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Handbook of ECT
A Guide to Electroconvulsive Therapy for
Practitioners
Handbook of ECT
A Guide to Electroconvulsive Therapy
for Practitioners
Charles H. Kellner, MD
New York Community Hospital
University Printing House, Cambridge CB2 8BS, United Kingdom
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Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the
pursuit of education, learning, and research at the highest international
levels of excellence.
www.cambridge.org
Information on this title: www.cambridge.org/9781108403283
DOI: 10.1017/9781108242028
© Charles H. Kellner 2019
This publication is in copyright. Subject to statutory exception and to the
provisions of relevant collective licensing agreements, no reproduction
of any part may take place without the written permission of Cambridge
University Press.
First published 2019
Printed and bound in Great Britain by Clays, Ltd, Elcograf S.p.A.
A catalogue record for this publication is available from the British Library.
ISBN 978-1-108-40328-3 Paperback
Cambridge University Press has no responsibility for the persistence or

accuracy of URLs for external or third-party internet websites referred to in
this publication and does not guarantee that any content on such websites
is, or will remain, accurate or appropriate.
Every effort has been made in preparing this book to provide accurate and
up-to-date information that is in accord with accepted standards and practice
at the time of publication. Although case histories are drawn from actual cases,
every effort has been made to disguise the identities of the individuals involved.
Nevertheless, the authors, editors, and publishers can make no warranties that
the information contained herein is totally free from error, not least because
clinical standards are constantly changing through research and regulation.
The authors, editors, and publishers therefore disclaim all liability for direct
or consequential damages resulting from the use of material contained in this
book. Readers are strongly advised to pay careful attention to information
provided by the manufacturer of any drugs or equipment that they plan to use.
To my wife, Andrea, with appreciation for her unending
patience and support.
Contents
Preface page ix
List of Abbreviations xi
1 Basic Concepts of ECT 1 4 ECT Treatment Course 87

Basic Concepts 1 Treatment Schedule 87
Overview 1 Clinical Monitoring 88
Theories of Mechanism Continuation/Maintenance
of Action 3 ECT 89
Basics of Electricity 7 5 Common Adverse Effects 95
Medical Physiology 9 Cognition 95
2 ECT: Patient Selection and Headache, Muscle Aches,
Preparation 19 and Nausea 98
Indications 19 6 The ECT Service 101
The ECT Consultation 21 Staffing and Administration 101
The ECT Consultation Note 23 The ECT Suite 102
The Pre-ECT Evaluation 25 Record Keeping 102
ECT in Specific Medical
Conditions 27 7 Special Issues 105
Concurrent Medications 31 Stigma 105
Informed Consent 36 Patient-Centered ECT 105
Malpractice Litigation and
3 ECT Technique 49 Insurance 106
Electrode Placement 49 Research 106
Stimulus Dosing 53
Practical Advice on Choosing the
Stimulus Dose 57
Electrode Site Preparation 57 Index 109
Physiological Monitoring 61
Anesthetics and Muscular
Relaxation 67
Cardiovascular Agents 73
Missed, Short, and Prolonged
Seizures 75
Treatment Procedure 79
vii
Preface
This book is a revision of Brain Stimulation in Psychiatry (Kellner, 2012), but

now with a return to its original title from the first edition and an exclusive focus
on electroconvulsive therapy (ECT). Despite the interest in other brain stimu-
lation modalities, ECT remains the only proven, clinically viable, noninvasive
brain stimulation technique for the treatment of very serious psychiatric illness.
Notwithstanding the unfortunate stigma surrounding ECT, the treatment has
continued to gain acceptance, and its use is growing in many countries around
the world; therefore, a dedicated handbook for the optimal practice of clinical
ECT is warranted.
ECT has a remarkable track record of safety and efficacy, and a large scien-
tific evidence base to support it. It remains a standard treatment in the modern
psychiatric armamentarium. Psychiatrists and other health professionals need
to be aware of the most recent advances in ECT technique and clinical indica-
tions that allow it to be effective and better tolerated than ever before.
This book is a handbook of clinical practice that is aimed both at practition-
ers and trainees who need a quick, up-to-date source about most aspects of clin-
ical ECT. It is not meant to be an exhaustive text, rather a primer of technique,
as well as a guide to the most important current reference articles in the field. I
have tried to interpret recent research for the practitioner in a way that allows
evidence-based practice decisions, but avoids unnecessary complications
that could actually impede clinical decision-making. The tendency to change
practice with each new study finding, before it has been adequately replicated,
should be avoided. With the citations at the end of each chapter of the manual,
the reader will find a concise reference guide to the current medical literature
for each aspect of ECT practice.
Contemporary ECT is extremely effective and safe, and the desire to provide
patients with the most tolerable form of ECT is, of course, each practitioner’s
goal. Efficacy, however, should not be sacrificed out of exaggerated concern for
transient cognitive side effects, given the severity of illness of most ECT patients
and the urgent need for relief of depressive and psychotic symptoms. The choice
of electrode placement and stimulus dosing strategy, both of which affect effi-
cacy and tolerability, should be decided for each patient based on a careful
assessment of the clinical situation and the patient’s preferences (see Chapter 3).
I am encouraged that the worldwide community of ECT clinicians and
researchers continues to contribute rapidly to the knowledge base about how
best to perform ECT and the understanding of how ECT exerts its therapeu-
tic actions (Martin et al., 2018; Oltedal et al., 2017). The state of ECT in the
ix
x Preface
United States was recently well summarized in an editorial in JAMA Psychiatry,

“Modern Electroconvulsive Therapy: Vastly Improved Yet Greatly Underused”
(Sackeim, 2017). It is my hope that the information in this book will enable
clinicians to practice state-of-the-art ECT, prescribing it appropriately to all
those seriously ill patients who need it.
References
Kellner, C. H. (2012). Brain stimulation in psychiatry. Cambridge: Cambridge
University Press.
Martin, D. M., Galvez, V., Lauf, S., Dong, V., Baily, S. A., Cardoner, N., . . . Loo, C. K.
(2018). The Clinical Alliance and Research in Electroconvulsive Therapy Network:
an Australian initiative for improving service delivery of electroconvulsive therapy.
J ECT, 34(1), 7–13. doi:10.1097/YCT.0000000000000435.
Oltedal, L., Bartsch, H., Sorhaug, O. J., Kessler, U., Abbott, C., Dols, A., . . . Oedegaard,
K. J. (2017). The Global ECT-MRI Research Collaboration (GEMRIC): establishing
a multi-site investigation of the neural mechanisms underlying response
to electroconvulsive therapy. Neuroimage Clin, 14, 422–432. doi:10.1016/
j.nicl.2017.02.009.
Sackeim, H. A. (2017). Modern electroconvulsive therapy: vastly improved
yet greatly underused. JAMA Psychiatry, 74(8), 779–780. doi:10.1001/
jamapsychiatry.2017.1670.
Abbreviations
ACT Association for Convulsive Therapy

ACTH adrenocorticotropic hormone
AMD anterograde memory dysfunction
APA American Psychiatric Association
BDNF brain-derived neurotrophic factor
BF bifrontal
BL bilateral
BT bitemporal
CNS central nervous system
CORE Consortium for Research in Electroconvulsive Therapy
CT computed tomography
DBS deep brain stimulation
DST dexamethasone suppression test
ECG electrocardiogram
ECS electroconvulsive shock, animal analog of ECT
ECT electroconvulsive therapy
EEG electroencephalogram
EFFECT European Forum for ECT
EMG electromyogram
FDA US Food and Drug Administration
GABA gamma-aminobutyric acid
GERD gastroesophageal reflux disease
HAM-D Hamilton Rating Scale for Depression
xi
xii List of Abbreviations
HPA hypothalamic-pituitary-adrenal
HRSD Hamilton Rating Scale for Depression
ISEN International Society for ECT and Neurostimulation
J joules
MADRS Montgomery-Asberg Depression Rating Scale
MAOI monoamine oxidase inhibitor
mC millicoulomb
MMSE Mini-Mental State Exam
MoCA Montreal Cognitive Assessment
MRI magnetic resonance imaging
MRS magnetic resonance spectroscopy
NIMH National Institute of Mental Health
NMS neuroleptic malignant syndrome
NPO nothing by mouth
PCP phencyclidine
PET positron emission tomography
QIDS Quick Inventory of Depressive Symptomatology
QIDS-SR Quick Inventory of Depressive Symptomatology-Self Report
RMD retrograde memory dysfunction
RUL right unilateral
SNRI serotonin–norepinephrine reuptake inhibitor
SSRI selective serotonin reuptake inhibitor
TCA tricyclic antidepressant
TSH thyroid-stimulating hormone
Chapter Basic Concepts of ECT
1
Basic Concepts
Electroconvulsive therapy (ECT) is a safe and reliably effective procedure; it
requires that the practitioner have a theoretical and practical background to
perform it well. Our hope is that this book will assist the practitioner in the
application of previously acquired knowledge of ECT. Our intent is that this
book should complement the existing, comprehensive texts on ECT, includ-
ing the report of the American Psychiatric Association (APA) Task Force on
Electroconvulsive Therapy (2001) (American Psychiatric Association, 2001),
Electroconvulsive Therapy by Richard Abrams (Abrams, 2002), Electroconvulsive
and Neuromodulation Therapies by Conrad Swartz (Swartz, 2009), and
Electroconvulsive Therapy: A Guide for Professionals and Their Patients by Max
Fink (Fink, 2009).
Our belief is that ECT is a well-standardized procedure that can be learned
quite easily. The body of knowledge that the practitioner must master is cir-
cumscribed and not overly complex. Of course, as in any clinical endeavor, situ-
ations arise that require expert judgment and some modification of standard
technique. There is no substitute for clinical experience, and consultation with
experts is recommended in difficult cases.
The goal of this text is to provide a practical and useful outline of the basics
of the treatment and to assist the reader in developing a well-informed, com-
monsense attitude to approaching the patient who needs ECT. At all times, tech-
nical excellence and patient comfort should be foremost considerations.
Overview
ECT remains the most reliably effective treatment for serious depression. Its efficacy
and speed of response compare favorably to those of antidepressant medications
(Husain et al., 2004). For these reasons, it must be considered a mainstream treat-
ment in modern psychiatric practice, not one that is optional or “on the fringe.” In the
past two decades, there has been a steady increase in ECT research, as evidenced by
the growing number of ECT-related citations in the scientific literature. In addition,
1
2 Chapter 1: Basic Concepts of ECT
renewed clinical interest in ECT has led to the growth of professional societies dedi-
cated to the advancement of ECT including the International Society for ECT and
Neurostimulation (ISEN, formerly the Association for Convulsive Therapy [ACT])
and the European Forum for ECT (EFFECT), among others worldwide. Exciting
developments include innovations in technique, such as the electrical dose titration
method of estimating seizure threshold (Sackeim et al., 1987); the use of ultrabrief
pulse stimuli (Sienaert et al., 2009); as well as new information about the use of ECT
in catatonia (Fink & Taylor, 2003), autistic self-injury (D’Agati et al., 2017), and as
a continuation/maintenance treatment for affective disorders (Kellner et al., 2006,
2016).
Despite the ongoing barrage of criticism of the treatment (based largely on
either outdated or incorrect information), ECT has remained in continuous use
since its introduction in Rome in 1938. But modern ECT is so far removed from
that primitive procedure that it should hardly be considered the same treatment.
Just as it would be unreasonable to equate surgery as performed in 1938 with
surgery as performed in 2018, so old-fashioned ECT is now of purely historical
interest. The remarkable popularity of the movie One Flew Over the Cuckoo’s
Nest (1975) is largely responsible for the continued public perception of ECT as
a barbaric, coercive procedure. Several books for the lay public, including Shock:
The Healing Power of Electroconvulsive Therapy by Kitty Dukakis and Larry Tye
(Dukakis & Tye, 2006); Shock Therapy: A History of Electroconvulsive Treatment
in Mental Illness by Edward Shorter and David Healy (Shorter & Healy, 2007);
Struck by Living: From Depression to Hope by Julie Hersh (Hersh, 2010); and
Each Day I Like It Better: Autism, ECT, and the Treatment of Our Most Impaired
Children by Amy Lutz (Lutz, 2014), are both informative and factually accurate;
they paint a realistic and positive picture of contemporary ECT.
Although ECT is an essential part of psychiatric practice, it remains a very
small part. According to data from the National Institute of Mental Health
(NIMH), in 1980, approximately 32,000 psychiatric inpatients received ECT
in the United States; in 1986, the number increased to approximately 37,000
(Thompson et al., 1994). The current figure of patients who receive ECT annu-
ally in the United States is almost certainly greater, although, surprisingly, pre-
cise data are unavailable. Hermann et al. (1995) estimated that 100,000 patients
received ECT in the United States in 1995; Abrams (2002) estimated that 1–2
million patients per year receive ECT worldwide. A recent large epidemiologi-
cal study reported that only 1.5% of inpatients with mood disorders receive ECT
in US psychiatric hospitals (Slade et al., 2017).
Health care reform has led to a greater emphasis on the ability to offer the
treatment to outpatients. Because ECT is likely to be more effective than anti-
depressant medications for many patients (Janicak et al., 1985), it stands to
reason that it would be viewed favorably in an increasingly cost- and efficiency-
conscious environment.
The old assumption that a course of ECT necessitates being in the hospital
is no longer valid. Of course, some patients will be so severely psychiatrically or
Chapter 1: Basic Concepts of ECT 3
medically ill as to require hospitalization. Many, however, with adequate family

support and close attention to the logistics of treatment (e.g., explicit written
instructions about concurrent medications, nothing by mouth [NPO] status,
prohibition of driving) can be safely and comfortably treated as outpatients
(Fink et al., 1996; Jaffe et al., 1990).
Because ECT requires specialized knowledge and technical skill, it is likely
to be performed by only a small minority of psychiatrists. Thus, local ECT
experts, to whom other practitioners refer patients, may be the norm.
Although there may be some controversy about what level of ECT exper-
tise should be required of all psychiatric residents, there can be little disagree-
ment that all psychiatrists should know enough about ECT to make informed
referrals to ECT practitioners (Kellner & Li, 2016). Furthermore, the report
of the APA Task Force on Electroconvulsive Therapy (American Psychiatric
Association, 2001, pp. 225–231, 242) makes specific recommendations about
minimum didactic and practical experiences for psychiatric residents and prac-
titioners who want to be privileged by a hospital to perform ECT.
ECT should be performed only by qualified personnel in an appropriate
setting. This setting has traditionally been a hospital or hospital-based clinic
where access to the equipment and personnel necessary to handle cardiopul-
monary emergencies is available. In the United States, the fact that ECT is not
reimbursed by Medicare or most private insurances unless it is performed in
a hospital has likely limited its availability. However, there is no good reason
why ECT could not be safely administered in a properly equipped and staffed
surgicenter or outpatient practice. Close cooperation with the staff who provide
anesthesia support is essential for optimal ECT. As in all medicine, the goal of
scientific and technical advancement remains improved patient care.
Theories of Mechanism of Action

ECT has multiple, profound effects on brain systems, and we continue to add to
our understanding of how it works to alleviate psychiatric illness. Patients and
practitioners, understandably, would be reassured to know exactly how ECT
exerts its therapeutic effects. While we are not yet able to explain this in an accu-
rate and comprehensive way, rather than settle for a stark “we don’t know,” it is
more reasonable to invoke one of the better-supported theories of mechanism
of action (see below). In truth, we know nearly as much about how ECT works as
we do about how antidepressant medications work. A full understanding of how
ECT (and other antidepressant treatments) works may need to await a more
thorough understanding of the etiology of the major psychiatric illnesses.
Research over the last several decades has provided a wealth of informa-
tion about specific changes in neurobiology induced by ECT (Mann, 1998;
Sackeim, 1989; Swartz, 2009). The classic research of Ottosson (Ottosson,
1960, 1962) using lidocaine-modified ECT helped to establish the seizure as
crucial to the efficacy of ECT. From time to time, this facet of ECT dogma is
challenged (Regenold et al., 2015). The finding that low-dose right unilateral
ECT may produce suboptimal clinical outcomes despite adequate seizure

duration confirmed that not all ECT seizures are equivalent (Sackeim et al.,
1987). It appears that both the anatomic location of seizure initiation as well as
intensity of the electrical stimulus affect both therapeutic efficacy and cogni-
tive effects (Nobler & Sackeim, 2008; Nobler et al., 2000). The search continues
for more sophisticated measures of seizure therapeutic adequacy other than
seizure duration (e.g., postictal electroencephalographic [EEG] suppression)
(Krystal & Weiner, 1994; Minelli et al., 2016; Nobler et al., 1993). It is generally
accepted that more robust EEG seizure expression (perhaps best characterized
by a combination of morphological features and other physiological character-
istics) is associated with better clinical outcomes.
The main theories are summarized below.
Neurotrophic Theory
The most exciting progress in the elucidation of ECT’s mechanism of action has
been the rapid accumulation of evidence for its neurotrophic effects. It is now
quite clear that the effects of ECT, in contradistinction to those of prolonged
depression, may be beneficial for the brain. In fact, it appears that ECT reverses
many of the structural abnormalities seen in severely depressed individuals.
Animal studies show that ECS (electroconvulsive shock, the animal analog
of ECT) results in increased neurogenesis and mossy fiber sprouting in the den-
tate gyrus of the hippocampus (Bolwig & Madsen, 2007; Lamont et al., 2005;
Madsen et al., 2000). This line of research continues rapidly, with frequent addi-
tions to the literature both replicating previous work and providing a more
nuanced understanding of the neurogenesis process (Olesen et al., 2017; Otabe
et al., 2014; Schloesser et al., 2015; Smitha et al., 2014; Svensson et al., 2016). It is
possible that advanced neuroimaging techniques, such as magnetic resonance
spectroscopy (MRS), may soon be able to provide evidence for neurogenesis in
humans after ECT. Evidence now shows that ECT leads to increases in neuro-
trophic factors such as brain-derived neurotrophic factor (BDNF) in depressed
patients (Piccinni et al., 2009; Rocha et al., 2016).
Whether neurogenesis is a principal part of the process by which ECT
induces structural brain changes is not yet clear; what is clear is that we now
have MRI evidence that ECT leads to increased volume in cortical and subcor-
tical structures. Dukart et al. (2014) showed gray matter volume increases in
hippocampus and subgenual cortex in a group of unipolar and bipolar patients.
Joshi et al. (2016) showed increases in hippocampus and amygdala volume in
depressed adult patients; Bouckaert et al. (2016) showed increased hippocam-
pal volume with ECT in a large group of geriatric depressed patients, with return
to baseline volumes after 6 months. Redlich et al. (2016) also demonstrated
increases in hippocampal volume with ECT, as well as a correlation between
baseline subgenual cingulate gyrus volume and ECT response. Preliminary evi-
dence shows that other basal ganglia structures are also increased in volume with
ECT (Wade et al., 2016). A meta-analysis reviewed the body of evidence (nine
studies, n = 174) that ECT is associated with volume increases of hippocampus

(Wilkinson et al., 2017). It has recently been suggested that the increase in hip-
pocampal volume may be associated with temporary cognitive effects as well as
antidepressant effects (van Oostrom et al., 2018).
Taken together, the above MRI data indicate that ECT has profound restora-
tive effects on the brain. Given the rapid pace of discovery in this field, future
research will likely soon elucidate which component of the procedure (stimulus,
electrode placement, current density, seizure, or other component) is respon-
sible for these structural changes; it may also soon be possible to better predict
who will respond to ECT and to which specific technique.
Classical (Monoamine) Neurotransmitter Theory

