Electroconvulsive Therapy

Updated: Jan 12, 2015
  • Author: Raj K Kalapatapu, 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. One review concluded that ECT is only marginally more effective than placebo (ie, sham ECT). [2] ECT has been viewed as harmful by the general public, [3] psychiatric patients, [4] and mental health professionals. [5]

ECT has also been perceived as a form of violence against women. [6] 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. [7]

Despite such debate, ECT is used in the United States and endorsed by the American Psychiatric Association. [8] Approximately 100,000 patients annually receive ECT in the United States. [9] Professional associations in Austria, Canada, Australia, Denmark, Netherlands, Germany, and India have offered professional guidelines for its use. [10]

The image below depicts electroconvulsive therapy.

Electroconvulsive therapy (ECT) can help some peop Electroconvulsive therapy (ECT) can help some people with bipolar disorder. ECT uses an electric current to cause a seizure in the brain and is one of the fastest ways to ease severe symptoms. It is usually a last resort when a patient does not improve with medication or psychotherapy.


In the 1500s, the Swiss physician Paracelsus (Auroleus Phillipus Theostratus Bombastus von Hohenheim) induced seizures by administering camphor by mouth to treat psychiatric illness. [9] The first published report of the use of seizure induction to treat mania using camphor was in 1785. [9]

In 1934, the Hungarian neuropathologist Ladislas Joseph von Meduna began the modern era of convulsive therapy by using intramuscular injection of camphor (soon replaced with pentylenetetrazol) to treat catatonic schizophrenia. [9] In 1938, Italian psychiatrist Lucio Bini and neurologist Ugo Cerletti performed the first electrical induction of a series of seizures in a catatonic patient and produced a successful treatment response. [9] One year later, ECT was introduced to the United States. [11]

Lack of adequate anesthesia or muscle relaxation during ECT led to fractures and dislocations, and insufficient knowledge about the dose parameters of electrical stimulation led to more severe cognitive adverse effects. [11] In 1940, curare was developed for use as a muscle relaxant during ECT. [9] Until effective antipsychotic drugs were developed in the 1950s, the only effective alternatives to ECT were insulin shock therapy and lobotomy. [11]

In the 1950s, Max Fink was the first to apply rigorous scientific research methods to ECT. [12] Succinylcholine, a depolarizing muscle relaxant, was introduced in 1951, and the first controlled study of unilateral ECT was conducted in 1958. [9] In the 1960s, randomized clinical trials of the efficacy of ECT versus medications in the treatment of depression showed response rates that were significantly higher with ECT. [9]

In 1978, the American Psychiatric Association 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. [9]

In 1988, randomized controlled clinical trials of ECT versus lithium showed that they were equally effective in treating mania. [9] In 2000, Sarah Lisanby and colleagues from Columbia University induced convulsive treatment with magnetic stimulation. [9]

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. [13]

The induction of a bilateral generalized seizure is required for both the beneficial and adverse effects of ECT. [9] An increase in gamma-aminobutyric acid (GABA) transmission and receptor antagonism has been observed, which raises the seizure threshold during ECT. [14] ECT may also lead to an increase of endogenous opioids, which may also have anticonvulsant properties. [12]

Positron emission tomography (PET) has been used to study the neurophysiological effects of ECT. [9] 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. [15]

Nearly every neurotransmitter system is affected by ECT, including beta-adrenergic, serotonin, muscarinic, cholinergic, and dopaminergic systems. [9] Brain-derived neurotrophic factor (BDNF), [16, 17] second-messenger systems, [9] and catechol-O-methyltransferase (COMT) polymorphisms [18] may play a role in ECT.

Although many biomarkers have been studied, no ECT biomarker is routinely used in clinical practice. [17]

Relevant Anatomy

In the central nervo/us 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 major depressive disorder, bipolar disorder, schizophrenia, and other disorders.

