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Literature review current through: Dec 2019. | This topic last updated: Aug 13, 2018.
INTRODUCTION
Electroconvulsive therapy (ECT) uses a small electric current to produce a generalized cerebral
seizure under general anesthesia. ECT is used mainly to treat severe depression, but is also
indicated for patients with other conditions, including bipolar disorder, schizophrenia,
schizoaffective disorder, catatonia, and neuroleptic malignant syndrome.
There is no question about the efficacy and safety of ECT, which is practiced widely in the United
States and the rest of the world [1]. Nevertheless, it remains controversial and stigmatized
because of misinformation and outmoded perceptions about how the treatment is performed [2].
This topic provides an overview of ECT. The indications for and efficacy of ECT in unipolar major
depression, technique for performing ECT, medical consultation for ECT, and indications for and
efficacy of ECT in bipolar disorder are discussed separately.
● (See "Unipolar major depression in adults: Indications for and efficacy of electroconvulsive
therapy (ECT)".)
● (See "Technique for performing electroconvulsive therapy (ECT) in adults".)
● (See "Medical consultation for electroconvulsive therapy".)
● (See "Bipolar disorder in adults: Indications for and efficacy of electroconvulsive therapy
(ECT)".)
HISTORY OF ECT
The use of seizures to treat psychiatric disorders has progressed over time, improving the efficacy
and tolerability of ECT.
ECT began with observations that patients with schizophrenia often improved temporarily after a
spontaneous seizure [3-5]. Initially, physicians induced seizures with medications. In 1938, Italian
psychiatrists used an electric current to induce seizures as a treatment for schizophrenia [6]. ECT
quickly spread around Europe and the rest of the world, and was first used in the United States in
1939. Patients suffered bone fractures occasionally and considerable anticipatory anxiety, but
advances in anesthesia techniques in the 1950s allowed for the use of general anesthesia and
muscle relaxation for ECT, which eliminated these problems.
The use of ECT in the United States has fluctuated [7,8]. ECT use declined in the 1970s, and
subsequently increased, possibly as a result of greater treatment resistance to pharmacotherapy
in depressed patients, increased recognition of the limitations of pharmacotherapy, and better
public acceptance.
Current use — ECT is offered at most major psychiatric treatment centers. However, a study of a
private insurance claims database in the United States found that among nearly one million
patients with unipolar major depression or bipolar disorder, ECT was administered to only 0.25
percent [9].
ECT patients today are more likely to be of higher socioeconomic status, white, and receive ECT
in a private sector psychiatric facility [7,10]. In addition, patients with mood disorders who are
treated with ECT have higher rates of psychiatric comorbidity, compared with patients who are not
treated with ECT [9]. State hospitals rarely offer the treatment, even though many of the patients
would meet indications for ECT.
NEUROBIOLOGY
Much is known about the neurobiology of ECT, although its exact mechanism of action remains to
be elucidated:
● Human and animal studies show that ECT increases release of monoamine
neurotransmitters, particularly dopamine, serotonin, and norepinephrine [2,11-13]. ECT also
enhances monoamine transmission by desensitizing presynaptic adrenergic autoreceptors.
● The neuroendocrine hypothesis suggests that ECT relieves depression by causing the
hypothalamus or pituitary gland to release hormones, including prolactin, thyroid stimulating
hormone, adrenocorticotropic hormone, and endorphins [2].
● The neurotrophic/tropic hypothesis suggests that ECT works by inducing neurogenesis (brain
structural plasticity) and increasing neurotrophic signaling, thus reversing many of the
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deleterious atrophic brain changes induced by severe, chronic depression [2,15-23]. Multiple
studies demonstrate increases in gray matter volume and cortical thickness in several brain
areas, most prominently the amygdala and hippocampus. In addition, brain-derived
neurotrophic factor appears to increase after ECT.
● ECT is reported to change brain connectivity [25]. One functional magnetic resonance
imaging study before and after successful treatment with ECT revealed a reduction in global
connectivity within the left dorsal lateral prefrontal cortex [26], whereas another functional
magnetic resonance imaging study found increased right hippocampal connectivity [27] and a
structural study found increased connectivity in dorsal fronto-limbic circuits [28]. Change in
connectivity is being studied as a potential predictor of ECT response [29,30].
PRE-ECT EVALUATION
● Determine whether ECT is indicated (table 1). (See "Unipolar major depression in adults:
Indications for and efficacy of electroconvulsive therapy (ECT)".)
● Establish baseline psychiatric and cognitive status to serve as reference points for evaluating
response and cognitive effects. (See 'Clinical monitoring' below.)
● Identify and treat any general medical conditions that might be associated with an increased
risk of adverse events from ECT (table 2). (See 'Patients with comorbid general medical
illness' below.)
● Initiate and continue the informed consent process. (See 'Informed consent' below.)
A complete medical history should be taken. Medical consultation prior to ECT is indicated for
most patients 40 years or older, and is frequently obtained in younger patients as well. Particular
attention should be paid to any history of cardiopulmonary and central nervous system disease
and prior surgeries (with inquiry about type of anesthesia and any complications). (See "Medical
consultation for electroconvulsive therapy" and "Technique for performing electroconvulsive
therapy (ECT) in adults", section on 'Electrode placement'.)
