Electroconvulsive Therapy

Updated: Sep 24, 2019
  • Author: Mehul V Mankad, MD; Chief Editor: Dennis M Popeo, MD  more...
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Electroconvulsive therapy (ECT) has been demonstrated to be an effective and safe treatment for many psychiatric disorders. [1] The use of ECT still generates significant controversy, however. It has been negatively portrayed in movies such as One Flew Over the Cuckoo's Nest, House on Haunted Hill, and Requiem for a Dream. [2]

Despite such debate, ECT is widely used in the United States and endorsed by the American Psychiatric Association (APA). [3]  Professional associations in Austria, Canada, Australia, Denmark, Netherlands, Germany, and India have offered professional guidelines for its use. [4]  Efficacy rates for the use of ECT in populations of treatment-resistant depression patients exceed 85%, eclipsing all other treatments for severe depression. [5]  In 2018, the United States Food and Drug Administration reclassified ECT devices from Category III (higher risk) to Category II (moderate risk) when used in severe depressive episodes and catatonia. [6]

The image below depicts electroconvulsive therapy.

Electroconvulsive therapy (ECT) is a safe and effe Electroconvulsive therapy (ECT) is a safe and effective treatment for major depressive disorder, bipolar disorder, catatonia, schizophrenia, and several other conditions. ECT uses an electric current to cause a seizure in the brain and is one of the fastest ways to treat severe symptoms of mental illness. It should be considered when a patient does not improve with medication or psychotherapy or when the severity of symptoms is life-threatening.


In 1934, the Hungarian neuropathologist Ladislas Joseph von Meduna began the modern era of convulsive therapy by using intramuscular injection of camphor and pentylenetetrazol to treat catatonic schizophrenia. This approach was dubbed chemical convulsive therapy (CCT). [7]  In 1938, Italian psychiatrist Lucio Bini and neurologist Ugo Cerletti performed the first electrical induction of seizures in a catatonic patient and produced a successful treatment response. Their electrical stimulation of the ictal response was more reliable than chemical stimulation. Initially the approach was given a variety of names, but the term electroconvulsive therapy was eventually identified as the leading nomenclature. Lothar Kalinowsky, one of Cerletti's assistants, left Italy in 1939 and performed the first ECT in the United States in 1940. [8]

In 1978, the APA published the first Task Force Report on ECT, with the goal of establishing standards for consent and the technical and clinical aspects of the conduct of ECT. [9]  In 1985, the National Institutes of Health and National Institute of Mental Health Consensus Conference on ECT endorsed a role for the use of ECT and advocated research and national standards of practice. [10]

Mechanism of Action

The mechanism of action of ECT is not fully known. ECT affects multiple central nervous system components, including hormones, neuropeptides, neurotrophic factors, and neurotransmitters. [11]  

One theory of ECT efficacy is related to the "hyperconnectivity hypothesis." Functional MRI (fMRI) data suggests that patients with depression experience a localized increase in connectivity within the left dorsolateral prefrontal cortex. This hyperconnectivity is decreased in patients treated with ECT in a similar fashion to those individuals treated with chemical antidepressant treatment. [12]  

Positron emission tomography (PET) has been used to study the neurophysiological effects of ECT. In a literature review of studies assessing possible changes in cerebral glucose metabolism by PET before and after ECT, reduction in glucose metabolism after ECT in bilateral anterior and posterior frontal areas represented the most consistent findings. [13]

Nearly every neurotransmitter system is affected by ECT, including adrenergic, serotonin, muscarinic, cholinergic, and dopaminergic systems. Brain-derived neurotrophic factor (BDNF), [14, 15] second-messenger systems, and catechol-O-methyltransferase (COMT) polymorphisms [16] may play a role in ECT. An increase in gamma-aminobutyric acid (GABA) transmission and receptor antagonism has also been observed. [17]  Finally, ECT may also lead to an increase of endogenous opioids. [18, 19]

Although many biomarkers have been studied, no ECT biomarker is routinely used in current clinical practice. [15]

Relevant Anatomy

In the central nervous system, the brain and spinal cord are the main centers where correlation and integration of nervous information occur. Both the brain and spinal cord are covered with a system of membranes, called meninges, and are suspended in the cerebrospinal fluid; they are further protected by the bones of the skull and the vertebral column.

