle relaxation; it is the most effective treatment available for severe, potentially life-threatening depression and for catatonia.
• Neuromodulation is the broader family of treatments that change brain activity with electricity or magnetism; alongside ECT it includes repetitive transcranial magnetic stimulation (rTMS, a coil against the scalp, outpatient, no anaesthetic) and implanted vagus nerve stimulation (VNS, a chest-wall pacemaker wired to the vagus nerve in the neck).
• ECT is used when speed and certainty matter: life-threatening depression, catatonia, a severe or prolonged manic episode, or depression that has not responded to adequate trials of medication and psychological treatment.
• The most feared side effect is memory impairment, usually transient anterograde difficulty and a patchy retrograde gap for events around the treatment; it is reduced by unilateral (non-dominant) electrode placement and briefer pulses, at some cost in speed of response.
• TMS is no better than sham for everyone but has an adequate short-term effect and a good safety profile, so NICE allows its normal use; VNS has frequent, well-recognised side effects and limited-quality evidence, so NICE restricts it to special arrangements.

By the end of this page you should be able to:

1. Explain what ECT and the main neuromodulation techniques are, and how they differ in invasiveness, setting and speed.
2. State the indications for ECT, including when it is first-line rather than a last resort. ^[5]
3. List the main contraindications and cautions, and explain why "no absolute contraindications" does not mean "no risk".
4. Describe a modern modified ECT procedure from preparation to recovery, including consent, dosing and seizure monitoring.
5. Recognise and manage the common and serious complications, especially the cognitive ones.
6. Compare ECT, rTMS and VNS using guideline evidence, and cite the NICE, APA and RCPsych positions.

ECT was introduced in 1938. In modified ECT the stimulus is delivered under general anaesthesia and muscle relaxation, so the body does not convulse visibly, but the brain still has a generalised seizure. The seizure, and the changes it produces in brain chemistry and connectivity, are the therapeutic event. The precise mechanism of ECT is not fully understood; candidate mechanisms include effects on monoamine transmission, neuroplasticity and network connectivity. ^[6] It remains, however, the most effective acute treatment for severe major depression. ^[2]

Neuromodulation is the umbrella term for treatments that alter nervous-system activity with physical energy. ^[7] The three relevant to psychiatry are:

• ECT: electrical stimulus to the brain, given as a course, usually twice a week for 6 to 12 sessions. ^[1]
• rTMS: a rapidly changing magnetic field from an electromagnetic coil held against the scalp, delivered as an outpatient course, usually daily, without anaesthesia. ^[3]
• Implanted VNS: a generator implanted under the skin below the collarbone, connected by a lead to the left vagus nerve in the neck, delivering brief pulses continuously for years. ^[4][7]

A fourth technique, transcranial direct current stimulation, exists but is outside the scope of this page; NICE has separate guidance on it. ^[7]

This page concentrates on ECT because that is the technique trainees most often encounter on a ward, and treats rTMS and VNS as the two other neuromodulation options to compare with it.

The most common misconception is that ECT is the treatment of last resort. The Indian Psychiatric Society guideline puts it directly: ECT is considered first-line when rapid and definite response is needed to avert harm, including high suicidality, catatonia, excitement, aggression, poor oral intake, acute psychotic exacerbations and severe physical debilitation secondary to psychiatric disorder. ^[5] The reasoning is that these are emergencies where waiting for a drug to work risks death; the harm of untreated illness then outweighs the procedural risk. ^[5]

NICE recommends ECT for severe depression when the person prefers it based on past experience, when a rapid response is needed (for example, life-threatening depression because the person is not eating or drinking), or when other treatments have been unsuccessful. ^[2] NICE technology appraisal TA59, which still governs this area, says ECT is for rapid and short-term improvement of severe symptoms after an adequate trial of other options has failed and/or when the condition is potentially life-threatening, in severe depressive illness, catatonia, or a prolonged or severe manic episode. ^[1]

For catatonia, NICE and RCPsych agree that benzodiazepines, usually lorazepam, come first, with ECT as the next step or immediately if the catatonia is malignant or the patient is not drinking. ^[1]

ECT is also used in psychotic depression, bipolar depression, and more rarely in schizophrenia (usually only when there is catatonia, intractable positive symptoms, or neuroleptic malignant syndrome). ^[5][6] The general management of schizophrenia with ECT alone is not recommended. ^[1]

