I

Review Article

Electroconvulsive Therapy: A Review of History,

Patient Selection, Technique, and Medication
Management
Stephen Taylor, MD

Abstract: Electroconvulsive therapy (ECT) is a safe and effective

treatment for severe and persistent depression, bipolar disorder and
schizophrenia. Though ECT is now over 60 years old, it remains an
underutilized treatment today. History, patient selection, safety, and
characteristics of the treatment stimulus, technique, and medications
used in ECT are reviewed. Dosing strategies, as pertaining to seizure
threshold, will be considered. Mechanisms of action, especially with
regard to serotonin, norepinephrine, and dopamine receptor expression will be discussed.
Key Words: electroconvulsive, seizure, depression, bipolar disorder, schizophrenia

lectroconvulsive therapy (ECT) has been shown to be a

highly effective, safe, and even life-saving treatment for
persistent and severe depression, bipolar disorder and schizophrenia. Over 50,000 ECT treatments are performed annually
in the United States,' The history of ECT, clinical indications
for ECT, patient outcomes, current practices in ECT administration, patient workup, and post ECT care will be reviewed.

History
Convulsive therapy, relevant to the practice of psychiatry, has its origins in the work of Ladislaus von Meduna,^
Meduna used pentylenetetrazol to induce seizures in patients
with catatonic schizophrenia,''^ This form of convulsive therapy was wide- spread in Europe in the 1930s, Electricity was
used successfully in 1938 by Ugo Cerietti and Lucio Bini for
the purpose of eliciting seizures to treat mental illness. In the
1950s, Max Fink, one of the most important figures in the

From the Department of Psychiatry and Behavioral Science, University of

Louisville School of Medicine, Louisville, Kentucky.
Reprint requests to Dr. Stephen Taylor, Department of Psychiatry, Behavioral Sciences, University of Louisville, School of Medicine, 501 E
Broadway, Med Center 1, Suite 340, Louisville, KY 40202. Email:
mmst@insightbb.com
Accepted December 8, 2006.
Copyright 2007 by The Southern Medical Association
0038-4348/0-2000/10000-0494

494

history of ECT, was the first to apply rigorous scientific

research methods to ECT, which gave the treatment scientific
legitimacy,'^
The anti-psychiatry movement and the promise that pharmacology would cure mental illness contributed to a decline
in ECT use in the ensuing decades. The anti-psychiatry movement was largely a by-product of popular philosophical ideology of the time, negative views that mental illness was a
mere invention, and negative views of ECT as a brutal practice. In spite of negative media depiction (the movie One
Flew Over the Cuckoos Nest, for example) contributing to a
decline in ECT use, ECT has shown a strong comeback in the
last decade, which is a testament to its continued efficacy and
safety,^'"

Patient Selection
It has long been known that ECT is an appropriate treatment for medication resistant depression. Patients who have
shown no response to pharmacotherapy, or psychotherapy,
will still respond to ECT at a rate that approaches 55%,'*
Recent studies have demonstrated that ECT is highly effective for the initial treatment of depression as well. The response rate for index depression has been reported as high as
80 to 90%,' Index depressions have been defined as depressive episodes that are currently occurring, with a discemable

Key Points
Electroconvulsive therapy (ECT) has been shown to
be a highly effective, safe, and even life-saving treatment for persistent and severe depression, bipolar disorder and schizophrenia,
ECT is safe for patients with comorbid medical conditions, as modem anesthesia techniques and medications have greatly reduced the morbidity and mortality
of ECT,
Experience and emerging research have made it clear
that ECT should be offered to patients as a viable
treatment option at all stages of their illness process.

2007 Southern Medical Association

Review Article

beginning and a clear history of the patient experiencing normal mood states before the onset of depression. These data
have led the APA to recommend that the use of ECT be
considered as an initial treatment option, in certain cases, for
patients with severe depression,^
For all patients treated with ECT, it should be stressed
that ECT represents a treatment that will bring remission, not
a cure, and in many cases, maintenance ECT should be discussed with patients because the effects of ECT are transient,^
These caveats are in part due to the nature of the treatment
itself, as well as the remitting nature of the illnesses for which
ECT is effective. The APA recommends that the patient receive ECT once a week for a month following the initial
treatment. Subsequent maintenance treatments should be
scheduled according to clinical judgment, patient preference,
and with regard to the patient's history of previous illness
relapses,^
ECT has been approved for the treatment of bipolar illness in mania, depression, and mixed states, ECT has also
been shown efficacious in the treatment of schizophrenia with
pharmacotherapy as psychotic symptom relapse prevention.*