This theory suggests that ECT works in a way similar to that of antidepressant
medications – that it enhances deficient neurotransmission in relevant brain
systems. This is a corollary of the classical monoamine depletion theory of
depression, a theory that has been updated to include the possibility of a mod-
ulatory role for monoamine systems, rather than a simple deficit-adequacy
model (Heninger et al., 1996). Specifically, ECT is known to enhance dopa-
minergic, serotonergic, and adrenergic neurotransmission. Animal stud-
ies using ECS have demonstrated increases in dopamine-related behaviors
(Fochtmann, 1994). The exact mechanism for this dopaminergic enhancement
is as yet unclear; however, it may involve increased dopamine release, receptor
changes, and/or changes in the blood–brain barrier (Fall et al., 2000). The fact
that ECT has clear antiparkinsonian effects argues strongly for dopaminergic
enhancement (Cumper et al., 2014; Popeo & Kellner, 2009). That ECT also has
profoundly antipsychotic effects (and we would expect decreases in dopamine
function to be associated with antipsychotic effects) argues against a single
theory of increased dopamine availability throughout the brain (Rosenquist
et al., 2014).
Numerous studies of the serotonin system in both animals (ECS) and
humans (ECT) have revealed a complex pattern of changes to pre- and post-
synaptic receptors, the serotonin transporter and serotonin metabolites in
the cerebrospinal fluid, not all of which are consistent with a simple theory of
serotonin enhancement with ECT (Swartz, 2009). For many years, based on
animal studies, the serotonin system was believed to be the only monoaminer-
gic system in which ECT had opposite effects from most antidepressant drugs.
ECS increases 5-HT2 receptor number, whereas antidepressant drugs decrease
5-HT2 receptor number (Mann & Kapur, 1992). A positron emission tomogra-
phy (PET) scan investigation found, in contrast to the ECS studies, that ECT
reduces brain 5-HT2 receptors in depressed patients (Yatham et al., 2010). These
authors speculated that “the ability of ECT to further down-regulate brain
5-HT2 receptors in antidepressant non-responsive individuals may explain its
efficacy in those people with antidepressant refractory depression.” Rudorfer
et al. (1988) demonstrated that 5-hydroxyindoleacetic acid (5HIAA), the major
metabolite of serotonin, was increased in the spinal fluid of patients after ECT.
A review in the special issue of the Journal of ECT dedicated to “Mechanisms
in ECT” (Volume 30, #2, 2014) contained a review of serotonin and dopamine
neurotransmission in ECT (Baldinger et al., 2014).
The adrenergic system is also affected by ECT; here, too, numerous pre-
clinical, as well as clinical studies have yielded complex, sometimes contra-
dictory findings. As with other antidepressant drugs, down regulation of
beta-adrenergic receptors has been a consistent finding in ECS studies. Some
studies suggest that ECS results in increased cortical norepinephrine transmis-
sion as a result of postsynaptic effects (Newman et al., 1998). However, human
studies have failed to find consistent alterations in norepinephrine turnover
with ECT (Rudorfer et al., 1988).
Other neurotransmitter systems, including glutamate and gamma-
aminobutyric acid (GABA), have been implicated in the mechanism of action
of ECT. Studies of glutamate, in both animals and human subjects, have yielded
conflicting results. Pfleiderer et al. (2003) showed reduced glutamate with MRS
in the anterior cingulate of depressed patients; glutamate levels normalized with
successful ECT. A more recent study showed the opposite in the rat hippocam-
pus, with glutamate levels decreasing after ECS (Dong et al., 2010). Glutamate
may be involved in both the antidepressant and the cognitive effects of ECT.
The GABA system has been implicated in the antidepressant and anticon-
vulsant properties of ECT (Swartz, 2009). Both animal (Ferraro et al., 1990) and
human studies (Esel et al., 2008) have demonstrated increases in GABA levels
after ECS or ECT. As a major inhibitory neurotransmitter that is measurable in
human serum, GABA is likely to be the focus of further investigations of ECT’s
mechanism of action in the future.
Neuroendocrine Theory
This theory suggests that ECT-induced release of hypothalamic or pituitary
hormones results in antidepressant effects (see Haskett, 2014, for a review).
The specific hormone(s) responsible for this therapeutic effect has yet to be iso-
lated. ECT results in release of prolactin, thyroid-stimulating hormone (TSH),
adrenocorticotropic hormone (ACTH), and endorphins, among other neuro-
humoral substances (Kamil & Joffe, 1991). A putative antidepressant neuropep-
tide, “antidepressin” or “euthymesin,” has been theorized to be released from the
hypothalamus during the ECT seizure, exerting beneficial effects on mood dis-
orders in a way similar to the diabetes/insulin model (Fink & Nemeroff, 1989).
Many investigations have confirmed both the dysregulation of the
hypothalamic-pituitary-adrenal (HPA) in melancholic depression and the
correction of this abnormality with successful antidepressant treatment, most
notably, ECT (Carroll, 1986). The dexamethasone suppression test (DST),
the endocrine test that identifies the HPA abnormality, has also been used as
a marker of the adequacy of continuation ECT; failure to normalize has been
shown to be an indication of the need for ongoing continuation ECT (for review,
see Bourgon and Kellner, 2000).
Anticonvulsant Theory
This theory suggests that the antidepressant effect of ECT is related to the fact
that ECT itself exerts a profound anticonvulsant effect on the brain. Several lines
of evidence indicate that this is so, including the facts that seizure threshold rises
(and seizure duration decreases) over a course of ECT and that some patients
with epilepsy have fewer seizures after ECT (Griesemer et al., 1997; Sackeim,
1999). ECT has even been used to treat resistant status epilepticus (Lisanby
et al., 2001; Miras Veiga et al., 2017). Neurohormones have been postulated to
mediate this anticonvulsant effect. The cerebrospinal fluid of animals receiving
ECS is anticonvulsant when given intraventricularly to recipient animals, possi-
bly as a result of endogenous opioids (Holaday et al., 1986). GABA has also been
proposed as a key mediator of ECT’s anticonvulsant effect (see above).
Connectivity Theory
Preliminary data suggest that abnormal baseline neural network connectivity
in patients with depression or schizophrenia is re-regulated by ECT. The signifi-
cance of this finding for explaining the mechanism of action of ECT remains to
be elaborated (Argyelan et al., 2016; Li et al., 2017; Mulders et al., 2016).
Basics of Electricity
The ECT practitioner should know the following basic facts about electricity
in ECT.
Stimulus Characteristics
Modern ECT devices use alternating current that delivers a stimulus in the form
of a series of bidirectional square-wave pulses. This is referred to as a brief pulse
or ultra-brief pulse (when the pulse width is below 0.5 ms) stimulus. Older ECT
devices delivered a sine-wave stimulus. The brief pulse or ultra-brief pulse stim-
ulus is more efficient at inducing seizures and consequently can produce sei-
zures with a lower “dose” of electricity. This results in less cognitive impairment.
Emerging data are promising that ultra-brief pulse stimuli will be much less
cognitively impairing, yet preserve efficacy (Kellner et al., 2016; Sienaert et al.,
2010; Tor et al., 2015; Verwijk et al., 2012).
Charge
Charge refers to the total number of electrons flowing through a conductor.
Many ECT experts agree that the dose of electricity used in ECT should be
expressed in terms of charge. The setting dials on some ECT devices vary the
charge (by increasing stimulus duration), although they are labeled “energy.”
The equation for charge is
charge = current × time
Charge is expressed in millicoulombs (mC).
Energy
Energy adds a term for voltage to the equation for charge. Thus,
energy = voltage × current × time
Voltage can be thought of as the pressure with which the electrons are “pushed”
through the conductor.
By rearranging the above equation with the substitution of an expanded
term for voltage
(voltage = current × resistance [Ohm’s law])
we arrive at
energy = current2 × resistance × time
Thus, as resistance increases, if current and time are kept constant, energy also
increases. Because modern ECT devices are mostly of the constant-current
type, a patient with a higher resistance will have more energy delivered than a
patient with lower resistance treated at the same setting. The constant-current
ECT device is designed to increase the voltage automatically (up to a prede-
termined safe maximum limit) to deliver the desired charge despite high
resistance. Because a patient’s resistance (impedance) during the delivery of a
stimulus is unknown until the stimulus is delivered, settings on an ECT device
in terms of joules (J) must necessarily be estimates based on an arbitrary fixed
“standard” impedance (e.g., 200 or 220 Ω). Remember that the dial on the ECT
device that controls the length of the stimulus is actually setting the charge and
only indirectly setting the energy.
Energy is expressed in terms of joules. Note that the number of joules used
in ECT is generally considerably smaller than that used in cardiac defibrillation.
ECT devices available in the United States deliver an allowable maximum of
101.4 J. Joules may be converted to millicoulombs by multiplying by 5.7 (assum-
ing fixed impedance of 220 Ω and current of 0.8 A).
Impedance may be highly variable between individual patients. The pri-
mary contributor to the impedance of the electrical circuit is not the brain, but
rather the skin, the underlying scalp soft tissues, and the skull. The contribution
of these elements to the inter-individual variability of seizure threshold for ECT
requires further research (Beale et al., 1994; Coffey et al., 1995; Petrides et al.,
2009; Sackeim et al., 1994).
Electrical Safety
The risk of injury to the patient or the practitioner from being shocked is very
small. Theoretically, if the patient’s impedance is too high, a skin burn at the
electrode site can occur. This possibility is virtually eliminated by the provision
of electrical self-test features in modern ECT devices, which allow the psychia-
trist to check impedance before delivering the stimulus (see section “Electrode
Site Preparation” in Chapter 3). The person delivering the stimulus is at no risk
for getting shocked unless he or she actually touches the metal or the conduct-
ing surface of one of the stimulus electrodes. The patient’s scalp may be touched
(e.g., to provide counter pressure on the left side of the forehead during a right
unilateral treatment) during the delivery of the stimulus without fear of being
shocked. Calls of “Stand clear!” are unnecessary. However, it is prudent to
ensure that anesthesia personnel or other personnel do not touch the electrodes
during the delivery of the stimulus.
Medical Physiology
Of greatest importance to the clinician are the physiological effects of ECT on
the central nervous and cardiovascular systems. As described in later sections,
modifications in ECT technique may be required in patients with neurological
or cardiovascular disease.
Cerebral Physiology of ECT

Seizure Induction
ECT involves the use of an electrical stimulus to depolarize cerebral neurons
and thereby produce a generalized seizure. The more completely generalized
the seizure, the more powerful the antidepressant effect is thought to be. The
mechanism by which ECT seizures are propagated is not well understood (Enev
et al., 2007). However, important differences in efficacy and cognitive effects
between bilateral and unilateral electrode placements may result from differing
routes of seizure generalization in the brain (Staton et al., 1981) and different
regional current density (Lee et al., 2016).
Ictal EEG
During the initial phase of the induced seizure, EEG activity is variable, consist-
ing of patterns of low-voltage fast activity and polyspike rhythms. These patterns
correlate with tonic or irregular clonic motor movements. With seizure progres-
sion, EEG activity evolves into a pattern of hypersynchronous polyspikes and
waves that characterize the clonic motor phase. These regular patterns begin
to slow and eventually disintegrate as the seizure ends, sometimes terminating
abruptly in a “flat” EEG (Weiner et al., 1991) (see Figure 3.8a–c in Chapter 3).
Interictal EEG
Transient, cumulative changes also occur in the interictal EEG in response to
a course of ECT. Increased predominance of delta activity on interictal EEG is
seen as a function of the number of ECT treatments given in a course of ECT
and their rate of administration (Fink, 1979). The interictal EEG typically
returns to baseline by approximately 1 month following the ECT course in most
patients. Generalized EEG slowing has been associated with a positive outcome
after ECT (Sackeim et al., 1996). Farzan et al. (2014) have suggested that EEG
changes with ECT may reflect resetting of aberrant functional connectivity
between brain regions.
Other Neurophysiological Effects of ECT

The ECT seizure is also associated with a variety of transient and benign changes
in cerebral physiology, including increases in cerebral blood flow, cerebral
blood volume (resulting in a transient rise in intracranial pressure), and cer-
ebral metabolism. The brief rise in intracranial pressure is rarely of clinical con-
sequence, but it is the reason for the historical proscription of ECT in patients
with space-occupying mass lesions. Postictally, cerebral blood flow and metab-
olism are decreased, often for several days after the seizure, and then return
to normal levels. Transient disruption of the blood–brain barrier also occurs,
possibly related to the hypertensive surge, but the significance of this is unclear
(Andrade & Bolwig, 2014; Bolwig et al., 1977).
Cardiovascular Physiology
Cardiac Rate and Rhythm
ECT results in a marked activation of the autonomic nervous system, and the
relative balance of parasympathetic and sympathetic nervous system activity
determines the observed cardiovascular effects. Vagal (parasympathetic) tone
is increased during and immediately after administration of the electrical stim-
ulus; it may be manifested by bradycardia or even a brief period of asystole.
This is generally benign and often resolves spontaneously without intervention
(Burd & Kettl, 1998). With development of the seizure, activation of the sympa-
thetic nervous system occurs, resulting in a marked increase in heart rate, blood
pressure, and cardiac workload. Peripheral stigmata of sympathetic activation
may also be observed; they include piloerection and gooseflesh. The tachycar-
dia and hypertension continue through the ictus and generally end along with
the seizure. Shortly after the seizure, there may be a second period of increased
vagal tone, which may be manifested by bradycardia and various dysrhythmias,
including the appearance of ectopic beats. As the patient awakens from anesthe-
sia, there may be an additional period of increased heart rate and blood pressure
as a result of arousal and further sympathetic outflow (Welch & Drop, 1989).
Cardiac Workload
The cardiovascular responses during ECT combine to produce an increase in
myocardial oxygen demand and a decrease in coronary artery diastolic filling
time. Transient electrocardiographic (ECG) changes in the ST segment and T
waves are seen in some patients during and shortly following the procedure,
although it is unclear whether these findings are related to myocardial ischemia.
A direct effect of brain stimulation on cardiac repolarization has been proposed
as an alternative mechanism (Welch & Drop, 1989). No corresponding rise in
cardiac enzymes has been found to accompany these ECG changes (Braasch &
Demaso, 1980; Dec et al., 1985). An echocardiographic study done during and
after ECT treatments found transient regional wall motion abnormalities more
often in patients with ST segment/T wave changes in ECG, suggesting a period
of demand myocardial ischemia (Messina et al., 1992). Kadoi et al. (2001), using
transthoracic echocardiography, showed transient left ventricular dysfunc-
tion after the ECT stimulus; the clinical significance of these findings remains
unknown.
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Chapter ECT: Patient Selection
2
and Preparation
Indications
The primary indications for electroconvulsive therapy (ECT) are major depres-
sion (both unipolar and bipolar types), mania, and schizophrenia (Table 2.1).
Catatonia, once considered rare, has reemerged as another important indication
for ECT (Fink et al., 2016a; Fink et al., 2016b; Fink & Taylor, 2003). Although
typically considered a secondary treatment after pharmacotherapy has failed,
ECT is an appropriate initial treatment in some circumstances (Table 2.2). Such
“primary use” of ECT is usually compelled by the urgency of the clinical situa-
tion; sometimes it is because the patient prefers ECT to other treatment options.
The rapidity with which ECT provides symptomatic relief (including relief of
suicidal intent) is often a major advantage in urgent clinical situations (Fink
et al., 2014; Husain et al., 2004; Kellner et al., 2005, 2010).
Major Depressive Episode

The most common indication for ECT is major depressive episode, in both uni-
polar and bipolar disorders. Most studies have found response rates of 80%–
90% for major depression treated with ECT, with remission rates often only
slightly lower (Kellner et al., 2006, 2010, 2016). Psychotic features and catato-
nia are markers of a particularly high ECT response rate in major depression
(American Psychiatric Association, 2001; Petrides et al., 2001). ECT may be
Table 2.1 Major indications for ECT

Major depressive episode (unipolar and bipolar)
Mania
Mixed affective state
Catatonia
Schizophrenia
Schizoaffective disorder
19
20 Chapter 2: ECT: Patient Selection and Preparation
Table 2.2 Indications for ECT as a first-line treatment

When there is a need for rapid improvement
• Suicidality
• Malnutrition
• Catatonia
• Severe psychosis with agitation
When other treatments are considered more risky
• In the elderly
• In pregnancy
When the patient prefers ECT
unique among medical treatments in that symptom severity predicts better out-
come; that is, the more severely ill a patient is at baseline, the more likely he/she
is to respond well to ECT (Brown, 2007).
Manic Episode
ECT is highly effective in the treatment of the manic phase of bipolar illness
(Kellner et al., 2015; Perugi et al., 2017). ECT is more rapidly effective than
lithium for mania and may be more effective in mixed or agitated manic states
(Small et al., 1988). The efficacy of bilateral as compared with right unilateral
ECT for mania remains controversial. Some practitioners advocate daily bilat-
eral ECT early in the treatment course for severe mania (Mukherjee et al., 1994).
Delirious mania, while rare, is considered by some practitioners to be a primary
indication for ECT (Jacobowski et al., 2013; Stromgren, 1997).
Schizophrenia
Worldwide, schizophrenia may be the most common indication for ECT (Xiang
et al., 2015). In the United States, ECT has typically been used for a subset of
schizophrenic patients with affective features, catatonia, neuroleptic malignant
syndrome (NMS), or a history of previous response to ECT. More recently, there
has been a reappraisal of the use of ECT for schizophrenia, with a tendency to
view it as a treatment for medication-refractory illness, irrespective of the pres-
ence of affective features (Petrides et al., 2015). ECT generally does not alleviate the
negative symptoms of schizophrenia. Combination therapy with antipsychotic
medication and ECT may synergistically improve psychosis in schizophrenia
(American Psychiatric Association, 2001, pp. 17–18, 87–88). First-episode
psychosis, in which it may not yet be clear whether the illness is affective or in
the schizophrenia spectrum, often responds very well to ECT (Kellner, 1995).
Continuation/maintenance ECT for schizophrenia, although common in clini-
cal practice, has a limited research evidence base to date (Iancu et al., 2015).
Other Indications
Both the mood and the motor manifestations of Parkinson’s disease often
improve with ECT. The treatment is typically used in the later phases of the
Chapter 2: ECT: Patient Selection and Preparation 21
disease when patients have become refractory to or intolerant of antiparkin-

sonian medication. Because it may be a viable alternative to deep brain stim-
ulation (DBS), dopaminergic tissue transplantation, or pallidotomy for many
patients, further study of ECT in Parkinson’s disease is warranted (Borisovskaya
et al., 2016; Cumper et al., 2014; Kellner et al., 1994; Popeo & Kellner, 2009).
Patients with severe depression and comorbid Parkinson’s disease may be par-
ticularly good candidates for ECT.
Post-stroke depression has been reported to respond well to ECT
(Harmandayan et al., 2012).
Catatonia, irrespective of etiology, responds well to ECT (Fink & Taylor,
2003).
NMS likewise responds well to ECT (see below).
An emerging indication for ECT is the treatment of self-injurious behavior
in children, adolescents, and young adults with severe autism. ECT has been
shown to decrease the number and severity of episodes of self-injury, as well as
provide mood stabilization in this population. While there are, as yet, no con-
trolled clinical trials, an accumulating case report evidence base attests to the
efficacy and tolerability of ECT for this indication. Most acute courses of ECT for
such patients are performed with bilateral electrode placement. It has become
clear that continuation/maintenance ECT is virtually always necessary to pro-
vide ongoing benefits (D’Agati et al., 2017; Lutz, 2014; Wachtel et al., 2011, 2018).
The ECT Consultation

Since only a small percentage of psychiatrists actually practice ECT (less than 10%),
most patients are referred by other psychiatrists to ECT practitioners for a consul-
tation. For outpatients, this is usually a single 45- to 90-minute session; for inpa-
tients, this may be done at the bedside by the hospital ECT service or the Psychiatry
Consultation-Liaison service. The consultation consists of four basic components:
(1) taking the history, both psychiatric and medical, (2) educating the patient and
significant other(s) about the benefits and risks of ECT, (3) synthesizing the infor-
mation obtained and providing the patient with an opinion/recommendation as to
the advisability of ECT, and (4) writing the consultation note. By the end of the visit,
the following three questions should have been answered:
1. Does the patient have an ECT-responsive illness?
2. Does the patient have any medical problems that might require
modifications of technique or increase the risks of the procedure?
3. Has appropriate informed consent been obtained?
Addressing each of the above questions requires specific, focused question-
ing during the consultation interview.
Does the Patient Have an ECT-Responsive Illness?

While the overall format of the consultation interview follows that of the stand-
ard diagnostic psychiatric interview, special attention must be paid to certain
aspects of the history of present illness. Since it is helpful to determine the extent
to which the illness is episodic versus chronic, asking the patient “When did
this episode of depression begin?” is a good way to start the interview. Current
depressive signs and symptoms should be comprehensively elicited, with spe-
cial emphasis given to vegetative signs (including amount of weight loss), loss of
function, suicidal ideation/intent, and psychotic thinking. Remembering that
urgency of illness is one of the factors that will compel your recommendation
for ECT, try to get a complete picture of the patient’s level of current distress and
dysfunction. Next, obtain the history of treatments (and response/tolerability
to them) tried to date in the current episode. An obsessionally exhaustive list
of every medication and dose is rarely necessary; rather, several examples from
various classes will usually serve to paint a picture of the number and strength of
treatment trials. Remember to ask about other treatment modalities, including
rTMS and ketamine, as well as psychotherapies.
The psychiatric history should include number, type, and duration of episodes;
treatment trials; hospitalizations; and suicide attempts. If the patient has had ECT
before, every effort should be made to elicit details of that prior treatment, includ-
ing electrode placement, number of treatments, response, and tolerability.
Family psychiatric history, often overlooked, is an important part of the ECT
consultation because of the heritability of severe mood disorders and the likeli-
hood that treatment response may be similar in family members (McGuffin et al.,
2003). The report of a relative with good response to ECT is reassuring both about
the integrity of the diagnosis and the likelihood of treatment response.
Does the Patient Have Any Medical Problems That

Might Require Modifications of Technique or Increase the Risks
of the Procedure?
The medical history is elicited to assess the patient’s risk for general anesthesia and
the need for any additional testing or consultations. One can begin this section
of the interview by simply asking the patient if he/she has any medical problems;
if yes, follow up with as many details of the illness, its evaluation, both past and
recent, and treatment, as possible. A surgical history is particularly important as
it will usually allow you to know if the patient has had exposure to general anes-
thesia. Ask the patient specifically how he/she tolerated the general anesthesia.
It is worthwhile to ask all patients specifically if they have ever had any heart
or lung problems as these two organ systems are the most common source of any
ECT or anesthesia complications. Older patients should be asked if they have
ever had a “heart attack” or chest pain. Asking the patient if they can walk up
a flight of steps without getting short of breath is a useful way to grossly assess
overall cardiopulmonary function.
A smoking history is an important part of the cardiopulmonary history; an
estimate of pack-years smoked should be made and noted.
The patient’s handedness (relevant for electrode placement), height and

weight in kilograms (needed for calculating anesthetic doses), and condition
of teeth (including presence of dentures, which may need to be removed before
ECT) should all be noted.
Drug allergies should also be noted.
Has Appropriate Informed Consent Been Obtained?

As stated above, the consultation interview includes the education of the patient
and significant other(s) about the potential risks versus benefits of ECT, so that
patients may provide informed consent if they wish to proceed with ECT (see
also “Informed Consent” section). In the consultation, explain that there are two
sets of risk associated with ECT: the medical risks of the general anesthesia (the
safety of the procedure) and the cognitive risks of the ECT (the tolerability of the
procedure). This is also the time to let the patient know about restrictions on
driving, the need to be NPO, and which medications should be discontin-
ued, held, or, conversely, given in conjunction with ECT (see “Concurrent
Medications” section). The patient should be advised of the need for any pre-
procedural medical or laboratory evaluation, as mandated by hospital policy or
needed because of the patient’s medical status.
Many practitioners, myself included, explain to the patient the differ-
ences in efficacy and tolerability between bilateral and unilateral electrode
placements, sometimes offering an opinion as to which seems advisable in
the present situation, and asking the patient if he/she has a preference. There
is no clear consensus about what level of technical detail is appropriate
(Rasmussen, 2011); clearly, this will vary based on the patient’s clinical situa-
tion and condition.
The ECT Consultation Note

The ECT consultation note is an important document in the medical record.
It should summarize the patient’s psychiatric and medical history, building
the case for your conclusion about whether or not ECT is appropriate for the
patient. The “impression” or “assessment” section typically starts with the psy-
chiatric and medical diagnoses, then states your opinion about the advisability
of ECT, then lists any medical issues of concern. It should then document that
risks versus benefits as well as any behavioral limitations (e.g., no driving) have
been discussed and whether the patient has expressed any preference for a par-
ticular type of ECT. The “plan” or “recommendations” section should state what
medical evaluation (including any consultations) are needed before proceeding
with ECT.
A sample ECT consultation note, modified from a real one, is shown
in Box 2.1 (please note that it is meant to show typical elements of the ECT
consultation note, not necessarily represent a “standard” or “typical” ECT
patient).
Box 2.1
Patient seen in the office for ECT consultation, referred by Dr. XX, in the company
of his father.
ID: 26-year-old single college graduate
CC: “I’ve been depressed for a while now.”
HPI: The patient reports he has been depressed for the past three years,
despite multiple medication trials. Symptoms include low mood, crying, lack of
motivation, bed clinging, anxiety, oversleeping, 15-pound weight gain, and intru-
sive suicidal fantasies. He notes that a month ago he had thoughts of throwing
himself down a stairwell, but that since resuming sertraline, his suicidal fantasies
have largely disappeared. He is assessed to be at low risk currently. He has been on
multiple selective serotonin reuptake inhibitors (SSRIs), as well as anticonvulsants
in the current episode. He reports only transient benefit and also that he is very
sensitive to medications. He currently rates his depression severity as 7/10, but it
has been as high as 9/10 recently. He considers it very disabling in his life.
Past psychiatric history: He reports social anxiety since childhood, but no prior
episodes of depression. He also reports some Obsessive Compulsive Disorder (OCD)
symptoms for many years, including counting and checking rituals. He has been in
psychotherapy that he has not found helpful. He has never been hospitalized, nor
made a suicide attempt. He reports one possible 10-day episode of hypomania that
may have been precipitated by a combination of escitalopram and cocaine.
Family psychiatric history: A maternal aunt has been treated for depression
with medications.
Medical history: He reports that he has had a series of concussions from sports,
resulting in one CT scan of his brain and 2 MRIs; the last MRI was 2 months ago,
and reportedly normal; he also had a normal EEG at that time.
He had an inguinal hernia repair at age 17 under general anesthesia; he
reports that he woke up agitated from the general anesthesia.
Left handed, 5’ 7”, 175 lbs., dentition intact.
Allergies: Negative.
Alcohol/drugs: He used to drink heavily and abuse drugs, but has been absti-
nent for the past three years.
Cigarettes: He has smoked five cigarettes a day for 3 years.
Social history: Born in Washington, DC, raised in Connecticut, the youngest of
three siblings. He graduated from a state university in 2014 with a degree in commu-
nications, but was only able to work for one day before having to quit because of his
depression. His hobbies include baseball and soccer. He lives at home with his parents.
Mental status examination: Alert, well groomed, slightly overweight, mood
depressed, affect restricted, thought content depressive, thought process logical,
oriented times three, cognition fully intact, no psychotic symptoms, denies cur-
rent suicidal ideation, insight, and judgment good.
Impression: Major depression, single episode, severe. Because of the sever-
ity of the patient’s current illness, and his failure to respond to multiple medica-
tion trials, ECT is a reasonable therapeutic option. Risks of ECT, both medical and
cognitive, discussed in detail. Patient told that he needs to be NPO prior to each
procedure. Patient told of need to refrain from driving during ECT course. Patient
told of the requirements of pre-procedural medical and laboratory evaluation. We

discussed the differences between bilateral and right unilateral electrode place-
ments; it is likely that we would start with right unilateral electrode placement,
noting that he is left-handed and might need to be switched to left unilateral ECT.
We discussed the fact that ECT will treat his current episode, but not cure him of
his underlying illness, and that he may need continuation ECT and will definitely
need ongoing medication management. We discussed the option of an monoam-
ine oxidase inhibitor (MAOI) trial instead of ECT.
Plan: Patient will discuss with his referring doctor whether or not he wishes to
proceed with a course of outpatient ECT.
The Pre-ECT Evaluation