The central nervous system is composed of large numbers of excitable nerve cells and their processes, called neurons, which are supported by specialized tissue called neuroglia. The long processes of a nerve cell are called axons or nerve fibers. The interior of the central nervous system is organized into gray and white matter. Gray matter consists of nerve cells embedded in neuroglia; it has a gray color. White matter consists of nerve fibers embedded in neuroglia; it has a white color due to the presence of lipid material in the myelin sheaths of many of the nerve fibers. The billions of neurons in the brain are connected to neurons throughout the body by trillions of synapses.

For more information about the relevant anatomy, see Central Nervous System Anatomy and Brain Anatomy.


ECT is indicated for selected patients with catatonia, major depressive disorder, bipolar disorder, schizophrenia, and other disorders.


Considered one of the most lethal psychiatric disorders, few treatments are currently available for the treatment of catatonia. No randomized controlled trials of ECT for the treatment of catatonia exist, likely due to the relative rarity and severity of the condition. Patients who have failed medical treatment with benzodiazepines still have at least an 80% likelihood of response to ECT. [20]  World Federation of Societies of Biological Psychiatry (WFSBP) clinical guidelines for the treatment of catatonia related to schizophrenia recommend the use of ECT upon failure of benzodiazepines. [21]

Major depressive disorder

ECT should be considered for patients in the acute phase of major depressive disorder who have a history of treatment resistance (as defined by greater than two antidepressant trials), high degree of symptom severity, or who have psychotic symptoms. [22]  ECT is more effective in patients with psychotic features accompanying their major depressive episode than nonpsychotic patients. [5]  ECT may also be the treatment of choice for patients in whom treatment response is urgently needed, such as patients who are acutely suicidal or those who are refusing food and are nutritionally compromised. These considerations of symptom severity should be given regardless of the number of prior antidepressant medication failures. [22]

ECT may be useful in patients with major depressive disorder for whom medication or psychotherapy has not been effective in maintaining stability during the continuation phase. [23, 22]  ECT should be considered in patients whose condition has failed to respond to medication trials, individuals who have not tolerated indicated medications, or those who have previously shown a response to ECT. [22]  ECT also should be considered in patients with melancholic and atypical depression. [24, 25]

Bipolar disorder

ECT may be considered for patients in the depressive phase, manic phase, or mixed phase of bipolar disorder, [26, 27, 28]  Response rates of depressive symptoms in bipolar patients are similar to unipolar patients, and response rates exceed 70% for the manic phase of the illness. [29] ECT also is a potential treatment for those experiencing severe mania or depression during pregnancy, particularly in the first trimester when teratogenic risks from traditional mood stabilizing medications may be greater. [28, 30] ECT may be efficacious in patients with rapid cycling bipolar disorder. [31] Mania resulting from ECT is uncommon. [1]  


ECT can be considered an adjunctive biological treatment for schizophrenia in combination with first- or second-generation antipsychotics. While treatment with clozapine should be considered in cases of treatment-resistant schizophrenia, the use of ECT may benefit patients already receiving antipsychotic medication. [32]  In those patients who are already receiving clozapine and experiencing breakthrough symptoms of psychosis, the addition of ECT can have adjunctive benefits. [33]

ECT may be particularly beneficial if mood symptoms (depression, mania, or suicidal ideation) are present. [34]

Comorbid disorders

ECT is not recommended for the treatment of obsessive-compulsive disorder (OCD) but may be considered for treating comorbid disorders such as major depressive disorder, mania, and schizophrenia in patients with OCD. [35]  The efficacy of ECT in the treatment of core symptoms of posttraumatic stress disorder (PTSD) is inconclusive. [36]

Other disorders and indications

ECT has been effective in the treatment of neuroleptic malignant syndrome, [37] depression associated with Parkinson disease, [38, 39]  and particular cases of delirium, [40] It has also been effective in treating patients with intellectual disabilities who have treatment-resistant mood or psychotic disorders. [41]


ECT has no absolute contraindications. Many medical conditions place patients at an increased risk for complications and warrant closer monitoring, however. In patients with medical comorbidities (discussed below) additional precautions can mitigate any additional risks associated with performing ECT in medically ill populations.