Appropriate physical examination (including dental evaluation) and laboratory evaluation, guided
by the relevant history, should be performed. The patient's handedness and any dental problems
should be noted. Specific laboratory tests are not indicated for patients without known medical
comorbidities. (See "Preoperative medical evaluation of the healthy adult patient".)
Inducing a seizure causes transient increases in blood pressure, pulse, and intracranial pressure,
which can have deleterious effects. Organ systems of most concern are [34]:
● Cardiovascular
● Pulmonary
● Central nervous system
Seizures increase cardiac workload and oxygen demand. Thus, it is important to try to maximize
the patient's cardiovascular status before ECT. Additionally, medication to blunt increases in heart
rate and blood pressure is indicated prior to ECT and during the procedure in patients for whom
these increases would be detrimental.
A separate topic discusses strategies to reduce the risk of cardiac complications and the use of
ECT in patients with coexisting cardiac disease (including hypertension, coronary heart disease,
heart failure, and valvular disease), patients with pacemakers or implantable defibrillators, and
patients who are anticoagulated, as well as patients with coexisting pulmonary disease, diabetes,
or neurologic disease. (See "Medical consultation for electroconvulsive therapy".)
PREGNANCY
ECT is sometimes indicated for pregnant patients, and the procedure can safely be used for these
patients. (See "Unipolar major depression in adults: Indications for and efficacy of
electroconvulsive therapy (ECT)" and "Bipolar disorder in pregnant women: Treatment of mania
and hypomania", section on 'Electroconvulsive therapy' and "Teratogenicity, pregnancy
complications, and postnatal risks of antipsychotics, benzodiazepines, lithium, and
electroconvulsive therapy", section on 'Electroconvulsive therapy' and "Technique for performing
electroconvulsive therapy (ECT) in adults", section on 'Pregnancy'.)
CONCURRENT MEDICATIONS
Antidepressants can improve the efficacy of ECT. A review of 10 systematic reviews, 7 meta-
analyses, and 3 practice guidelines found that for depressed patients, a tricyclic may improve the
antidepressant effect of ECT [37]. As an example, a randomized trial assigned depressed patients
(n = 319) receiving an acute course of ECT to concomitant nortriptyline, venlafaxine, or placebo.
Remission occurred in more patients who received nortriptyline or venlafaxine compared with
placebo (63 and 60 versus 49 percent) [38], with a significant difference between nortriptyline and
placebo.
Antidepressants are generally safe to use with ECT and do not affect its tolerability. As an
example, a randomized trial of depressed patients receiving an acute course of ECT with
concomitant nortriptyline, venlafaxine, or placebo found the number of adverse events did not
differ significantly between the three groups [38]. Other types of antidepressants are also well
tolerated during ECT, including selective serotonin reuptake inhibitors, tetracyclics, and
monoamine oxidase inhibitors [39,40].
Antipsychotic medications are often continued during ECT and may provide a synergistic
antipsychotic effect, especially second-generation antipsychotics [41]. In addition, antipsychotics
generally do not appear to affect the tolerability of ECT. Second-generation antipsychotics and
high potency first-generation antipsychotics are thought to be safe. A review found that early
reports warned of hypotension and cardiac complications from combining chlorpromazine and
ECT, but later reports did not substantiate these problems [42]. Nonetheless, combining of low
potency, first-generation antipsychotics with ECT should be done cautiously.
Lithium has the potential to increase the adverse cognitive effects of ECT and to prolong the
effects of succinylcholine (which is typically used during ECT to reduce tonic-clonic movements),
but these problems are rare [43]. A review of several case series found that concomitant lithium
and ECT is safe [43]. We suggest reducing lithium levels below the full therapeutic range at the
time of each ECT treatment by withholding one or two doses of lithium prior to each treatment.
Benzodiazepines should be tapered and discontinued whenever possible during ECT because of
their anticonvulsant properties, which can increase seizure threshold, shorten seizure duration,
and decrease the intensity of the ECT seizure [44]. These effects may decrease the clinical
efficacy of ECT.
However, for patients who need to continue their benzodiazepine during ECT, it is reasonable to
switch from drugs with long half-lives to one with a short half-life, and withhold the evening dose
before each ECT treatment. In addition, small doses of benzodiazepines may not be a problem.
Patients who are very anxious about the ECT procedure itself may take a benzodiazepine (eg, 1
mg of lorazepam sublingual) 30 to 60 minutes before the treatment.
Another reasonable alternative for patients who continue their benzodiazepine is to use
intravenous flumazenil, which reverses the anticonvulsant effect of benzodiazepines and is given
one to three minutes before anesthetic induction [45]. The typical dose of flumazenil is 0.4 to 0.5
mg, but doses up to 1.0 mg may be necessary for patients who have been chronically taking high
doses of benzodiazepines. If patients receiving flumazenil manifest symptoms of benzodiazepine
withdrawal within one hour post-ECT, subsequent ECT treatments should be followed by
administration of intravenous midazolam (eg, 1 mg).