The goals of the pre-ECT evaluation are to (1) determine whether ECT is
indicated, (2) establish baseline psychiatric and cognitive status to serve as a
reference point for assessing patient response and cognitive side effects, (3)
identify and treat (optimize) any medical factors that may be associated with
an increased risk of adverse effects from ECT, and (4) initiate the process of
informed consent (see “Informed Consent” section).
Once the indication for ECT has been clearly identified, baseline symp-
tom severity scores, which will be used as markers for clinical response, should
be established. We recommend the use of standardized measures of clinical
response during a course of ECT. These include (1) the Hamilton Rating Scale for
Depression (HRSD) (Hamilton, 1960); (2) the Montgomery-Asberg Depression
Rating Scale (Montgomery & Asberg, 1979); and (3) a self-rating scale, examples
of which are the Beck Depression Inventory (Beck et al., 1961), the Carroll Rating
Scale for Depression (Carroll et al., 1981), and the Quick Inventory of Depressive
Symptomatology-Self report (QIDS-SR) (Rush et al., 2003), for evaluation of
depressive symptoms. A baseline (pre-ECT) assessment of cognitive function is
needed to monitor the extent of adverse cognitive effects that may develop dur-
ing the treatment course. We recommend the Mini-Mental State Exam (Folstein
et al., 1975) or the Montreal Cognitive Assessment (MoCA) (Nasreddine et al.,
2005) for this purpose. Other, short, bedside cognitive assessment tools are being
designed and tested for use during ECT, but currently none has been widely
accepted. More formal neuropsychological assessment of cognitive function
should be considered for selected cases (e.g., patients with preexisting cogni-
tive impairment or patients who are deemed likely to report subjective memory
dysfunction). Both objective and subjective cognitive assessments are con-
sidered important for assessing overall cognitive outcomes with ECT (Kumar
et al., 2016). It is possible that the US Food and Drug Administration (FDA) will
mandate specific cognitive testing to be done before, and during, a course of ECT.
Of course, a basic medical and psychiatric workup is an essential part of
the pre-ECT evaluation. This should include medical history, physical exami-
nation, psychiatric history, mental status examination, and limited laboratory
Table 2.3 Pre-ECT Evaluation

– Medical and psychiatric history
– Physical examination
– Mental status examination
– Laboratory evaluation (in selected cases)
Electrocardiogram
Complete blood count
Basic or comprehensive metabolic panel
Other tests specific to patient’s medical condition (e.g., theophylline level, lithium level)
– Anesthesia consultation
– Consider (in selected cases)
Computed tomography or magnetic resonance imaging of the brain
Chest X-ray
Electroencephalogram
evaluation (in selected cases, an electrocardiogram [ECG], a complete blood

count, electrolytes, and liver function tests). Young, healthy patients may not
require any laboratory evaluation, in accordance with recently liberalized poli-
cies governing ambulatory surgical procedures at many institutions (Sundsted
et al., 2014; Tess & Smetana, 2009).
A computed tomography (CT) or magnetic resonance imaging (MRI) scan
of the brain is sometimes necessary to confirm or rule out a space-occupying
lesion or increased intracranial pressure (Table 2.3). While many psychiatric
patients will have had a brain structural image in the course of the evaluation
of their psychiatric illness, routinely ordering such scans as part of the pre-ECT
evaluation is unnecessary and wasteful (Sajedi et al., 2016). An electroencepha-
logram (EEG) may be helpful in detecting previously undiagnosed organic
brain disease (e.g., toxic/metabolic encephalopathy) and serves as a record of
the patient’s brain electrical activity before ECT.
Anesthesia consultation is an important part of the pre-ECT evaluation,
and cooperation between the ECT and anesthesia teams is essential. Other
consultations may be helpful (e.g., neurology, cardiology) if history, physical
examination, or laboratory findings suggest that further evaluation is needed.
Optimizing the patient’s medical status, with the help of these consultants, is an
important part of preparing the patient for ECT.
Although there are no absolute medical contraindications to ECT, there are
situations of increased risk (Table 2.4). Careful consideration of risks and ben-
efits is critical when the clinician encounters a patient with serious medical ill-
ness who is referred for ECT. The report of the American Psychiatric Association
(APA) Task Force on ECT (2001) lists situations of substantial risk, including (1)
space-occupying cerebral lesion or other conditions with increased intracranial
Table 2.4 Situations of increased risk

– Space-occupying cerebral lesion
– Increased intracranial pressure
– Recent myocardial infarction
– Recent cerebrovascular accident
– Aneurysm
– Retinal detachment
– Pheochromocytoma
Table 2.5 Common medical conditions that may necessitate modifications in ECT

technique
– Chronic obstructive pulmonary disease
– Asthma
– Hypertension
– Coronary artery disease
– History of myocardial infarction
– Cardiac arrhythmia
– History of cerebrovascular accident (stroke)
– Osteoporosis
– Renal failure on dialysis
pressure, (2) recent myocardial infarction with unstable cardiac function, (3)
recent intracerebral hemorrhage, (4) bleeding or unstable vascular aneurysm
or malformation, (5) retinal detachment, (6) pheochromocytoma, and (7)
American Society of Anesthesiologists physical status classification of 4 or 5.
Some common medical conditions that may contribute additional risk and may
require modifications in ECT technique are listed in Table 2.5.
ECT in Specific Medical Conditions

In this section, we discuss the use of ECT in patients with specific medical ill-
nesses. For a review of ECT in the high-risk patient, see Abrams (1989) and
Alexopoulos et al. (1989).
Central Nervous System (CNS) Disease

For a more comprehensive review of this topic, please see also Kellner and
Bernstein in Coffey (1993) as well as Ducharme et al. (2015).
Parkinson’s Disease
Nearly half of all patients with Parkinson’s disease will experience major depres-
sion (Brown & Wilson, 1972). A growing literature supports the use of ECT for
the treatment of both depression and the Parkinson’s disease itself in patients
with Parkinson’s disease (Andersen et al., 1987). It has been postulated that the
dopamine-enhancing effects of ECT are related to its efficacy in the treatment
of the motor systems of Parkinson’s disease (Cumper et al., 2014; Fochtmann,
1988). In patients who are taking Sinemet (carbidopa-levodopa) at the time of
their ECT, adjustments in dose (typically, decreasing by 50%) may be required
to decrease the likelihood of dyskinesias and post-ECT delirium (Figiel et al.,
1991; Rasmussen & Abrams, 1991). Since Parkinson’s disease is a continuous
illness (as opposed to an episodic one, such as recurrent depression or bipolar
disorder), it stands to reason that the benefits of ECT would be of finite duration
and likely require maintenance treatment to be sustained. While better defini-
tion of the overall role of ECT in the treatment of Parkinson’s disease must await
further clinical research (Kellner et al., 1994; Popeo & Kellner, 2009), it is sur-
prising that the substantial benefits of ECT in Parkinson’s disease are not more
widely known and accepted (Borisovskaya et al., 2016). This is likely due to the
lingering stigma surrounding ECT in the neurology community.
Dementia
ECT has an important role in treating the depression that often accompanies
dementing illness and can be dramatically helpful in patients with pseudo-
dementia. Differentiating dementia from pseudo-dementia in elderly persons
is often a difficult task (Pier et al., 2012). When dementia coexists with depres-
sion, cognitive function may improve after treatment of the depression. Patients
with preexisting dementia who are given ECT may experience transient cogni-
tive worsening (Dybedal et al., 2015; Hausner et al., 2011). These effects can be
minimized by modifications in ECT technique, including (1) decreasing the
treatment frequency from three times weekly to once or twice weekly, (2) using
unilateral electrode placement, (3) using ultra-brief stimulus parameters, (4)
avoiding excessive stimulus doses, and (5) minimizing exposure to anticho-
linergic premedications. Also, elderly patients may be particularly sensitive to
ECT–drug interactions. ECT to treat the agitation that is often part of the clini-
cal picture of advanced dementia is clearly helpful and becoming more wide-
spread, but remains somewhat controversial (Acharya et al., 2015; Burgut et al.,
2010; Glass et al., 2017; Oudman, 2012).
Brain Tumor
A transient rise in intracranial pressure is associated with ECT-induced sei-
zures, an effect most likely related to the increase of cerebral blood flow. This
increase in intracranial pressure may put patients with space-occupying brain
lesions at risk for brain herniation. The presence of a brain tumor, once an abso-
lute contraindication to ECT, is now no longer thought of as such. Although
clearly one of the most significant risks, not all brain tumors are equally prob-
lematic (Maltbie et al., 1980). Large edematous tumors causing mass effect
are clearly extremely dangerous. However, small calcified meningiomas with-
out associated edema probably pose little risk (Abrams, 2002; Goldstein &
Richardson, 1988; Kellner et al., 1991; McKinney et al., 1998; Teraishi et al.,
2012). Neurosurgical consultation should be considered in patients with brain

tumors referred for ECT.
Stroke
Patients who have had a recent hemorrhagic stroke and who need ECT may be
at risk for re-bleeding during the procedure. There is little information about
the risks of ECT to patients who have had recent ischemic strokes. Generally,
withholding ECT for a period of weeks to months is recommended if the patient
has had a stroke. However, this delay must be weighed against the severity of the
psychiatric illness itself. Extremes of blood pressure, both hyper- and hypoten-
sion, should be avoided during ECT in stroke patients. The use of intravenous
antihypertensives during ECT may be helpful in safely managing some cases
(Allman & Hawton, 1987).
Stroke as a consequence of ECT (either ischemic, embolic, or hemorrhagic)
is a very rare event (Bruce et al., 2006; Lee, 2006).
Epilepsy
Patients with concurrent epilepsy and depression can be safely treated with
ECT. It is recommended that epileptic patients continue to receive their anti-
convulsant medications during the course of ECT (Abrams, 2002). The rise in
seizure threshold that accompanies ECT may actually reduce the frequency of
spontaneous seizures in patients with epilepsy (Dubovsky, 1986; Griesemer
et al., 1997; Sackeim et al., 1983; Schnur et al., 1989). ECT has been used as a
treatment for status epilepticus (Cline & Roos, 2007; Kamel et al., 2010; Miras
Veiga et al., 2017; Zeiler et al., 2016). Consideration may be given to adjusting
anticonvulsant medication during a course of ECT if eliciting adequate seizures
becomes difficult.
Cardiovascular Disease
Myocardial Infarction/Ischemic Heart Disease
Although rare, cardiac complications during ECT represent the most common
cause of fatality associated with the treatment (Zielinski et al., 1993). The cat-
echolamine surge and subsequent hypertension and tachycardia that accom-
pany ECT-induced seizures may put patients with prior cardiac disease at risk
for myocardial ischemia. Also, patients who have had a recent myocardial
infarction may be at risk for further myocardial damage. The use of intravenous
beta-blockers, nitrates, and other antihypertensive agents and careful atten-
tion to oxygenation are important risk-reducing strategies in this population.
The goal of treatment should be the blunting of the hypertensive/tachycardic
response, rather than its full elimination, to avoid the risk of over-correcting
and inducing hypotension. We recommend the use of labetalol (5–20 mg IV) or
esmolol (5–60 mg IV) for patients with a history of hypertension and/or tachy-
cardia if there is concern about their ability to tolerate the hemodynamic effects
of ECT safely (Boere et al., 2014). An alternative strategy is to treat patients with
coronary artery disease with nitroglycerin, either before the procedure (trans-
dermally or sublingually) or during the procedure (intravenously) (Saito et al.,
2000; Villalonga et al., 1989). Also, regularly prescribed cardiac medications
(e.g., antihypertensives or antiarrhythmics) should be taken with a small sip of
water 2 h before ECT (see also sections “Cardiovascular Medications” in this
chapter and “Cardiovascular Agents” in Chapter 3).
Arrhythmias
To protect against bradyarrhythmia, anticholinergic medication (e.g.,
glycopyrrolate 0.2 mg IV or atropine 0.4 mg IV) may be given before ECT.
Anticholinergic premedication may be recommended when stimulus dose
titration is performed because of the risk of subconvulsive stimuli inducing
bradycardia, although this risk is modest (Mizen et al., 2015). Patients receiving
beta-blockers may be at higher risk of bradycardia. Significant tachyarrhyth-
mias may be treated with intravenous beta-blockers, as previously discussed.
Transient benign hypertension, tachycardia, and premature ventricular con-
tractions may occur for several minutes following ECT. These arrhythmias tend
to resolve spontaneously and to have little clinical significance. Therefore, unless
these conditions are sustained or deemed particularly severe, close observation
may be the only necessary action.
Other Medical Conditions

Pulmonary Disease
Patients with preexisting chronic obstructive pulmonary disease or asthma
can be treated safely with ECT; they should receive their inhalant bronchodila-
tors before each ECT treatment (Mueller et al., 2006). Theophylline should be
avoided or kept in the low therapeutic range to prevent prolonged seizures or
status epilepticus (Schak et al., 2008).
Pregnancy
ECT has been used safely during all trimesters of pregnancy. ECT may be pre-
ferred over psychopharmacological methods because of the brief exposure of
the fetus to pharmacological agents during ECT, in comparison to the prolonged
exposure to potentially teratogenic agents during the course of a pregnancy.
The risks of ECT increase toward the end of pregnancy. These risks include the
induction of premature labor and the increased risk of pulmonary aspiration
due to the uterus pressing upon the stomach. Tracheal intubation is recom-
mended for ECT during the third trimester. Fetal monitoring is recommended,
and the rapid availability of an obstetric consultant is prudent (Abrams, 2002;
Anderson & Reti, 2009). Additional details of management strategies may be
found in recent reviews (Leiknes et al., 2015; Sinha et al., 2017; Spodniakova
et al., 2015).
Neuroleptic Malignant Syndrome

ECT is effective for NMS, even when pharmacological treatments have failed.
Many authors believe that aggressive treatment with ECT, similar to that rec-
ommended for catatonic patients, is appropriate for patients with NMS (Chiou
et al., 2015; Fink, 1994; Trollor & Sachdev, 1999; Verdura Vizcaino et al., 2011).
Patients with NMS should not receive neuroleptics during ECT.
Gastrointestinal Disorders
Pretreatment with histamine-2 (H2) blockers, proton pump inhibitors, meto-
clopramide, or sodium citrate is usually sufficient aspiration prophylaxis for
most patients with clinically significant gastroesophageal reflux. Patients are
typically asked to take their anti-reflux medication before the treatment, either
at bedtime if this is their usual dosing routine, or with a small sip of water upon
awakening the morning of the treatment. Anesthesiologists may elect to intu-
bate patients who have severe reflux disease or those who have a known history
of incompetent gastroesophageal sphincters (Tess & Smetana, 2009).
Musculoskeletal Disorders
Appropriate muscle relaxation virtually eliminates risk of fracture during
ECT, even in patients with fragile bones (e.g., osteoporosis or recent fracture).
However, in patients with severe osteoporosis, it is advisable to use the higher
dose range of 1.0–1.50 mg/kg of succinylcholine to ensure complete muscular
blockade (Bryson et al., 2012; Li et al., 2016; Mirzakhani et al., 2016). It is also
advisable not to use the cuffed-limb method in these cases. Patients with any
loose or fractured teeth or with a history of temporomandibular joint disease
should have these conditions stabilized before ECT.
Concurrent Medications
A careful evaluation of the patient’s concurrent medications is required before
ECT. Concurrent medications may affect both the safety and efficacy of ECT.
Decisions about which medicines to discontinue, taper, or temporarily withhold
prior to each ECT should start to be made during the initial ECT consultation.
In this section, we review the interactions of psychotropic and other medica-
tions with ECT. See Haskett and Loo (2010), Kellner et al. (1991), and Zolezzi
(2016) for more in-depth reviews. Discontinuation before ECT is required for
some agents, whereas modified dosing is recommended for other agents.
Psychotropic Medications
In the past, it was recommended that most psychotropic medications be tapered
and discontinued before beginning ECT. Nowadays, practitioners are much
more liberal in combining ECT and psychotropic medications. This is due to
accumulating evidence of additive efficacy with some antidepressants, as well as
safety data for many drugs combined with ECT (Kellner et al., 2016; Lauritzen
et al., 1996; Sackeim et al., 2009). Antipsychotic medications (originally first
generation, and now the “atypicals”) may act synergistically with ECT in the
treatment of psychotic patients, and have for a long time been co-prescribed
with ECT.
We review below the major categories of psychotropic medications and
their interactions with ECT.
Lithium
Recent data suggest that the coadministration of lithium and ECT is relatively
safe and that earlier warnings about the combination were overly conservative
(Dolenc & Rasmussen, 2005; Thirthalli et al., 2011; Volpe & Tavares, 2012).
Nonetheless, the combination has been associated with the development of
delirium or prolonged seizures (Sadananda et al., 2013; Sartorius et al., 2005;
Weiner et al., 1980). The transient increase in permeability of the blood–brain
barrier following ECT (Bolwig et al., 1977) has been proposed as a possible
mechanism by which increased concentrations of lithium can enter the CNS.
In general, it is advisable to hold lithium for at least 24 h before ECT, so that
patients can be treated with lithium blood levels at the lower end of the thera-
peutic range. The occasional patient who presents for treatment having inad-
vertently taken his/her lithium dose the day before should generally still be
treated, as the risk is quite low, unless the lithium level is very high.
Antidepressants
The combination of ECT and antidepressant medications, once frowned upon,
is now encouraged, both because newer generation antidepressants are safer
and because there is accumulating evidence for antidepressant synergy (Kellner
et al., 2016; Sackeim et al., 2009) and possibly enhanced relapse prevention.
While some question the practice of continuing previously “ineffective” antide-
pressants during ECT, in many cases antidepressants have not been completely
ineffective and it may be possible to continue an agent that has provided some
symptom relief. There is also the possibility that an agent that was not “power-
ful” enough to treat an acute depressive episode may still confer some relapse
prevention benefit in the period after remission with ECT (van den Broek et al.,
2006). If a patient begins an acute course of ECT on no antidepressant medica-
tion, some practitioners believe that an agent should be started before the end of
the acute course of ECT, so that the patient is not left unprotected (i.e., without
therapeutic blood levels) when ECT is stopped. The agent may be either one
that has been partially effective in the past, or one that is new for the patient.
The newer selective serotonin reuptake inhibitors (SSRIs) and serotonin-
norepinephrine reuptake inhibitors (SNRIs) pose less cardiac risk when given
with ECT than the older tricyclic antidepressants (TCAs). In practice, the com-
bination of these agents and ECT has become widespread.
While TCAs are much less commonly used than in the past, when they are
used, there is still concern about cardiovascular effects of interactions between
these antidepressants and ECT or the anesthetic agents used during the proce-
dure. The issue of potential adverse effects of TCAs given in conjunction with
ECT has generated a plethora of case reports and small case series (Pritchett
et al., 1993). Discontinuation of a TCA shortly before beginning ECT may be
particularly problematic (Raskin, 1984). A recent case report of the synergy
between ECT and imipramine is supportive of the combination (Birkenhager &
Pluijms, 2016).
The use of monoamine oxidase inhibitors (MAOIs) in patients receiving
ECT, previously somewhat controversial, is now viewed more favorably. A
critical reading of the literature suggests that the combination is not nearly as
risky as once thought. It has been recommended in the anesthesia literature
that MAOIs be discontinued up to 2 weeks before elective surgery or ECT, but
this is considered unnecessary by some authors (Dolenc et al., 2004). Early case
reports describe hyper- and hypotension, fever, hyperreflexia, seizures, and
hepatotoxicity in patients receiving general anesthesia while taking MAOIs
(Jenkins & Graves, 1965). Investigators have documented the safety of ECT in
patients receiving chronic MAOI therapy (el-Ganzouri et al., 1985).The newer
transdermal delivery form of the MAOI selegiline has been reported to be safe
in conjunction with ECT (Horn et al., 2010).
We routinely treat patients on MAOIs with ECT, with the suggestion that
the dose be kept fairly constant before and during the ECT course. Part of the
“time out” procedure for such patients is a reminder to the treating team that the
patient is on an MAOI and the known drug contraindications must be observed.
Benzodiazepines
In addition to raising the seizure threshold, benzodiazepines may also decrease
the intensity or generalization of the ECT seizure. They may also shorten seizure
duration, and their use may increase the number of ECT treatments required
for recovery (Stromgren et al., 1980; Tang et al., 2017). Pettinati et al. (1990)
carried out a comprehensive study of the combined use of benzodiazepines
and ECT. They found a significant relationship between therapeutic failure of
unilateral ECT and concomitant benzodiazepine use. This lack of efficacy may
have been related to the increase in seizure threshold caused by the concur-
rent benzodiazepines and the low stimulus dosing techniques used. The authors
recommended discontinuing benzodiazepines before unilateral ECT is given.
This interaction is likely less important when bilateral or high-dose unilateral
ECT is used. We believe it is prudent to taper and/or discontinue benzodiaz-
epines before ECT, if possible. However, it is quite permissible to continue low-
or moderate-dose benzodiazepines, if anxiety is a troublesome symptom for
the patient. Certainly, if anxiety about the procedure itself might jeopardize the
treatment course, the patient may be given benzodiazepines, even on the morn-
ing of treatment. We recommend the use of 0.5 or 1 mg lorazepam sublingual,
approximately 30 min before ECT to treat pre-procedure anxiety. For patients
who have been taking long half-life benzodiazepines, such as clonazepam, it
may be advisable to switch to a shorter half-life drug, such as lorazepam, before
starting ECT. This way, benzodiazepine blood levels will be lower at the time of
ECT, after the prior evening’s dose.
If a patient has taken more than a small dose of benzodiazepine the day
prior to ECT, consideration may be given to the use of the reversal agent, fluma-
zenil. Although the total literature is small, several authors encourage the use
of pretreatment doses of flumazenil (dose range 0.2–1.0 mg, typical dose 0.4–
0.6 mg) for seizure enhancement (Bailine et al., 1994; Krystal et al., 1998). It is
injected 1–3 min prior to anesthesia induction; consideration should be given
to the additional administration of 1–2 mg of midazolam after the seizure has
ended to preclude any post-ECT discomfort from potential benzodiazepine
withdrawal. One group has reported the use of flumazenil for seizure enhance-
ment in patients not taking any benzodiazepine, on the theoretical assumption
that reduction of endogenous GABA-ergic tone will lead to seizure enhance-
ment (Yi et al., 2012).
Anticonvulsants
Similar to benzodiazepines, anticonvulsants also raise the seizure threshold and
may theoretically interfere with the efficacy of ECT. In patients with epilepsy,
anticonvulsants should be continued during a course of ECT. Consideration
may be given to adjusting dosage or type of anticonvulsant if it becomes difficult
to elicit adequate seizures. Anticonvulsants prescribed for psychiatric indica-
tions may be tapered and discontinued before beginning ECT; another strategy
is to withhold only the prior day’s dose and see if adequate seizures are easily
obtained. One report suggests that concomitant treatment with an anticonvul-
sant may require longer ECT treatment courses (Virupaksha et al., 2010). There
is, as yet, no consensus about whether or not ECT and anticonvulsants may have
additive or synergistic effects (Rakesh et al., 2017; Rubner et al., 2009; Sienaert &
Peuskens, 2007).
Antipsychotic Medications
Antipsychotic medications have long been regarded as synergistic with ECT
in the treatment of psychotic symptoms. It has been speculated that this effect
may be related to their lowering of the seizure threshold (Coffey et al., 1995),
although this is far from certain. Low-potency antipsychotic medications (e.g.,
chlorpromazine) have been reported to cause hypotensive reactions when
given with ECT (Grinspoon & Greenblatt, 1963). High-potency antipsychotic
medications (e.g., haloperidol or fluphenazine) are considered safe when used
concurrently with ECT. This combination is indicated particularly in the treat-
ment of psychotic depression. Also, when ECT is used to treat schizophrenia,
the combination of ECT and antipsychotic medications may be more effective
than ECT alone (American Psychiatric Association, 2001, pp. 17–18, 87–88; see
also below).
Atypical Antipsychotic Medications
Atypical or “second generation” antipsychotic medications are now routinely
combined with ECT and the combination is not thought to involve significantly
increased risk (Oulis et al., 2011). Additive or synergistic benefit for schizophre-
nia is likely, as it is with first-generation drugs (Zheng et al., 2016). Numerous
reports document the efficacy and safety of clozapine combined with ECT
(Grover et al., 2015; Lally et al., 2016; Petrides et al., 2015).
Psychotropic Medications During Continuation/Maintenance ECT