The ECT treatment and recovery areas should contain equipment to monitor vital signs and provide initial management of medical emergencies. An optimal treatment site includes separate functional areas for waiting, treatment, and recovery. [1]

A stethoscope, a blood pressure measurement device, electrocardiographic and pulse oximetry measurement devices, and an oxygen delivery system should be present. Supplies for inducing anesthesia, providing ventilation, monitoring physiologic functions (including seizure activity), and performing resuscitation should be present.

Examples of ECT machines available in the United States include the Thymatron System IV (Somatics, LLC, Lake Bluff, Ill) and the MECTA Spectrum 5000Q (MECTA Corporation, Lake Oswego, Ore). Extensive details on equipment, physiologic monitoring, and treatment site can be found in the American Psychiatric Association's Task Force Report. [1]

Electrode Placement

Common electrode positions in ECT include the bitemporal, right unilateral (also known as the d'Elia placement), and bifrontal positions. [42]  Bitemporal electrode placement is often referred to as bilateral electrode placement. However, since both bitemporal and bifrontal electrode placements are bilateral, particular care should be given to nomenclature. Further research is needed for the asymmetric bilateral placement and other novel electrode placements. [1, 43]

With bitemporal position, electrodes are placed bifrontotemporally, with the center of each electrode approximately 1 inch above the midpoint of an imaginary line drawn from the tragus to the external canthus. [42]

With unilateral electrode placement, one electrode is typically placed over the nondominant frontotemporal area, and the other electrode is placed just lateral to the midline vertex on the nondominant side. [42]  As the left hemisphere is dominant in most people, unilateral electrode placement is almost always over the right hemisphere and is commonly referred to as right unilateral ECT.

In the bifrontal position, the placement of an electrode on each side of the head is more frontal than in bitemporal placement.


In the first several years of use, ECT was performed without anesthesia. Since the late 1950s, however, ECT has been performed under general anesthesia. [18] The goal is to produce a brief period of general anesthesia accompanied by muscle relaxation. The level of desired sedation exceeds so-called conscious sedation. Inadequate anesthesia may lead to problems such as incomplete unconsciousness and autonomic arousal.

Induction anesthetic agents used in ECT include the following: [1, 44]

  • Methohexital (barbiturate)

  • Thiopental (barbiturate)

  • Etomidate (nonbarbiturate)

  • Ketamine (nonbarbiturate)

  • Fentanyl and analogues (opioid)

  • Propofol (nonbarbiturate)

Methohexital is most commonly used and is the preferred anesthetic for ECT because of its established safety record, effectiveness, and low cost. Propofol, while an effective induction anesthetic, has the greatest anticonvulsant properties of commonly used agents for ECT. Ketamine and etomidate have the least negative impact on seizure duration [1, 44] Inhalational anesthesia with medications such as sevoflurane may also be an option, but such approaches are uncommon. [45]

The cognitive outcome after ECT may be affected by the choice of the anesthetic medication. [46] No matter which anesthetic medication is used, the appropriate dose should be established at each treatment session, and adjustments should be made at subsequent treatment sessions. [1]  As seizure quality is directly affected by the choice of induction anesthetic agent, the ECT treatment team and the anesthesia team should discuss choice of induction agent and should consider seizure efficacy when considering changes to the anesthesia care plan. [47]

Neuromuscular Blockade

Neuromuscular blockers are administered to prevent musculoskeletal complications (fractures or dislocations) related to motor activity during the seizure that occurs with ECT. [18]  This is especially important if the patient has osteoporosis or a history of spinal injury. [48, 18]

Muscle relaxation is traditionally performed with succinylcholine. This agent is the most commonly administered neuromuscular blockade during the ECT procedure. However, rocuronium and other nondepolarizing neuromuscular blockade agents can also be considered particularly when followed by reversal using sugammadex. [49]

A nondepolarizing muscle relaxant may be indicated in patients with pseudocholinesterase deficiencyhypercalcemia, severe neuromuscular disease, severe osteoporosis, or a personal or family history of malignant hyperthermia. [1]

Prior to electrical stimulation, the sufficiency of muscle relaxation is determined by the reduction or loss of deep tendon reflexes; loss of plantar reflexes; loss of muscle tone; the reduction or failure to respond to a nerve stimulator; or any combination of these factors. [1]


ECT is associated with significant, but brief, shifts in autonomic nervous system response. After the electrical stimulus is administered during ECT, the patient experiences a parasympathetic response with a short period of bradycardia. This parasympathetic response typically lasts for a few seconds and is followed by a longer sympathetic nervous system response with tachycardia and a transient rise in blood pressure.

