Electroconvulsive therapy (ECT) and other biological non-pharmacological treatments: mechanism of action, indications, contraindications, and procedures

01Electroconvulsive therapy

Electroconvulsive therapy (ECT) induces a brief generalised seizure by passing a small electric current between electrodes on the scalp, while the patient is under a short general anaesthetic and a muscle relaxant. It is the most effective treatment for severe depression, acts faster than antidepressants, and remains one of the most stigmatised treatments in medicine.

Convulsive treatment grew from a mistaken belief that epilepsy and schizophrenia rarely occur together, so that seizures might cure psychosis. They did not cure schizophrenia, but worked remarkably in depression and catatonia.

1. 1934

   Chemical convulsions

   Ladislas Meduna in Budapest induces seizures with camphor, then pentylenetetrazol, in catatonic schizophrenia.

2. 1938

   Electrical convulsions

   Ugo Cerletti and Lucio Bini in Rome induce the first seizure with electricity, which is easier to control and soon becomes standard.

3. 1940s–50s

   Modified ECT

   Curare and then suxamethonium, with short anaesthesia, prevent the fractures and fear of unmodified treatment.

4. 1975

   Stigma

   The film One Flew Over the Cuckoo's Nest fixes a punitive picture of ECT in the public mind; use declines.

5. 1980s

   Brief pulses

   Brief-pulse machines replace sine-wave current, with EEG monitoring and dose titration, cutting cognitive side effects.

6. 2003

   Evidence and standards

   A meta-analysis confirms that real ECT beats sham ECT and drugs; in the UK, NICE guidance and an accreditation service set standards.

Use varies widely across Europe: each Nordic country treats more than 200 people per million a year, most of western Europe 30 to 100, Poland about 13 and Italy about 3, differences that reflect history and attitudes more than evidence.

02Mechanism of action

How ECT works is not settled, but several lines of evidence point the same way. The seizure itself is needed: sham ECT, an anaesthetic without a seizure, is clearly less effective. It is not sufficient, though: right unilateral ECT at a dose just above threshold produces full seizures yet works poorly, so where and how strongly the brain is stimulated matters too.

Older explanations are rejected: that ECT works through fear or punishment, through memory loss, or through brain injury. Imaging, post-mortem and animal studies show no structural damage from modern ECT.

03Indications

ECT is chosen when a fast, reliable response is needed, when other treatments have failed or cannot be tolerated, or when the patient prefers it because it worked before.

In the UK, NICE’s 2003 ECT guidance limits ECT to rapid, short-term improvement of severe symptoms when other treatments have failed or the illness is potentially life-threatening, in catatonia or a prolonged or severe manic episode, and does not support its general use in schizophrenia. For depression its advice was replaced in 2009 and now sits in the 2022 depression guideline: consider ECT for severe depression if the patient prefers it, often after a past good response, if a rapid response is needed, or if other treatments have failed. A 2025 NICE review proposed withdrawing TA59 and moving its advice on mania, catatonia and schizophrenia into the guidelines for each condition.

ECT is a reasonable choice in two groups often thought too fragile for it. In older people it is well tolerated and often works better than in younger ones. In pregnancy, and for severe postpartum illness, it avoids drug exposure and acts fast, with obstetric and anaesthetic input.

04Contraindications and high-risk conditions

There are no absolute contraindications: the risk of ECT is weighed against the risk of the illness, which in severe depression can be death. The risks come from the anaesthetic and from what the seizure does to the body: a brief surge of vagal tone (slow heart, even asystole), then a sympathetic surge (fast heart, sharp rise in blood pressure), and a rise in cerebral blood flow and intracranial pressure.

Drugs matter as well, because they change the seizure threshold or the seizure:

05The procedure

Consent and capacity

ECT is given with the patient's informed consent wherever possible. The explanation covers why it is proposed, what happens, the likely benefit, the risks of the anaesthetic and the cognitive effects, the alternatives and the risk of having no treatment. Consent is given for a course, can be withdrawn at any time, and is checked before every session.