Most patients are treated with combined medication–ECT strategies during the
maintenance phase; controlled data are beginning to emerge for the develop-
ment of useful guidelines in this area (Kellner et al., 2016; Lisanby et al., 2008).
Combined antidepressant and/or mood stabilizer and ECT treatment should
be considered in patients who have responded to acute-phase ECT but have a
history of frequent and severe relapses. These patients may withhold their lithium,
anticonvulsants, and benzodiazepines 12–36 h before each continuation/main-
tenance ECT and resume them after their ECT. Tapering/discontinuation regi-
mens should be individualized with the aim of reducing the drug level before ECT,
while paying attention to the possible development of withdrawal symptoms.
Other Agents
Cardiovascular Medications
Patients should receive their routine antihypertensive and antianginal/antiar-
rhythmic medications with a small sip of water approximately 2 h before ECT.
Transdermal nitrates should be in place at least 30 min before treatment (Parab
et al., 1992). Medications that should be avoided before ECT include diuret-
ics (because of the increased risk of incontinence, or, rarely, bladder rupture in
patients with a full bladder), reserpine (because of the risk of hypotension and
death), and lidocaine (because of its potent anticonvulsant properties).
Hypoglycemics
For patients with diabetes, adjustments in the dosage of insulin and oral hypo-
glycemics may be required on the morning of ECT because of the overnight fast.
Holding the morning insulin dose until after the patient has had breakfast is the
usual approach. In severe diabetic patients with a propensity toward ketoacido-
sis, half of the patient’s usual morning dose of insulin may be given with running
intravenous dextrose before ECT; this, however, is rarely required (Rasmussen
et al., 2006). A fingerstick glucose measurement should be made before and
after ECT in patients with severe diabetes. Consultation with an endocrinolo-
gist about management strategies may be helpful.
Antiasthmatics
Steroids and β-adrenergic agonists should be given before ECT, as required, to
prevent bronchoconstriction. Patients may be asked to bring their inhalers to the
ECT suite, so that they may use them just before anesthesia induction. Because
of an association with prolonged seizures during ECT, theophylline should be
stopped before ECT in most cases. If theophylline is medically required, blood
levels should be monitored closely during a course of ECT and kept in the low
therapeutic range (Rasmussen & Zorumski, 1993; Schak et al., 2008).
Table 2.6 Morning medications that should be given (and those that

should NOT) before ECT
Medication Exclusions
Antihypertensives Diuretics
Antianginals, antiarrhythmics, digoxin Lidocaine
Anti-gastric reflux agents
Glaucoma eyedrops Echothiophate
Bronchodilators Theophylline
Glaucoma Medications
Patients should receive their glaucoma eye drops before ECT because of the
transient increase in intraocular pressure during the procedure (Good et al.,
2004). The prominent caveat is that ECT patients should not receive echothio-
phate (an irreversible cholinesterase inhibitor) because of the risk of prolonged
apnea in patients given succinylcholine.
Gastrointestinal Medications
Patients with peptic ulcer disease or gastroesophageal reflux disease (GERD)
should receive their H2 blocker, proton pump inhibitor, or metoclopramide
with a sip of water at least 2 h before ECT. Sodium citrate (30 cc po) may be given
immediately before treatment to neutralize any acid remaining in the stomach
(see also section “Gastrointestinal Disorders”).
Anticoagulant Medications
Anticoagulants typically do not cause any problem with ECT; patients may be
safely treated while anticoagulated. For the older warfarin-type anticoagulants,
coagulation times may be followed during a course of ECT, to ensure that they
are in range (Mehta et al., 2004; Petrides & Fink, 1996; Tancer & Evans, 1989).
The newer generation of oral anticoagulants (factor Xa or direct thrombin
inhibitors) are very likely safe in conjunction with ECT (Schmidt et al., 2014;
Shao et al., 2017; Shuman et al., 2015).
Most other medications can be held until 1–2 h following each ECT, unless
the medication is clearly physiologically protective for the patient during the
treatment (Table 2.6).
Informed Consent
Obtaining informed consent from the patient and his or her family is an essen-
tial part of the pre-ECT workup. Informed consent requires (1) the provision of
adequate information, (2) a patient who is capable of understanding and acting
intelligently upon such information, and (3) the opportunity to provide consent
in the absence of coercion (American Psychiatric Association, 2001, pp. 97–98).
This APA report contains an excellent four-page sample informed consent doc-
ument (pp. 319–322). The ECT practitioner should ensure that the ECT consent
conforms to all applicable laws, statutes, and hospital policies. Essential infor-
mation to be included for ECT informed consent includes the following items:
• The indication for ECT
• The effectiveness of ECT for the condition
• Description of the procedure itself
• Routine side effects
• More rare adverse events (e.g., major anesthetic complications)
• Any condition that may place the patient at increased risk
The patient should understand that consent can be withdrawn at any point
and should know whom to contact with questions during the treatment course.
The patient should be cautioned that major personal or financial decisions
should not be made during or immediately after a course of ECT. The patient
should not drive until the cognitive effects of ECT have largely resolved and,
in the case of continuation/maintenance ECT, until 24 h after treatment (see
also “Has Appropriate Informed Consent Been Obtained?” for a discussion of
informed consent during the ECT consultation).
Consent for the Depressed Patient

Self-disparagement and uncertainty often make treatment decisions difficult
for depressed patients. Educating family members is invaluable in helping the
depressed patient decide whether to receive ECT. Educational videotapes, pro-
vided through each of the major ECT device manufacturers and available from
other sources, are often very helpful.
Involuntary ECT
As with any other medical procedure, informed consent for ECT may need to
be waived in acute emergencies. ECT may be a lifesaving procedure for acutely
suicidal, catatonic, or dangerously malnourished patients. For these patients,
and for any patients who lack capacity to provide consent, some form of substi-
tuted consent (with surrogate decision makers) is required, as defined by local
jurisdiction.
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Chapter ECT Technique
3
Electrode Placement
There are three commonly used electrode placements in current ECT prac-
tice: bilateral (BL), also known as bitemporal (BT); right unilateral (RUL); and
bifrontal (BF), although the role of BF placement remains to be fully established
(Bansod et al., 2017; Kellner et al., 2010a; Kellner et al., 2010b). We believe that
in many cases the decision about which electrode placement to use should be
made in collaboration with the patient, after a discussion of the likely advan-
tages and disadvantages of each. In clinical practice, it should be relatively easy
to decide whether to use bilateral or unilateral electrode placement. The deci-
sion should be based primarily on the severity and urgency of the patient’s con-
dition. Bilateral electroconvulsive therapy may act more rapidly or completely
than right unilateral ECT, but bilateral ECT will have greater cognitive side
effects.
Strong opinions expressed in the ECT medical literature about one electrode
placement being “better” than others for all clinical situations have perpetuated
unnecessary controversy. ECT practitioners should be skilled at delivering all
three electrode placements and offer patients the type of ECT best suited to
their individual clinical situation. In a busy ECT service with the typical range
of ECT patient severity, it is common for about half of the patients to be started
with right unilateral placement and about half with bilateral or BF placement.
Bilateral ECT
Once the decision to proceed with ECT has been made, bilateral ECT should be
considered for patients who are judged to be most seriously ill. For depressed
patients, indicators of such severity include acute suicidality, poor nutritional
status, and severe agitation or psychosis. Some experts suggest that mania should
be treated with bilateral ECT (Small et al., 1985). Certainly, bilateral ECT should
be considered for patients with severe mania whose extent of psychomotor agi-
tation places them at risk for dehydration and physical exhaustion. Catatonia,
in any diagnostic category, is generally considered an indication for bilateral
49
50 Chapter 3: ECT Technique
ECT. A recent case series reporting successful treatment of catatonia with right
unilateral electrode placement, while interesting, is not compelling enough to
change practice. Although severity of depression must be judged individually
for each patient, some general guidelines may be helpful. If a standardized rat-
ing scale is used, a score in the upper ranges of the scale may help to confirm
the severity of illness. For example, a Hamilton Rating Scale for Depression
(HRSD) rating score of 30 or greater (Hamilton, 1960) might favor the use of
bilateral electrode placement. Weight loss of greater than 10% of body weight or
suicidal preoccupation requiring constant observation might also favor the use
of bilateral ECT. Patients who want to be assured of receiving the most powerful
and effective form of treatment may express a preference for bilateral over uni-
lateral ECT. Finally, patients with severe medical conditions that might increase
the risks of repeated anesthesia sessions should be considered for bilateral elec-
trode placement because it is most reliably effective and typically has more rapid
therapeutic effects, minimizing the number of anesthesia inductions.
Right Unilateral ECT

Unilateral electrode placement should be used for the majority of patients who
do not fall into the above category, “most seriously ill.” In general, these patients
will still be very seriously depressed, but without potentially life-threatening
complications of the illness. If the patient fails to show initial response after 4–6
unilateral ECT treatments at adequate stimulus dose, then a switch to bilateral
ECT should be strongly considered (Abrams, 2002; Lapidus & Kellner, 2011).
Individuals with particular concerns about cognitive impairment, such as those
with cognitively demanding jobs, should receive unilateral ECT unless a clear
indication for bilateral ECT is present. Those with preexisting cognitive impair-
ment, such as dementia, who have less cognitive reserve should preferably
be treated with unilateral electrode placement, unless they meet the severity
criteria listed above.
Left-Handedness
Left-handed patients who are being considered for right unilateral ECT pose
an interesting problem. (For a comprehensive review, see Kellner et al., 2017.)
Because language function is predominantly located in the left hemisphere in
approximately 98% of right-handed people and in 70%–90% of left-handed
people (Bryden, 1982), it is reasonable to begin unilateral ECT on the right side,
even in left-handed patients. If the patient experiences unusually severe confu-
sion or memory impairment after the first treatment, consideration should be
given to switching to left unilateral electrode placement for the second treat-
ment and comparing the speed of recovery of orientation between the two. A
simple test of hemispheric dominance can also be done, comparing the time
elapsed following an ECT treatment until the patient can name simple objects
(American Psychiatric Association, 2001, pp. 154–155; Kellner et al., 2017; Pratt
et al., 1971). Treatments can be continued with the laterality that causes the least
Chapter 3: ECT Technique 51
immediate cognitive impairment. It should also be remembered that another

option is switching to bilateral electrode placement, with the expectation that
efficacy will be enhanced and that cognitive side effects may not be substantially
increased (Lapidus & Kellner, 2011).
Bifrontal ECT
BF electrode placement has become widely used because it is believed to com-
bine the efficacy of BT placement, with a cognitive effect profile similar to
that of RUL placement. Several moderate-sized studies support these conten-
tions (Bailine et al., 2000; Letemendia et al., 1993) while a larger study by the
Consortium for Research in Electroconvulsive Therapy (CORE) group failed
to confirm these advantages (Kellner et al., 2010). Technically, BF placement
is the easiest to use because there is no hair to interfere with the placement of
electrodes. We believe that it is likely that BF placement is more similar to BT
than to RUL in both efficacy and cognitive effects. Given the smaller evidence
base supporting its use, it is difficult to recommend it as the placement of choice;
however, it is certainly a viable option (Bansod et al., 2017). Future studies may
help clarify its optimal place in treatment technique.
Location of Electrodes
Although many different electrode sites have been used in the past, in modern
ECT almost all practitioners use three standard placements. For bilateral ECT,
the electrode positions are symmetrically located on either side of the forehead
just above the midpoint of a line running from the outer canthus of the eye to
the external auditory meatus. If a circular metal electrode is used and its inferior
edge is placed on this line, the center of the electrode will be approximately 1 in.
above the line. As noted above, this placement is synonymously referred to as
either “bilateral,” “bitemporal,” or sometimes, “bifrontotemporal” (Figure 3.1).
Figure 3.1 Bilateral electrode placement

Vertex
electrode
Figure 3.2 Right unilateral electrode placement
Figure 3.3 Patient set up for right unilateral ECT (d’Elia placement), using disposable,
adhesive stimulus pads
For right unilateral ECT, the right electrode position is the same as for bilat-
eral ECT, and the other (vertex, or bregma) electrode is placed with the left
(medial) electrode edge touching a line that runs down the middle of the skull at
its intersection with a perpendicular line connecting the two external auditory
canals (Figure 3.2). If the left edge of the electrode disc is at this vertex position,
the center of the electrode will be approximately 1 in. to the right of the ver-
tex. This configuration is known as the d’Elia placement, after the psychiatrist
who developed it (d’Elia, 1970) (Figure 3.3). For BF electrode placement, the
Figure 3.4 Bifrontal electrode placement
location of the electrodes is on the forehead, with the center of the electrode
placed approximately 5 cm above the outer canthus of the eye. Given the ana-
tomical differences between peoples’ foreheads, the exact location will differ
slightly between patients (Figure 3.4).
It is important to remember that optimal electrode placement will allow for
the greatest distance between the two electrodes while staying as closely as pos-
sible to the anatomical landmarks outlined above. The technique of preparing
the electrode sites is covered in the section “Electrode Site Preparation.”
Stimulus Dosing
Choosing the appropriate strength of the stimulus (the electrical “dose”) has
become an important part of contemporary ECT practice. Nowadays, the prac-
titioner needs to make decisions about both stimulus characteristics (primarily
pulse width) and intensity (primarily expressed in terms of charge). Obviously,
the stimulus has to be sufficient to induce a generalized seizure – the therapeutic
goal of ECT – but beyond that, the situation becomes more complex. Some gen-
eralized ECT seizures, if induced with a stimulus very close to seizure thresh-
old (particularly with right-sided electrode placement), may not be maximally
therapeutic; thus, in certain situations, it may be advantageous to give stimuli
that are several times greater than the seizure threshold (see below). On the
other hand, stimuli that are far in excess of the seizure threshold (particularly
with bilateral electrode placement) may contribute to excess cognitive impair-
ment. Several options are available to the ECT practitioner in attempting to
deal with this clinical dilemma. Despite its having been widely adopted in clini-
cal practice, a recent commentary calls into question the evidence base of the
dose titration method, suggesting that it has not yet been adequately researched
(Rosenman, 2017). We will review the available methods below, including (1)
stimulus dose titration, (2) age-based dosing, (3) fixed high-dose therapy, and
(4) dosing estimates based on patient characteristics (e.g., age, sex). The issue
of the use of ultrabrief pulse stimuli will be discussed in a separate section (see
below).
Stimulus Dose Titration

First, let us define seizure threshold. Quite simply, seizure threshold is the mini-
mum amount of electrical stimulus needed to induce a seizure. But “amount”
in terms of what? Charge is probably the best unit of measurement to describe
the stimulus, although, unless the stimulus characteristics are fully described
(frequency, pulse width, duration, and current), even charge does not tell the
whole story. Some ECT devices describe their output in terms of joules (J), with
the assumption that a patient’s impedance will be close to the standard value of
220 Ω. It should be remembered, however, that even though such devices indi-
cate the “energy” setting in joules, they are constant-current devices, and, there-
fore, this setting will be an approximation, and you are really setting the amount
of charge to be delivered. Thus, patient seizure threshold may be expressed in
terms of either charge or joules, but more commonly charge. With dose titration,
a patient’s seizure threshold is determined at the first ECT session. This “method
of limits” involves starting at low stimulus levels and administering a series of
increasingly strong stimuli until a seizure occurs (Beale et al., 1994; Coffey et al.,
1995; O’Neill-Kerr et al., 2017; Sackeim et al., 1993; Tiller & Ingram, 2006).
After the delivery of each stimulus, one observes the patient and the EEG
recording on the ECT device to determine if a seizure has been elicited. If both a
robust motor and EEG seizure are observed, then the patient’s seizure threshold
has been found. If no motor or EEG seizure are detected, continue to observe
the patient and run the EEG recording paper for at least 20 s (this is to not miss a
possibly delayed-onset seizure). In the case of an equivocal EEG seizure and no
observed motor seizure, we recommend that one conclude that no seizure has
occurred. In the case of a well-developed EEG seizure and no motor seizure, the
field is divided as to what to do. We recommend restimulating at the next step
in the titration algorithm, which usually then results in both a robust motor,
as well as EEG, seizure. Of course, if there is an explanation for the absence
of the motor seizure, for example, if the cuff was not properly inflated on the
ankle, then restimulation may not be advisable. When restimulating, the ECT
device paper strip is stopped, impedance is rechecked, the bite block is again
positioned, the ECT device is set to the next (higher) stimulus in the algorithm
and the stimulus is delivered.
To some extent, the choice of stimulus settings in a dose titration sequence
is arbitrary and specific to the ECT device being used. The general principle is
quite simple, however, and should be universally applicable: start with a setting
near the lowest output of the device and increase that by 50%–100% for each
subsequent stimulus. Remember to consult the instruction manual of your ECT
device to help in establishing the specific sequence you will use in your practice.
Most patients will have a seizure within the first two steps in the titration
sequence. Virtually all patients will have had a seizure by the third setting in
your dose titration sequence. For the very rare situation in which a patient does
not have a seizure with the third stimulus, you will have to decide whether it is
safe to deliver a fourth stimulus at the maximal setting on the ECT device. This
decision will depend on several factors, including the patient’s medical condi-
tion, the type and amount of anesthesia given, and the urgency of the psychiatric
illness. Your overriding concerns should be (1) patient safety and (2) eliciting a
seizure. The vast majority of ECT patients should not leave the ECT suite with-
out having had a seizure. Multiple stimuli may be associated with greater side
effects, such as headache, nausea, and hypertension.
Some patients require modification of the general principles outlined
above. Most important, young patients will probably require a very low stimu-
lus charge. Unless there are extenuating circumstances, adolescents and young
adults (<30 years old) should be stimulated first near the lowest setting of the
device.
At the other end of the spectrum, very elderly patients or patients who are
being treated while continuing to take anticonvulsant medication(s) may need
a higher stimulus charge than the standard sequence.
What should you do with the seizure threshold information obtained at
the first ECT session? The general principle is that you should use the infor-
mation to make a rational choice of stimulus dose for subsequent treatments.
Stimulus dosing differs for right unilateral and bilateral electrode placements.
For right unilateral, one should be liberal with stimulus dosing, for bilateral, one
should be conservative. With bilateral electrode placement, the stimulus need
only exceed the seizure threshold by a moderate amount (e.g., 1.5–2 × seizure
threshold). With right unilateral electrode placement, the stimulus dose should
be several multiples of the seizure threshold, most commonly, about 6 × seizure
threshold (McCall et al., 2000; Sackeim et al., 2009).
Age-Based Dosing
An alternative to dose titration is to make an educated estimate of the patient’s
seizure threshold and then choose a stimulus charge that is likely to be suffi-
ciently above that threshold to produce effective antidepressant results, while
minimizing cognitive effects. Because seizure threshold increases with age,
the most commonly recommended system has been to select a dose based
on the patient’s age. Petrides and Fink (1996) recommended a specific type of
age-based dosing that they call the “half age” method: setting the charge on
the ECT device at the percentage of “energy” one-half the patient’s age. This
method decreases the likelihood of administering grossly suprathreshold stim-
uli (Petrides et al., 2009; Swartz & Michael, 2013). Abrams and Swartz (2016), in
the Thymatron® System IV Instruction Manual, now also suggest setting the per-
centage of “energy” at approximately half the patient’s age for bilateral electrode
placements, and at the patient’s age for unilateral electrode placement. The same
strategy can, of course, be used on MECTA devices, with appropriate calcula-

tion and setting of total charge.
Fixed High-Dose Therapy

A third method of stimulus dosing involves giving a fixed high charge to all
patients without determination of their seizure threshold (Abrams et al.,
1991; McCall et al., 2000). Many practitioners believe this strategy exposes
the patient to unnecessarily high stimulus doses, which may lead to more
cognitive impairment. However, this method is useful in severely ill patients
in whom a rapid, definitive response is needed. For example, treating a cata-
tonic or agitated manic patient at 80%–100% stimulus charge for the dura-
tion of the ECT course may provide a more rapid and sustained response
than near-threshold dosing.
Dosing Estimates Based on Patient Characteristics

Some practitioners use stimulus dosing charts to determine the appropriate
dose for a given patient. These charts are based on patient characteristics known
to be associated with seizure threshold. These include the patient’s age, sex,
laterality of electrode placement, and other variables (refer to the ECT device
manufacturer instruction manuals; for example, MECTA provides stimulus
titration and preselected dosing tables).
Ultrabrief Pulse Stimuli

Ultrabrief pulse stimuli are becoming more commonly used in contempo-
rary ECT. By arbitrary convention, “ultrabrief ” is defined as a pulsewidth less
than 0.5 ms; brief pulse is defined as a pulsewidth between 0.5–2.0 ms. Both
the MECTA and Thymatron ECT devices are capable of delivering ultrabrief or
brief pulsewidth stimuli. There is no reason to believe that 0.5 ms is a magical
dividing line between brief and ultrabrief stimuli; rather, it is more likely that
there is a continuum of effects, with narrower pulsewidths possibly associated
with lesser cognitive effects.
There is increasing evidence that the use of ultrabrief pulse stimuli is asso-
ciated with diminished cognitive impairment, compared with standard brief
pulse stimuli (Sienaert et al., 2010; Verwijk et al., 2012). While the emerging
data also support the clinical efficacy of ultrabrief pulse stimuli, it remains to be
seen if the antidepressant efficacy and speed of response are, in fact, comparable
to standard brief pulse stimuli.
Several reports document the use of ultrabrief stimuli with RUL ECT.
At least one study documents the efficacy of ultrabrief stimuli with BF ECT
(Sienaert et al., 2009). There is no reason to doubt the efficacy of ultrabrief
stimuli with bilateral electrode placement, despite one report with a small sam-
ple suggesting it is ineffective; it is more likely that this result was anomalous
(Sackeim et al., 2008).
Seizure thresholds are markedly lower with ultrabrief pulse stimuli and
dose titration algorithms and subsequent dosing strategies may need to be
adjusted accordingly (Kellner et al., 2016).
Practical Advice on Choosing the Stimulus Dose

While research studies and theory inform the practice of stimulus dose selec-
tion, clinical experience and common sense should be used to guide proto-
cols in the ECT suite. It is certainly not necessary to obsessionally determine
a patient’s seizure threshold using a dose titration procedure with numerous
closely spaced steps. Rather, a procedure with a few moderately spaced steps will
provide a reasonable estimate of the patient’s seizure threshold.
Dose titration makes more sense for right unilateral than for bilateral elec-
trode placement because there is more evidence that underdosing lessens effi-
cacy with right unilateral. For bilateral electrode placement, using the patient’s
age as a guide, and treating at approximately half that age, is a reasonable initial
dosing strategy.
In practice, when using ultrabrief stimuli (0.25 or 0.3 ms) with right unilat-
eral electrode placement, most patients will seize at the 5% setting (25 mC) at
the first treatment, and can be treated at 30% (6 × seizure threshold, 150 mC)
for subsequent treatments.
With bilateral electrode placement, most young patients can be successfully
treated with initial stimuli around 20% (100 mC) and most older patients with
initial stimuli around 40% (200 mC).
Of course, these are just guidelines that can, and should, be modified for
individual patient needs.
What about the stimulus dose in treatments 3 and beyond? Most practition-
ers would continue treatments at the same stimulus dose unless (1) the patient
is not improving as expected, (2) the seizures become “inadequate” (i.e., missed,
very short, or of very low EEG amplitude), or (3) the patient is having excessive
cognitive effects. For situations 1 and 2, the stimulus dose could be adjusted up
by increments of 25%–50%. For situation 3, the stimulus dose could be low-
ered, or other steps taken to decrease the cognitive effects of the treatment (e.g.,
increasing the time interval between treatments).
Electrode Site Preparation

The preparation of the scalp for stimulus delivery and EEG monitoring is a cru-
cial part of the ECT procedure. The reader should supplement the instructions
for site preparation reviewed here with the particular recommendations of the
ECT device manufacturer. To verify proper skin contact, a self-test procedure
should be a standard part of the preparation for ECT stimulus delivery.
EEG Recording Electrodes

A minimum of two-channel (4 leads) EEG recording should be standard pro-
cedure for all ECT. One lead is placed on the left side of the forehead, one on
1 inch
Frontal EEG lead placement Mastoid EEG lead placement
Figure 3.5 Electroencephalogram (EEG) placement
the right side of the forehead, one behind the left ear, over the mastoid bone,
and one behind the right ear. This lead placement, referred to as left and right
frontomastoid, allows monitoring of seizure activity in the both hemispheres;
this is appropriate for both bilateral and right unilateral ECT.
The frontal leads should be placed 1 in. above the eyebrow in the mid-
pupillary line. The mastoid leads should be placed behind the ear, as high on the
mastoid process as allowed by the patient’s hairline. This location helps to avoid
artifact from the carotid artery (see Figure 3.5). EEG recording sites should be
cleaned with alcohol and then dried. Disposable, self-adhesive electrodes are
then applied; make sure that they adhere tightly.
Electromyogram (EMG) Recording Electrodes