Prior to anesthesia, administration of anticholinergics (eg, atropine, glycopyrrolate) can reduce the risk of vagally mediated bradyarrhythmias or asystole and minimize oral and respiratory secretions. [1]

Anticholinergics can increase preexisting tachycardia and can cause constipation, fecal impaction, and urinary retention. Anticholinergic medication use is also associated with delirium. [1]

Beta Blockade

Due to tachycardia and associated rise in blood pressure (and presumably intracranial pressure) during ECT, clinicians may choose to proactively address the sympathetic nervous system response in patients prone to hypertension. Ideally, the patient's oral antihypertensive regimen would be optimized prior to their initiation of ECT. Once in the treatment room, clinicians can consider delivery of intravenous beta blockers prior to anesthesia induction. While esmolol is an effective intravenous beta blocker, it's anticonvulsant properties negatively impact seizure duration for the purposes of ECT. Other beta blockers, such as labetolol, are known to have less effect on seizure duration. [50]

Pretreatment Evaluation

A collaborative approach between the ECT psychiatrist, medical consultants, and anesthesia provider is a more meaningful and inclusive method than simply asking for clearance. [51]

A pre-ECT evaluation should include the following components: [1, 18, 42, 51]

  • A thorough psychiatric history and examination, including history of response to ECT and other treatments

  • Documentation of results of medication trials with speical attention to dose and duration

  • An indication of hand dominance (i.e., right v. left)

  • A medical history and examination, with special attention to cardiovascular, pulmonary, neurological, and musculoskeletal systems

  • A history of dental problems and examination for loose or missing teeth

  • A history of personal and family experiences with anesthesia

  • A cognitive assessment (at minimum, evaluation of orientation and memory)

Though no routine set of laboratory tests for patients before undergoing ECT has been established, commonly ordered tests prior to initiation of ECT may include the following:

  • Complete blood count

  • Serum chemistry

  • Renal function

  • Electrocardiogram

  • Urinalysis

  • Chest radiograph (especially with cardiovascular or pulmonary disease or history of smoking)

  • Brain imaging (CT or MRI)

  • Electroencephalogram (guided by history and examination)

  • Neuroradiological/neuropsychological tests (guided by history and examination)

  • Spinal radiograph (especially with known or suspected spinal disease)

  • Consultation with medical specialties such as cardiology, neurology, neurosurgery, or endocrinology as required by special medical conditions

Informed Consent

Informed consent is an important part of the process for ECT. In a descriptive systematic review of papers and reports that included 134 testimonies, approximately half the patients reported that they had received sufficient information about ECT and adverse effects. In that review, approximately one third of patients did not feel they had freely consented to ECT, even when they had signed a consent form. [52]

No patient with a capacity to give voluntary consent should be treated with ECT without his or her written, informed consent. The capacity to consent has generally been interpreted as evidence that the patient can understand information about the procedure and can act responsibly on the basis of this information. [1, 53]

The use of involuntary ECT is uncommon but may be critical in life-threatening situations such as catatonia, severe mania, or psychosis. Clinicians must be familiar with local state laws about the use of ECT in patients lacking the ability to provide informed consent. [54]

The informed-consent process should be documented in the patient's medical record and should include a discussion of the disorder, its natural course, and the option of receiving no treatment. [53]  Printed literature and videotapes about ECT may be useful. The family of the patient should be included in the discussion. [55]

The consent form for ECT should include the following information: [1, 53]

  • A description of the ECT procedure with proposed benefits and potential risks

  • A description of treatment alternatives including a discussion of no treatment

  • A discussion of options regarding electrode placement and stimulus type

  • The typical range for the number of treatments

  • A statement concerning the need for continuation or maintenance treatment including pharmacotherapy and/or maintenance ECT

  • Discussion of the possible risks, including death, cardiac dysfunction, confusion, and memory impairment

  • A listing of patient requirements during the ECT course, such as taking nothing by mouth after midnight and stopping driving

  • A statement that consent is voluntary and can be withdrawn at any time

Medical Comorbidity and ECT

Concurrent medical conditions and their treatments may affect the response to and risks associated with electroconvulsive therapy. [1]