Anticonvulsants may theoretically interfere with the efficacy of ECT, similar to benzodiazepines,
although the evidence for this is sparse [46]. Most patients on anticonvulsants for mood
stabilization can be successfully treated by withholding the prior evening or night’s dose, without
the need to discontinue the medication [47]. However, if seizures are difficult to elicit or too short,
we reduce the dose and/or discontinue the medication. The duration of an adequate ECT seizure
is discussed separately. (See "Technique for performing electroconvulsive therapy (ECT) in
adults", section on 'Seizure duration'.)
Patients with epilepsy should continue their anticonvulsants during a course of ECT. Clinicians
should reduce the dose if ECT seizures are difficult to elicit or too short, or withhold a dose the
evening or night before the ECT treatment.
Other drugs
INFORMED CONSENT
The psychiatrist should ensure that the consent process conforms to all state and local laws and
statutes, and hospital policies. Informed consent requires that the patient [39]:
ECT consent forms are more detailed compared with those for most other medical procedures
because ECT is closely scrutinized. The American Psychiatric Association Task Force report
provides a sample template for ECT consent that has been widely adopted [39] (table 3 and table
4).
Informational material written for the layperson is typically provided to patients and family
members as part of obtaining informed consent. In addition, patients and family members may
watch video to augment the written material and discussion with the psychiatrist recommending
ECT. (See 'Outside sources of patient education' below.)
The vast majority of ECT is administered with fully informed consent given by the patient for a
series of treatment [2]. In circumstances when the patient is too ill (eg, catatonic or psychotic) and
lacks capacity to provide consent, and the need for ECT is urgent or emergent, the psychiatrist
should seek substitute consent by a court [49].
The patient should be cautioned not to make major personal or financial decisions during or
immediately after the acute course of ECT. In addition, the patient should not drive until the
cognitive effects of ECT have resolved. Patients who are receiving continuation or maintenance
ECT should not drive until 24 hours after each treatment [50].
TREATMENT COURSE
Number of treatments — There is no standard number of treatments for an acute ECT course
and no way to predict how many treatments a particular patient will need. Most patients remit with
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6 to 12 treatments, but some require only three while others require 20 or more [39].
In a study of 184 patients with unipolar major depression, the mean number of treatments needed
to reach remission was 7 (standard deviation 3) [51]. A second study of 230 patients with unipolar
or bipolar major depression found that 90 percent or more of the remissions occurred with nine or
fewer treatments, depending upon the type of electrode placement [52]. (See "Technique for
performing electroconvulsive therapy (ECT) in adults", section on 'Electrode placement'.)
Acute ECT should last until the patient remits, reaches an improvement plateau, or develops
limiting adverse effects. It is becoming more common to taper the frequency of ECT treatments,
rather than abruptly stop a course.
Once remission is achieved, however, ongoing continuation and maintenance treatments are
frequently indicated. (See 'Continuation and maintenance ECT' below.)
Treatment frequency — The frequency of treatments varies by country and the clinical urgency.
Standard practice in the United States is to give ECT three times per week on a Monday-
Wednesday-Friday schedule. The routine in many other countries is twice a week, particularly for
elderly patients. Urgently ill patients (eg, catatonic or severely malnourished) may be given daily
bilateral ECT until some improvement is evident [50].
Meta-analyses of five randomized trials (169 patients with unipolar major depression) found that
symptomatic improvement, remission, and number of ECT treatments were comparable for twice-
weekly and thrice-weekly ECT; however, duration of treatment was significantly longer for twice-
weekly ECT (by nearly five days) [53]. The data were insufficient to analyze differences in
cognitive impairment; nevertheless, some randomized trials indicate that cognitive impairment is
greater with bilateral, brief pulse ECT administered three times/week compared with two
times/week [54,55].
Clinical monitoring — Depressive symptoms and cognition should both be monitored, and we
encourage clinicians to serially measure severity of symptoms with a standardized scale
(measurement based care). Several depression rating scales are available; we suggest that
clinicians use clinician-administered rating scales rather than patient self-report scales because
the validity of self-report scales can be compromised by confusion and amnesia from ECT. The
scale should be administered at baseline, weekly during the course of ECT, and when the ECT
course is completed. The most commonly used clinician-administered scale is the Hamilton Rating
Scale for Depression (form 1A-C) [56]. A reasonable alternative is the Montgomery-Asberg
Depression Rating Scale (figure 1A-C) [57]. Measurement based care for treating depression is
discussed separately. (See "Using scales to monitor symptoms and treat depression
(measurement based care)".)
Many scales are also available for monitoring cognition; the most common is the Mini-Mental State
Examination [58]. It is easy to use and adequate for routine clinical use, although its sensitivity
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may be limited [59]. More comprehensive neuropsychologic testing may be indicated for selected
patients (eg, those with known cognitive deficits at baseline). (See "The mental status examination
in adults", section on 'Cognitive screening tests'.)
ADVERSE EFFECTS
The adverse effects of ECT may be divided into general medical and cognitive effects.
Adverse general medical effects — ECT is one of the safest procedures performed under
general anesthesia.
Mortality is mostly related to cardiopulmonary events. Patients with coronary heart disease may be
at risk for cardiac ischemic events because the seizure increases cardiac workload and oxygen
demand. The cardiovascular effects of ECT are discussed separately. (See "Medical consultation
for electroconvulsive therapy", section on 'Cardiovascular effects'.)
● Aspiration pneumonia – Risk is increased in patients who do not have an empty stomach [50].