One ECT device (the Thymatron) uses a two-lead, single-channel EMG to
measure motor seizure activity. The EMG electrodes should be placed approxi-
mately 3 in. apart on the dorsum of the right foot (see Figure 3.6). The sites are
cleaned with alcohol and allowed to dry, and the same type of disposable, stick-
on electrodes used for the EEG are applied. The MECTA ECT device uses an
optical motion sensor wrapped around the patient’s finger or toe to detect the
motor seizure, in a manner analogous to the EMG.
Stimulus Site Preparation

The preparation of the stimulus sites is crucial for safe and effective ECT (see
section “Electrode Placement” for an anatomical guide to stimulus electrode
location). The practitioner should refer to the instruction manual of his or her
ECT device for further details of site preparation.
Figure 3.6 Patient set up showing electromyogram and blood pressure cuff on right
foot, nerve stimulator on left calf
Right Unilateral Considerations

For site preparation in right unilateral ECT, attention must first be given to part-
ing the hair at the vertex. This part must provide sufficient scalp exposure for
good electrode-to-scalp contact. As noted below, a metal handheld electrode
is sometimes easier for the vertex site, rather than a disposable stick-on. Other
aspects of site preparation are identical for unilateral and bilateral ECT.
Metal Stimulus Electrodes

When using metal electrodes, both scalp sites are first cleansed with a gauze
pad soaked in saline. Conductive gel is then applied to the stimulus electrodes
and, when manual electrode paddles are used, the electrodes are placed on the
stimulus site after the patient is anesthetized; sufficiently firm pressure must be
maintained to allow good skin contact throughout the delivery of the stimulus.
This sequence may be somewhat different when a headband is used to hold elec-
trodes in place. Refer to the ECT device instruction manual for further direc-
tion in the use of the headband, if this method is to be used. The vertex metal
electrode is handheld with a paddle, whereas the frontotemporal electrode may
be either handheld or held in place with a headband.
Disposable, Stick-on Electrodes

Many practitioners choose to use disposable stimulus electrodes, which adhere
to the patient’s scalp. When these electrodes are used, the site should be moistened
with saline, then dried, followed by the application of a few drops of “pre-tac”
conductive solution. Additional “pre-tac” can be directly applied to the adhesive
side of the electrode before application. The practitioner should then press the
electrodes into place, with special attention to good skin adherence across the
entire surface. The vertex electrode, for unilateral ECT, may require a handheld
cupped paddle over the site to maintain adequate contact. Both pads may be
held firmly in place during the delivery of the stimulus with a gloved hand.
See Figure 3.7 for a summary of the placement of recording and stimulus
electrodes.
4 channel setup – 2 EEG, 1 EMG, 1 ECG channel *
On mastoid
– Iso
Ch1 2 3 4
+ Gnd
BP cuff inflated
*Electrode connections for channel 1, 2 EEG, channel 3 EMG, channel 4 ECG recording
Figure 3.7 Patient set-up showing recording (EEG, EMG, ECG) and stimulus electrodes
used on a contemporary ECT device. (Used with permission from Somatics, LLC.)
The Self-Test Procedure

Following placement of the stimulus electrodes and before delivery of the stim-
ulus, adequate integrity of the electrical circuit should be documented by a self-
test procedure. This procedure involves the passage of a small amount of current
(below the patient’s sensory threshold) to measure the impedance of the circuit.
The cause of an abnormal impedance value should be fully evaluated and corrected
before stimulus delivery.
High Impedance
An abnormally high impedance (e.g., greater than 2800 Ω) represents a failure
of smooth current flow through the circuit. Common causes include improper
skin preparation and/or inadequate skin-to-electrode contact and inadequate
connection of the stimulus cable to the electrodes or the ECT device.
Low Impedance
An impedance that is too low (e.g., less than 100 Ω) is very rare and indicates an
accessory pathway for current flow. This shunt may be due to communicating
conductive gel between the electrodes or conduction occurring through some
other substance, such as hair gel or excessive perspiration. A short circuit in
the stimulus cable is another possible cause. In the case of either too low or too
high impedance, the cause of the problem should be remedied before delivery of the
stimulus.
Physiological Monitoring
Vital signs, blood oxygen saturation, electrocardiogram (ECG), EEG, and EMG
are all continuously monitored during ECT. In addition, a nerve stimulator
should be used to monitor the effects of succinylcholine.
Vital Signs
Pulse and blood pressure should be followed at close intervals before, during,
and after ECT. An automated blood pressure cuff is ideal for these purposes and
is strongly recommended. A baseline pressure and pulse should be recorded
before any medication is given. If pretreatment antihypertensive agents (e.g.,
esmolol or labetalol) are given, several minutes should be allowed for the
agent(s) to work and a repeat set of vital signs should be recorded. Poststimulus
vital signs should be recorded every 3–5 min until a stable baseline is achieved
(usually approximately 10 min). More frequent or longer monitoring schedules
can be used for patients for whom there are particular concerns about cardio-
vascular management.
Pulse Oximetry
It is now standard anesthesia practice to monitor blood oxygen saturation by
pulse oximetry continuously before and during ECT and in the immediate
post-ECT recovery period. This simple, noninvasive monitoring procedure

provides the practitioner with crucial information about the patient’s respira-
tory status. Most patients should have an oxygen saturation at, or near, 100%
during most of the procedure.
The pulse oximeter probe can be placed on a finger, toe, or earlobe. It should
be on a limb without a blood pressure cuff because inflation of the cuff inter-
rupts the probe’s functioning.
Electrocardiogram
The ECG is monitored using standard leads. The tracing is continuously dis-
played on an oscilloscope screen and may also be printed out. The ECG can be
printed out by the ECT device itself.
Electroencephalogram
EEG monitoring is a crucial part of modern ECT practice. It enables the prac-
titioner to confirm that a cerebral seizure has occurred and that the seizure has
ended in a timely manner. This is a crucial point and bears repeating: EEG moni-
toring is most important for determining that the seizure is over.
Although the 4-lead, two-channel EEG used in most ECT cannot provide
the sophisticated information of a standard 16-lead EEG, it is adequate for the
requirements of ECT.
The now-standard left and right frontomastoid recording sites fulfill the
important criteria of adequate interelectrode distance and, with right unilat-
eral electrode placement, the ability to know that the seizure has generalized to
the left hemisphere (Figure 3.5). Furthermore, these sites eliminate the possible
problem of one side canceling out the other, as can occur when two frontal (one
on either side of the forehead) leads are used for the same channel.
Interpretation of the EEG has been the subject of considerable discus-
sion and controversy in the ECT literature (Farzan et al., 2014; Minelli et al.,
2016). In practice, it should become a matter of routine for the practitioner to
adequately record and interpret the EEG. Adequate recording is ensured by
careful attention to recording site location and preparation, setting of amplifier
gain, and exclusion of artifact (see sections “Electrode Site Preparation” and
“Treatment Procedure”). Interpretation of the ECT EEG is largely a matter of
common sense: the seizure ends when the EEG goes flat. Most of the time, this
determination is a very simple one. Sometimes, however (e.g., when the EEG
amplitude decreases gradually rather than abruptly), it is difficult to determine
exactly when the seizure ends (although after a few seconds it will become clear
that the seizure is over). In rare instances, the EEG, despite one’s best efforts, is
uninterpretable. In such cases, the practitioner will need to rely on clinical signs
(resumption of spontaneous breathing, return to baseline heart rate) to know
that the seizure is over. See Figures 3.8 and 3.9 for sample tracings from modern
ECT devices.
EEG1 200 μV/cm
EEG2 200 μV/cm
EMG 1000 μV/cm
14b/m 0b/m
ECG 1000 μV/cm

0s 1s 2s 3s 4s 5s 6s 7s 8s 9s 10s
(a)
Figure 3.8a Sample ECT tracing. Seizure initiation

72b/m 68b/m 64b/m
40s 41s 42s 43s 44s 45s 46s 47s 48s

(b)
Figure 3.8b Well-developed EEG seizure and end of the motor seizure

42b/m 41b/m 57b/m
75s 76s 77s 78s 79s 80s 81s 82s 8

(c)
Figure 3.8c End of the EEG seizure

Figure 3.9 Computer monitor showing seizure in progress. Top two lines are left and
right frontomastoid EEG, third line is electromyogram (EMG), and bottom line is electro-
cardiogram (ECG)
A major part of EEG interpretation is being able to distinguish artifact from

true cerebral activity. Examples of the most commonly encountered artifacts are
shown in Figure 3.10.
Electromyogram
Monitoring EMG is a way to provide a backup measurement (and hard-copy
tracing) of the length of the motor seizure. The Thymatron device provides a
channel specifically for EMG monitoring, the MECTA device has an analo-
gous feature, the “Optical Motion Sensor,” which serves the same function. Two
extra-long leads are attached to the dorsum of the right foot (see Figure 3.6) to
record the EMG of the motor seizure. The tracing is interpreted in the same way
as is the EEG. When the EMG tracing goes flat, the motor seizure is over; the
length of the seizure is noted from the timing marks on the recording paper. See
Figures 3.8a–c for an example of EMG patterns during each phase of the ECT
seizure.
EMG recordings may also be subject to artifact. Most commonly, moving
the patient or the EMG leads during recording produces artifact. At times, the
muscles of patient’s right foot may remain slightly contracted after the motor
seizure ends; gently pushing up on the toes to relax the foot will usually allow
the EMG line to go flat.
Nerve Stimulator
A peripheral nerve stimulator is used to assess the muscle relaxant effect of suc-
cinylcholine (Kellner, 2011). Several anatomical sites can be used: in the arm,
Carotid pulse EEG artifact
EEG
EMG
42s 43s 44s 45s 46s 47s

(a)
EEG lead disconnection artifact
EEG
EMG
(b)
Figure 3.10 Recording artifacts
along the radial or ulnar nerves; in the leg, along the posterior tibial nerve; or
on the dorsum of the foot. We recommend placement of the nerve stimulator
along the posterior tibial nerve, as pictured in Figure 3.6. Using a site on the leg
rather than on the arm allows more accurate assessment of when the effects of
succinylcholine are maximal because the drug works in a rostrocaudal progres-
sion. We also recommend a nerve stimulator with an automatic setting such that
the progressive decrement in response can be easily observed. Alternatively,
one can simply monitor the plantar reflexes or repeatedly check the tone of the
limbs. Generally, it takes approximately 1 min for the succinylcholine to have
maximal effect in a young patient, and about 2 min in many older patients (see
section “Muscular Relaxation”).
Anesthetics and Muscular Relaxation

A professional trained in anesthesia is a required member of the ECT treatment
team. The anesthesia experience should be brief and uncomplicated for most
patients; the primary goals are patient safety and comfort.
Standard dosing (using the ranges listed in this chapter) is initiated at the
first treatment session for both the induction agent and the muscle relaxant.
Any recommended adjustments to these doses, either increases or decreases,
should be noted, and implemented at subsequent treatment sessions.
Anesthetics
Brief, light general anesthesia is used during ECT to achieve absence of discom-
fort and anxiety for the procedure, and to allow the use of succinylcholine for
Table 3.1 ECT anesthetics

Agent Usual dose (mg/kg) Relative Comments
anticonvulsant
effect
Methohexital 0.75–1.2 1 Standard agent for ECT;
rapid recovery; pain
on injection
Thiopental 2.0–5.0 2 Cardiovascular
depression
Propofol 1.0–2.0 3 Pain on injection; may
shorten seizures
Etomidate 0.2–0.4 0 Myoclonus; adrenal
suppression; less
cardiovascular
depression
Ketamine 1.0–2.0 –1 (proconvulsant) Hypertension;
tachycardia;
hallucinations
Alfentanil 0.010–0.015 1 Increased duration
(adjunctive) of apnea; reduced
hypertension and
tachycardia; reduced
hypnotic dose
Remifentanil 0.001–0.008 –1 (proconvulsant) Reduced hypnotic
(adjunctive) dose; attenuated
hemodynamic
response
muscular relaxation (see Table 3.1 for a comparison of various agents used in

ECT anesthesia). (Please see Bryson et al., 2017, and Kellner and Bryson, 2013,
for reviews of ECT anesthesia).
Methohexital
Methohexital has become the standard anesthetic for ECT because it has rapid
onset, brief duration, and causes minimal postanesthesia confusion. It is less
anticonvulsant than other barbiturates. Dosing is typically 0.75–1.0 mg/kg
body weight, given as an intravenous bolus of a 1% solution (i.e., 10 mg/mL).
The minimum required dose is often lower in elderly patients. Methohexital is
a local irritant and often burns upon intravenous injection; however, it causes
only brief discomfort because unconsciousness rapidly ensues.
Thiopental
Thiopental has a longer duration of action and is more anticonvulsant than
methohexital. The early suggestion that thiopental produced more cardiac
arrhythmias than methohexital (Pitts et al., 1965) is controversial and has not
been born out in subsequent usage.
Propofol
Propofol has become the second most commonly used induction agent in
ECT. It has the advantages of causing less hypertension and tachycardia than
methohexital as well as less postictal agitation. Patients may experience a
“smoother” anesthesia experience with this agent. However, it is markedly more
anticonvulsant than other induction agents and is associated with shorter sei-
zures and increased seizure thresholds. Because of these anticonvulsant proper-
ties, it may be the agent of choice for ECT in children and adolescents (Bailine
et al., 2003), many of whom may have prolonged seizures early in their treat-
ment course.
Etomidate
Etomidate is a good alternative anesthetic with acceptably low anticonvulsant
properties. It has less negative effect on cardiac contractility than methohexital
and may be preferable in patients with heart failure. Myoclonic jerks are often
seen during the drug’s onset of action. Repeated doses have been reported to
cause adrenocortical insufficiency, although this is probably an uncommon
occurrence.
Ultrashort-Acting Narcotics
Recently, ultrashort-acting narcotics, such as alfentanil and remifentanil, have
been used in combination with propofol, methohexital, or etomidate to induce
anesthesia for ECT. In general, using an adjunctive narcotic reduces hypnotic
dose, increases seizure duration, and attenuates hemodynamic responses to
ECT (Recart et al., 2003; Takekita et al., 2016).
Ketamine
Ketamine is interesting as an alternative ECT anesthetic because of both its pro-
convulsant and intrinsic antidepressant properties (Wan et al., 2015). It is an
NMDA antagonist compound related to phencyclidine (PCP) and can induce
psychotic symptoms. Practitioners have long used it without encountering such
problems (Rasmussen et al., 1996). There have been reports that its use in ECT
can accelerate antidepressant response and possibly reduce cognitive adverse
effects, but the evidence for this is inconsistent (Kellner & Iosifescu, 2017;
McGirr et al., 2017; Okamoto et al., 2010). It is associated with a higher inci-
dence of hypertension during the procedure and possibly increased agitation on
emergence. Some practitioners switch from other induction agents to ketamine,
as an augmentation strategy in patients who are not responding adequately dur-
ing a course of ECT.
Muscular Relaxation
Muscular relaxation is used during ECT to eliminate musculoskeletal injury
from the seizure and to facilitate airway management. Complete paralysis is not
required except in cases of severe osteoporosis or an unstable vertebral column.
Succinylcholine
The preferred neuromuscular blocking agent for ECT is succinylcholine, pri-
marily because of its rapid onset and brief duration of action. Succinylcholine
dosing is usually 0.75–1.0 mg/kg of lean body mass (Bryson et al., 2012). When
complete paralysis is required, the dose of succinylcholine may be increased
by 40%–50% (Bryson et al., 2012). Succinylcholine is typically given as a rapid
intravenous bolus of a solution of 20 mg/mL, which should be refrigerated
until just before use. Succinylcholine should only be given after the patient is
unconscious. A patent airway should be present before succinylcholine dosing
because the drug paralyzes the diaphragm.
Assessment of Muscular Relaxation
The adequacy of muscular relaxation may be measured by a peripheral nerve
stimulator and by the loss of tone and reflexes in a distal extremity. Because
succinylcholine is a depolarizing agent, muscle fasciculations occur as the
drug reaches the neuromuscular junction. The disappearance of fasciculations
(usually last seen in the toes) is a marker that full circulation of the drug has
occurred. Elderly patients often have a longer latency of action than younger
patients (Beale et al., 1994; Bryson et al., 2012). Waiting approximately 60 s
following injection of succinylcholine in young patients, and 120 s in geriatric
patients is usually adequate.
Fasciculation Muscle Pain

Especially after the first treatment, diffuse musculoskeletal pain due to fascicu-
lations may occur. The pain is responsive to simple analgesics (e.g., nonsteroidal
anti-inflammatory drugs) and typically lessens with subsequent treatments. If
the pain persists after subsequent treatments, fasciculations may be attenuated
by pretreatment with a small dose of a nondepolarizing muscle relaxant.
Cuff Technique
Before succinylcholine injection, a blood pressure cuff on the right ankle should
be inflated above the patient’s systolic pressure to prevent succinylcholine access
to that foot. This procedure allows focal observation of the motor seizure. The
right side of the body is used to document seizure generalization to the contralat-
eral hemisphere in the case of right unilateral ECT, and, of course, is also suitable
for use with bilateral placements. In situations where the right leg cannot be used
(e.g., severe edema, skin infection) the left foot or a forearm may be used.
Nondepolarizing Muscle Relaxants

Nondepolarizing muscle relaxants (e.g., mivacurium, rocuronium, cisatracu-
rium, and vecuronium) have a slower onset and a longer duration of action
than succinylcholine. They are used in ECT for special situations, including
pseudocholinesterase deficiency (usually a familial disorder) and risk of exces-
sive potassium release with succinylcholine, as is seen in cases of severe burns,
massive tissue trauma, or severe spasticity or paralysis (American Psychiatric
Association, 2001, pp. 134–136). Reversal agents (e.g., neostigmine) and an
anticholinergic agent (e.g., glycopyrrolate) will also need to be given. Recently,
a novel reversal agent for rocuronium and vecuronium, sugammadex, has
become available on the American market (Kadoi et al., 2013).
Anticholinergic Agents
The routine use of anticholinergic premedication to prevent vagal bradyar-
rhythmias during ECT is controversial. Preexisting cardiac conduction delay,
the use of β-adrenergic antagonists, and dose titration procedures, which may
involve multiple subconvulsive stimuli, all argue for anticholinergics to be used.
Arguments against their use include the induction of increased heart rate and
blood pressure, constipation, urinary retention, and potential amnestic effects.
A reasonable practice would be to administer an anticholinergic agent at the
first treatment in a course if a dose titration procedure is being done, and then
omit it at subsequent treatments. Even such targeted use, however, is often
unnecessary; many practitioners forego routine anticholinergic use.
Glycopyrrolate
Glycopyrrolate (a peripheral anticholinergic that does not cross the blood–
brain barrier) is given in doses of 0.2–0.4 mg intravenously at the time of the
procedure. Note that glycopyrrolate is either given for the purpose of preventing
bradycardia or for decreasing airway secretions. For preventing bradycardia,
it may be given immediately before anesthesia induction; for drying up secre-
tions, it should be given approximately 10 min before the procedure.
Atropine
Atropine is a more potent vagolytic agent than glycopyrrolate. Atropine doses
range from 0.4 to 1.0 mg intravenously at the time of the procedure.
Oxygenation
The patient should receive supplemental oxygen, 100%, by means of mask,
throughout the procedure. It is prudent to start oxygen supplementation before
the procedure, especially in patients with a history of myocardial ischemia. For
all patients, as soon as unconsciousness is produced by the barbiturate, positive-
pressure ventilation at 15–20 breaths/minute should begin and continue until
spontaneous respiration resumes. Oxygen saturation should be maintained
at or near 100% throughout the procedure. Vigorous hyperventilation should
be given for patients in whom a longer seizure is desired (Aksay et al., 2014;
Gomez-Arnau et al., 2018). This can be started immediately after the succinyl-
choline is injected, and continued (with a break for the insertion of the bite block
and stimulus delivery) until the desired seizure length is achieved. For some
patients, it may be particularly effective to ask them to start hyperventilating
for about a minute before the induction agent is given (de Arriba-Arnau et al.,
2017); the anesthesiologist can then take over the hyperventilation when the
patient is unconscious.
Airway Management and NPO Status

Airway Management
The anesthetist should carefully evaluate the patient’s mouth and airway before
ECT for any potential problem areas. Loose teeth should be documented and
may need extraction before the procedure. Solitary teeth, loose teeth, or asym-
metrical bite bearing by teeth may require evaluation by a dentist before ECT.
For some patients who are initially not easy to ventilate, the insertion of an oral
airway may facilitate ventilation. The oral airway must be removed prior to
the insertion of the bite block (see below), and can be reinserted after stimulus
delivery.
Bite Block
When the patient is ready for stimulus delivery, the oxygen mask should be
removed while a protective foam or rubber bite block is inserted into the mouth.
The bite block should be inserted so as to push the tongue inferiorly and pos-
teriorly into the mouth, behind the teeth. The bite block should then be placed
against the upper teeth, and the lower teeth and jaw should be held up to firmly
meet the bottom surface of the bite block. The lips should be pulled safely over
the bite block. The chin should be pushed upward with firm pressure during the
stimulus. This action absorbs the jaw flexion that occurs as a result of the direct
effects of the stimulus on, and the poor succinylcholine blockade of, these mus-
cles. The bite block is usually removed after stimulus delivery. For some patients
it may be left in place to facilitate ventilation by the anesthetist. It may also be left
in place if delivery of a second stimulus is being considered.
Nothing by Mouth (NPO)

Because of concern about aspiration of gastric contents during anesthesia,
patients are to have nothing by mouth (NPO) for 8 h before the procedure.
When a patient has taken small amounts of liquids or clear liquids the morning
of ECT, the anesthesiologist should be consulted and consideration should be
given to treating the patient after a short (e.g., 2 h) waiting period.
Intubation
Patients very rarely require intubation for ECT. In certain situations (e.g., the
third trimester of pregnancy, severe gastroparesis, or severe gastroesopha-
geal reflux), the anesthesiologist may elect to intubate the patient. In the large
majority of cases of gastroesophageal reflux, pretreatment with an anti-acid
medication (H2 blocker or proton pump inhibitor), taken with a sip of water
approximately 2 h before ECT, should be sufficient aspiration prophylaxis.
Cardiovascular Agents
It is helpful to conceptualize two categories of cardiovascular drugs for ECT
patients:
1. Those that are taken regularly to treat chronic hypertension, arrhythmias,
ischemia, or other cardiac conditions, and
2. Those that are given adjunctively just before or during the ECT procedure
to blunt the hypertensive, tachycardic response to the seizure.
In general, a patient’s regular cardiovascular medication should be contin-
ued during a course of ECT, including antihypertensives and antiarrhythmics.
Exceptions to this rule are diuretics on the mornings of treatment (because
a patient should not have a full bladder at the time of treatment) and reser-
pine at any point during an ECT course (because of the risk of hypotension).
Fortunately, reserpine is no longer in routine use. Medications can be given by
mouth with a sip of water 1–2 h before ECT. The most important adjunctive
cardioactive agents are discussed below.
The main goals of the use of adjunctive agents are to reduce the risk of myo-
cardial ischemia (a possible result of the increased oxygen demand associated
with tachycardia) and to reduce the risk of systemic hypertension. It should be
kept in mind that (although it seems intuitively obvious that careful control of
heart rate and blood pressure would be beneficial) few data exist comparing
cardiovascular morbidity in ECT done with and without adjunctive antihyper-
tensive agents.
Beta-Blockers
Esmolol
Esmolol is an ultrashort-acting drug (half-life 9 min) that decreases heart rate
but has relatively less effect on blood pressure. Its rapid onset and short dura-
tion of action make it a nearly ideal agent for use in ECT. Typical bolus doses are
10–50 mg, but higher doses are sometimes used (Boere et al., 2014).
Labetalol
Labetalol is a short-acting combined alpha- and beta-blocker (half-life 5 h) that
decreases both heart rate and blood pressure. Typical bolus doses range from 5
to 20 mg. Because its duration of action is longer than that of esmolol, there is
a risk of inducing hypotension in the post-ECT period (Shrestha et al., 2007).
Beta-blockers should be used with caution in patients with asthma, cardiac
conduction delay, or heart failure.
Other Antihypertensives (Calcium Channel