Neurological comorbidities

Caution is advised for patients with space-occupying intracranial lesions, as these individuals are at increased risk for edema and brain herniation after ECT. Patients with intracerebral lesions that lack a mass effect can safely undergo ECT. [56]

ECT increases intracranial pressure and blood flow to the brain. Patients who have increased intracerebral pressure or are at theoretical risk for cerebral bleeding, such as those with cerebrovascular disease and aneurysms, may be at increased risk during ECT. Patients with very recent strokes may be an area of special concern. However, patients with remote history of cerebrovascular accident have not shown adverse effects from ECT when studied. [56]

ECT has been safely used after coil embolization of a cerebral aneurysm. [57] ECT has been used in the presence of Charcot-Marie-Tooth disease, [58] arachnoid cysts, [59, 60] epilepsy, [1, 61] myasthenia gravis, [1] and multiple sclerosis. [1]

Cardiac comorbidities

Patients with cardiac disease can be evaluated by a cardiologist who can provide recommendations for the patient’s management during the course of ECT. [1, 18, 62] In patients with unstable angina, uncompensated congestive heart failure, uncontrolled hypertension, high-grade atrioventricular block, and symptomatic ventricular arrhythmias, ECT raises the risk of symptoms from these cardiac conditions. [1] Patients with hypertension should be stabilized with antihypertensive medications before undergoing ECT. [63] Patients with a recent myocardial infarction (MI) may be at higher risk of cardiac complications such as MI, although the risk decreases as the time interval between the MI and ECT increases.

With a proper pre-ECT cardiac and pacemaker/defibrillator assessment, patients with cardiac pacemakers and implantable cardioverter defibrillators can safely undergo ECT. [64] ECT has been used in the presence of severe aortic stenosis [65] , and it has been used after heart transplantation, though further studies are needed. [66]

Other comorbidities

Patients who have medical disorders associated with autonomic sensitivity (eg, clinically evident hyperthyroidism, pheochromocytoma), with sensitivity to anesthesia (eg, amyotrophic lateral sclerosis, porphyria, pseudocholinesterase deficiency), or with cognitive sensitivity (eg, traumatic brain injury) may require more extensive workup and closer monitoring during ECT. [48]

Patients with gastroesophageal reflux disease may experience worsening symptoms during ECT, due to stimulation of the vagus nerve. [18]

Patients with diabetes, metabolic disorders (eg, hyperkalemia, hypokalemia, hyponatremia), chronic obstructive pulmonary disease, hypercoagulable states, glaucoma, and renal disease require close monitoring during ECT. [1, 67]

Electroconvulsive Therapy and Medications

Some medications may be continued during ECT, some medications are decreased or withdrawn, and some augment ECT. [1]

In general, medications that decrease acute risks from general anesthesia or the ECT procedure should be given prior to treatment. Medications such as antihypertensives, antianginals, antiarrhythmics (except lidocaine), bronchodilators (except theophylline), glaucoma medications (except long-acting cholinesterase inhibitors), and corticosteroids [1] may be safely given prior to ECT. Antacid medications and proton pump inhibitors may be safely used. [18]

Diuretics and hypoglycemics may be withheld until after an ECT treatment. [1, 48] Theophylline should be discontinued if possible given the proconvulsant effect of that medication. [1, 48]

Anticonvulsants should be lowered in dose as much as clinically possible during ECT, because antiepileptics may raise seizure threshold, adversely affect seizure expression, or possibly affect clinical efficacy. [1] One review found that the combination of various anticonvulsants and ECT was safe and effective, though no evidence indicated that this combination increased efficacy. [68]

Monoamine oxidase inhibitors (MAOIs) can be continued during the course of ECT. Nevertheless, some clinicians withdraw MAOIs 7–14 days before ECT. [1]

The combination of ECT and antipsychotics may be more effective in schizophrenia than either treatment alone. [1, 33] Although definitive conclusions cannot be made, the combination of ECT and antipsychotics is safe and effective in schizophrenia, especially in patients whose symptoms are refractory to conventional treatments. [69, 70]  Although clozapine is known to induce spontaneous seizures, this adverse effect was not increased in populations receiving ECT and clozapine simultaneously. [33]

Debate about the safety of lithium during ECT is ongoing, as some patients have no problems but others may have a higher risk for delirium or prolonged seizures. [1, 42, 71]  A study of maintenance ECT included lithium as a long-term medication without increased cognitive adverse effects in the patients receiving lithium and ECT. [23]  Benzodiazepines should be discontinued if possible. If benzodiazepines cannot be discontinued, then the dose should be reduced to the lowest effective dose. [1]