The Indian Psychiatric Society guideline lists common and uncommon indications in table form. ^[5] In summary:

• Major depression: poor oral intake, high suicidal risk, high distress needing rapid remission, psychotic or melancholic features, peripartum depression, treatment resistance, severe mixed affective features. ^[5]
• Mania: requiring rapid clinical improvement, persisting clinically significant agitation or aggression, treatment-resistant mania, severe mixed or delirious mania. ^[5]
• Schizophrenia and related disorders: acute psychosis needing high-intensity management, good previous response, treatment-resistant or clozapine-resistant schizophrenia, postpartum psychosis. ^[5]
• Catatonia: benzodiazepine-resistant, good past response, malignant catatonia. ^[5]
• Uncommon: severe self-injurious behaviour in autism, agitation in dementia, difficult-to-treat obsessive-compulsive disorder before neurosurgery, certain Parkinson's disease phenomena, neuroleptic malignant syndrome. ^[5]

Predictors of a good response include older age, psychotic symptoms, shorter episode duration, melancholic features and greater baseline severity; a past good response to ECT is also predictive. ^[5]

NICE is explicit that ECT should not be used as maintenance therapy in depressive illness. ^[1] This is a frequent exam trap: NICE TA59 says continuation or maintenance ECT is not recommended for depression, although clinically, after a good acute response, pharmacological relapse prevention (antidepressant, plus lithium augmentation) is started. ^[1][2] Continuation ECT up to six months and maintenance ECT after six months are discussed in other guidelines and in practice, particularly in recurrent severe illness, but in NICE's terms maintenance ECT for depression is not recommended. ^[5] State both positions honestly and be clear which guideline you are quoting. ^[1][2][5]

There are no absolute contraindications to ECT: the risk of the untreated illness is weighed against the procedural risk, and the patient has a say. ^[5] What exists is a list of conditions that raise risk and demand specialist anaesthetic, medical or surgical input and documented counselling. ^[5]

Other risk-raising factors noted in clinical guidance include poorly compensated heart failure, valvular disease, bradycardia or heart block, cardiac pacemakers, vascular (aortic or intracranial) aneurysms, epilepsy, osteoporosis, retinal detachment and glaucoma, thyrotoxicosis, abnormal serum potassium, poor dentition, obesity, asthma or chronic obstructive pulmonary disease, skull defects or plates, older age, and pregnancy. ^[1]

• Pregnancy and the postpartum period. ECT is often safer than psychotropic medication in pregnancy, because psychotropic drugs cross the placenta, but the risks of ECT (including seizure-induced uterine contractions) are also enhanced, so it is used with particular caution, obstetric input, left lateral positioning and lower anaesthetic doses. ^[1][6]
• Older adults. Older people respond very well, but cognitive recovery may be slower and post-ictal confusion more likely; NICE specifically flags the older age group for enhanced risk discussion. ^[1][2]
• Children and adolescents. ECT is rare in this age group. The Indian guideline requires two independent psychiatrists (or a psychiatrist plus a physician) and permission from the mental health review board. ^[5]

ECT needs less anatomy than a lumbar puncture but three points matter:

1. The seizure is generalised. The stimulus spreads from the cortex to involve both hemispheres and the diencephalon, including the hippocampus and amygdala. The therapeutic effect is believed to come from the diencephalic seizure and the neurochemical and neuroplastic changes that follow it, not from the peripheral convulsion. ^[6]
2. Electrode placement is defined relative to cranial landmarks. Unilateral placement is one electrode on the right fronto-temporal region and the other 1 inch right of the vertex (the point where the interauricular line meets the nasion-inion line). Bitemporal placement puts one electrode in each fronto-temporal region; bifrontal placement puts electrodes on the frontal regions. ^[5]
3. The vagus nerve, used in VNS, is the tenth cranial nerve; the left vagus is chosen for stimulation because right-sided stimulation risks bradycardia more. ^[7]

A modern ECT treatment suite has three adjacent areas: a waiting and preparation room, the administration room, and a recovery room. ^[5]

In the administration room the essentials are:

• ECT apparatus with a constant-current device producing brief or ultrabrief rectangular pulses, plus EEG and ECG monitoring, bite block, and pulse oximetry. ^[5]
• Anaesthetic agents (for example propofol, thiopentone, etomidate, ketamine or sevoflurane) and a muscle relaxant, ideally succinylcholine, with a non-depolarising alternative available. ^[5]
• Oxygen with intermittent positive pressure ventilation capability, suction, and a defibrillator. ^[5]
• An emergency drug tray covering severe hypertension, hypotension, arrhythmia, cardiopulmonary arrest, anaphylaxis, prolonged seizure and status epilepticus. ^[5]

For TMS, the equipment is a purpose-made electromagnetic coil held against the scalp, with a comfortable chair, ear plugs for the noise, and often a neuronavigation system or the F3 (10-20 EEG) or 5 cm rule to locate the dorsolateral prefrontal cortex. ^[3]

For implanted VNS, the equipment is a pulse generator (about the size of a watch) implanted below the clavicle and a lead tunnelled to the left vagus nerve in the neck; settings are adjusted with an external hand-held programmer. ^[4][7]

Preparation separates ECT from a medication review: it is an anaesthetic procedure with a seizure, and the checklist reflects that.

Psychiatric evaluation must confirm the indication and, if the patient has had ECT before, record the previous electrode placement, parameters, response and cognitive side-effects. ^[5] Drug review matters: anticonvulsants raise seizure threshold; chlorpromazine and clozapine are proconvulsant; lithium increases post-ictal delirium risk; tricyclic antidepressants increase the risk of cardiac events during ECT. ^[5]

Physical evaluation identifies relative contraindications: fundoscopy, cardiovascular, neurological and respiratory examination, dental check for loose teeth, and an assessment of any spinal or skeletal risk. ^[5]

Pre-anaesthetic evaluation then plans the anaesthetic and muscle relaxant, and liaison with physicians is mandatory whenever significant medical comorbidity exists. ^[5]

Investigations are guided by comorbidity rather than routine: full blood count, glucose, electrolytes, renal function and ECG are common, with echocardiography or further imaging when indicated. ^[5]

A baseline cognitive screen is useful, because change can only be interpreted against a pre-treatment measure. ^[5]

NICE is prescriptive about consent, and its wording is worth learning. Valid consent is needed whenever the person can grant or refuse it; the decision is made jointly by the patient and the treating clinician on the basis of an informed discussion. ^[1][2] Consent must be obtained without pressure or coercion (including the pressure created by the clinical setting), the patient must be reminded of the right to withdraw consent at any point, and an advocate or carer should be involved to facilitate discussion. ^[1][2]

Where a patient cannot consent, advance directives (advance decisions) must be respected and the patient's advocate or carer consulted. ^[1][2] In the Indian guideline, the same principle appears: written informed consent before the course, with caregivers included unless the patient objects, and re-consent before continuation or maintenance ECT because the purpose and character of treatment have changed. ^[5]

For minors, assent is taken in addition to parental consent, and two independent psychiatrists plus permission from the mental health review board are required. ^[5]

The information given must cover the general risks of ECT, the risks and benefits specific to that patient, the risks of the anaesthetic, current comorbidities, and the risks of not having treatment, with the assessment documented. ^[1][2]

Patients are fasting (clear liquids for at least 2 hours, milk and light meals 6 hours, fried, fatty or meat meals 8 hours), the head is clean and dry, and prescribed medications are managed individually. ^[5] Lithium, anticonvulsants, theophylline and benzodiazepines are usually withheld; morning doses of antihypertensives, thyroxine and bronchodilators are not. ^[5]

The procedure is the same every day, and the steps are reported to the patient and the notes.