Blockers, Hydralazine, Nitroglycerin)
While far less commonly used than beta-blockers, several other antihyperten-
sive agents have been used effectively in conjunction with ECT at the time of the
procedure. These include calcium channel blockers (e.g., nicardipine), hydrala-

zine, and nitroglycerin.
Nicardepine (Cardene) has replaced sublingual nitrates and, to some extent,
other calcium channel blockers to control blood pressure during ECT because
it can be given IV and titrated more deliberately than sublingual medications
(Zhang et al., 2005). Diltiazem (Cardizem) (Wajima et al., 2001) and verapamil
(Isoptin) (Wajima et al., 2002) are two other calcium channel blockers that are
available in intravenous preparations.
Hydralazine is an older “classic” agent, not commonly used any more, which
works well to reduce blood pressure but may cause tachycardia. Typical doses
are 5–40 mg. Because the average maximal vasodilation occurs after 10–80 min,
hypotension in the post-ECT period could be a risk.
Nitroglycerin is an extremely helpful agent used to decrease the risk of
myocardial ischemia and to reduce blood pressure. It is available as a transder-
mal paste, a sublingual tablet or spray, or an intravenous infusion. While we
previously recommended transdermal or sublingual use before the procedure,
we now limit our recommendations mainly to the use of intravenous nitro-
glycerin to control hypertension in at-risk patients during and shortly after the
procedure. When used intravenously, nitroglycerin provides nearly immedi-
ate lowering of blood pressure and can be titrated for effective blood pressure
control.
Lidocaine
This potent antiarrhythmic is also a potent anticonvulsant and thus is prob-
lematic to use in conjunction with ECT. When serious ectopy or ventricular
arrhythmias appear during or after the seizure, a bolus dose of 50–100 mg may
be given. If possible, to prevent interference with the seizure, the injection of
lidocaine should be delayed until the motor seizure ends. Low doses of lido-
caine are sometimes injected just prior to anesthesia induction, or mixed with
the induction agent (propofol or methohexital), to decrease the pain of the irri-
tating induction agent. It is unclear if this has any significant effect on seizure
duration or quality (MacPherson et al., 2010).
It should be emphasized that decisions about the use of potent cardioac-
tive agents should be made in concert with the anesthesia staff. Exactly which
patients to treat or pretreat remains a matter of clinical judgment and some con-
troversy. Patients with a history of angina or myocardial infarction should be
most carefully assessed, and steps taken to avoid excessive oxygen demand on the
heart. Elderly patients with hypertension may be best treated with small doses of
labetalol or esmolol. The risks of side effects of these drugs (mainly hypotension)
need to be balanced against the potential risks of the treatment itself.
Often, we do not use these agents at the first treatment, preferring merely to
observe whether clinically significant rises in heart rate or blood pressure occur.
If these changes are deemed problematic, medication can be given immediately,
then prophylactic use of antihypertensives can be instituted for subsequent

treatments. This would typically consist of giving 5 or 10 mg IV labetalol, or
20–40 mg of esmolol shortly before the procedure.
Missed, Short, and Prolonged Seizures

The vast majority of ECT seizures last between 20 and 70 s. Some weak evidence
suggests that very short seizures (less than 15–20 s) may be less therapeutic
than longer seizures, particularly if they are elicited by near-threshold stimuli.
Stronger evidence suggests that very long seizures (more than 2–3 min) may be
associated with more cognitive impairment than shorter seizures, particularly if
they are elicited by stimuli far in excess of seizure threshold. Very long seizures
may also be more difficult to terminate.
The issue of how to define seizure length requires comment. Because both
the motor seizure and the EEG seizure are measured, which one to use to deter-
mine seizure length is quite important, albeit arbitrary (Howsepian, 2011). We
will define seizures as follows:
• A missed seizure is one in which no motor activity develops following
delivery of the stimulus.
• A short seizure is one in which the motor manifestations of the seizure last
<15 s.
• A prolonged seizure is one in which motor or EEG seizure activity persists
>180 s. (Note that this definition of prolonged seizure is taken from the
report of the APA Task force on ECT (American Psychiatric Association,
p. 171) but in practice, it is more appropriate to consider any seizure >120
seconds “prolonged.” See section “Prolonged Seizures.”)
Interestingly, we choose the motor seizure to define a short seizure and the
EEG seizure to determine a prolonged seizure. This is a conservative position
because it tends to favor restimulation at the short end of the spectrum and
definitive intervention at the long end of the spectrum. It should be remem-
bered that the EEG seizure typically lasts longer (e.g., 10%–30% longer) than the
motor seizure and that one occasionally sees the development of an EEG seizure
without a motor seizure, but only very rarely a motor seizure without an EEG
seizure (and when this occurs, it is probably due to a technical failure to record
the EEG properly). It is important that the ECT practitioner be prepared to deal
with these three situations.
Missed Seizures
Most missed seizures occur during the stimulus dose titration procedure done
at the first treatment (see section “Stimulus Dosing”). If dose titration is carried
out, and stimuli are appropriately chosen at successive treatments, missed sei-
zures (other than those seen during dose titration) will be uncommon. When
they do occur, it will probably be toward the end of a treatment course in an
elderly patient with a very high seizure threshold or in a patient taking anticon-
vulsants. A missed seizure should prompt a routine sequence of steps. These
steps are discussed below.
Missed Seizure During Dose Titration
See the section “Stimulus Dose Titration.”
Missed Seizure in the Middle of an ECT Course
Follow the steps below, in order.
1. Be sure to observe the patient long enough (approximately 20 s) to
ascertain that a delayed seizure does not occur. (The seizure may be delayed
when the stimulus is just at threshold.)
2. Continue to hyperventilate the patient while checking the printed output
on the ECT device to be sure that the desired stimulus was actually given.
(Premature release of the stimulus delivery button is one cause of missed
seizures in the middle of an ECT course.)
3. Check the electrical connections to the stimulus electrodes for tightness
and continuity. Check the stimulus electrode delivery sites for adequate
preparation, repeating any of the site preparation steps deemed necessary
(see section “Electrode Site Preparation”).
4. After a 20- to 30-s wait, repeat the impedance check, reinsert the bite block,
and restimulate the patient at a higher stimulus intensity. How much higher
will depend on the level of the previous (subconvulsive) stimulus. (Note
that this can be determined by the use of a stimulus dosing algorithm,
examples of which appear in the ECT device manufacturers’ instruction
manuals). If, for example, a patient has a missed seizure at a stimulus dose
of 285 mC, it would be reasonable to restimulate at a 50% higher stimulus,
approximately 425 mC. If this procedure is also ineffective, it is reasonable
to restimulate at the highest setting on the ECT device. If a determination
of a high initial seizure threshold has been made for a given patient, and
that patient reaches the maximum setting on the ECT device through
incremental dosing and then misses a seizure, it is reasonable to give a
period of vigorous hyperventilation and then a second maximal stimulus. If
this second maximal stimulus is also ineffective, we recommend no further
stimuli at that treatment session.
5. If the patient is to have additional treatments, thoroughly review the factors
likely to have contributed to the missed seizure. These factors include
(1) excessive anesthetic dose, (2) concurrent anticonvulsant drug(s), (3)
an older patient late in the course of treatment, and (4) technical factors
(premature release of the stimulus button, poor electrical connections)
unrelated to the patient’s seizure threshold. Appropriate corrective
measures (e.g., lowering the dose of the anesthetic or the anticonvulsant)
can then be carried out before the next treatment.
Short Seizures
Seizures lasting less than 15 s are a fairly common occurrence, particularly late
in the course of treatment of an elderly patient. Short motor seizures are also
more common with the use of ultrabrief stimuli. Because short seizures may
be less effective, it is reasonable to attempt to increase seizure length into the
“acceptable” range. However, some patients may do well despite short seizures, and
in such cases, no technical modifications are required.
A motor seizure of less than 15 s should prompt the following routine steps:
1. Decide whether to restimulate. Restimulation should ordinarily be
attempted, unless there is some unusual overriding concern (e.g.,
development of a cardiovascular complication such as arrhythmia or severe
hypertension) or the patient is doing well clinically and their typical seizure
length is very short.
2. Hyperventilate the patient vigorously for approximately 60 s.
3. Reinsert the bite block, do a repeat impedance check, and restimulate at
an approximately 50% higher stimulus level, or the maximum setting on
the ECT device (if the previous stimulus was in the upper range of the ECT
device).
4. If the patient is to have additional treatments, thoroughly review the factors
likely to have contributed to the short seizure. Most commonly, these are
(1) excessive anesthetic dose, (2) a concurrent anticonvulsant (either a
“true” anticonvulsant, such as phenytoin [Dilantin] or carbamazepine, or
another drug with anticonvulsant properties, such as a benzodiazepine or
lidocaine), (3) lack of good hyperventilation, and (4) inadequate electrical
stimulus dose. Occasionally, a patient will have a short seizure because the
stimulus dose is way above (many multiples of) seizure threshold; in this
case, a paradoxical lowering of the stimulus dose may result in a longer
seizure.
It should be emphasized that some patients (particularly elderly patients near
the end of a course of treatment) have short seizures regardless of modifications
in technique. Most of these patients do very well, and drastic measures to increase
seizure length are clearly unwarranted.
There is evidence that for a given charge, prolonging the stimulus dura-
tion can lead to more efficient seizure elicitation (Sackeim et al., 1994).
Contemporary ECT devices offer several different stimulus program options
that allow for longer stimulus durations. This type of adjustment may be used as
an option when patients have short seizures.
In the past, another strategy commonly used for seizure prolongation was
the intravenous administration of caffeine (available as caffeine sodium benzo-
ate), an adenosine antagonist, 5 min before ECT (Coffey et al., 1987). Cardiac
rate controlling agents may be required with caffeine, and caution must be
exercised when using caffeine in patients with a history of cardiac ischemia or
arrhythmia. The dose of caffeine for this usage ranges from 125 to 2,000 mg,
starting with lower doses and increasing at subsequent treatments as needed.
There is debate over whether caffeine lowers the seizure threshold or prolongs
seizure duration or both (McCall et al. 1993). While some practitioners con-
tinue to use caffeine as an adjunctive medication in ECT, we no longer recom-
mend it, given the uncertainty of the risk–benefit ratio (Pinkhasov et al., 2016).
Prolonged Seizures
Prolonged seizures are of greater concern than short seizures because of their
potential to lead to adverse effects, particularly cognitive impairment. Therefore,
it is crucial to be vigilant for seizures lasting more than 2 or 3 min. The report
of the APA Task Force on ECT states, “a prolonged seizure is one that is longer
than 3 minutes by motor or EEG manifestations. Some practitioners use a more
stringent definition of 2 minutes” (American Psychiatric Association, 2001,
p. 171). We begin to become concerned when a seizure lasts more than 120 s,
and we begin to intervene by 130 s. Seizure prolongation should be determined
by the EEG because the most common occurrence is the continuation of EEG
seizure activity after the motor seizure has ended. Non-convulsive status epi-
lepticus refers to the condition in which the cerebral seizure persists despite the
lack of motor manifestations. Of course, if the motor seizure is also prolonged,
or if for some reason the EEG cannot be recorded or interpreted, the motor
seizure is obviously used to determine seizure prolongation.
Once the decision to terminate a prolonged seizure is made, the following
steps should be taken:
1. Administer an anticonvulsant drug. We recommend giving approximately
50% of the dose of the anesthetic drug when methohexital or propofol have
been used. For example, if a patient had been given 60 mg of methohexital
for induction, now a 30 mg intravenous bolus should be given. An
alternative would be to give an intravenous benzodiazepine (e.g., 1–2 mg
IV lorazepam [Ativan] or midazolam [Versed]).
2. Continue to oxygenate (but not hyperventilate) and carefully monitor the
cardiovascular status of the patient while watching the EEG for cessation of
epileptiform activity.
3. If after 1–2 min the seizure is still ongoing, repeat the medication given
above.
4. Continue pharmacological interventions along with full medical support of
the patient until seizure activity is ended.
A prolonged seizure should prompt a thorough review of the factors likely
to have contributed to its occurrence, including (1) concurrent administration
of a proconvulsant medication (e.g., theophylline), (2) metabolic disturbance
(e.g., hyponatremia), and (3) structural brain disease. It should be remembered
that some young patients have long seizures at the lowest stimulus settings on
the ECT device, particularly in the first several treatments. Such patients may
routinely require administration of additional doses of the anesthetic agent

to end their seizures. Propofol may be a particularly good choice of induction
agent in these patients (Bailine et al., 2003).
Treatment Procedure
Outlined below is a list of steps required for a typical ECT procedure:
(Note that some details of the sequence may need to be modified for the
particular requirements of the ECT device you are using; remember to consult
the instruction manual of your device for details.)
1. Confirm that the patient has had nothing to eat or drink that morning, has
taken the appropriate premedications, and has signed informed consent
(Table 3.2). Then have him or her lie down on the treatment bed.
2. Start the intravenous line. Although it may seem obvious, it cannot be
overstated that a well-functioning intravenous line is the cornerstone
of safe ECT. This does not necessarily suggest that the intravenous line
must be a large-bore catheter attached to an intravenous bag; a small
butterfly or catheter, if carefully inserted and well secured in place, works
just as well. Typical sites are the dorsum of the hand, the forearm, and the
antecubital region. The larger the vein, the less likely it is that the injection
of methohexital or propofol will be painful. For this reason, an antecubital
vein is the preferred site.
3. Attach the blood pressure cuff and the ECG leads.
4. Record vital signs.
5. Place a second blood pressure cuff on the right ankle.
6. Prepare the EEG recording sites and stimulus electrode sites as per the
ECT device instruction manual.
7. Select the electrical stimulus dose on the ECT device (Figures 3.11 and 3.12).
8. Attach the EEG, ECG, and EMG electrodes of the ECT device, following
the sequence recommended by the device manufacturer. Apply stimulus
electrodes if using stick-on type.
9. Tap with a finger on the EEG and EMG electrodes to check that they are
properly connected and that amplifier sensitivity is in the proper range.
You should see a large positive and negative deflection of the tracing on
the computer monitor, with a quiet baseline between taps.
Table 3.2 Pre-ECT orders

NPO after midnight
– Take cardiovascular and anti-gastric reflux medications with sip of water approximately 2
hours before ECT (if prescribed)
– Void just before ECT
Note: NPO = nothing by mouth.
Figure 3.11 The MECTA spECTrum 5000Q. Used with the manufacturer’s permission
Figure 3.12 The Thymatron System IV device. Used with permission from Somatics, LLC
10. Administer anesthetic induction agent intravenously.

11. Apply stimulus electrodes if using handheld type (note that this step
may be delayed until the muscle relaxant has worked, per practitioner
preference).
12. Perform impedance test on the ECT device.
13. Begin assisted ventilation with 100% oxygen.
14. Inflate the blood pressure cuff on the right ankle to above systolic
pressure.
15. Ensure that the patient is unconscious, then administer succinylcholine,
0.75–1.0 mg/kg intravenously.
16. Start nerve stimulator to assess muscular relaxation. Observe for
decrement and eventual disappearance of response.
17. Simultaneously observe for fasciculations. Wait until they subside in the
calves and toes.
18. Insert the bite block, making sure that the tongue is pushed inferiorly and
posteriorly in the mouth, away from the teeth, and that the chin is held
firmly against the bite block.
19. Recheck for proper impedance, confirm positioning of the bite block, and
deliver the electrical stimulus.
20. Remove the bite block and resume ventilation. Observe the motor and the
EEG seizures, noting the duration of both.
21. When the motor seizure ends, deflate the blood pressure cuff on the right
ankle.
22. Allow the patient to awaken in as unstimulating an environment as
possible.
23. Monitor vital signs in the treatment and then recovery areas.
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Chapter ECT Treatment Course
4
Treatment Schedule
Number of Treatments
There is no standard number of ECT treatments in a course, and a patient can-
not be told in advance exactly how many treatments he/she will need to remit.
Most patients will require between 6 and 12 treatments, but some will require as
few as 3 or 4 and some as many as 20. There are reports of rare complete recov-
eries, or resolution of suicidality, after one or two treatments (Fligelman et al.,
2016; Kobeissi et al., 2011; Thomas & Kellner, 2003; Tran et al., 2017).
The patient should be treated until one of the following therapeutic end
points is achieved:
1. Full recovery.
2. A plateau in improvement is reached, and no further gains have been seen
after the last two treatments.
A treatment course should be interrupted in the case of any of the following

events:
1. Unacceptably serious cognitive effects occur.
2. A medical complication occurs that renders further treatment unsafe at the
time.
3. Consent is withdrawn.
4. Additionally, some practitioners suggest that when a bipolar depressed
patient switches into hypomania, a quite rare event (Bailine et al., 2010), the
treatment course be stopped. Others argue that, because ECT also treats
mania, the course should be continued until the patient is euthymic. We
believe continuing the course is appropriate in most situations.
87
88 Chapter 4: ECT Treatment Course
Length of ECT Course by Diagnosis

There are few convincing data showing that a particular diagnosis requires more
or fewer treatments in a course. The exception to this is the evidence that bipolar
depression responds slightly more quickly than unipolar depression (Sienaert
et al., 2009). Some practitioners believe, on the basis of clinical experience, that
patients with schizophrenia require longer treatment courses and also that
some patients with catatonia require prolonged courses for full recovery. In
most cases, application of the previously mentioned two criteria for therapeutic
end points will allow for rational, flexible decision-making about how long to
continue ECT.
Treatment Frequency
Routine practice in the United States is to give ECT three times a week on a
Monday–Wednesday–Friday schedule. This schedule was probably originally
designed around the schedule of the treating physician, but it works very well to
balance good speed of recovery with some between-treatment time for recovery
from side effects (Stromgren, 1990).
Elderly patients, or those for whom there are particular concerns about cog-
nitive adverse effects, may be treated twice a week (e.g., Monday and Friday).
Recovery from depression may be expected to be slower (Lerer et al., 1995). A
twice-a-week ECT schedule is routinely used in the United Kingdom and other
countries.
Some practitioners have suggested that right unilateral ECT, because it
causes less cognitive impairment than bilateral ECT, may be given more fre-
quently than three times a week (four or even five times a week) (Abrams, 1967).
Ultrabrief pulse right unilateral ECT, with its particularly benign cognitive side
effect profile, may provide opportunities for such flexible treatment scheduling
(Rasmussen et al., 2016).
Very seriously ill patients, including those who are severely manic, cata-
tonic, or malnourished, can be given daily bilateral ECT until some evidence of
recovery is seen.
Clinical Monitoring
To be able to make informed decisions about when to stop or continue treat-
ment, close clinical monitoring of the patient is required. This monitoring
should be done by frequent interviews (at a minimum, before each treatment),
paying attention to the patient’s report of mood, energy level, reduction in psy-
chotic symptoms (if present), and memory function. Reports by hospital staff
(for inpatients) or family (for outpatients) of the patient’s behavior and ability to
function are also essential.
Information gathered from patient, staff, and family should be supple-
mented by objective rating scales. Many excellent depression rating scales
are available, including the Hamilton Rating Scale for Depression (HRSD or
Chapter 4: ECT Treatment Course 89
Table 4.1 Strategies to consider if substantial cognitive dysfunction develops

– Switch from bilateral to unilateral electrode placement
– Decrease treatment frequency (from three times weekly to twice or once weekly)
– Decrease stimulus dose or decrease stimulus pulsewidth
– Review concurrent medications for contribution to cognitive dysfunction
“HAM-D”) (Hamilton, 1960) the Montgomery-Asberg Depression Rating Scale

(MADRS) (Montgomery & Asberg, 1979) or Quick Inventory of Depressive
Symptomatology (QIDS) (Rush et al., 2003). Such a scale should be given before
ECT is begun, at least once weekly during the course of ECT, and at the comple-
tion of the ECT course – preferably by the same person – and the score should
be recorded in the patient’s medical record.
Objective measures of cognitive functioning are also important to follow
during a course of ECT. Again, many test instruments are available and accept-
able, including the Mini-Mental State Exam (MMSE) (Folstein et al., 1975) and
the Montreal Cognitive Assessment (MoCA) (Moirand et al., 2018; Nasreddine
et al., 2005). Although they provide only a rough estimate of cognitive function-
ing, such tests have the advantage of being simple and quick to administer. They
should be given before the ECT course is begun; weekly during the course of
ECT (optional), preferably on non-treatment days or in the morning before the
next treatment; and at the completion of the ECT course. Significant declines
should prompt more detailed clinical assessment of the patient and considera-
tion of interrupting the treatment course. If cognitive dysfunction develops,
other strategies may also be helpful (Table 4.1).
It will come as a pleasant surprise to the beginning ECT practitioner that
many patients show improvement, rather than deterioration, in their MMSE
scores, because the cognitive impairments of depression (“depressive pseudo-
dementia”) resolve with ECT (Biedermann et al., 2016).
Continuation/Maintenance ECT
Affective disorders are increasingly recognized as recurrent, lifelong, illnesses.
Decades ago, patients would remit with a course of ECT and remain well for
many years without maintenance therapy; this, unfortunately, is no longer the
case for many patients. The concept of “treatment resistance” has been offered
as an explanation for this phenomenon, but in truth, we do not fully understand
this apparent change in the natural history of mood disorders (Sackeim et al.,
1990). Choices for principal modalities of continuation/maintenance treatment
after acute ECT are medications or ECT, singly or in combination, with adjunc-
tive psychotherapy, when indicated (Wilkinson et al., 2017). Medications may
be given as monotherapy, but more commonly as combinations. When given as
continuation/maintenance therapy after remission of the index episode, med-
ication (either monotherapy or combination therapy) clearly reduces relapse
rates of unipolar depression (Frank et al., 1990; Sackeim et al., 2001). The CORE
continuation ECT versus pharmacotherapy study demonstrated that continua-
tion ECT, given without medications, was as effective in preventing relapse after
successful ECT as the combination pharmacotherapy lithium and nortriptyline
(Kellner et al., 2006). Earlier studies found continuation/maintenance ECT to
reduce hospitalization rates in patients with recurrent mood disorders (Petrides
et al., 1994).
ECT is unique among psychiatric treatments in that it is typically withdrawn
once it has proved effective. The lesson to be learned from the above discussion
is that some type of continuation/maintenance therapy (either medication(s)
or ECT, or both), is necessary after ECT to maximize the chances of sustained
remission. Our practice is to taper most acute ECT courses over a couple of weeks
and then to offer continuation (arbitrarily defined as therapy in the 6-month
period following the index course of ECT) or maintenance (defined as therapy
continuing beyond 6 months after the index course) ECT to patients with a his-
tory of relapse on medication following response to ECT. Continuation or main-
tenance ECT involves single treatments, given at increasing intervals, tailored
to deliver the minimum number of treatments required to maintain remission
(Lisanby et al., 2008; Monroe, 1991).The PRIDE (Prolonging Remission in
Depressed Elderly) study results suggest that continuation ECT with concomi-
tant antidepressant and mood-stabilizing medications, followed by additional
continuation/maintenance ECT when needed, can help further reduce relapse
rates (Kellner et al., 2016).
Frequency of Treatments/Electrode Placement

There is no single continuation/maintenance ECT schedule that is applica-
ble to all patients; some degree of individualization and clinical judgment is
required. The acute course (3×/week) can be followed by a taper to 2×/week,
then weekly for several weeks. The interval between treatments can then be
gradually extended, the goal being to determine the maximal interval that
results in maintenance of full remission. Most patients will end up on a schedule
of a single treatment every 3–6 weeks, although some will require more frequent
treatment.
The electrode placement used in continuation/maintenance ECT is almost
always that which was used in the index course of ECT, although an argument
could be made for the use of bilateral electrode placement because single treat-
ments at long intervals are not expected to cause significant cognitive impair-
ment, and, theoretically, might be more protective (Kellner et al., 1991).
Inpatient Versus Outpatient Treatment

Most maintenance ECT patients can be treated as outpatients; however, an over-
night stay in the hospital is required in some circumstances. These instances include
the patient who cannot reliably avoid taking anything by mouth before treatment
and the patient who requires close medical management before or after ECT.
For a full review of issues related to ambulatory ECT, the reader should con-
sult a task force report on ambulatory ECT (Fink et al., 1996).
Monitoring During Maintenance ECT

The patient’s medical status should be followed closely during maintenance
ECT. Laboratory data (e.g., electrolytes and ECG) should be obtained at appro-
priate intervals. Cognitive status and depressive symptoms should be followed
and rated.
Continuation or Maintenance ECT End Point