Electroconvulsive Therapy and Pediatrics

Many child and adolscent psychiatrists have little training or knowledge of ECT. The American Academy of Child and Adolescent Psychiatry published an overview of ethical issues in January 2012. The guidelines suggest that written, informed consent be obtained from the parents and that a second opinion on the necessity of ECT be obtained from an independent psychiatrist not involved in the treatment of the minor. [72]

Diagnostic considerations for ECT in an adolescent patient [73] include severe or persistent major depression or mania [74] with or without psychotic features, schizoaffective disorder, schizophrenia, catatonia, [75] or neuroleptic malignant syndrome. The symptoms must be severe, persistent, and disabling.

Before considering ECT in children and adolescents, lack of treatment response should be documented. Lack of treatment response is defined as failure to respond to at least 2 adequate trials of appropriate psychopharmacological agents accompanied by other appropriate treatment modalities. [73]  

The response rate for mood disorders to ECT in the pediatric population is 63% and 80% for catatonia according to the largest review of ECT use in the pediatric population. [76]  A more recent systematic review from 2013 found similar results. [77]

Electroconvulsive Therapy in the Elderly

Geriatric patients can be particularly sensitive to adverse effects from daily medications, including psychotropic medications. The use of ECT in the elderly population may reduce risks associated with polypharmacy if the number of psychotropic medications can be reduced. A high proportion of patients who receive ECT are in the geriatric age group. [1] In elderly patients, ECT has been used to treat catatonia, [78] bipolar mania, [79] and psychotic disorders. [78]

Generally, geriatric patients with depression have better outcomes with ECT than do younger patients. [1] ECT is especially indicated for patients with depression who are at risk for harm because of psychosis, suicidal ideation, or severe malnutrition, [80, 81, 82] but it is also helpful for treatment-resistant nonpsychotic major depression. [83, 84]

Seizure threshold may rise with increasing age, and effective seizures may be hard to induce. [1] Geriatric patients may be at a higher risk for persistent confusion and greater memory deficits during and after ECT. [1]

Electroconvulsive Therapy in Pregnancy

ECT is considered safe and effective for the mother and fetus in the treatment of major depressive disorder during pregnancy. [22, 63] ECT is a potential treatment for patients with bipolar disorder who are experiencing mixed episodes [27] , severe mania, or severe depression during pregnancy. [28]

ECT can be considered as an option to decrease extended exposure to psychotropic medication during pregnancy [85] or for those pregnant women whose symptoms fail to respond to standard therapy. [86] Obstetric consultation should be obtained and fetal monitoring should be used, when appropriate.

Patients in late pregnancy should lie on their left side during ECT to ensure adequate blood flow to the fetus. Hyperventilation is to be avoided. [87]

Transmission of anesthesia medications across the maternal-fetal barrier is considered to be minimal. [18] ECT is considered relatively safe in terms of teratogenicity and neonatal toxicity. [1] Because of an increased risk of gastric reflux and possible aspiration, pregnant women may be premedicated with a nonparticulate antacid, such as sodium citrate. [1]

Generally, breastfeeding does not need to be interrupted during ECT. Anesthetic agents pose little risk to the nursing infant. Exposure of nursing infants to medications may be decreased if the mother delays feeding for several hours after an ECT treatment. Alternatively, breast milk may be collected and stored before an ECT treatment and given via bottle after an ECT treatment. [1]




The electrical stimulus must be sufficient to induce a seizure. Modern ECT devices use either a brief square wave pulse (approximately 1 milisecond) or ultra-brief square wave pulse (less than 0.5 milisecond). Data suggests that brief pulse ECT requires fewer treatments but that ultra-brief pulse ECT is associated with fewer cognitive adverse effects. [88]  The dose is measured in millicoulombs of charge delivered. [42]

Three methods are used to determine stimulus intensity and dosing, as follows: [1, 42]

  • Empirical titration

  • Formula-based titration

  • Fixed dosages

In empirical titration, progressively higher doses are given during the first ECT session until seizure threshold is reached. This provides the most precise method for determining seizure threshold. [1] In formula-based titration, the dose is based on factors such as age, gender, and electrode placement. In the third method, a fixed dose is given independent of patient or other factors.