● Fracture – Patients with severe osteoporosis are at increased risk of fracture, and extra care
should be taken to ensure excellent muscle relaxation [65].
● Dental and tongue injuries – These may occur when the oral bite block is not fully protective
[66]. Loose teeth are at risk for dislodgement during the procedure and possible aspiration,
and should be stabilized or extracted before ECT.
● Headache – This is the most common, nonserious adverse medical effect of ECT [67-69].
Patients should be told to expect some headache after each treatment. It is typically managed
with acetaminophen or ibuprofen given after the treatment. Prophylaxis with intravenous
ketorolac 30 mg may be considered for patients with significant post-ECT headache [70].
● Nausea – Transient, postprocedure nausea is common and is the result of the anesthesia and
airway manipulation, which may introduce air into the stomach. Prophylaxis with intravenous
● Other somatic symptoms – Patients sometimes complain of other somatic symptoms such as
myalgias, which may be a result of the fasciculations induced by succinylcholine. Myalgias
are common immediately after the first treatment and less common thereafter. Temporary jaw
and neck discomfort may also occur after the first treatment, as a result of the jaw clench
during the stimulus and/or fasciculations in these muscles [50]. However, one study assessed
a group of depressed patients both pre-ECT and during an acute course of ECT, and found
that the frequency of somatic symptoms other than headache did not increase [71]. The
authors suggested that these other somatic symptoms may have been due to the depressive
illness, the use of psychotropic medications, or withdrawal from such medications.
Concerns that ECT causes structural brain damage have been dispelled by multiple human and
nonhuman primate studies [1,37].
Adverse cognitive effects — Concern about adverse effects on cognition, primarily memory,
remains an impediment to prescribing ECT [72]. However, the risks of major depression and the
potential benefits of ECT outweigh the potential memory loss from ECT.
The patient’s pretreatment cognitive status appears to be associated with ECT induced memory
loss. As an example, a study of patients (n = 50) who were treated with ECT found that memory
loss was greater in patients with low cognitive reserve, based upon years of education and
occupational attainment, than patients with high cognitive reserve [73].
In addition, the adverse cognitive effects of ECT are affected by electrode placement, stimulus
type and dose, and anesthesia [74]. (See "Technique for performing electroconvulsive therapy
(ECT) in adults".)
We monitor cognition during an acute course of ECT by administering the Mini-Mental State
Examination (MMSE) at baseline prior to onset of ECT, and again after the last ECT treatment. In
addition, we assess patients with the MMSE at any point if we are concerned about cognition.
Given that the MMSE is not in the public domain, many clinicians use the Montreal Cognitive
Assessment (MoCA) instead. The MoCA is accessible online and in multiple languages at
www.mocatest.org. Details regarding the MMSE and MoCA are discussed separately. (See
"Evaluation of cognitive impairment and dementia", section on 'Cognitive testing'.)
Incidence and course — Many patients report some adverse cognitive effects during and after
a course of ECT:
● A 2003 review of seven observational studies (n >1100 patients treated with ECT) found that
the proportion of patients who reported any memory loss ranged from approximately 50 to 80
percent [75]. Memory loss for at least six months beyond the end of ECT was reported by
about 30 to 55 percent.
● A national registry study identified patients (n >1200; mean age 53 years) who were treated
with brief-pulse ECT between 2011 and 2014 and found that subjective memory worsening
was endorsed by approximately 25 percent (and subjective memory improvement in 10
percent) [76]. After adjusting for each of the study variables, the analyses showed that
memory worsening was more likely to occur in:
• Patients aged 18 to 39 years than patients 65 years or older (32 versus 22 percent)
• Patients without subjective memory disturbance before ECT than patients with memory
disturbance (39 versus 17 percent)
• Patients concurrently treated with lithium than patients not treated with lithium (31 versus
25 percent)
• Patients who did not remit, compared with patients who remitted (28 versus 22 percent)
Factors not associated with memory worsening included the major depression diagnosis
(unipolar or bipolar), presence of psychotic features or personality disorder, and the use of
psychotropic medications other than lithium.
However, objective tests indicate that cognitive abnormalities caused by ECT are generally short
lived. A meta-analysis of 84 observational studies evaluated neuropsychological function (24
cognitive tests, eg, MMSE and Word List learning) in 2981 depressed patients who were treated
with ECT and assessed with standardized tests at baseline and after the course of ECT was
completed; all post-ECT assessments were compared with baseline assessments. The primary
findings were as follows [77]:
● Up to 3 days post-ECT, cognitive performance was impaired on most tests, and many of the
effects of ECT were clinically moderate to large.
● 4 to 15 days post-ECT, impairment was observed on one test, whereas small to moderate
improvement of cognition was observed on several tests.
● More than 15 days posttreatment, cognitive performance was improved on most tests; the
effects were clinically small to moderate.
● A retrospective study examined routinely collected data from patients (n = 126) assessed
prior to ECT and for up to six months afterwards [79]. The large majority of patients were
treated for unipolar major depression; all patients received bilateral ECT twice weekly at a
dose two times seizure threshold. Assessments included an objective test of visuospatial
memory. Compared with baseline, visuospatial memory was worse one month and three
months post-ECT, but was superior at the six-month assessment.