Major depressive disorder

ECT should be considered for patients in the acute phase of major depressive disorder who have a high degree of symptom severity and functional impairment or who have psychotic symptoms or catatonia. [19, 20] ECT may also be the treatment of choice for patients in whom treatment response is urgently needed, such as patients who are suicidal [19, 21] or those who are refusing food and are nutritionally compromised. [19]

Bipolar disorder

ECT may be considered for patients with severe or treatment-resistant manic or mixed episodes of bipolar disorder, [22, 23] or (in consultation with the psychiatrist) for patients who prefer this treatment modality. [24] ECT also is a potential treatment for those experiencing severe mania or depression during pregnancy. [24] ECT may be efficacious in patients with rapid cycling bipolar disorder. [25] Mania resulting from ECT is rare. [1]

In patients with life-threatening inanition (the exhausted condition that results from lack of food and water), suicidality, [21] or psychosis, ECT is a reasonable alternative treatment. [24] For patients who have depression with psychotic or catatonic features, ECT should be considered. [24] Maintenance ECT may be considered for patients whose acute episode of depression responded to ECT. [24]


ECT is effective for symptoms of acute schizophrenia but is not effective for chronic schizophrenia. [9] In combination with antipsychotics, ECT may be considered for patients with severe psychosis that has not responded to treatment with antipsychotic medications. [26]

The greatest therapeutic benefit appears to occur when ECT is administered concurrently with antipsychotic medications. [26, 27, 28] ECT also should be considered for patients with prominent catatonic features that have not responded to lorazepam. [26]

For patients with comorbid depression, ECT may be beneficial if depressive symptoms are treatment-resistant or if features such as suicidal ideation and behaviors or inanition are present. [26]

In the stable phase of schizophrenia, ECT may benefit some patients whose condition has responded to ECT in the acute phase but for whom pharmacological prophylaxis alone has been ineffective or cannot be tolerated. [26] ECT may be especially effective when marked positive and affective symptoms are present. [29]

Other psychotic disorders

ECT is effective for psychotic disorders related to schizophrenia, such as schizophreniform disorder and schizoaffective disorder. [1] In combination with antipsychotics, ECT may be considered for patients with schizoaffective disorder with severe psychosis that has not responded to treatment with antipsychotic medications. [26]

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. [30]

Other disorders and indications

ECT has been effective in the treatment of catatonia, [31] neuroleptic malignant syndrome, [32] depression associated with Parkinson disease, [33, 34] pain, [35] particular cases of delirium, [36] and acute confusion psychosis. [37] It has also been effective in treating patients with intellectual disabilities who have treatment-resistant mood or psychotic disorders. [38]

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. [19] 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. [9, 19] ECT also should be considered in patients with melancholic [39] and atypical [40] depression.


ECT has no absolute contraindications. Many medical conditions place patients at an increased risk for complications and warrant closer monitoring, however. [9]

In a study of patients with major depressive disorder and comorbid borderline personality disorder (BPD), patients with BPD did not experience the same degree of improvement when treated with ECT as did patients with other personality disorders or with no personality disorder. [41]




In the first several years of use, electroconvulsive therapy (ECT) was performed without anesthesia. Since the late 1950s, however, ECT has been performed under general anesthesia. [12] The goal is to produce a "light level" of anesthesia. Excessive anesthesia may cause problems such as prolonged unconsciousness and cardiovascular complications, and too little anesthesia may cause problems such as incomplete unconsciousness and autonomic arousal. [1, 9]

Anesthetic medications used in ECT include the following [1] :

  • Methohexital (barbiturate)
  • Thiopental (barbiturate)
  • Etomidate (nonbarbiturate)
  • Ketamine (nonbarbiturate)
  • Alfentanil (opioid)
  • Propofol (nonbarbiturate)

Methohexital is most commonly used [9] and is the preferred anesthetic for ECT because of its established safety record, effectiveness, and low cost. [1] Inhalational anesthesia with medications such as sevoflurane may also be an option. [42]

The cognitive outcome after ECT may be affected by the choice of the anesthetic medication. [43] 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]


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]


Common electrode positions in ECT include the bifrontotemporal, right unilateral, and bifrontal positions. [44] Further research is needed for the asymmetric bilateral position. [1, 45]

In the bifrontotemporal position [44] (commonly referred to as bilateral), 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. [9]

In the right unilateral position, one electrode is typically placed over the nondominant frontotemporal area, and the other electrode is placed on the nondominant centroparietal scalp, just lateral to the midline vertex. [9] As the left hemisphere is dominant in most people, unilateral electrode placement is almost always over the right hemisphere. [9]

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

In the asymmetric bilateral position, [45] the left electrode is moved about 6 cm anterior from the standard frontotemporal position, and its lateral edge is medial to the bony intersection ridge between the temple and the forehead. The right electrode is in the standard frontotemporal position.