Mechanism of Action
Though ECT has proven efficacy and safety, the mechanism of action is difficult to elucidate, A full discussion of
the proposed mechanisms of action is well covered elsewhere,^ There are three mechanisms that seem to hold the
most favor among researchers: 1) Modulation of monoamines,
2) Change in neurotrophic factors, and 3) Anticonvulsant
factors,^'''
It has been shown that monoamine levels increase in
animal models treated with ECT,^'' It may also be that increases in serotonin levels have an indirect impact on levels
of endogenous opioids,' The increase in dopamine levels with
ECT may explain why ECT improves symptoms of Parkinson
disease,'**
Little is known about the intracellular impact of ECT,
though researchers have looked at neurotrophic mechanisms and
possible relation to therapeutic response. This theory of neurotrophic mechanism states that cyclic AMP (cAMP) is up regulated with ECT,^ which increases brain derived neurotrophic
factor (BDNF)," BDNF regulates neuron cell strength, growth
and survival, as well as norepinephrine and serotonin receptor
expression.
Increase in GABA transmission and receptor antagonism
has been observed in ECT,'^ This anticonvulsant action raises
the seizure threshold during ECT. Also, ECT causes an increase of endogenous opioids that may also have anti-seizure
properties.

sidered safe, with a mortality of approximately 1/10,000 patients or 1/80,000 treatments. This puts the ECT risk at the
level of childbirth or minor surgery,' There are no recommendations regarding the total number of ECT treatments.
However, some case reports have examined patients who
have had thousands of lifetime treatments with no ill effects,'^
The most commonly expressed worries and criticisms
center on memory loss, Anterograde amnesia, or the inability
to form new memories, has been reported, though it tends to
be short-lived and resolves rapidly within a few weeks of the
procedure,''' Retrograde amnesia, or loss of past memories,
tends to affect recent memories more than remote memories.
Loss of memories of the events immediately surrounding the
procedure is not uncommon and usually resolves within weeks
of the treatment,'^ Loss of remote memories is quite rare, and
for that reason, is difficult to quantify. Permanent memory
loss is extremely rare,'*
Other reported side effects include headache, nausea, and
muscle soreness. Muscle soreness is often due to the use of
succinylcholine; however, inadequate muscle blockade also
causes muscle soreness,'^ Nausea is common with ECT given
that ECT stimulates the vagus nerve. Proton pump inhibitors
can be used safely in such patients.
Missed or short seizures can occur. It is also noted that
seizure induction can be difficult, particularly in the elderly.
In addition to hyperventilation, pharmacologic methods have
been shown to be of help. Augmentation with caffeine or
switching anesthetic agents may also
"*'^

Seizure Characteristics, Dosing, and

Frequency of Treatment

Much of the current bias and controversy surrounding

ECT is with regard to safety and side effects, ECT is con-

ECT functions to induce a seizure, and characteristics of

a therapeutic seizure have been reported. Some important
points to mention here are: 1) Length of ictal motor response,
2) Length of the EEG seizure, and 3) Intensity of the electrical stimulus.
An appropriate ictal response has been reported to be
between 20 to 25 seconds in duration,' Direct observation of
the ictal motor seizure is the best method of measure; however, newer ECT devices have the capacity to monitor EMG
activify, which is recorded by the ECT device and analyzed
by the onboard computer (MECTA Corp.; Somatics LLC),
A therapeutic seizure is generally accepted to be one that
is greater than 30 seconds in length,' During the clonic phase
of the seizure, spike and slow waves will be observed on the
EEG, Seizure termination will often be followed with post ictal
suppression, observed as a flattening on the EEG monitor.
Stimulus intensity has been a topic of much ongoing
research and controversy. Current data suggest that a moderately suprathreshold seizure offers the best clinical response
for the patient.^"'^' Seizure threshold is difficult to measure in
patients; however, newer dosing strategies have improved ca-

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495

Safety and Side Effects

Taylor Electroconvulsive Therapy: A Review

pacities to determine the seizure threshold with greater accuracy.