After 6–12 months of successful continuation or maintenance ECT, the treat-
ment plan can be reassessed, in discussion with the patient, family, and other
healthcare providers. A risk–benefit analysis should be carried out, weighing
the risks of relapse against the risks of continuing ECT, versus switching to other
modalities (medications and psychotherapy). Some patients with severe and
highly recurrent illness will require maintenance ECT for extended periods,
and sometimes indefinitely.
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Frank, E., Kupfer, D. J., Perel, J. M., Cornes, C., Jarrett, D. B., Mallinger, A. G., . . .
Grochocinski, V. J. (1990). Three-year outcomes for maintenance therapies in
recurrent depression. Arch Gen Psychiatry, 47(12), 1093–1099.
Hamilton, M. (1960). A rating scale for depression. J Neurol Neurosurg Psychiatry, 23,
56–62.
Kellner, C. H., Burns, C. M., Bernstein, H. J., & Monroe, R. R., Jr. (1991). Electrode
placement in maintenance electroconvulsive therapy. Convuls Ther, 7(1), 61–62.
V., . . . Group, C. P. W. (2016). A novel strategy for continuation ECT in geriatric
doi:10.1176/appi.ajp.2016.16010118
Gen Psychiatry, 63(12), 1337–1344. doi:10.1001/archpsyc.63.12.1337
Kobeissi, J., Aloysi, A., Tobias, K., Popeo, D., & Kellner, C. H. (2011). Resolution of
severe suicidality with a single electroconvulsive therapy. J ECT, 27(1), 86–88.
doi:10.1097/YCT.0b013e3181da842a
Lerer, B., Shapira, B., Calev, A., Tubi, N., Drexler, H., Kindler, S., . . . Schwartz, J. E.
(1995). Antidepressant and cognitive effects of twice- versus three-times-weekly
ECT. Am J Psychiatry, 152(4), 564–570. doi:10.1176/ajp.152.4.564
Lisanby, S. H., Sampson, S., Husain, M. M., Petrides, G., Knapp, R. G., McCall, W. V., . . .
Kellner, C. H. (2008). Toward individualized post-electroconvulsive therapy care:
piloting the Symptom-Titrated, Algorithm-Based Longitudinal ECT (STABLE)
intervention. J ECT, 24(3), 179–182. doi:10.1097/YCT.0b013e318185fa6b
Moirand, R., Galvao, F., Lecompte, M., Poulet, E., Haesebaert, F., & Brunelin, J. (2018).
Usefulness of the Montreal Cognitive Assessment (MoCA) to monitor cognitive
impairments in depressed patients receiving electroconvulsive therapy. Psychiatry
Res, 259, 476–481. doi:10.1016/j.psychres.2017.11.022
Monroe, R. R., Jr. (1991). Maintenance electroconvulsive therapy. Psychiatr Clin North
Am, 14(4), 947–960.
Montgomery, S. A., & Asberg, M. (1979). A new depression scale designed to be
sensitive to change. Br J Psychiatry, 134, 382–389.
Nasreddine, Z. S., Phillips, N. A., Bedirian, V., Charbonneau, S., Whitehead, V., Collin,
I., . . . Chertkow, H. (2005). The Montreal Cognitive Assessment, MoCA: a brief
screening tool for mild cognitive impairment. J Am Geriatr Soc, 53(4), 695–699.
doi:10.1111/j.1532-5415.2005.53221.x
Petrides, G., Dhossche, D., Fink, M., & Francis, A. (1994). Continuation ECT: relapse
prevention in affective disorders. Convuls Ther, 10(3), 189–194.
Rasmussen, K. G., Johnson, E. K., Kung, S., Farrow, S. L., Brown, S. K., Govrik, M.
N., & Citronowicz, R. I. (2016). An open-label, pilot study of daily right unilateral
ultrabrief pulse electroconvulsive therapy. J ECT, 32(1), 33–37. doi:10.1097/
YCT.0000000000000261
Rush, A. J., Trivedi, M. H., Ibrahim, H. M., Carmody, T. J., Arnow, B., Klein, D. N., . . .
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The impact of medication resistance and continuation pharmacotherapy on
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Stromgren, L. S. (1990). Frequency of ECT treatments. Convuls Ther, 6(4), 317–318.
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33(1), 52–57. doi:10.1097/YCT.0000000000000348
Chapter Common Adverse Effects
5
Cognition
The most talked-about effect of ECT is memory loss. In fact, ECT typically
causes predictable, largely temporary, memory loss and other cognitive effects
that are generally not serious and are very acceptable, given the substantial relief
from severe depression that most patients can expect from ECT (Semkovska &
McLoughlin, 2010). Modern ECT techniques have markedly reduced the effects
on memory for most patients (Kellner & Farber, 2016).
An older, detailed review of the effects of ECT on memory function can be
found in the Annals of the New York Academy of Sciences (Squire, 1986). A more
recent, comprehensive reference is the special issue of the Journal of ECT on
cognition (Loo, 2008).
Most recently, Kellner and Farber, in an editorial in Acta Psychiatrica
Scandinavica (Kellner & Farber, 2016), sought to contextualize the issue of
cognitive adverse effects of ECT, weighed against the risks of depressive or
psychotic illness. We wrote:
We believe that the adverse cognitive effects of ECT should be considered a
tolerability and not a safety issue. In medicine, safety refers to the risk of physical
injury or death. To elevate cognitive adverse effects to this level perpetuates
the stigma surrounding ECT. In medicine, treatment decisions always involve
a risk–benefit calculation. The risks of the condition are weighed against the
risks of the treatment or no treatment. It is imperative that the dangers of mood
disorders are understood when considering the side-effect profile of ECT or
any other antidepressant treatment. Depression can result in disability and
exacerbation of medical comorbidities. In rare cases, depressive loss of appetite
may lead to serious medical consequences; catatonia, a complication of mood
disorder, may be a life-threatening medical emergency. Moreover, untreated or
inadequately treated depression may be lethal due to suicide.
The most apt analogy to properly contextualize the seriousness
of depressive illness weighed against the risks of ECT is cancer and
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96 Chapter 5: Common Adverse Effects
chemotherapy. Many cancers are lethal, life-threatening illnesses for which

treatments (surgery, chemotherapy, and radiation) carry considerable risks.
Patients rarely categorically refuse cancer treatments because of concerns
about adverse effects, yet this happens frequently with ECT. Our contention
is that refusing ECT because of concerns about memory loss is equivalent
to refusing cancer chemotherapy because of concerns about hair loss. These
effects are unpleasant and upsetting, but not worth risking one’s life over. Just
as the side-effects of chemotherapy abate, so too do those of ECT; most of the
hair grows back, most of the memories return, and the patient’s life is saved.
Practitioners are charged with providing their patients the safest, most
tolerable, and effective treatments. For ECT, this means using the most
appropriate technique (optimizing electrode placement, stimulus dosing, and
anesthesia technique) and fully informing patients about treatment options
and potential risks. It can be explained to patients that convalescence from a
serious episode of depression, as well as from the effects of the treatment, will
take time and patience. Most patients will have been sick in their depressive
episode for a very long time; full recovery will take some time as well.
For our purposes, we can summarize ECT’s effects on memory and cogni-
tion as follows:
ECT affects memory/cognition in three ways. It causes
1. an acute postictal confusional state,
2. anterograde memory dysfunction (AMD), and
3. retrograde memory dysfunction (RMD).
Postictal Confusional State

All patients have some degree of confusion and disorientation immediately
following ECT. This side effect is more pronounced with bilateral ECT than
with right unilateral ECT, and it may be more prolonged in elderly patients.
Generally, within a very few minutes of awakening, patients are able to follow
simple commands and then begin to speak. Initial disorientation and confu-
sion generally subside within 10–20 min and typically are resolved within an
hour. With ultrabrief pulse right unilateral ECT, reorientation may occur in sev-
eral minutes. Some data suggest that longer disorientation on awakening from
the first treatment may be a predictor of greater retrograde amnesia from the
entire acute ECT course, although this is not well confirmed (Sobin et al., 1995).
Patients must be carefully supervised and monitored by nursing staff during
the immediate post-ECT period. A quiet, low-stimulus environment is optimal.
Postictal Agitation
Approximately 10% of patients will develop marked agitation and restlessness
immediately postictally (“emergence delirium”) (Abrams, 2002). This is usu-
ally easily managed with a short-acting, rapid-onset benzodiazepine such as
Chapter 5: Common Adverse Effects 97
midazolam (typically 2 mg, range: 1–4 mg) administered intravenously. If a

patient has become agitated at a previous treatment session, at the next ses-
sion, to prevent the development of agitation, the benzodiazepine may be given
as soon as spontaneous respirations resume following the treatment. Patients
should be monitored for continuation of spontaneous respirations following
administration of benzodiazepines in this setting. Another strategy for the
management of postictal agitation is switching to propofol as the induction
agent, or giving small boluses of propofol on emergence (Tzabazis et al., 2013).
Recently, several authors have reported the successful use of dexmedetomidine,
a selective alpha-2 adrenoceptor agonist with sedative effects, for prevention of
postictal agitation (Aksay et al., 2017; Bryson et al., 2013; O’Brien et al., 2010).
It is given via infusion pump, one protocol suggesting a dose of approximately
1 µg/kg, infused over 10 min immediately after seizure termination, but other
dosing strategies may also be effective. Blood pressure needs to be monitored
carefully when using dexmedetomidine. Pretreatment with sublingual olanzap-
ine (5–10 mg, given 30–45 minutes before treatment) has also been reported to
reduce postictal agitation (Hermida et al., 2016).
Finally, the behavioral measure of placing the recovery stretcher in the
Trendelenberg position (“gravitational restraint”) may be helpful in the man-
agement of the agitated patient (O’Brien et al., 2010).
Anterograde Memory Dysfunction

AMD refers to the impaired ability to record new memories after receiving ECT.
It can be thought of as disruption of current memory function. Usually this
amnesia involves patients’ inability to remember things that they have done or
were told on the days of, or following, ECT. AMD is worst immediately after
ECT and subsides within days or a few weeks. AMD is more severe after a course
of bilateral ECT than a course of right unilateral ECT (and probably less severe
with ultrabrief pulse than brief pulse right unilateral) and is more severe after a
course of ECT (either type) than after a single maintenance treatment.
Retrograde Memory Dysfunction

RMD refers to the forgetting of memories from the pre-ECT period. Because
our memories are precious to us and central to our sense of self and individu-
ality, this particular memory effect of ECT is of greatest concern to patients.
Fortunately, RMD is usually limited to the weeks or few months before the start
of ECT. The principle of last-in, first-out applies; that is, memories recorded
most proximally to the start of ECT are most vulnerable to being lost, and
memories recorded in the more remote past are less vulnerable. We make it a
practice to tell patients to expect that they will have little recollection of events
during the weeks of their ECT course and they may have spotty memory loss for
the 3–6 months or so before that. It must be emphasized that there is tremen-
dous variability in this regard: most patients report that the amount of memory
loss is acceptable, given the benefit of recovery from severe depression, and
that as more time elapses, they are less bothered by any residual memory gaps.
We encourage family members to remind patients repeatedly of events that
occurred in the pre-ECT interval so that any gaps can be filled in. Occasionally,
patients report that they do not want to be reminded of events from the period
during which they were severely depressed. This behavior should not be con-
fused with the erroneous notion that ECT works by causing patients to forget
how depressed they were.
Occasionally, reports appear of persistent, severe memory loss after ECT
(Donahue, 2000). Such reports are often sensationalized by the media and anti-
psychiatry groups. Adverse cognitive outcomes are much less likely in contem-
porary practice, with modern ECT techniques, than they were in the distant past.
Headache, Muscle Aches, and Nausea

Headache
A substantial proportion of patients report headache following ECT. This side
effect may be related to the contraction of the temporalis and masseter mus-
cles or to the cerebral hemodynamic changes that accompany the treatment.
Although the exact etiology of the headache is unclear, it is typically transient
and responds well to acetaminophen, ibuprofen, aspirin, or other nonsteroidal
anti-inflammatory agents. Rarely, triptans or opiates may be required
(Markowitz et al., 2001).
A common treatment strategy is the administration of 15–30 mg intrave-
nous ketorolac (Toradol) just before the ECT procedure. Generally, this is not
done at the first treatment; rather, if the patient reports a significant headache
after the first treatment, ketorolac may be offered before subsequent treatments.
Another preemptive analgesia strategy is to give either ibuprofen or acetami-
nophen po, about 2 h before ECT (Isuru et al., 2017; Leung et al., 2003).
Muscle Aches
Diffuse myalgias are most commonly seen after the first ECT session and then
subside following subsequent treatments. This symptom is likely due to muscle
fasciculations from succinylcholine. Typically, the myalgias are transient and
respond well to the same symptomatic treatment used for headaches. If myal-
gias persist after subsequent treatments and the patient’s muscular block is ade-
quate, the practitioner should consider a small reduction in the succinylcholine
dose or, in rare situations, blocking fasciculations by pretreatment with a small
dose of a nondepolarizing muscle relaxant.
Nausea
A minority of patients are nauseated after ECT. This side effect may be related
to the anesthetic, the seizure itself, or air in the stomach from assisted ventila-
tion. When it is a regular occurrence, nausea may be treated with intravenous
Chapter 5: Common Adverse Effects 99
ondansetron (Zofran) (typically 4 mg, range 4–8 mg), given shortly before the
procedure. Ondansetron may also be given IV or po after the treatment for
persistent nausea. Drinking a carbonated beverage, such as ginger ale, in the
recovery period, is also often helpful.
References
University Press.
Aksay, S. S., Bumb, J. M., Remennik, D., Thiel, M., Kranaster, L., Sartorius, A., & Janke,
C. (2017). Dexmedetomidine for the management of postictal agitation after
electroconvulsive therapy with S-ketamine anesthesia. Neuropsychiatr Dis Treat, 13,
1389–1394. doi:10.2147/NDT.S134751
Bryson, E. O., Briggs, M. C., Pasculli, R. M., & Kellner, C. H. (2013). Treatment-
resistant postictal agitation after electroconvulsive therapy (ECT) controlled with
dexmedetomidine. J ECT, 29(2), e18. doi:10.1097/YCT.0b013e3182717610
Donahue, A. B. (2000). Electroconvulsive therapy and memory loss: a personal
journey. J ECT, 16(2), 133–143.
Hermida, A. P., Janjua, A. U., Tang, Y., Syre, S. R., Job, G., & McDonald, W. M. (2016).
Use of orally disintegrating olanzapine during electroconvulsive therapy for
prevention of postictal agitation. J Psychiatr Pract, 22(6), 459–462. doi:10.1097/
PRA.0000000000000185
Isuru, A., Rodrigo, A., Wijesinghe, C., Ediriweera, D., Premadasa, S., Wijesekara, C., &
Kuruppuarachchi, L. (2017). A randomized, double-blind, placebo-controlled trial
on the role of preemptive analgesia with acetaminophen [paracetamol] in reducing
headache following electroconvulsive therapy [ECT]. BMC Psychiatry, 17(1), 275.
doi:10.1186/s12888-017-1444-6
Kellner, C. H., & Farber, K. G. (2016). Electroconvulsive therapy and cognition: a
salutary reappraisal. Acta Psychiatr Scand, 134(6), 459–460. doi:10.1111/acps.12658
Leung, M., Hollander, Y., & Brown, G. R. (2003). Pretreatment with ibuprofen to
prevent electroconvulsive therapy-induced headache. J Clin Psychiatry, 64(5),
551–553.
Loo, C. (2008). Cognitive outcomes in electroconvulsive therapy: optimizing current
clinical practice and researching future strategies. J ECT, 24(1), 1–2. doi:10.1097/
YCT.0b013e318165dccb
Markowitz, J. S., Kellner, C. H., DeVane, C. L., Beale, M. D., Folk, J., Burns, C., &
Liston, H. L. (2001). Intranasal sumatriptan in post-ECT headache: results of an
open-label trial. J ECT, 17(4), 280–283.
O’Brien, E. M., Rosenquist, P. B., Kimball, J. N., Minor, L. N., & Arias, L. M. (2010). A
novel positioning technique for the agitated patient after electroconvulsive therapy:
gravitational restraint. J ECT, 26(3), 158. doi:10.1097/YCT.0b013e3181ec0d75
O’Brien, E. M., Rosenquist, P. B., Kimball, J. N., Dunn, G. N., Smith, B., & Arias, L. M.
(2010). Dexmedetomidine and the successful management of electroconvulsive
therapy postictal agitation: a case report. J ECT, 26(2), 131–133. doi:10.1097/
YCT.0b013e3181b07c26
Semkovska, M., & McLoughlin, D. M. (2010). Objective cognitive performance

associated with electroconvulsive therapy for depression: a systematic review and
meta-analysis. Biol Psychiatry, 68(6), 568–577. doi:10.1016/j.biopsych.2010.06.009
Sobin, C., Sackeim, H. A., Prudic, J., Devanand, D. P., Moody, B. J., & McElhiney, M. C.
(1995). Predictors of retrograde amnesia following ECT. Am J Psychiatry, 152(7),
995–1001. doi:10.1176/ajp.152.7.995
Squire, L. R. (1986). Memory functions as affected by electroconvulsive therapy. Ann N
Y Acad Sci, 462, 307–314.
Tzabazis, A., Schmitt, H. J., Ihmsen, H., Schmidtlein, M., Zimmermann, R.,
Wielopolski, J., & Munster, T. (2013). Postictal agitation after electroconvulsive
therapy: incidence, severity, and propofol as a treatment option. J ECT, 29(3),
189–195. doi:10.1097/YCT.0b013e3182887b5b
Chapter The ECT Service
6
Staffing and Administration
The ECT staff consists of a multidisciplinary team working together to provide
optimal patient care. The ECT-trained psychiatrist leads the team, working in a
collaborative relationship with anesthesia and nursing personnel.
Perhaps the most important issue in ECT-related patient care is the quality
of the working relationship between psychiatrist and anesthetist. The develop-
ment of a mutually respectful, trusting relationship is as important as a good
intravenous line! Such a relationship takes some time to develop and is facili-
tated by having only a few anesthesia personnel rotate through the treatment
suite and by reaching agreement regarding consistency of the anesthetic plan
among all staff members.
Nursing staff play a key role in the delivery of ECT. Depending on how a
particular ECT service is staffed and organized, nursing roles may include both
administrative and direct clinical care responsibilities. One designated nurse
should be in charge of all nursing issues related to ECT. She or he should super-
vise the other recovery or treatment area nurse(s) and see to it that the specific
nursing functions of the treatment procedure are carried out. These include
performing the “time out” patient and procedure recognition process (where
mandated), recording of vital signs and medications given, and insertion of
the bite block (unless the insertion of the bite block is the responsibility of the
anesthesiologist, as it is in many ECT services). Other nursing functions may
include other medical record keeping, patient education, and clinical assess-
ment, as well as responsibility for maintaining equipment and supplies in the
treatment room.
As the leader of the treatment team, the psychiatrist is responsible for main-
taining the medical standards and professional atmosphere of the ECT suite. To
this end, he or she should feel comfortable in politely reminding his or her col-
leagues that voices should be kept low and that there is no place for discussion of
other “interesting cases” within earshot of patients. At all times, the overriding
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principle should be that patients will be treated in the way we would want to be
treated were we in their situation.
The ECT Suite

Ideally, ECT should be done in a suite of rooms specially designed to provide
separate treatment, recovery, and waiting areas. Adequate space should be avail-
able to provide privacy for patients and a calm, quiet environment for post-
treatment recovery. Waiting areas for family members should be nearby and
hospitable. The experience of having ECT should be similar to a visit to a well-
run private internist’s or dentist’s office.
The location of the ECT suite is also very important. There is no absolute
need to do ECT in an expensive operating room or general post-anesthesia
recovery area. Such areas tend to be busy, hectic, public, and potentially fright-
ening to patients. A location on the psychiatry unit or a separate area in an out-
patient surgery facility is preferable. In some instances, consideration should be
given to treating a severely medically ill patient in the hospital operating room
or main recovery room suite, for optimum access to emergency equipment and
medical staff.
The equipment necessary for an ECT suite, well described in the report of
the American Psychiatric Association (APA) Task Force on ECT (American
Psychiatric Association, 2001, pp. 121–122) includes the following:
• Suction and oxygen are needed in both treatment and recovery areas.
• An anesthesia device, although preferred by many, is not necessary,
and wall oxygen with disposable breathing circuits and masks is fully
satisfactory.
• Pulse oximeters should be available for both treatment and recovery areas.
• An ECG/automatic blood pressure monitor should be located in the
treatment room.
• A nerve stimulator should be available.
• A fully stocked drug and emergency equipment cabinet should be at hand
in the treatment room, and responsibility for deciding on which drugs to
include should be shared by the psychiatric and anesthesia staff. Restocking
of supplies is usually the responsibility of the nursing staff.
• Finally, the ECT device, with all necessary supplies (including a copy of the
instruction manual for quick reference) should be located on a countertop
or a cart near the treatment stretcher.
Record Keeping
Documentation of the ECT evaluation and treatment process is essential for
good patient care and for medicolegal purposes. The two primary records to be
kept are the patient’s medical record and the ECT service’s record.
Chapter 6: The ECT Service 103
The Medical Record

The patient’s medical record should contain the ECT consultation sheet, detail-
ing the indications for treatment, pertinent medical issues, and recommenda-
tions about consent. All the required pre-ECT workup should be in the medical
record, as well as the completed consent form. There should be a procedure note
for each ECT treatment. This note should include doses of treatment medica-
tions, electrode placement, treatment number, stimulus parameters and dose,
motor and EEG seizure durations, and any complications noted and their man-
agement. The anesthesia staff and the recovery nursing staff should also include
appropriate documentation of the patient’s clinical status during treatment and
recovery, including serial vital signs. The ECT team’s appraisal of the patient’s
clinical status and the plan for ongoing management should be included in the
chart at least once a week during the ECT course.
The ECT Service’s Record

The ECT service may maintain a separate record of the pre-ECT evaluation,
procedure parameters, clinical response and/or complications, and recommen-
dations for continuation therapy. Such separate ECT records facilitate retrieval
of ECT information that may be needed for future patient care, for transmit-
tal to other hospital facilities, or for monitoring trends in ECT practice. As
electronic medical records become the norm, it is likely that both clinical and
research ECT databases will be fully computerized in the near future.
Reference
American Psychiatric Association. Committee on Electroconvulsive Therapy., &
Chapter Special Issues
7
Stigma
Stigma remains the biggest impediment to the acceptance of ECT. The burden
of the abuses of the past, irrational fears of the electrical stimulus, and exagger-
ated concerns about memory loss all contribute to the stigma surrounding ECT.
An example of how destructive this stigma can be is the despicable discrediting
of 1972 vice-presidential candidate Thomas Eagleton, when his history of ECT
treatment was revealed. Fortunately, courageous efforts to counter stigma also
exist; one example is television personality Dick Cavett’s disclosure that ECT
effectively reversed his serious depression. In recent years, many patients have
spoken and written courageously about their positive experiences with ECT
(Dukakis & Tye, 2006; Hersh, 2010; Manning, 1994).
Perhaps the best way to counter the stigma surrounding ECT is to educate
ourselves well and to insist on high standards in the performance of ECT. We
hope that this book is helpful in achieving those goals.
Patient-Centered ECT
An innovative clinical practice gaining popularity in the United States is to allow
a family member to be present in the ECT suite during the patient’s treatment
(Coffey & Coffey, 2016; Evans & Staudenmeier, 2005) This practice requires the
agreement of all the professionals on the ECT healthcare team; the ECT psy-
chiatrist should take the lead in explaining the benefits to other members of the
team. While still uncommon in most of clinical medicine, ObGyn physicians
have allowed fathers to be present in the delivery room for several decades; for
ECT, such a model of family involvement can be comforting for the patient and
serve to demystify and destigmatize the treatment process. While not appro-
priate in all situations, if the patient wishes it, a selected family member can be
invited to stay in the room during the treatment. The family member should
be briefed in advance about what to expect, and informed that in the very rare
case of an emergency, might be asked to leave the room. Feedback from family
members who have observed ECT is typically very positive; most observers are
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surprised at how uncomplicated and routine ECT appears, and are comforted
to know exactly what is happening to their family member.
Malpractice Litigation and Insurance