After the electrical stimulus is administered during ECT, a short period of bradycardia occurs, which then converts to tachycardia during the seizure. Prior to anesthesia, administration of anticholinergics (eg, atropine, glycopyrrolate) can reduce the risk of vagally mediated bradyarrhythmias or asystole [1] and minimize oral and respiratory secretions. [9]

Anticholinergics may be especially useful for patients taking beta-adrenergic receptor blockers. [1, 9] Due to lack of an evidence base in moderating the cardiovascular effects of ECT, however, not all clinicians routinely use anticholinergics. [1]

Anticholinergics can increase preexisting tachycardia and can cause constipation, fecal impaction, and urinary retention. [1]

Neuromuscular Blocking

Neuromuscular blockers are administered to prevent bone fractures and physical injury related to motor activity during the seizure that occurs with electroconvulsive therapy. [9, 11, 12] This is especially important if the patient has osteoporosis or a history of spinal injury; [11, 12] in these cases, complete relaxation may be indicated. [1]

Anesthesia support is needed for administration of neuromuscular blocking agents. The preferred neuromuscular blocker is succinylcholine, a depolarizing drug. [1] Atracurium, mivacurium, rocuronium, and rapacuronium are alternatives to succinylcholine. [1]

A nondepolarizing muscle relaxant may be indicated in patients with pseudocholinesterase deficiency, hypercalcemia, 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 knee, ankle, or plantar withdrawal reflexes; loss of muscle tone; the reduction or failure to respond to a nerve stimulator; or any combination of these factors. [1]

Pretreatment Evaluation

No routine pretreatment evaluation for patients undergoing ECT is established. A collaborative approach between the ECT psychiatrist, medical consultants, and anesthesia provider is a more meaningful and inclusive method than simply asking for clearance. [46]

A pre-ECT evaluation should include the following components [1, 9, 11, 12, 44, 47, 46] :

  • A thorough psychiatric history and examination, including history of response to ECT and other treatments
  • 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 include the following:

  • Complete blood count
  • Serum chemistry
  • Renal function
  • Electrocardiogram
  • Urinalysis
  • Chest radiograph (especially with cardiovascular or pulmonary disease or history of smoking)
  • 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. [48]

No patient with a capacity to give voluntary consent should be treated with ECT without his or her written, informed consent. No clear consensus about how to determine capacity to consent has been established. 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, 47]

The use of involuntary ECT is rare. Involuntary ECT should be reserved for patients who need emergency treatment and who have a legally appointed guardian who has agreed to the use of ECT. [9] Clinicians must be familiar with local, state, [49] and federal laws about the use of ECT. [9]

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. [9] Printed literature and videotapes about ECT may be useful. [9] The family of the patient should be included in the discussion. [50]

The consent form for ECT should include the following information [1, 47] :

  • Who is recommending ECT and why
  • A description of treatment alternatives
  • A detailed description of how, when, and where ECT will be carried out
  • A discussion of options regarding electrode placement
  • The typical range for the number of treatments
  • A statement that the treatment is not guaranteed to be successful
  • A statement concerning the need for continuation or maintenance treatment
  • Discussion of the possible risks, including death, cardiac dysfunction, confusion, and memory impairment
  • A statement that the consent also applies to emergency treatment that may be clinically necessary during periods when the patient is unconscious
  • A listing of patient requirements during the ECT course, such as taking nothing by mouth after midnight
  • A statement that the patient has had an opportunity to ask questions and indication of who can be contacted with further questions
  • A statement that consent is voluntary and can be withdrawn at any time

Electroconvulsive Therapy with Comorbidity

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. [9] Patients with intracerebral lesions that lack a mass effect can safely undergo ECT. [12]

ECT increases intracranial pressure and blood flow to the brain. [12] Patients who have increased intracerebral pressure or are at risk for cerebral bleeding, such as those with cerebrovascular disease and aneurysms, are at increased risk during ECT. [9] Patients with very recent strokes are of special concern. [1]

ECT has been safely used after coil embolization of a cerebral aneurysm. [51] ECT has been used in the presence of Charcot-Marie-Tooth disease, [52] arachnoid cysts, [53, 54] epilepsy, [1, 55] myasthenia gravis, [1] and multiple sclerosis. [1]