Research indicates that a seizure stimulus that is 150% above the
seizure threshold for bilateral ECT, and 200 to 250% above the
seizure threshold for unilateral ECT, offers the best clinical response with the least cognitive impairment,^'"'^
Though a complete discussion of different dosing strategies in ECT is beyond the scope of this paper, a brief word
about dose titration and other dosing techniques will be offered here. There are three basic approaches to selecting stimulus energies: 1) Pre-selected dosing, 2) Age-based dosing
and half-age dosing, and 3) Dose titration.
Preselected dosing involves making an assumption about
what stimulus intensity has the best chance of inducing a
seizure in the greatest number of patients. Often, the device
will be set at 75% of its maximum energy and left there until
the energy stimulus is no longer adequate to produce a seizure, A variation of this technique is to use the patient's age
as a determinant of stimulus settings. For example, a 30-yearold would start with an energy setting of 30%, or roughly
150 mC, This stimulus dose is continued until it is no longer
adequate for seizure production. The half-age method uses an
energy setting equal to half the patient's age.
The dose titration method divides the stimuli of the ECT
device into 8 levels. The first level is the lowest energy setting of the device. Each subsequent level is approximately
50% greater in energy than the previous level. An assumption
of what stimulus intensify has a fair chance of inducing a
seizure in a patient is selected first. If the first stimulus dose
does not induce a seizure, then the next level is selected, and
so on. This method often fails to produce a seizure on the first
stimulus, but it does help the clinician narrow the range of
energy that is required to induce a seizure. On subsequent
treatments, the energy is increased, as stated earlier, to achieve
a moderate suprathreshold seizure,^'^^
Dosing frequency has differed in the United States and
Europe. By convention, ECT is performed three times a week
in the US, while in Europe it is performed twice a week.
Twice weekly treatments result in slower improvement, decreasing cognitive side effects, while thrice weekfy treatments
will bring a patient to remission faster. Patients will typically
receive between six and twelve treatments with ECT, It is not
uncommon for patients to respond after their first treatment,
though it can take more than twelve treatments to see an
adequate response in some patients. Balance and risk-benefit
analysis is always necessary when selecting any treatment
strategy for a patient. One must always keep the severity of
illness, as well as patient preference, in mind when setting a
treatment strategy for ECT,

Electrode Placement
When ECT was first used, the electrodes were placed on
either side of the head at the temples. By the mid 1950s,
practitioners began to experiment with unilateral electrode

496

placement. The electrodes were placed over the nondominant

hemisphere, which resulted in less post treatment confusion
and memory loss. Though somewhat controversial, right unilateral electrode placement has been demonstrated to be as
effective as bilateral placement in some studies; however,
higher stimulus intensify is needed to achieve a therapeutic
response. 1,22

Medications in ECT
ECT was performed without anesthesia in the first several years of its use, but by the late 1950s, anesthesia had
become commonplace. Early use of barbiturates carried the
risk of cardiac arrhythmias, as well as decreasing seizure
duration.^'' Today, methohexital, a short-acting barbiturate,
has become the anesthetic of choice among ECT practitioners. Though barbiturates increase seizure threshold and decrease seizure duration, among barbiturates, methohexital appears to have the least impact on these factors.
The use of muscle blockers has greatly reduced the likelihood of physical injury during ECT,'^'^'* The dmg of choice
among psychiatrists and anesthesiologists is succinylcholine.
This dmg has a quick onset of action, is short-acting, and
does not need to be reversed, as is the case with many nondepolarizing blockers,
ECT causes a significant change in autonomic function.
Initially, the patient experiences a parasympathetic surge,
which can cause significant bradycardia, hypotension, and, in
some cases, brief asystole,^^ To prevent this, anticholinergic
dmgs such as glycopyrrolate are often used. Although atropine has been the dmg of choice in the past, glycopyrrolate
offers the advantage over atropine in that it does not cross the
blood-brain barrier and therefore does not cause unwanted
cognitive side effects,^"*