1. Arrival and verification. Patient identified, consent confirmed, fasting status checked, identity and procedure re-verified.
2. Pre-treatment assessment. Brief pulse, blood pressure, oxygen saturation and a cognitive/clinical check; the patient is reassured. ^[5]
3. Anaesthesia. Intravenous access secured; the patient is pre-oxygenated; a short-acting induction agent (propofol 0.75 to 1 mg per kg, thiopentone 3 to 5 mg per kg, etomidate 0.15 to 0.3 mg per kg or methohexitone 0.5 to 1 mg per kg) is given, and succinylcholine 0.3 to 1 mg per kg relaxes the patient. ^[5]
4. Ventilation and positioning. The patient is ventilated by mask until spontaneous breathing returns; a mouth guard protects the teeth. ^[5]
5. Electrode placement. Either right unilateral or bilateral (bitemporal or bifrontal) electrodes are applied to the scalp as documented in the treatment plan. ^[5]
6. Dosing. The operator delivers a brief (0.5 to 2 ms) or ultrabrief (0.2 to 0.4 ms) rectangular pulse at a current of about 800 to 900 mA. The standard is the stimulus titration method, finding the seizure threshold in the first session and then giving 1.5 times threshold for bilateral brief-pulse ECT, 4 to 6 times threshold for unilateral brief-pulse ECT, and 6 times threshold for ultrabrief right unilateral ECT. ^[5]
7. Seizure. A generalised seizure is induced; motor and EEG activity are monitored (the Hamilton cuff method on the isolated ipsilateral limb, plus bilateral EEG). ^[5]
8. Missed or inadequate seizure. If no seizure occurs within 20 seconds of the stimulus, re-stimulation at a higher dose is undertaken, up to four or five attempts; vigorous hyperventilation may help. ^[5]
9. Prolonged seizure. If the seizure lasts more than 180 seconds, terminate with benzodiazepines, phenytoin, valproate or the induction barbiturate, and monitor airway and respiration until it ceases. ^[5]
10. Recovery. Lateral position until spontaneous breathing returns; the patient is transferred to the recovery room with continuous vital signs monitoring, and feeding is withheld until fully conscious. ^[5]

ECT is given as a course, usually twice a week. ^[1] The Indian guideline recommends not fewer than 8 to 12 sessions in an acute course before concluding that ECT has failed, with switching from unilateral to bilateral, or from ultrabrief to brief pulse, after 4 to 8 sessions if there has been no response. ^[5] A clinical assessment is made after every session, and at least weekly with rating scales. ^[5]

Adequacy is more about quality than duration: a graduated onset, tonic contraction, bilateral clonic activity and clear post-ictal suppression on the EEG. ^[5] Seizures of adequate quality, even when brief, work in older depressed patients. ^[5] A 15-second motor threshold was the old rule of thumb but is now recognised to be of little prognostic value. ^[5]

rTMS needs no anaesthetic; it is done in a chair. ^[3] The patient sits while an electromagnetic coil is held against the scalp, usually over the left dorsolateral prefrontal cortex (identified by the 5 cm rule, the F3 EEG site, or neuronavigation). ^[3] Daily sessions of about 30 minutes are given, typically for 2 to 6 weeks. ^[3] NICE IPG542 covers both conventional rTMS and theta-burst stimulation; the coil can be placed unilaterally or bilaterally. ^[3] Intermittent theta-burst stimulation shortens the session and has been found no worse than conventional rTMS for depression outcomes in a non-inferiority trial. ^[3]

Implanted VNS requires surgery under general or local anaesthetic. ^[4][7] Two components are placed under the skin near the clavicle: a battery and stimulator (about the size of a watch) and a wire tunnelled to the left vagus nerve in the neck. ^[7] The stimulator then runs continuously, usually for 30 seconds every 5 minutes, with settings adjusted by an external programmer. ^[7] It is intended to be long-term: the battery lasts 7 to 10 years depending on settings. ^[7]

Immediate aftercare after ECT includes recovery and safety: ensure spontaneous respiration, control post-ictal agitation with verbal reassurance and, if needed, benzodiazepines, and withhold food until full consciousness has returned. ^[5] Orientation, gait, vital signs and any dental, musculoskeletal or other injuries are checked before leaving the recovery unit. ^[5]

After the course:

• NICE says that when depression has responded, an antidepressant or psychological intervention should be started or continued to prevent relapse, with lithium augmentation considered. ^[2]
• Clinical status is assessed following each session, and treatment is stopped when a response is achieved or sooner if adverse effects appear. ^[1] Cognitive function is monitored continuously and at minimum at the end of a course. ^[1][5]
• After the course, patients should be asked about memory problems and, if present, referred for detailed neuropsychological assessment. ^[5]
• RCPsych and the RCPsych patient information literature encourage continuing medication, talking therapy such as cognitive behavioural therapy, and continuation or maintenance ECT in recurrent cases. ^[6][7]