Cardiac comorbidities

Patients with cardiac disease should be evaluated by a cardiologist who can assist with the patient’s management during the course of ECT. [1, 12, 56] 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. [9]

Patients with a recent myocardial infarction (MI) are at high risk of cardiac complications such as MI, although the risk is greatly decreased 2 weeks after the MI and is further reduced 3 months after the MI. [9]

With a proper pre-ECT cardiac and pacemaker/defibrillator assessment, patients with cardiac pacemakers and implantable cardioverter defibrillators can safely undergo ECT. [57] ECT has been used in the presence of severe aortic stenosis [58] , and it has been used after heart transplantation, though further studies are needed. [59]

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. [11]

Patients with gastroesophageal reflux disease may experience worsening symptoms during ECT, due to stimulation of the vagus nerve. [12]

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, 60]

Electroconvulsive Therapy and Medications

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

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. [12]

Diuretics and hypoglycemics may be withheld until after an ECT treatment. [1, 11] Theophylline should be discontinued if possible. [1, 11]

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. [61]

Monoamine oxidase inhibitors (MAOIs) are generally safe. 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] 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. [62, 63]

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, 12, 44, 64] Benzodiazepines should be lowered in dose or discontinued if possible. [1, 12]

Most antidepressants can be safely combined with ECT. [46] Caution is recommended with high doses of bupropion. [1]

Electroconvulsive Therapy and Pediatrics

The use of ECT in the pediatric population is controversial. [65] The American Academy of Child and Adolescent Psychiatry published a practice parameter for the use of ECT with adolescents in December 2004.

Diagnostic considerations for ECT in an adolescent patient [66] include severe or persistent major depression or mania [67] with or without psychotic features, schizoaffective disorder, schizophrenia, catatonia, [68] or neuroleptic malignant syndrome. The symptoms must be severe, persistent, and significantly disabling, and they may include life-threatening symptoms.

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. [66] Every child or adolescent patient being considered for ECT should receive an independent evaluation from a psychiatrist who is not directly responsible for the patient's treatment and who is knowledgeable about ECT. [66]

The response rate for mood disorders to ECT in the pediatric population is 75-100%. The response rate for psychotic disorders is 50-60%. [66]

Electroconvulsive Therapy in the Elderly

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, [69] bipolar mania, [70] and psychotic disorders. [69]

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, [71, 72, 73] but it is also helpful for treatment-resistant nonpsychotic major depression. [74]

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]

A 2003 Cochrane Database review of ECT for elderly patients with depression found that solid conclusions could not be drawn as to whether ECT was more effective than antidepressants or regarding the safety and adverse effects of ECT in these patients. [75]

Electroconvulsive Therapy in Pregnancy

ECT is considered safe and effective for the mother and fetus in the treatment of major depressive disorder during pregnancy. [19] ECT is a potential treatment for patients with bipolar disorder who are experiencing mixed episodes [23] , severe mania, or severe depression during pregnancy. [24]

ECT should be considered for women who prefer to avoid extended exposure to psychotropic medication during pregnancy [76] or for those pregnant women whose symptoms fail to respond to standard therapy. [76, 77] 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. [78]

Transmission of anesthesia medications across the maternal-fetal barrier is considered to be minimal. [12] 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. A brief pulse waveform is used in modern electroconvulsive therapy (ECT) machines. [9] The dose is measured in millicoulombs of charge delivered. [44]

Three methods are used to determine stimulus intensity and dosing, as follows [1, 44] :

  • 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.

A fourth method, called the glissando technique, in which the stimulus intensity is progressively increased during delivery from a subconvulsive to a convulsive level, has not been justified. It is now of only historical interest. [1]

When determining stimulus intensity and dosing, changes in seizure threshold during the course of treatment should also be considered. A patient's seizure threshold may increase anywhere from 25-200%. [1]

Seizure Quality

Seizure duration has little bearing on efficacy of electroconvulsive therapy, and seizure duration has a complex association with stimulus intensity. 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 seizure activity and to document seizure duration. [44] Seizure motor activity is monitored using the "cuff" procedure, in which distribution of a muscle relaxant is blocked to the hand or foot via a tourniquet to maintain the potential for muscle contraction. [1, 44]