● Another prospective observational study enrolled patients who were hospitalized for unipolar
major depression and treated with ECT (n = 22) or usual care (n = 24); neuropsychological
testing showed that verbal memory was impaired in both patient groups, compared with
healthy controls (n = 35) [83]. Improvement of verbal memory was greater in patients who
received ECT than usual care.
Although randomized trials suggest that concurrent treatment with different medications may
mitigate the adverse cognitive effects of ECT, the use of these medications is not part of standard
treatment with ECT. Adjunctive medications that were superior to placebo in reducing cognitive
impairment include exogenous triiodothyronine [84] and acetylcholinesterase inhibitors such as
donepezil, galantamine, and rivastigmine [85]. However, the sample sizes in the trials were small
and further replication is required.
It does not appear that ECT is associated with an increased risk of dementia. A national registry
study identified patients with a first time diagnosis of a mood disorder (n >162,000), including
patients who were treated with ECT (nearly 6000), and followed them for a median of five years
[86]. After adjusting for the probability (propensity) to receive ECT, based upon potential
confounding factors such as sex, educational level, and use of psychotropic medications, the
analyses found that the subsequent risk of dementia was comparable for patients treated with
ECT and those not treated with ECT, including patients aged 70 years or older at baseline. This
finding is consistent with other evidence that suggests ECT improves (rather than injures) brain
structure and function. (See 'Neurobiology' above.)
Types of impairment — ECT causes three basic types of cognitive impairment [72]:
● Acute confusion
● Anterograde amnesia
● Retrograde amnesia
The acute confusional state is the result of both the seizure and the anesthesia. It typically
resolves 10 to 30 minutes after the procedure. The confusional state may include postictal
agitation, which typically can be managed with a single intravenous dose of midazolam (eg, 1 to 3
mg) [87] or propofol (eg, 0.5 mg/kg) [88].
Anterograde amnesia is the decreased ability to retain newly acquired information. It occurs during
a course of ECT and typically resolves within two weeks after completing the course. We thus
suggest that patients refrain from driving during an acute course of ECT and for at least 24 hours
after a single ECT (during continuation and maintenance ECT), or from making important business
or personal decisions for one to two weeks after completing an acute course of ECT [89].
Retrograde amnesia involves forgetting recent memories and is the most anxiety-producing
cognitive effect of ECT. The memories are for events that occur during the course of ECT and a
period of weeks to a few months prior to that; however, some patients report retrograde amnesia
that extends back for years [90]. The deficits are greatest and most persistent for knowledge about
public or world events (impersonal memory) compared with knowledge about the self (personal
memory) [91]. Bilateral ECT causes more retrograde amnesia than right unilateral [74,90].
Retrograde amnesia recovers more slowly than anterograde amnesia [91].
Some of the lost memories of events prior to the course of ECT may be expected to return, while
others may not. A systematic review found four studies in which the proportion of patients who
reported persistent or permanent memory loss ranged from 29 to 55 percent [75]. The existence
and etiology of more severe memory impairments than typically experienced is controversial
[74,90,92-94]. Regardless, the typical ECT patient is profoundly depressed and accepts some
degree of memory loss as a reasonable tradeoff for resolution of the depressive episode.
Continuation ECT is the practice of providing a single ECT treatment, at an interval of one to eight
weeks, during the first six months after remission. The purpose is to prevent relapse of the mood
or psychotic episode that prompted the acute course of ECT. Maintenance ECT refers to ECT
given beyond continuation ECT, to patients who have recovered from the acute mood or psychotic
episode but require treatment to prevent recurrence of a new episode. Continuation and
maintenance ECT are usually outpatient procedures.
Mood and psychotic disorders are chronically recurring illnesses. Therefore, continuation and
maintenance treatment (with pharmacotherapy, ECT, psychotherapy, or a combination) are
required for most patients who recover from an initial episode. As an example, in a prospective,
observational study of 154 patients with major depression who remitted after successful treatment
with ECT in community hospitals, 64 percent relapsed during 24 weeks of follow-up [95].
We suggest continuation and maintenance ECT for depressed patients who have successfully
completed a course of acute ECT and:
The electrode placement used for continuation and maintenance ECT should be the same as that
used for acute ECT. (See "Technique for performing electroconvulsive therapy (ECT) in adults",
section on 'Electrode placement'.)
Pharmacotherapy is often combined with continuation and maintenance ECT, with improved
outcomes [96,97].
The schedule for continuation and maintenance ECT generally starts with weekly treatments for
several weeks and gradually tapers to the maximal interval that allows the patient to remain
euthymic. Following an acute course of ECT three times per week, we suggest treatments be
administered weekly for one to three weeks, followed by gradually increasing the interval between
treatments (eg, biweekly for four weeks and then monthly for two months) [51]. Some patients
continue to taper down to one treatment every three months, depending upon their clinical status
and preference. There is no single continuation/maintenance ECT schedule that is best for all
patients; the schedule should be flexible and adjusted to the needs of the patient, taking into
account the patient’s history of relapse and the severity of prior depressive episodes. As an
example, patients who suffer subsyndromal symptoms short of a full recurrence may temporarily
require more frequent treatments. Patients who benefit from maintenance ECT can receive it
indefinitely. Use of self-report and clinician administered rating scales to monitor the patient’s
clinical status is discussed separately. (See "Using scales to monitor symptoms and treat
depression (measurement based care)".)