• Headache, muscle soreness, joint pain, nausea and fatigue, usually mild and responsive to simple analgesia. ^[5]
• Post-ictal confusion or delirium, usually resolving in 5 to 45 minutes; if it persists, support the airway, secure an intravenous line, reduce stimulation, use benzodiazepines or, if needed, low-dose haloperidol, and exclude non-convulsive status epilepticus. ^[5]
• Manic or hypomanic switch. ^[5]

ECT produces a parasympathetic surge during and immediately after the stimulus, then a sympathetic surge with tachycardia and hypertension during the seizure, followed by a return to baseline. ^[1] Serious complications occur mainly in the post-ictal period. ^[1] They include sinus arrest, arrhythmias, myocardial ischaemia and infarction, pulmonary oedema and aspiration. ^[1] That is why NICE insists the risk-benefit assessment documents the anaesthetic risk and comorbidities, and why an ECG and specialist input are needed in patients with cardiac disease. ^[1][2]

Memory impairment is the adverse effect patients worry about most. ^[5] It takes three forms:

1. Acute disorientation immediately after a seizure, usually lasting minutes.
2. Anterograde difficulty, impaired acquisition of new verbal and non-verbal material, which is most marked during the course and generally recovers after treatment ends. ^[5]
3. Retrograde (autobiographical) memory loss, in which events around the time of treatment become less accessible. This is the most distressing and the hardest to measure objectively. ^[5]

Retrograde loss is more likely with bitemporal placement, higher doses above threshold, more treatments and older age. ^[5] Switching to unilateral placement, briefer (0.5 to 1 ms) pulses or reduced stimulus doses can mitigate it, at some cost in efficacy. ^[5] For these reasons many services use right unilateral brief-pulse or ultrabrief-pulse ECT first, escalating to bitemporal only when speed is paramount or there has been no response. ^[5]

Subjective memory complaints should be taken seriously alongside objective testing, because standard cognitive tests are not sensitive to the autobiographical loss patients describe. ^[5]

• Prolonged seizure or status epilepticus (seizure more than 180 seconds). ^[5]
• Tardive seizure appearing hours later. ^[5]
• Airway, aspiration and respiratory complications, including in asthmatic or obese patients. ^[5]
• Musculoskeletal injury such as jaw dislocation, fracture or dislocation in patients with osteoporosis, and tongue bite. ^[5]
• Nausea and vomiting, often with headache. ^[5]
• Death. Mortality is comparable to that of minor procedures requiring general anaesthesia, largely from cardiac causes in physically ill patients. ^[1]

TA59 is the core NICE technology appraisal. ^[1] It says ECT is only for rapid, short-term improvement of severe symptoms after adequate alternatives have failed, or when the illness is life-threatening, in severe depressive illness, catatonia, or a prolonged or severe manic episode. ^[1] It requires a documented risk-benefit assessment covering the anaesthetic, comorbidities, cognitive side effects and the risks of not treating; particular caution in pregnancy, older adults and children; valid consent without coercion; reassessment after every session; stopping once response is achieved or if adverse effects appear; and avoidance of repeated courses except after previous good response or after all other options have been considered. ^[1] It states that ECT should not be used as maintenance therapy for depression and should not be used in the general management of schizophrenia. ^[1]

NG222 updates the depression-specific recommendations. ^[2] ECT should be considered for severe depression if the patient prefers it from past experience, if a rapid response is needed (for example, life-threatening depression with refusal to eat or drink), or if other treatments have failed. ^[2] Clinics providing ECT must be ECTAS accredited and follow ECTAS standards. ^[2] After response, antidepressant or psychological treatment should be started to prevent relapse, with lithium augmentation considered. ^[2]

NICE judged that rTMS for depression has no major safety concerns and adequate short-term efficacy, although the clinical response is variable; it may be used with normal clinical governance and audit. ^[3] The meta-analytic effect size was a Hedges g of 0.55 across 40 randomised trials including 1,592 patients (rTMS n=751 versus sham n=632). ^[3] rTMS reduces HDRS scores by about 37 percent in mixed depression and 48 percent in treatment-resistant depression, compared with about 22 to 23 percent with sham. ^[3] Against ECT, the mean HDRS reduction was 34 percent with rTMS and 46 percent with ECT. ^[3] NICE asks clinicians to tell patients about other treatment options and to make clear that the treatment may not help them. ^[3]