Drug Interactions in ECT

There are a few dmg interactions with ECT that are
worthy of some discussion, Anticonvulsant medications,
which are commonly used in the psychiatric patient, act to
raise the seizure threshold and decrease the length of the
seizure,^''-^^ As data are making it clear that efficacy is linked
to the degree to which the seizure exceeds the seizure threshold, anticonvulsants may increase the seizure threshold in
some patients, such that the seizure will no longer be therapeutic. Stopping the anticonvulsant is advised if it can be
done safely. If it is not possible to stop anticonvulsant medications, then decreasing the dose to the lowest therapeutic
level is recommended.
Lithium, a dmg commonly used to treat bipolar disorder,
has the potential to both increase seizure duration and cause
intense postictal confusion. Though a full discussion of the
proposed mechanism of action is beyond the scope of this
paper, a previous study has examined this in some detail^^
showing that the concomitant use of lithium with ECT is not
recommended.
2007 Southern Medical Association

Review Article

Theophylline is a dmg that can increase seizure duration

and increase the risk of status epilepticus. Discontinuation of
the medication is advised. If the patient cannot stop the medication, then decreasing it to the lowest therapeutic dmg level
will at least decrease the risk of interaction with ECT,^^
Patients who are taking a benzodiazepine should stop the
medication before ECT, if possible, Benzodiazepines increase
the seizure threshold, decrease seizure duration, and consequently decrease the potential efficacy of ECT, If stopping
benzodiazepines does not seem wise or possible, then the use
of flumazenil just before ECT can temporarily reverse the
effects of benzodiazepines,

Workup and Patient Considerations

The APA recommends that each patient receive a complete psychiatric and medical evaluation before ECT, No specific recommendations regarding laboratory workup exist;
however, a minimum of an electrolyte panel and a complete
blood count should be obtained. A thorough history of the
illness process, as well as treatments tried in the past, is
necessary for a complete evaluation. Patients who have tried
ECT in the past with a favorable response have a greater
chance of responding to treatment in the future. As stated
earlier, patients with medication resistant depression often
respond favorably to ECT, However, patients with dysthymia
or comorbid personality disorders often do not have a robust
response to ECT,^
Though there are no absolute contraindications to ECT,
some medical conditions do complicate the use of ECT, Care
should be used with ECT on patients with space occupying
intracranial lesions. Past convention indicated that patients
with intracerebral masses should not receive ECT,^ ECT
increases intracranial pressure, as well as a transient increase
in blood flow to the brain. Current studies suggest that patients with intracerebral masses that lack a mass effect can
safely receive ECT (eg, patients with meningiomas),'" Head
Computed Tomography (CT) is not necessary unless there is
clinical suspicion.
Patients with cardiac disease can receive ECT, but evaluation by a cardiologist should be obtained and may help in
managing the patient. When considering ECT in patients who
have recently had a myocardial infarction, care should be
taken to ensure that further damage to the cardiac muscle is
not done due to the increased work demands of the procedure.
However, ECT does not appear to cause malignant arrhythmias or cardiac ischemia,^^ Patients with cardiac pacemakers
may safely receive ECT, A cardiologist should be consulted,
as the older demand type pacemakers may need to be converted to a fixed rate pacing or deactivated before ECT,'''''''''
ECT is considered safe in pregnancy. Obstetric consult
should be obtained and fetal monitoring used when appropriate. Avoidance of hyperventilating the patient will ensure
adequate oxygenation of the fetus during the treatment. In
Southern Medical Journal Volume 100, Number 5, May 2007

late pregnancy, the patient should lie on her left side, which
will ensure adequate blood flow to the fetus. Transmission of
anesthetic agents across the matemal fetal barrier is considered to be minimal,
A careflil dental examination should be part of the patient workup. Modifications to the bite block may be necessary for chipped or broken teeth. Loose teeth may need to be
extracted before ECT to avoid injury to the oral cavity and
aspiration.
Patients with gastroesophageal reflux disease may experience worsening symptoms during ECT, as the treatment
stimulates the vagus nerve. Antacid medications can be safely
used. Patients who are on proton pump inhibitors may safely
use them before and after ECT, Some anesthesiologists argue
that intubation may be called for in rare cases in which the
patient suffers from severe reflux disease.