Efficacy — Following acute ECT, continuation and maintenance treatment with ECT plus
pharmacotherapy is more effective than pharmacotherapy alone. Evidence supporting the use of
ECT plus medication includes the following [96]:
● In one study, geriatric patients with unipolar major depression were acutely treated with ECT
plus venlafaxine; those who remitted (n = 120) were randomly assigned to six months of
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● A one-year, open-label, randomized trial compared maintenance ECT (weekly for six weeks
and then every two weeks) plus pharmacotherapy (antidepressants in nearly all patients;
lithium and antipsychotics were used in varying numbers of patients) with pharmacotherapy
alone in 56 patients who responded to an acute course of ECT for unipolar or bipolar major
depression [97]. Relapse occurred in fewer patients who received combination treatment than
pharmacotherapy alone (32 versus 61 percent).
Cognitive effects of continuation and maintenance ECT are generally minor or nonexistent:
● A controlled trial randomly assigned depressed patients who remitted with an acute course of
ECT to continuation ECT or continuation pharmacotherapy and evaluated them with an
extensive battery of memory tests at baseline and after 24 weeks of treatment [51,99].
Neurocognitive performance was comparable for the two groups.
Stigma — Stigma remains the biggest impediment to the appropriate use of ECT. The level of
knowledge about modern ECT among patients and medical practitioners is low [101]. The
portrayal of ECT in the media as a crude and coercive treatment remains problematic, frightening
off patients who might benefit from it. Improved education about ECT among health care
professionals will lead to more favorable perceptions about its use [102]. In addition, allowing
family members to watch administration of ECT in the treatment suite can be reassuring and help
diminish stigma [103,104].
Access — Access to ECT in the United States is variable and very limited in some rural areas. It
is rarely available to patients in state psychiatric hospitals. Patients with no or limited insurance
coverage may be unable to pay for ECT, leading to a situation in which ECT is preferentially
available to more affluent patients with better insurance [9].
Training — ECT is a standard part of training in general psychiatry residency programs in the
United States, and many programs offer in-depth hands-on training. Guidelines for curriculum are
suggested by the American Psychiatric Association [39]. Several post-residency hands-on training
courses are offered throughout the United States. These may be identified by contacting the
American Psychiatric Association at 888-357-7924.
Individual United States hospitals issue privileges to psychiatrists to perform ECT, but there is no
board certification for ECT in the United States [1].
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Depressive disorders".)
UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.”
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
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These articles are best for patients who want a general overview and who prefer short, easy-to-
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Here are the patient education articles that are relevant to this topic. We encourage you to print or
e-mail these topics to your patients. (You can also locate patient education articles on a variety of
subjects by searching on “patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Electroconvulsive therapy (ECT) (The Basics)")
● Beyond the Basics topics (see "Patient education: Electroconvulsive therapy (ECT) (Beyond
the Basics)")
One of the requirements for obtaining informed consent for ECT is that patients receive adequate
information about the procedure. Additional written material is available for patients and family
members to augment discussions with the psychiatrist at http://jama.ama-
assn.org/cgi/reprint/285/10/1390.
Educational material explaining ECT is also available as part of a document entitled "Brain
Stimulation Therapies" that is published by the National Institute of Mental Health. This publication
can be obtained through a toll-free number, 866-615-6464, or online at the website
http://www.nimh.nih.gov/health/topics/brain-stimulation-therapies/brain-stimulation-therapies.shtml.
The website also provides information about depression in language intended for the lay public.
SUMMARY
● Indications for electroconvulsive therapy (ECT) include severe unipolar depression, bipolar
disorder, schizophrenia, schizoaffective disorder, catatonia, and neuroleptic malignant
syndrome. (See "Unipolar major depression in adults: Indications for and efficacy of
electroconvulsive therapy (ECT)" and "Bipolar disorder in adults: Indications for and efficacy
of electroconvulsive therapy (ECT)" and "Evaluation and management of treatment-resistant
schizophrenia" and "Catatonia: Treatment and prognosis" and "Neuroleptic malignant
syndrome", section on 'Electroconvulsive therapy'.)
● Although the exact mechanism of action of ECT is unknown, accumulating data suggest that
ECT reverses many of the deleterious atrophic brain changes induced by severe central
nervous system illnesses. (See 'Neurobiology' above.)
● Inducing a seizure causes transient increases in blood pressure, pulse, and intracranial
pressure, which can have deleterious effects. Organ systems of most concern are
cardiovascular, pulmonary, and central nervous system. Medication to blunt increases in heart
rate and blood pressure is indicated prior to ECT and during the procedure in patients for
whom these increases would be detrimental. (See 'Patients with comorbid general medical
illness' above and "Medical consultation for electroconvulsive therapy".)
● Many psychotropic medications may be continued during a course of ECT for their synergistic
effect without compromising safety, including antidepressants, antipsychotics, and lithium.
Morning doses on the day of ECT are given after the patient has recovered from that day's
procedure. Anticonvulsants and benzodiazepines often interfere with ECT and may need to
be tapered and discontinued. (See 'Psychotropic drugs' above.)