NICE found no major safety concerns for implanted VNS but frequent well-recognised side effects, with limited-quality efficacy evidence; it may only be used with special arrangements for clinical governance, consent and audit or research. ^[4] That is why VNS remains available in only a small number of UK centres, usually after at least two other treatments have failed. ^[4][7]

The American Psychiatric Association Task Force on ECT published the third edition of The Practice of Electroconvulsive Therapy in 2024, the first revision since 2001. ^[8] Its 24 chapters cover indications, staffing, location and equipment, pre-ECT evaluation, special populations, consent, preparation, anaesthesia, medications during ECT, stimulus parameters and electrode placement, seizure monitoring, post-ictal recovery, outcome evaluation, frequency and number of treatments, adverse events, cognitive side effects and management of prolonged or inadequate seizures, as well as a chapter on emerging neuromodulation techniques including TMS and VNS. ^[8]

The Royal College of Psychiatrists published the fourth edition of The ECT Handbook in 2019, edited by Ferrier and Waite, integrating UK legal frameworks, ECTAS and SEAN accreditation, and chapters on TMS and other brain stimulation treatments. ^[6]

The open-access Indian guideline was used for the technical details in this page: fasting and preparation, anaesthetic and muscle relaxant doses, electrode placement, pulse width and dosing multiples, seizure adequacy, prolonged seizure management and cognitive side-effect mitigation. ^[5] Its indication table and consent framework were also used. ^[5]

• TA59 and the older literature describe ECT as after other options have failed; the Indian guideline and many clinicians describe certain indications (suicidality, catatonia, malignant neuroleptic syndrome) as first-line because speed matters. Both are compatible: the practical question is whether the situation can safely wait. ^[1][5]
• TA59 says ECT should not be used as maintenance therapy in depression; other textbooks and practice descriptions discuss continuation and maintenance ECT in recurrent severe illness. ^[1][5] Follow your local guideline and, in the UK, NICE.
• Efficacy numbers from ECT trials come from different meta-analyses with different definitions of treatment resistance and response; quote them with their source when you need them. ^[2]

• ECT is low-tech once a constant-current machine, a mask, oxygen and a basic anaesthetic and muscle relaxant are available; it can be given safely in a district hospital with a trained psychiatrist, an anaesthetist and an ECT nurse. ^[5]
• Where TMS or VNS is unavailable, ECT remains the neuromodulation treatment of choice for severe depression; psychological and pharmacological alternatives should be optimised. ^[5]
• Outcome monitoring does not need electronic systems: a weekly clinician assessment, a brief cognitive screen (for example the Montreal Cognitive Assessment) and the standard ECT audit dataset are enough. ^[5]

Related MedGrasp topics that a reader will want next include depression and major depressive disorder, bipolar disorder and mania, catatonia, schizophrenia and psychotic disorders, neuroleptic malignant syndrome, and dementia. (These topics are listed as plain text pending verification of their slugs.)

• ECT is a generalised seizure induced by a brief electrical stimulus under general anaesthesia and muscle relaxation, and it is the most effective acute treatment for severe depression.
• It is first-line when speed matters: life-threatening depression, refusal to eat or drink, catatonia, severe mania, neuroleptic malignant syndrome and similar emergencies.
• Otherwise it comes after adequate trials of other treatment, or when the patient prefers it from past experience.
• Common indications include severe, psychotic, melancholic and peripartum depression, bipolar depression, treatment-resistant depression, and mania and catatonia.
• There are no absolute contraindications, but raised intracranial pressure, recent cardiac and cerebrovascular events, unstable arrhythmias, and pregnancy raise risk and require specialist input.
• Consent must be valid, informed, uncoerced and documented, with reassessment after every session and a right to withdraw at any time.
• ECT needs no elaborate imaging; the electrodes are placed on the scalp, and dosing is individualised to the seizure threshold.
• Twice-weekly courses usually run for 6 to 12 sessions, with switching or escalation if there is no response.
• After response, antidepressant or psychological treatment (and lithium augmentation) is started to prevent relapse.
• Memory impairment (acute disorientation, anterograde difficulty, patchy retrograde loss) is the main adverse effect; it is reduced by unilateral placement and briefer pulses.
• TMS is an outpatient magnetic option with a moderate effect size and a good safety profile, allowed by NICE.
• Implanted VNS is a years-long neuromodulation device for treatment-resistant depression, with frequent side effects and limited-quality evidence, restricted by NICE.