When a patient lacks capacity, the law decides, and it differs between countries. In England and Wales, the Mental Health Act allows ECT for a detained patient who has capacity only with their consent; for one who lacks it, an independent second-opinion doctor must approve it, and it cannot be given against a valid advance decision refusing it. Only an emergency, to save life or prevent serious deterioration, allows treatment before these steps. Elsewhere in Europe the rules differ widely: in a 2024 survey of 18 countries, practitioners in 7 could give ECT without consent to a patient about to die of psychotic depression without anyone else's approval, while in the other 11 the law barred it or first required a court, an ethics committee or an independent second opinion.

Electrodes, pulses and dose

The current is given in short pulses. Brief pulses of about 0.5 to 1.5 milliseconds have replaced the old sine wave, which caused more confusion. Ultrabrief pulses, below 0.5 milliseconds and usually about 0.3, with right unilateral placement spare memory further, at the cost of a few more sessions.

The dose is set against the seizure threshold, the smallest charge that produces a seizure, which varies many-fold between people. It is higher in older people and men and is raised by benzodiazepines and anticonvulsants. At the first session the threshold is found by titration, starting low and stepping up. Later sessions use about one and a half to two and a half times the threshold for bitemporal or bifrontal ECT and much more, often about six times, for right unilateral ECT, which barely works near threshold. Because ECT raises the threshold, the dose usually rises during the course.

A session

1. 1

   Prepare

   Physical work-up, blood tests and, where indicated, an ECG; baseline depression rating and cognitive test; drugs reviewed; consent checked; fasted as for any anaesthetic, bladder emptied, dentures out.
2. 2

   Anaesthetise

   IV access; ECG, oxygen saturation, blood pressure and EEG monitoring; oxygen by mask, a short-acting anaesthetic such as propofol or methohexital, then a muscle relaxant, usually suxamethonium.
3. 3

   Stimulate

   A bite block protects the teeth and tongue, because the current makes the jaw clench directly. The electrodes are placed and checked, and the stimulus is given.
4. 4

   Watch the seizure

   The EEG seizure, typically lasting from about 20 seconds to two minutes, shows the treatment was adequate; a cuff on one limb, inflated before the relaxant, lets its movements be seen. A seizure lasting more than about two to three minutes is stopped with an IV benzodiazepine or more anaesthetic.
5. 5

   Recover

   Airway and vital signs are monitored by a recovery nurse until the patient is awake and oriented, usually within an hour.

The course

ECT is usually given twice a week in the UK and much of Europe, and often three times a week in the USA; more frequent sessions bring faster recovery but more cognitive effects. Depression usually needs 6 to 12 sessions, mania sometimes more, and catatonia often fewer. Mood and cognition are rated through the course, which stops when the patient has remitted, when two or three further sessions bring no more gain, or when side effects outweigh benefit.

sessions in a usual course

2a weeksessions in a usual course

for depression, typically

6–12sessionsfor depression, typically

treatments, the death rate in a pooled analysis

2.1per 100,000treatments, the death rate in a pooled analysis

06Adverse effects and outcome

Adverse effects

Most short-term effects are mild and pass within hours:

• Headache, in about half, and aching muscles, from suxamethonium; nausea; jaw pain.
• Confusion after waking, more common in older people, after bitemporal ECT and with high doses; it can need a calm room, reassurance and sometimes a benzodiazepine.
• Rarely a prolonged seizure, an arrhythmia, aspiration, damage to teeth, or a switch into mania in bipolar depression.
• Death is very rare, mostly cardiac in people with heart disease, and no commoner than with a general anaesthetic for surgery.

Cognitive effects are the main concern for patients:

The effects are less with right unilateral placement, ultrabrief pulses, doses based on titration and fewer sessions a week. Cognition is checked before the course and during it, and the technique is changed if it falls. Depression itself impairs memory, and many patients' memory and concentration are better after recovery than before ECT.

Outcome

In a meta-analysis, real ECT clearly beat both sham ECT and antidepressants in depression, and recovery often comes within three to four weeks.