● Most cardiac, antihypertensive, and anti-reflux medications should be taken with a small sip of
water approximately two hours before each ECT treatment. (See 'Other drugs' above.)
● The consent process should conform to all state and local laws and statutes, and hospital
policies. Informed consent requires that patients receive adequate information about their
illness and ECT, are capable of understanding and acting reasonably on this information, and
are given the opportunity to consent in the absence of coercion. (See 'Informed consent'
above.)
● Standard practice in the United States is to give ECT three times per week. The routine in
many other countries is twice a week. (See 'Treatment frequency' above.)
● Continuation and maintenance ECT is the practice of providing a single, intermittent ECT
treatments after remission to prevent recurrence of the mood or psychotic episode that
prompted the acute course of ECT. (See 'Continuation and maintenance ECT' above.)
● The mortality rate of ECT is at most 2 to 4 deaths per 100,000 treatments, making it one of
the safest procedures performed under general anesthesia. Mortality is mostly related to
cardiopulmonary events. Other adverse medical effects include aspiration pneumonia,
fracture, dental and tongue injuries, headache, and nausea. (See 'Adverse general medical
effects' above.)
● Many patients experience some adverse cognitive effects during and after a course of ECT,
including acute confusion, anterograde amnesia, and retrograde amnesia. However, objective
tests indicate that neuropsychological impairment caused by ECT is generally short lived, and
impaired cognition due to depression typically improves after a course of ECT. In addition,
ECT does not appear to be associated with an increased risk of dementia. We monitor
cognition with a standardized instrument. (See 'Adverse cognitive effects' above.)
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55. Shapira B, Tubi N, Drexler H, et al. Cost and benefit in the choice of ECT schedule. Twice
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GRAPHICS
Definitely effective
Unipolar major depression
Refractory or resistant to antidepressant therapy
Need exists for rapid treatment response, such as in pregnancy, persistent suicidal intent, or food refusal leading to
dehydration or nutritional compromise
Medical comorbidities prevent the use of antidepressant medication
Previous response to ECT
Psychotic features (eg, delusions or hallucinations)
Catatonia
Persistent suicidal intent
Aortic stenosis Echocardiography should be performed to Limited data suggest that ECT is safe with
assess severity if not done within the past the use of short-acting intravenous beta-
year or if there is a change in symptoms. If blockers to minimize procedure-related
stenosis is severe, then consult cardiologist hypertension and tachycardia. [1]
before proceeding with ECT.
Asthma or chronic Discontinue theophylline by tapering the Theophylline increases the risk of status
obstructive dose, if possible. Continue outpatient epilepticus after ECT. [2]
pulmonary disease regimen of bronchodilators and inhaled
glucocorticoids. Provide standard treatment
during an asthma exacerbation (inhaled
beta-agonists and, if necessary,
glucocorticoids, before proceeding with ECT).
Atrial fibrillation Continue outpatient medications for control ECT appears to be safe in patients with atrial
of heart rate. Control heart rate with fibrillation. Patients may have conversion to
calcium-channel blockers if needed. Manage and from sinus rhythm during ECT. The
anticoagulation as described below. effect of spontaneous rate conversion on
embolization rates is unknown.
Diabetes Measure blood glucose levels before and The effect of ECT on blood glucose is
after ECT treatment. If breakfast is likely unpredictable because of changes in diet,
only delayed, patients may delay taking their appetite, and energy level that may result
usual morning insulin until after ECT and from ECT. Individual ECT treatments raise
before eating. If ECT happens later in the blood glucose levels in patients with
morning, where breakfast and lunch are diabetes to the same degree as in patients
likely to be missed, then give one-half the without diabetes.
usual total morning dose as intermediate-
acting insulin. Withhold oral agents and
short-acting insulin until patient can eat.
Perform ECT early in the morning if possible.
Hypertension (poorly Start or intensify antihypertensive Blood pressure increases during the postictal
controlled) medications; delay ECT until blood pressure phase of ECT. Beta-blockers may shorten the
is <140/90 mmHg. Avoid beta-blockers. seizure duration and reduce the efficacy of
ECT. [3]
Hypertension (well- Continue usual antihypertensive
controlled) medication(s).
Implantable Turn off detection mode of ICD during ECT. ECT appears to be safe in patients with an
cardioverter- Perform continuous electrocardiographic ICD. [4]
defibrillator (ICD) monitoring throughout treatment. Place
resuscitative equipment by the patient's
bedside in the event that external
defibrillation is necessary. Make sure that
ICD has been interrogated routinely.
Need for long-term Continue anticoagulation to maintain an ECT appears to be safe in patients who
anticoagulation international normalized ratio of up to 3.5, require long-term anticoagulation. [5]
unless there is an increased risk of
intracranial hemorrhage (eg, intracranial
mass or aneurysm).
Pregnancy The informed-consent and risk-stratification Pregnancy would require modification of the
process should include an obstetrician and anesthetic technique, positioning of the
an anesthesiologist. In addition to standard patient, and monitoring requirements.
monitoring of the patient, noninvasive fetal
monitoring should be used after 14 to 16
weeks. After 24 weeks, a nonstress test with
a tocometer should be performed before and
after treatments.
Sources:
1. Mueller PS, Barnes RD, Varghese R, et al. The safety of electroconvulsive therapy in patients with severe aortic
stenosis. Mayo Clin Proc 2007; 82:1360.