Post Treatment Considerations

ECT can be done on both an inpatient as well as an outpatient basis. Routine monitoring of vital signs is done for 30
minutes following treatment, A designated ECT suite equipped
with blood pressure monitoring, oxygen level assessment, and a
crash cart is sufficient for ECT, Access to medications used in
ECT, as well as the appropriate medications used to abort prolonged seizures and manage cardiovascular abnormalities, is also
needed.
Observation of spontaneous respiration and normal blood
pressure is good clinical evidence that the patient is not having a tardive seizure. However, it is good practice to leave the
EEG monitor in place for several minutes following treatment
so the patient can be monitored for any subsequent seizure
activity.
The patient may resume her/his normal activity, as she/he
is able. Some practitioners advise against driving on the day
of treatment, and others tell patients not to drive until the
entire treatment series is complete.
Periodic assessment of the patient's memory should be
done. If the patient is having excessive memory problems,
then decreasing the frequency of treatments, changing anesthesia, or discontinuation of treatment should be considered.
Medications that have been held during ECT should be
resumed after treatment. If a patient with a seizure disorder
has been treated and their anticonvulsant medication dose
lowered for ECT, increasing the anticonvulsant medication to
pre-ECT doses can be done after the ECT series is complete,
ECT is a beneficial treatment for catatonia and neuroleptic malignant syndrome.

Discussion
ECT is a safe and effective treatment option for patients.
It has proven efficacy in treating medication resistant depression. It is also an excellent treatment option for patients with
severe suicidal ideation, ECT currently exists as an option for

497

Taylor Electroconvulsive Therapy: A Review

patients with bipolar disorder in all phases of the illness. It

has proven beneficial in patients with psychosis due to schizophrenia, as well as other related mental disorders,
ECT has been safely used in patients with comorbid
medical conditions. Careful management of their medical
complications makes ECT relatively safe to use. More modem anesthesia techniques and medications have greatly reduced the morbidity and mortality of ECT,
Although current wisdom has relegated ECT to a last
treatment option in many cases, experience and emerging
research have made it clear that ECT should be offered to
patients as a viable treatment option at all stages of their
illness process.

15. O'Connor M, Brenninkmeyer C, Morgan A, et al. Relative effects of

repetitive transcranial magnetic stimulation and electroconvulsive therapy on mood and memory: a neurocognitive risk-benefit analysis. Cogn
Behav Neurol 2003;16:118-127.
16. Reid WH Electroconvulsive therapy. Tex Med 1993;89:58-62.
17. Werawatganon T, Kyokong O, Charuluxananan S, et al. Muscular injury
after succinylcholine and electroconvulsive therapy. Anesth Analg 2004;
98:1676-1679.
18. Datto C, Rai AK, Ilivicky HJ, et al. Augmentation of seizure induction
in electroconvulsive therapy: a clinical reappraisal. J ^ C r 2002; 18:118125.
19. Krystal AD, Dean MD, Weiner RD, et al. ECT Stimulus intensity: are
present ECT devices too limited? Am J Psychiatry 2000; 157:963-967

Acknowledgments

20. McCall WV, Reboussin DM, Weiner RD, et al. Titrated moderately
suprathreshold vs fixed high-dose right unilateral electroconvulsive therapy: acute antidepressant and cognitive effects. Arch Gen Psychiatry
2000;57:438-444.

Special thanks to Dr. David Casey at the University of

Louisville for his guidance in organizing and preparing this
manuscript for publication.

21. Sackeim HA, Prudic J, Devanand DP, et al. A prospective, randomized

double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Arch Gen Psychiatry 2000;
57:425^34.

References

22. Heikman P, Tuunainen A, Kuoppasalmi K. Value of the initial stimulus

dose in right unilateral and bifrontal electroconvulsive therapy. Psychol
Med 1999;29:1417-1423.

1. Beyer JL, Weiner RD, Glenn MD, Eiectroconvulsive Therapy: A Programmed Text. 2nd edition. Washington, DC, American Psychiatrie
Press, Ine, 2001,
2. Abrams R. Electroconvuisive Therapy. 4th edition. Oxford, Oxford University Press, 2002.
3. Glass RM. Electroconvulsive therapy: time to bring it out of the shadows. JAMA 2001;285:1346-1348.
4. Sackeim HA, Haskett RF, Mulsant BH, et al. Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy;
a randomized controlled trial. JAMA 2001;285:1299-1307.
5. Weiner RD, Coffey CE, Fochtmann LJ, et al. The Practice of Eiectroconvulsive Therapy Recommendationsfor Treatment, Training, and Privileging. 2nd edition. Washington, DC, American Psychiatric Association, 2001.
6. Tharyan P, Adams CE. Electroconvulsive Therapy for Schizophrenia.
Cochrane Database of Systemic Reviews. (2):CD000076, March 2005.
7. Sadock BJ, Sadock VA. Kaplan and Sadock's Synopsis of Psychiatry:
Behavioral Sciences/Clinical Psychiatry. 9th edition. New York, Lippincott Williams & Wilkins, 2003.