Frequency of Treatments

In the United States, ECT is most commonly performed 3 times per week regardless of electrode placement. [1] More frequent regimens are not justified. [1] Treatments 2 times per week may result in less memory impairment than treatments 3 times per week. [1, 9] 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]

Multiple monitored ECT (MMECT) involves treatment in which more than one adequate seizure is induced in the same session under continuous anesthesia. [1, 9] Urgent clinical scenarios such as neuroleptic malignant syndrome may warrant MMECT, but routine use is not recommended. [1, 9]

Number of Treatments

The number of treatments needed to achieve a full clinical response in patients varies widely. Although the typical number of treatments is 6-12, [12, 44] 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 the severity of cognitive adverse effects. [1] Treatment is stopped when maximal improvement is reached. [1, 11]




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


Cardiovascular complications (eg, arrhythmias [79] ) 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 patients or 1 per 80,000 treatments. This is about the same as that associated with minor surgery. [1] The mortality rate may be higher in patients with severe medical disorders, though it may be lower than that with tricyclic antidepressant therapy. [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. [1] Individual patients vary significantly in the extent and severity of cognitive adverse effects experienced after ECT. [1] Various biochemical, electrophysiological, and neuroimaging correlates of the cognitive adverse effects of ECT exist. [80]

The particular ECT technique used has a significant impact on cognitive deficits, and modifications may need to be made, [81] such as switching to unilateral ECT, lowering the stimulus dose, increasing the time interval between treatments, or stopping medications that may increase cognitive adverse effects. [1]

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] Postictal delirium may occur in a minority of patients. [1]

A prospective, naturalistic, longitudinal study of clinical and cognitive outcomes in patients with major depression treated at 7 facilities found that cognitive outcomes varied across facilities and that differences in ECT technique largely accounted for these differences. [82] A recent review in older adults found mixed results regarding the impact of ECT on cognitive domains, aside from interictal slowing of information processing speed. [83]

Other adverse effects

Asystole has been reported in patients who undergo ECT. [84, 85] Prolonged seizures and status epilepticus may be more likely when patients receive medications that lower seizure threshold. [1] 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, [86] and, rarely, more potent analgesics such as codeine. [1] Muscle soreness and nausea may occur. [1] Mania resulting from ECT is rare. [1]

Continuation Electroconvulsive Therapy

Continuation ECT is used for prevention of relapse. [46] Because of the high risk of relapse after ECT, especially during the first few months, the argument for aggressive continuation therapy is compelling. [1]

Indications for continuation 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]

In a small study of patients with schizophrenia or schizophreniform disorder, continuation ECT plus neuroleptics was effective and safe for relapse prevention, even in patients with medication-resistant schizophrenia who relapsed after responding to acute ECT. [87]

A comparison multisite randomized parallel design study of continuation ECT and the combination of lithium and nortriptyline for relapse prevention in major depression found that both these modes of therapy had limited efficacy but were superior to placebo. [88] In a randomized controlled trial of continuation pharmacotherapy in patients with depression after response to ECT, a lower relapse rate was found with nortriptyline plus lithium (39%) than with nortriptyline alone (60%) or placebo (84%). [89]

Maintenance Electroconvulsive Therapy

Maintenance ECT is for prevention of recurrence. [46] Indications are the same as those for continuation ECT. [1] In a longitudinal, randomized, single-blind study of elderly patients with unipolar psychotic depression who remitted to ECT plus nortriptyline, the mean survival time was significantly longer in the continuation/maintenance ECT plus nortriptyline subgroup than in the nortriptyline subgroup. [90]

Pharmacological Therapy

Pharmacological therapy after ECT varies with a patient's diagnosis. [1] Patients with major depressive disorder and whose symptoms are resistant to pharmacological therapy may benefit prophylactically from the same class of medication during maintenance therapy after ECT. [91]

Regarding clinical predictors, lower remission rates after acute ECT may be associated with medication resistance and chronicity in patients with major depression but are not associated with age or burden of physical illness. [92] Melancholic features may not predict response to ECT. [93] In patients with nonpsychotic major depression, antidepressant medication failure may not predict acute remission with ECT. [94]


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 may lengthen the antidepressant effects of ECT. [95]