2. Devanand DP, Decina P, Sackeim HA, Prudic J. Status epilepticus following ECT in patient receiving theophylline. J
Clin Psychopharmacol 1988; 8:153.
3. Rumi DO, Solimene MC, Takada JY, et al. Electrocardiographic and blood pressure alterations during
electroconvulsive therapy in young adults. Arg Bras Cardiol 2002; 79:149.
4. Dolenc TJ, Barnes RD, Hayes DL, Rasmussen KG. Electroconvulsive therapy in patients with cardiac pacemakers
and implantable cardioverter defibrillators. Pacing Clin Electrophysiol 2004; 27:1257.
5. Mehta V, Meuller PS, Gonzalez-Arriaza HL, et al. Safety of electroconvulsive therapy in patients receiving long-term
warfarin therapy. Mayo Clin Proc 2004; 79:1396.
Name of Patient:
often related to the number and type of treatments given. A smaller number of treatments is likely to produce less
memory difficulty than a larger number. Shortly following a treatment, the problems with memory are greatest. As
time from treatment increases, memory improves.
I may experience difficulties remembering events that happened before and while I received ECT. The spottiness in
my memory for past events may extend back to several months before I received ECT, and, less commonly, for
longer periods of time, sometimes several years or more. Although many of these memories should return during
the first few months following my ECT course, I may be left with some permanent gaps in memory.
For a short period following ECT, I may also experience difficulty in remembering new information. This difficulty in
forming new memories should be temporary and typically disappears within several weeks following the ECT course.
The majority of patients state that the benefits of ECT outweigh the problems with memory. Furthermore, most
patients report that their memory is actually improved after ECT. Nonetheless, a minority of patients report
problems in memory that remain for months or even years. The reasons for these reported long-lasting
impairments are not fully understood. As with any medical treatment, people who receive ECT differ considerably in
the extent to which they experience side effects.
Because of the possible problems with confusion and memory, I should not make any important personal or
business decisions during or immediately after the ECT course. During and shortly after the ECT course, and until
discussed with my doctor, I should refrain from driving, transacting business, or other activities for which memory
difficulties may be troublesome.
The conduct of ECT at this facility is under the direction of Dr. ______________________. I may contact him/her at
_______________________ if I have further questions.
I am free to ask my doctor or members of the ECT treatment team questions about ECT at this time or at any time
during or following the ECT course. My decision to agree to ECT is being made voluntarily, and I may withdraw my
consent for further treatment at any time.
I have been given a copy of this consent form to keep.
Signature: Date:
Name: Signature:
Reprinted with permission from the Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and
Privileging. Copyright © 2001 American Psychiatric Association.
Name of Patient:
I understand that memory loss is a common side effect of ECT. The memory loss with ECT has a characteristic
pattern, including problems remembering past events and new information. The degree of memory problems is
often related to the number and type of treatments given. A smaller number of treatments is likely to produce less
memory difficulty than a larger number. Shortly following a treatment, the problems with memory are greatest. As
time from treatment increases, memory improves.
I may experience difficulties remembering events that happened before and while I received ECT. The spottiness in
my memory for past events may extend back to several months before I received ECT, and, less commonly, for
longer periods of time, sometimes several years or more. Although many of these memories should return during
the first few months following continuation/maintenance ECT, I may be left with some permanent gaps in memory.
For a short period following each treatment, I may also experience difficulty in remembering new information. This
difficulty in forming new memories should be temporary and will most likely disappear following completion of
continuation/maintenance ECT.
The effects of continuation/maintenance ECT on memory are likely to be less pronounced than those during an
acute ECT course. By spreading treatments out in time, with an interval of a week or more between treatments,
there should be substantial recovery of memory between each treatment.
Because of the possible problems with confusion and memory, it is important that I not drive or make any important
personal or business decisions the day that I receive a continuation/maintenance treatment. Limitations on my
activities may be longer depending on the side effects I experience following each treatment and will be discussed
with my doctor.
The conduct of ECT at this facility is under the direction of Dr. ______________________. I may contact him/her at
_______________________ if I have further questions.
I am free to ask my doctor or members of the ECT treatment team questions about ECT at this time or at any time
during or following the ECT course. My decision to agree to continuation/maintenance ECT is being made voluntarily,
and I may withdraw my consent for future treatment at any time.
I have been given a copy of this consent form to keep.
Signature: Date:
Name: Signature:
Reprinted with permission from the Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and
Privileging. Copyright © 2001 American Psychiatric Association.
Montgomery, SA. A new depression scale designed to be sensitive to change. Br J Psychiatry 1979; 134:382.
Montgomery, SA. A new depression scale designed to be sensitive to change. Br J Psychiatry 1979; 134:382.
Montgomery, SA. A new depression scale designed to be sensitive to change. Br J Psychiatry 1979; 134:382.
Contributor Disclosures
Charles Kellner, MD Other Financial Interest: Cambridge University Press (royalties, for the book,
"Handbook of ECT"); Psychiatric Times (paid contributor for articles on ECT); Northwell Health (honoraria for
teaching ECT course). Peter P Roy-Byrne, MD Employment: Mass Medical Society (Journal Watch). David
Solomon, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.