Electroconvulsive Therapy (ECT) — Indications, Contraindications, Procedure, Side Effects and Mechanism

Electroconvulsive therapy (ECT) is the controlled electrical induction of a generalised cerebral seizure under general anaesthesia to treat psychiatric illness. Convulsive treatments go back almost a century — insulin shock, camphor and metrazol were used first — but in 1938 Ugo Cerletti and Lucio Bini introduced electrically induced seizures as a more reliable and controllable method. General anaesthesia and muscle relaxants were added later.

The therapeutic effect depends on the seizure, not on the current or the convulsion. That is why modern ECT abolishes the visible convulsion with a muscle relaxant while the EEG still records the seizure. A typical course is an index phase of several sessions to produce remission, sometimes followed by continuation or maintenance ECT to prevent relapse.

The primary indication is severe or treatment-resistant major depressive disorder — depression that has not responded to multiple adequate antidepressant trials or that seriously impairs daily living. ECT also has established efficacy in several other severe conditions:

UK guidance is more restrictive. NICE technology appraisal TA59 recommends ECT only to achieve rapid, short-term improvement of severe symptoms after an adequate trial of other treatments has failed and/or when the condition is potentially life-threatening — naming catatonia and a prolonged or severe manic episode. It asks for a documented risk–benefit assessment (anaesthetic risk, comorbidities, cognitive impairment, and the risk of not treating), valid informed consent whenever the person has capacity, extra caution in pregnancy, older people and young people, reassessment after every session, and stopping once a response is achieved.

Benefits can last months to years, particularly with maintenance treatment and appropriate pharmacotherapy. For the drug side of mood disorders, see depression and bipolar disorder; for refractory psychosis, see schizophrenia and antipsychotics.

ECT has no absolute contraindications. The induced seizure transiently raises blood pressure, heart rate, myocardial oxygen demand and intracranial pressure, so the risks lie in patients who cannot tolerate those surges.

ECT is given by a team of at least a psychiatrist, an anaesthesiologist and a nurse, usually as an outpatient after an overnight fast, with standard ASA monitoring (ECG, blood pressure, pulse oximetry) plus EEG and EMG.

1. Pre-ECT work-up: history, examination, medication review. Theophylline is avoided (prolonged seizures); anticonvulsants, benzodiazepines, Z-drugs, gabapentin and lithium may raise the seizure threshold or add post-ECT delirium and may need adjustment.
2. Pre-oxygenation; an anticholinergic may be given to prevent bradycardia, asystole and secretions.
3. Induction: methohexital (0.75–1 mg/kg) is the gold-standard agent — rapid, short-acting, minimal effect on seizure threshold. Propofol and thiopental are anticonvulsant and shorten seizures; etomidate lengthens them.
4. Muscle relaxation: succinylcholine (0.75–1 mg/kg) is the usual agent; rocuronium or vecuronium if succinylcholine is contraindicated (hyperkalaemia risk, neuromuscular disease, malignant hyperthermia).
5. A cuff inflated on one ankle before the relaxant keeps that foot unparalysed, so the motor seizure can be seen. A bite block is essential — the relaxant does not stop masseter contraction from direct stimulation.
6. Stimulus: brief-pulse (0.5–2 ms) or ultrabrief (<0.5 ms) current through bitemporal, bifrontal or right unilateral electrodes. Brief hyperventilation before the stimulus can increase seizure intensity.
7. Seizure monitoring: an adequate seizure usually lasts 15–70 seconds (EEG seizure about 25% longer than the motor seizure). Seizures under 15 seconds may be ineffective; seizures beyond 2 minutes are terminated with half the induction dose of propofol or methohexital, or a benzodiazepine.

The stimulus first produces a parasympathetic discharge lasting about 15–20 seconds during the tonic phase, which can cause bradycardia, premature beats, AV block and even transient asystole — more likely with a subconvulsive (failed) stimulus. This is followed by a sympathetic surge with tachycardia and hypertension, raised myocardial oxygen consumption and raised intracranial pressure.

• Short-acting IV beta-blockers can blunt hypertension and tachycardia but may shorten the seizure.
• Blood glucose can rise transiently — monitor diabetic patients.
• Pacemakers and ICDs are not contraindications; detection functions are temporarily switched off and external defibrillation kept ready.
• In pregnancy: avoid hyperventilation, use left uterine displacement after 20 weeks, and monitor the fetal heart and uterine activity after 24 weeks.

Despite these effects, the American Heart Association and American College of Cardiology class ECT as a low-risk procedure, and its overall mortality is extremely low in a controlled medical setting. The remaining barrier to its use is stigma from historical, unmodified practice and media portrayals.

The mechanism is incompletely understood. The main hypotheses involve changes in cerebral blood flow and metabolism, neurotransmitters, neuroplasticity and neuroendocrine function:

• Neurotransmitter (monoamine) theory: ECT causes a widespread reduction in cortical 5-HT2 receptor density, paralleling antidepressant effects, and modulates dopamine and noradrenaline signalling.
• Neurotrophic / neuroplasticity theory: BDNF levels — often low in depression — rise after ECT, and imaging shows increased hippocampal volume, suggesting neurogenesis.
• Neuroendocrine theory: ECT acts on a hyperactive hypothalamic–pituitary–adrenal axis with impaired cortisol feedback.
• Functional connectivity and blood flow: changes in frontal, hippocampal and amygdala circuits that are abnormal in severe depression.

The Mental Healthcare Act, 2017 places specific limits on ECT:

• Section 95(1)(a): ECT without muscle relaxants and anaesthesia is prohibited.
• Section 95(1)(b): ECT for minors is prohibited — but under section 95(2), if the psychiatrist in charge considers it necessary, it may be given with the informed consent of the guardian and prior permission of the concerned Board (the Mental Health Review Board).
• Section 94(3): emergency treatment under the Act does not permit a medical officer or psychiatrist to use ECT.
• The same section also prohibits sterilisation as a treatment for mental illness and chaining in any form.