Seizure Quality

Motor seizure duration (i.e., witnessed seizure activity) has little bearing on efficacy of ECT. Nevertheless, if the seizure duration is less than 15 seconds in motor and EEG manifestations, the seizure was very likely limited by insufficient electrical stimulation. [1]

The EEG is used to confirm total seizure activity and to document seizure duration. [42]  Motor seizure duration can be difficulty to ascertain during the modern ECT procedure due to the use of neuromuscular blockade (succinylcholine or nondepolarizing blockers). Therefore, motor seziure activity can be monitored using the "cuff technique," in which the circulation of the neuromuscular blocking agent is restricted from the hand or foot via a temporary tourniquet. This restriction of blood flow allows visual or instrumented observation of motor activity to confirm the presence of a seizure. [1, 42]  Such redundancy can be useful in the rare event of EEG failure during ECT.

Frequency of Treatments

In the United States, ECT is most commonly performed 3 times per week regardless of electrode placement. [1]  Treatments 2 times per week may result in less memory impairment than treatments 3 times per week and can be used in patients who are sensitive to adverse effects from ECT or general anesthesia. [1]  Compared with treatments administered 3 times per week, twice-weekly treatments result in the same degree of final clinical improvement, although possibly at a slower rate of response. [1]

Number of Treatments

The initial phase of treatment to induce maximum response is commonly referred to as index ECT. The number of treatments needed to achieve a full clinical response in patients varies widely. Although the typical number of treatments is 6–12, [63, 42] some patients may respond after a few treatments, and some patients may not respond until after 10 treatments. [1] The total number should be a function of the patient's degree and rate of clinical improvement, as well as tolerance of the procedure. [1] Index ECT is stopped when maximal improvement is reached. [1]  ECT has a high rate of relapse if no continuation treatment (medications or less frequent ECT) is provided (see Post-Procedure below). [89]

Continuation and Maintenance Electroconvulsive Therapy

Continuation ECT is used for prevention of relapse. [51]  Because of the high risk of relapse after ECT, especially during the first few months, the argument for aggressive continuation therapy is compelling. [1]  The term Continuation ECT is often used to describe less frequent treatments delivered in the months immediately following a successful index course of ECT. Maintenance ECT is sometimes used as the term for less frequent treatments delivered several months after an index course of ECT. These terms are often combined under the rubric of maintenance ECT.

Indications for maintenance ECT include a history of ECT-responsive illness, patient preference, resistance or intolerance to medications alone, and ability of the patient (or surrogate consenter) to provide informed consent and adhere to the treatment plan. [1]

Maintenance ECT is often combined with medication therapy as well. Combined trials of pharmacotherapy and maintenance ECT have included nortriptyline, lithium, and venlafaxine. Results from these studies are mixed. Some data suggests that the combination of ECT and maintenace medication is superior to medication alone. Other data suggest that the two approaches are equal. [90, 91, 23]

Maintenance Medication

Pharmacological therapy after ECT varies with a patient's diagnosis. [1]  Patients with major depressive disorder and whose symptoms are resistant to pharmacological therapy to induce remission of symptoms still may benefit from the same class of medication during the maintenance phase after ECT. [92]  Alternately, clinicians and patients may choose a medication from a different drug class during the maintenance phase due to lack of efficacy during prior medication trials with pharmacologic agents known to the patient. As with any antidepressant medication trial, adequate duration and dosage should be considered in design of the maintenance medication plan.


Individual, family, or group psychotherapy is helpful for some patients after ECT to treat residual symptoms, cope with stress, and encourage a return to normal life. [1]  Preliminary evidence suggests that cognitive-behavioral therapy and other psychotherapies may lengthen the antidepressant effects of ECT. [93, 94]




The principal complications of electroconvulsive therapy (ECT) are confusion and cognitive adverse effects.