23. Mokriski BK, Nagle SE, Papuchis GC, et al. Electroconvulsive therapyinduced cardiac arrhythmias during anesthesia with methohexital, thiamylal, or thiopental sodium. J Clin Anesth 1992;4::208-212.
24. Ding Z, White PF. Anestheisa for electroconvulsive therapy. Anesth
Analg 2002,94.\35\-\364.
25. Tang WK, Ungvari GS. Asystole during electroconvulsive therapy: a
case report. Aust N Z J Psychiatry 2001;35:382-385.
26. Coffey CE, Lucke J, Weiner RD, et al. Seizure threshold in electroconvulsive therapy, II: the anticonvulsant effect of ECT. Bioi Psychiatry
1995;37:777-788.
27. Sackeim HA, Decina P, Prohovnik I, et al. Anticonvulsant and antidepressant properties of electroconvulsive therapy: a proposed mechanism
of Action. Bioi Psychiatry 1983;18:13Ol-131O.
28. El-Mallakh RS. Complications of concurrent lithium and electroconvulsive therapy: a review of clinical material and theoretical considerations.
Biol Psychiatry 1988;23:595-601.
29. Fink M, Sackeim HA. Theophylline and the risk of status epilepticus in
ECT. JECT 1998;14:286-290.

8. Gur E, Dremencov E, Garcia F, et al. Functional effects of chronic

electroconvulsive shock on serotonergic 5-HT(l A) and 5-HT(lB) receptor activity in rat hippocampus and hypothalamus. Brain Res 2002;952:
52-60.

30. Krystal AD, Coffey CE. Neuropsychiatric considerations in the use of

electroconvulsive therapy. J Neuropsychiatry Ciin Neurosci 1997;9:283292.

9. Benkelfat C. Biochemical effects of electroconvulsive therapy. Encephale 1988;14:273-281.

31. Kellner CH, Ramas L. Dexamethasone pretreatment for ECT in an elderly patient with meningioma. Clin Gerontol 1990;10:67-72.

10. Dam H, Pakkenberg H, Bolwig TG. Electric stimulation (ECT) in Parkinson disease. Ugesk Laeger 1992;154:183-187.

32. Takada JY, Solimene MC, da Luz PL, et al. Assessment of the cardiovascular effects of electroconvulsive therapy in individuals older than 50
years. Braz J Med Bioi Res 2005;38:1349-1357.

11. Li B, Suemaru K, Cui R, et al. Repeated electroconvulsive stimuli increase brain derived neurotrophic factor in ACTH-treated rats. Eur
JPharmacoi 2006;529:l 14-121.
12. Palmio J, Huuhka M, Saransaari P, et al. Changes in plasma amino acids
after electroconvulsive therapy of depressed patients. Psychiatry Res
2005;137:183-I90.
13. Devanand DP, Dwork AJ Hutchinson ER, et al. Does ECT alter brain
structure? Am J Psychiatry 1994; 151:957-970.
14. Moscrip TD, Terrace HS, Sackeim HA, et al. A primate model of anterograde and retrograde amnesia produced by convulsive treatment.
JECT 2004;20:26-36.

498

33. Giltay EJ, Kho KH, Keijzer LT, et al. Electroconvulsive therapy (ECT)
in a patient with a dual-chamber sensing, VDDR pacemaker. JECT
2005;21:35-38.
34. Dolenc TJ, Barnes RD, Hayes DL, et al. Electroconvulsive therapy in
patients with cardiac pacemakers and implantable cardioverter defibrillators. Pacing Ciin Eiectrophysiol 2004;27:1257-1263.

Please see James N. Kimball's editorial on page

462 of this issue.
2007 Southern Medical Association