The weakness is relapse. Without continuation treatment, most patients relapse within months: in one trial, 84 per cent on placebo relapsed within 24 weeks, against 39 per cent on nortriptyline with lithium. Even with continuation drugs, about a third relapse within six months and half within a year. After a course, an antidepressant or psychological treatment is started or continued, and lithium is considered; continuation ECT, sessions spaced out over months, is an option for people who have relapsed despite drugs.

07Other brain stimulation

Several newer treatments stimulate the brain without a seizure or an anaesthetic. They are less effective than ECT but much better tolerated.

Repetitive transcranial magnetic stimulation

Repetitive transcranial magnetic stimulation (rTMS) uses a rapidly changing magnetic field from a coil held on the head to make neurons fire in the cortex beneath. High-frequency stimulation, around 10 Hz, excites the left dorsolateral prefrontal cortex, which is underactive in depression; low-frequency stimulation over the right side has the opposite effect. Theta-burst stimulation delivers a session in about three minutes instead of about 40 and was as effective in a large trial, and accelerated schedules of several sessions a day are being tested.

European guidelines rate high-frequency left-sided rTMS as definitely effective in depression, and it is offered in many European countries, though funding varies. It needs no anaesthetic and has no effect on memory, but it is less effective than ECT, especially in psychotic depression. Metal in or near the head, such as cochlear implants or aneurysm clips, rules it out, and epilepsy raises the risk of a seizure.

Transcranial direct current stimulation

Transcranial direct current stimulation (tDCS) does not make neurons fire; it shifts their resting potential, the anode making the cortex beneath it more excitable. It is cheap and portable, and a fully remote, sham-controlled trial of home treatment was positive, but results across trials are mixed.

Vagus nerve and deep brain stimulation

Vagus nerve stimulation (VNS), first used for epilepsy, is reserved for chronic, treatment-resistant depression.

Deep brain stimulation (DBS), established for Parkinson's disease, has been tried in the most resistant depression, with targets such as the subcallosal cingulate cortex, and in severe obsessive-compulsive disorder, with targets in the ventral capsule and striatum. Early open studies in depression were promising, but sham-controlled trials have given mixed results, and it remains experimental, done in a few specialist centres.

08Light therapy and chronotherapy

The circadian clock in the suprachiasmatic nucleus is set mainly by light reaching the retina, and many depressed patients have disturbed sleep and rhythms. Chronotherapies act on that clock.

Bright light therapy

Bright light therapy was first used for seasonal affective disorder, depression that recurs each winter, with oversleeping, overeating and carbohydrate craving. Morning light advances the circadian rhythm and suppresses melatonin.

Evening light is less effective and delays sleep. Most trials are small and short, so the size of the benefit is uncertain.

Sleep deprivation

Staying awake through one night, total sleep deprivation or wake therapy, lifts depression within hours in about half of patients, faster than any other treatment. The effect is usually lost after the next night's sleep, even a short nap.

09Neurosurgery for mental disorder

Psychosurgery, now called neurosurgery for mental disorder, is mainly history. In 1935 the Portuguese neurologist Egas Moniz, with the surgeon Almeida Lima, cut the white matter of the frontal lobes in patients with severe mental illness, and Moniz shared the Nobel Prize in 1949. In the USA Walter Freeman and James Watts spread the standard prefrontal lobotomy from 1936, and from 1946 Freeman's quick transorbital operation, done outside operating theatres. Tens of thousands of people were operated on in Europe and North America, often with severe apathy, personality change and epilepsy, before antipsychotics in the 1950s and changing attitudes ended it.

Modern procedures are different: small, precise lesions, placed stereotactically with MRI guidance in the circuits linking the frontal lobes and the limbic system.

It is considered only for severe, chronic depression or OCD that has resisted every other treatment, including ECT and psychological therapy, in a patient who wants it and has capacity to consent. It is tightly regulated: in England and Wales any patient, detained or not, needs their own consent plus approval by an independent panel. Only a handful of operations are done in the UK each year, and in many countries none, as reversible deep brain stimulation has largely taken its place.