In general, ECT is an exceedingly safe procedure. The morbidity and mortality risks of ECT should be weighed against the acute and chronic risks of medications often used in patients with treatment-resistant psychiatric disorders. The same risks should also be weighed against the risk to the patient of continued symptoms of their treatment-resistant psychiatric disorder. Cardiovascular complications (eg, arrhythmias [95] ) and pulmonary complications are the leading causes of mortality due to ECT. [1]  The mortality rate for ECT is estimated to be 1 per 10,000 to 1 per 80,000 treatments. This rate is about the same as that associated with minor surgery. [1] The mortality rate may be higher in patients with severe medical disorders. [1]

Cognitive adverse effects

Cognitive adverse effects are the major limitations to the use of ECT. [1] The most severe effects are observed postictally, with a brief period of disorientation and impairments in attention, praxis, and memory. [1] The effects reverse over time and are considered mild in most patients who experience them. [96]  Individual patients vary significantly in the extent and severity of cognitive adverse effects experienced after ECT. Most data support the conclusion that bilateral (specifically bitemporal) ECT is associated with greater frequency and severity of cognitive adverse effects than nondominant unilateral ECT. [1, 96]  Additional data supports the association between fewer cognitive adverse effects in patients receiving ultra-brief pulse ECT as compared to brief pulse ECT. [88]  Various biochemical, electrophysiological, and neuroimaging correlates of the cognitive adverse effects of ECT exist. [97]

Anterograde and retrograde amnesia may result from ECT. [1] After ECT, anterograde amnesia resolves rapidly. With retrograde amnesia, deficits are greatest for events closest to the time of treatment. [1, 63] Postictal delirium, exemplified by disorientation and confusion, may occur in a minority of patients. [1]  This form of delirium may be related in part to the ECT procedure or may be secondary to repeated episodes of general anesthesia. Use of dexmedetomidine or other agents to mitigate adverse effects of ECT may be effective but can also lengthen the anesthesia recovery period. [47]

Other adverse effects

Prolonged seizures and status epilepticus may be more likely when patients receive medications that lower seizure threshold. [1]  ECT treatment programs should become familiar with emergency treatment of status epilepticus and maintain ready access to anticonvulsant medications in the event of such an adverse effect. Prolonged apnea is rare but may occur in patients who metabolize succinylcholine slowly. [1]

Headache is common. It can be treated with medications such as aspirin, acetaminophen, nonsteroidal anti-inflammatory drugs, sumatriptan, [98] and, rarely, more potent analgesics such as codeine. [1] Muscle soreness and nausea may occur. [1] Mania resulting from ECT is rare. [1]


Questions & Answers


What is electroconvulsive therapy (ECT)?

How has electroconvulsive therapy (ECT) evolved over time?

What is the mechanism of action for electroconvulsive therapy (ECT)?

What is the anatomy relevant to performing electroconvulsive therapy (ECT)?

When is electroconvulsive therapy (ECT) indicated?

What are the contraindications for electroconvulsive therapy (ECT)?

What equipment is needed to perform electroconvulsive therapy (ECT)?

What are the electrode placements for electroconvulsive therapy (ECT)?

What is the role of anesthesia in electroconvulsive therapy (ECT)?

What is the role of neuromuscular blockades in electroconvulsive therapy (ECT)?

What is the role of anticholinergics in electroconvulsive therapy (ECT)?

What is the role of beta blockade in electroconvulsive therapy (ECT)?

What is included in the preprocedural evaluation for electroconvulsive therapy (ECT)?

What information is included in the informed consent for electroconvulsive therapy (ECT)?

How do medical comorbidities affect electroconvulsive therapy (ECT)?

How do medications affect electroconvulsive therapy (ECT)?

What is the role of electroconvulsive therapy (ECT) in the treatment of children and adolescents?

What is the role of electroconvulsive therapy (ECT) in the treatment of the elderly?

What is the role of electroconvulsive therapy (ECT) in the treatment of pregnant women?

How is electroconvulsive therapy (ECT) performed?

How does seizure duration affect the efficacy of electroconvulsive therapy (ECT)?

What is the frequency of electroconvulsive therapy (ECT) treatments?

What is index electroconvulsive therapy (ECT)?

What is continuation electroconvulsive therapy (ECT)?

What is the role of medication following electroconvulsive therapy (ECT)?

What is the role of psychotherapy following electroconvulsive therapy (ECT)?

What are the possible complications of electroconvulsive therapy (ECT)?

What are the morbidity and mortality risks associated with electroconvulsive therapy (ECT)?

What are the possible cognitive adverse effects of electroconvulsive therapy (ECT)?

Which patients are at risk for prolonged seizures and status epilepticus following electroconvulsive therapy (ECT)?

What are possible adverse effects following electroconvulsive therapy (ECT)?