Because of the safety of the procedure, ECT generates remarkably little in the
way of malpractice litigation. This topic has been very well covered by Richard
Abrams in his textbook (Abrams, 2002). He provides a list of commonsense
rules of good medical practice that will help reduce the (already low) risk of
malpractice litigation.
In recent years, there have been several instances of the elimination of
insurance surcharges for ECT because of the absence of successful suits. When
these surcharges were challenged, it was demonstrated that, in fact, ECT did not
contribute to higher malpractice insurance costs.
Research
The extensive ECT literature attests to an 80-year history of productive clinical
and basic science research in ECT. We know a tremendous amount about many
aspects of ECT (Fink, 2011; Loo et al., 2006; Sienaert, 2011); see also the special
issue of The Journal of ECT on mechanisms of action (JECT, 2014). Indeed, there
are over 15,000 citations on PubMed about ECT; these are being added to at a
rate of about 5 per week. However, we need to know much more, both about the
way ECT works and about how to further improve its tolerability.
Important areas of ongoing research include the following:
• Mechanism(s) of action (please see Chapter 1 for review of exciting new
developments in neuroimaging research), through both basic and clinical
research
• Prediction of responders to right unilateral versus bilateral electrode
placement
• Adjunctive drugs to further decrease adverse cognitive effects
• Further determination of optimal stimulus parameters
• Safety of specific ECT–drug combinations in specific patient populations
• Further refinement of continuation/maintenance ECT and medication
protocols after acute ECT
• Neuropsychiatric indications for ECT, including Parkinson’s disease and
self-injurious behavior in autism
References
University Press.
Coffey, M. J., & Coffey, C. E. (2016). Patient-centered electroconvulsive therapy care: a
call to action. J ECT, 32(2), 78–79. doi:10.1097/YCT.0000000000000266
Chapter 7: Special Issues 107
Dukakis, K., & Tye, L. (2006). Shock: the healing power of electroconvulsive therapy. New
York: Avery.
Evans, G. E., & Staudenmeier, J. J. (2005). Family member presence during
electroconvulsive therapy: patient rights versus medical culture. J ECT, 21(1),
48–50.
Fink, M. (2011). Electroconvulsive therapy resurrected: its successes and promises after
75 years. Can J Psychiatry, 56(1), 3–4. doi:10.1177/070674371105600102
Hersh, J. K. (2010). Struck by living: from depression to hope. Dallas, TX: Brown Books
Publishing Group.
JECT. (2014). The Journal of ECT [Special Issue]. J ECT, 30(2).
Loo, C. K., Schweitzer, I., & Pratt, C. (2006). Recent advances in optimizing
electroconvulsive therapy. Aust N Z J Psychiatry, 40(8), 632–638. doi:10.1080/
j.1440-1614.2006.01862.x
Manning, M. (1994). Undercurrents: a therapist’s reckoning with her own depression
(1st edn). New York, NY: HarperCollins Pub.
Sienaert, P. (2011). What we have learned about electroconvulsive therapy and
its relevance for the practising psychiatrist. Can J Psychiatry, 56(1), 5–12.
doi:10.1177/070674371105600103
Index
ACT. See Association for Convulsive antiarrythmics, 35

Therapy (ACT) antiasthmatics, 35
ACTH. See adrenocorticotropic anticholinergic agent, 71
hormone (ACTH) anticholinergics, 28, 30, 71
acute-phase ECT, 35 anticoagulants, 36
additional treatments, 76, 77 anticonvulsant effect, 7
adolescents, 21, 55, 69 anticonvulsant theory, 7
adrenocorticotropic hormone (ACTH), 6 anticonvulsants, 6, 7, 24, 29, 34, 35, 55,
advantages, 49, 51, 69 68, 69, 74, 76, 77, 78
adverse effects, 25, 32, 69, 78, 88, 95, 96 antidepressants, 1, 2, 3, 5, 6, 7, 9, 31, 32,
adverse events, 37 35, 55, 56, 69, 90, 95
affect restricted, 24 antihypertensive agents, 29, 61, 73
affective features, 20 antihypertensives, 29, 30, 36, 73, 75
age, 24, 54, 55, 56, 57 antipsychotic effects, 5, 20, 34
age-based dosing, 54, 55 antipsychotics, 31, 34
agitation, 20, 28, 49, 69, 96 anxiety, 24, 33, 67
airway, 70, 71, 72 APA Task Force on Electroconvulsive
airway management, 70, 72 Therapy, 3
airway secretions, 71 apnea, 36, 68
alcohol, 24 appropriate dose, 56
alfentanil, 68, 69 arousal, 10
algorithms, 54, 76 arrhythmias, 30, 73, 74
allergies, 23 artifact, 58, 62, 66, 67
AMD. See anterograde memory aspiration, 31, 72
dysfunction (AMD) assessment, 23, 25, 67, 89, 101
amygdala, 4 Association for Convulsive Therapy
analgesics, 70 (ACT), 2
anatomical factors, 52, 58, 66 asthma, 27, 30, 73
anesthesia, 3, 9, 10, 22, 23, 24, 26, 33, 34, asystole, 10
35, 50, 55, 61, 67, 69, 71, 72, 74, 96, Ativan, 78
101, 102, 103 atropine, 30, 71
anesthetic agents, 79 auditory meatus, 51
anesthetics, 67, 68 augmentation, 69
aneurysm, 27 autism, 21, 106
angina, 74 availability, 3, 5, 30
animal studies, 4, 5 awakening, 31, 96
ankle, 54, 70, 79, 80, 81
antecubital vein, 79 barbiturates, 68
anterograde memory dysfunction basal ganglia, 4
(AMD), 96, 97 basics of the treatment, 1
antianginals, 36 Beck Depression Inventory, 25
antiarrhythmics, 30, 36, 73 benefits, 21, 23, 26, 28, 105
109
110 Index
benzodiazepine, 33, 34, 35, 77, 78, 96, 97 Cardizem, 74

beta-blockers, 29, 30, 73 carotid artery, 58
bifrontal ECT, 51 Carroll Rating Scale for Depression, 25
bifrontal electrode placement, 53 catatonia, 2, 19, 20, 21, 49, 50, 88, 95
bilateral ECT, 20, 49, 50, 51, 52, 59, 88, central nervous system, 9, 27
96, 97 cerebral neurons, 9
bilateral electrode placement, 50, 51, 53, cerebrospinal fluid, 5, 7
57, 90 charge, 7, 8, 52, 54, 55, 77, 101
bipolar patients, 4, 19, 20, 28, 87, 88 chemotherapy, 96
bite block, 54, 71, 72, 76, 77, 80, 81, 101 childhood, 24
bladder, 35, 73 children, 21, 69
bleeding, 27, 29 chin, 72, 80
blood flow, 10, 28 cholinesterase inhibitor, 36
blood oxygen saturation, 61 chronic obstructive pulmonary disease,
blood pressure, 10, 29, 59, 61, 62, 70, 71, 27
73, 74, 79, 80, 81, 102 cigarettes, 24
blood volume, 10 cisatracurium, 70
blood–brain barrier, 5, 10, 32, 71 classical monoamine depletion theory,
bolus, 68, 70, 73, 74, 78 5
bradyarrhythmia, 30 clinical monitoring, 88
bradycardia, 10, 30, 71 clonic motor phase, 9
brain, 3, 4, 5, 7, 8, 9, 10, 24, 26, 28, 32, cognitive assessments, 25
71, 78 cognitive dysfunction, 89
brain disease, 26, 78 cognitive effects, 4, 5, 6, 9, 25, 37, 51, 55,
brain electrical activity, 26 56, 57, 87, 95, 106
brain herniation, 28 cognitive functioning, 25, 28, 89
brain tumor, 28, 29 cognitive impairment, 7, 25, 50, 51, 53,
breathing, 62, 102 56, 75, 78, 88, 90
brief pulse stimuli, 7, 56 cognitive risks, 23
bronchodilators, 30, 36 combination therapy, 20
burns, 68, 71 comfort, 1, 67
comorbidities, 95
caffeine, 77 complete blood count, 26
calcium channel blockers, 73, 74 complications, 22, 29, 37, 50, 77, 87, 95,
calves, 80 103
cancer, 95 concurrent medications, 31
canthus, 51, 52 conduction, 61, 71, 73
carbamazepine, 77 confusion, 50, 68, 96
Cardene, 74 connection, 61
cardiac arrhythmia, 27, 69 connectivity theory, 7
cardiac disease, 29 Consortium for Research in
cardiac enzymes, 10 Electroconvulsive Therapy (CORE),
cardiac function, 27 51, 89
cardiac repolarization, 10 constant-current, 8, 54
cardioactive agents, 73, 74 consultation, 1, 21, 22, 23, 24, 26, 29, 31,
cardiovascular agents, 30, 73 37, 103
cardiovascular depression, 68 consultation note, 21, 23
cardiovascular disease, 29 continuation, 20, 35, 89, 90, 91
cardiovascular medications, 30, 35 continuation treatment, 2, 6, 21, 25, 35,
cardiovascular system, 9, 10, 32, 61, 68, 37, 78, 89, 90, 91, 97, 103, 106
73, 77, 78, 79 controversy, 3, 49, 62, 74
Index 111
CORE. See Consortium for Research in duration, 4, 7, 22, 28, 33, 54, 56, 68, 69,
Electroconvulsive Therapy (CORE) 70, 73, 74, 81
coronary artery disease, 27 dyskinesias, 28
cortical structures, 4, 6 dysrhythmias, 10
crying, 24
CT, 24, 26 ear, 58
cuff technique, 70 ECG, 10, 26, 60, 61, 62, 66, 79, 91, 102
cuffed-limb method, 31 echothiophate, 36
current density, 5, 9 ECS. See electroconvulsive shock (ECS)
current flow, 61 ECT
cerebral physiology of, 9
d’Elia placement, 52, 53 Consultation, 21, 23
DBS. See deep brain stimulation (DBS) course, 9, 24, 33, 56, 73, 76, 89, 96, 97,
death, 35, 95 103
deep brain stimulation (DBS), 21 device, 7, 8, 37, 54, 55, 56, 57, 58, 59,
delirium, 28, 32, 96 60, 61, 62, 76, 77, 78, 79, 80, 102
delivery, 8, 9, 33, 54, 59, 60, 61, 71, 72, 75, as a First-Line Treatment, 20
76, 101, 105 ECT Treatment Course, 87
delta activity, 9 ECT–drug interactions, 28
dementia, 28, 50, 89 ectopic beats, 10
dentate gyrus, 4 Ect-Responsive Illness, 21
depolarizing agent, 70 education, 23, 101
depressive symptoms, 19, 22, 24, 25, 32, EEG, 4, 9, 24, 26, 54, 57, 58, 60, 61, 62, 64,
89, 91, 95, 96 65, 66, 75, 78, 79, 81, 103
deterioration, 89 EEG Recording Electrodes, 57
dexamethasone suppression test (DST), 6 EFFECT. See European Forum for ECT
dexmedetomidine, 97 (EFFECT)
diabetes, 6, 35 efficacy, 1, 3, 5, 7, 9, 20, 21, 23, 28, 31, 33,
diagnostic psychiatric interview, 21 34, 35, 51, 56, 57
diaphragm, 70 elderly, 20, 28, 55, 68, 76, 77, 96
digoxin, 36 electrical circuit, 8, 61
Dilantin, 77 electrical dose-titration, 2
Diltiazem, 74 electrical safety, 8
disadvantages, 49 electricity, 7
discomfort, 34, 67, 68 basics of, 7
disorientation, 96 electroconvulsive shock (ECS), 4, 5, 6, 7
distress, 22 Electroconvulsive Therapy
diuretics, 35, 36, 73 basic concepts of, 1
dopamine, 5, 6, 28 electrode edge, 52
dopaminergic tissue transplantation, 21 electrode paddles, 59
dorsum, 58, 66, 67, 79 electrode placement, 5, 9, 21, 22, 23, 25,
dose titration, 53, 54, 55, 57, 71, 75 28, 49, 50, 51, 52, 55, 56, 57, 58, 62,
dose titration procedure, 57, 71, 75 89, 90, 96, 103, 106
dose titration sequence, 54, 55 electrode site preparation, 57
dosing estimates, 54, 56 electrode sites, 8, 51, 52, 79
dosing strategies, 57, 97 electrolytes, 26, 91
dosing tables, 56 emergencies, 3, 37
driving, 3, 23, 25 EMG, 58, 60, 61, 66, 79
drugs, 5, 6, 24, 31, 34, 70, 73, 74, 102, 106 EMG electrodes, 58, 79
DST. See dexamethasone suppression EMG Recording Electrodes, 58
test (DST) EMG tracing, 66
112 Index
endorphins, 6 Hamilton Rating Scale for Depression

energy, 7, 8, 54, 55, 88 (HRSD), 25, 50, 88
environment, 2, 81, 96, 102 handedness, 23
epilepsy, 7, 29, 34 handheld electrode, 59
escitalopram, 24 headache, 55, 98
esmolol, 29, 61, 73, 74, 75 headband, 59
Etomidate, 68, 69 heart, 10, 22, 62, 69, 71, 73, 74
European Forum for ECT (EFFECT), heart rate, 10, 62, 71, 73, 74
2 hemispheres, 58, 70
euthymesin, 6 hemodynamic responses, 69
eye, 36, 51, 52 hepatotoxicity, 33
eyebrow, 58 heritability, 22
high impedance, 61
family, 3, 22, 36, 37, 88, 91, 98, 102, 105 high stimulus doses, 56
fasciculations, 70, 80, 98 hippocampus, 4, 6
FDA, 25 history, 20, 21, 22, 23, 25, 26, 29, 31, 35,
fever, 33 71, 74, 77, 89, 90, 105, 106
first treatment, 50, 57, 67, 70, 71, 74, 75, hobbies, 24
96, 98 hormones, 6
fixed high charge, 56 hospital ECT, 21
fixed high-dose therapy, 54, 56 hospitalization, 3, 90
flumazenil, 34 hospitals, 2, 3, 21, 23, 37, 88, 90, 102, 103
fluphenazine, 34 HPA. See hypothalamic-pituitary-
foot, 58, 59, 66, 67, 70 adrenal (HPA)
forearm, 70, 79 HRSD. See Hamilton Rating Scale for
forehead, 9, 51, 52, 58, 62 Depression (HRSD)
frequency of treatments, 90 hydralazine, 73, 74
frontal leads, 58 hyperreflexia, 33
frontomastoid, 58, 62, 66 hypersynchronous polyspikes, 9
frontotemporal electrode, 59 hypertension, 10, 27, 29, 30, 33, 55, 68,
69, 73, 74, 77
GABA, 6, 7, 34 hyperventilation, 71, 76, 77
gastroesophageal reflux, 36, 72 hypnotic dose, 68, 69
gastroesophageal reflux disease (GERD), hypoglycemics, 35
36 hypomania, 24, 87
gastrointestinal disorders, 31, 36 hypotension, 29, 33, 35, 73, 74
gauze pad, 59 hypothalamic-pituitary-adrenal (HPA), 6
gel, 59, 61
GERD. See gastroesophageal reflux imipramine, 33
disease (GERD) impedance, 8, 54, 61, 76, 77, 80, 81
glaucoma, 36 improvement, 20, 87, 89
glutamate, 6 incontinence, 35
glycopyrrolate, 30, 71 indications, 19, 20, 34, 103, 106
gooseflesh, 10 individualization, 90
gray matter, 4 induction agent, 67, 69, 72, 74, 79, 80, 97
guidelines, 35, 50, 57 informed consent, 21, 23, 25, 36, 37, 79
initial stimuli, 57
H2 blocker, 36, 72 insight, 24
hairline, 58 insurances, 3
hallucinations, 68 intensity, 4, 33, 52, 76
haloperidol, 34 interelectrode distance, 62
Index 113
International Society for ECT and manic episode, 20

Neurostimulation (ISEN), 2 MAOI, 25, 33
intervention, 10, 75 mastoid bone, 58
intracerebral hemorrhage, 27 mastoid process, 58
intracranial pressure, 10, 26, 27, 28 mechanism of action, 3, 4, 6, 7
intubation, 30, 72 MECTA, 56, 58, 66, 80
involuntary ECT, 37 MECTA devices, 56
irritant, 68 medical condition, 26, 27, 30, 50, 55
ischemia, 11, 73, 77 medical factors, 25
ISEN. See International Society for ECT medical issues, 23, 103
and Neurostimulation (ISEN) medical physiology, 9
Isoptin, 74 medical problems, 21, 22
medical risks, 23
jaw, 72 medical status, 23, 26, 91
joules, 8, 54 Medicare, 3
judgment, 1, 24, 74, 90 medication, 20, 21, 22, 24, 29, 30, 31, 32,
36, 55, 61, 72, 73, 74, 78, 89, 90, 106
ketamine, 22, 68, 69 medication management, 25
ketoacidosis, 35 medication–ECT strategies, 35
ketorolac, 98 medications, 1, 2, 3, 5, 23, 24, 29, 30, 31,
32, 34, 35, 36, 74, 79, 89, 90, 91, 101,
labetalol, 29, 61, 73, 74, 75 103
laboratory evaluation, 23, 25, 26 memory dysfunction, 25
language function, 50 memory function, 88, 95, 97
laterality, 50, 56 memory loss, 95, 96, 97, 98, 105
left hemisphere, 50, 62 meningiomas, 28
left-handedness, 50 mental status examination, 25, 26
leg, 67, 70 metabolic panel, 26
length of ECT course, 88 metabolism, 10
lesions, 10, 26, 27, 28 metal electrodes, 59
lidocaine, 3, 35, 36, 74, 77 metal stimulus electrodes, 59
limitations, 23 methohexital, 68, 69, 74, 78, 79
lips, 72 metoclopramide, 31, 36
lithium, 20, 26, 32, 35, 90 midazolam, 34, 78, 97
liver, 26 Mini-Mental State Exam (MMSE), 25, 89
location of electrodes, 51 missed seizures, 75
long seizures, 75 mivacurium, 70
lorazepam, 33, 78 mixed affective state, 19
low impedance, 61 MMSE. See Mini-Mental State Exam
lung, 22 (MMSE)
MoCA, 25, 89
maintenance, 35, 89, 91 modifications, 9, 21, 22, 27, 28, 77
maintenance treatment, 2, 20, 21, 28, 35, monitoring, 30, 57, 58, 61, 62, 66, 88,
37, 89, 90, 91, 97, 106 91, 103
major depression, 19, 27 monoamine systems, 5
major depressive episode, 19 Montgomery-Asberg Depression Rating
major psychiatric illnesses, 3 Scale, 25, 89
malnutrition, 20 Montreal Cognitive Assessment
mania, 19, 20, 49, 87 (MoCA), 25, 89
mania, delerious, 20 mood, 2, 6, 20, 21, 22, 24, 35, 88, 89, 90,
mania, severe, 20, 49 95
114 Index
mood disorders, 2, 6, 22, 89, 95 nitroglycerin, 30, 73, 74

motivation, 24 NMDA antagonist, 69
motor systems, 28 NMS. See neuroleptic malignant
mouth, 72, 73, 80, 90 syndrome (NMS)
MRI, 4, 5, 24, 26 nondepolarizing muscle
MRS, 4 relaxants, 70
Muscle Aches, 98 nortriptyline, 90
muscle relaxant, 66, 67, 70, 80, 98 nothing by mouth, 72
muscle relaxant effect, 66 nothing by mouth status (NPO), 3, 23,
muscle relaxation, 31 25, 72, 79
muscles, 66, 72, 98 NPO. See nothing by mouth status
muscular relaxation, 67, 70 (NPO)
assessment of, 70 number of treatments, 22, 87, 90
musculoskeletal disorders, 31 nutritional status, 49
musculoskeletal injury, 70
myalgias, 98 OCD, 24
myocardial infarction, 27, 29, 74 olanzapine, 97
myocardial ischemia, 10, 29, 71, 73, 74 older patients, 57, 67
myoclonic jerks, 69 ondansetron, 99
myoclonus, 68 opiates, 98
opioids, 7
narcotics, 69 osteoporosis, 27, 31, 70
National Institute of Mental Health outcomes, 4, 25, 98
(NIMH), 2 outpatient ECT, 3, 25, 102
nausea, 55, 98 oversleeping, 24
near-threshold dosing, 56 oxygen demand, 10, 73, 74
neostigmine, 71 oxygen saturation, 62
nerve stimulator, 59, 61, 66, 70, 80, 102 oxygenation, 29, 71
neural networks, 7
neurobiology, 3 pallidotomy, 21
neuroendocrine theory, 6 paralysis, 70, 71
neurogenesis, 4 Parkinson’s disease, 20, 27, 106
neurohormones, 7 patient care, 3, 101, 102, 103
neurohumoral substances, 6 patient characteristics, 54, 56
neuroleptic malignant syndrome (NMS), patient selection, 19
20, 21, 31 patterns, 9, 66
neuroleptics, 31 PCP. See phencyclidine (PCP)
neurological aspects, 9 peptic ulcer disease, 36
neuromuscular junction, 70 perspiration, 61
neuropeptide, 6 PET, 5
neurophysiologic effects, 10 pharmacological interventions, 78
neuropsychological assessment, 25 pharmacotherapy, 19, 90
neurotransmission, 5, 6 phencyclidine (PCP), 69
neurotransmitters, 6 phenytoin, 77
neurotrophic effects, 4 pheochromocytoma, 27
neurotrophic theory, 4 physical examination, 25, 26
nicardepine, 74 physiological effects, 9
nicardipine, 74 physiological monitoring, 61
NIMH. See National Institute of Mental piloerection, 10
Health (NIMH) placement, 49, 50, 51, 58, 60, 61, 67
nitrates, 29, 35, 74 poor electrical connections, 76
Index 115
post-ECT, 28, 34, 62, 73, 74, 96 relapse prevention, 32

postictal agitation, 96, 97 relapse rates, 89, 90
postictal confusional state, 96 relapses, 35
postsynaptic effects, 6 remifentanil, 68, 69
pre-ECT evaluation, 25, 26, 103 remission, 19, 32, 89, 90
pregnancy, 20, 30, 72 renal failure, 27
premedication, 28, 30, 71, 79 reserpine, 35, 73
preparation, 8, 19, 52, 76 resistance, 8, 89
pre-procedural evulations, 23, 25 respiration, 71, 97
pretreatment, 34, 61, 70, 72, 98 response, 1, 4, 9, 19, 20, 22, 25, 29, 50, 56,
PRIDE study, 90 67, 68, 69, 73, 80, 90, 103
prior treatment, 22 response rate, 19
proconvulsant, 68, 69, 78 restimulation, 75
prolactin, 6 restlessness, 96
prolonged seizure, 75, 78 retinal detachment, 27
prophylaxis, 31, 72 retrograde memory dysfunction (RMD),
propofol, 68, 69, 74, 78, 79, 97 96, 97
proton pump inhibitor, 36, 72 reversal agents, 71
pseudocholinesterase, 71 rhythms, 9
psychiatric history, 22, 25, 26 right unilateral ECT, 50, 53, 88, 96
Psychiatry Consultation-Liaison service, right unilateral electrode placement,
21 52, 57
psychosis, 20, 49 risk, 8, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31,
psychotherapy, 22, 24, 89, 91 32, 34, 35, 36, 37, 49, 71, 73, 74, 78,
psychotic symptoms, 22, 24, 32, 34, 69, 91, 95, 106
88, 95 risk–benefit ratio, 91, 95
psychotropics, 31, 32, 35 risks, 21, 22, 23, 25, 26, 28, 29, 30, 50, 74,
public, 2, 102 91, 95, 96
pulmonary aspiration, 30 rituals, 24
pulmonary disease, 30 RMD. See retrograde memory
pulse, 56, 61, 102 dysfunction (RMD)
pulse oximetry, 61 rocuronium, 70
pulse width, 7, 52, 54, 56, 89 rTMS, 22
QIDS-SR. See Quick Inventory of safety, 23, 31, 33, 35, 55, 67, 95, 106
Depressive Symptomatology-Self saline, 59
report (QIDS-SR) scalp, 8, 9, 57, 59
Quick Inventory of Depressive Schizoaffective disorder, 19
Symptomatology-Self report schizophrenia, 7, 19, 20, 34, 88
(QIDS-SR), 25 seizure, 2, 3, 4, 5, 6, 7, 8, 9, 10, 28, 29, 30,
32, 33, 34, 35, 52, 54, 55, 56, 57, 58,
rapid and sustained response, 56 62, 64, 65, 66, 68, 69, 70, 71, 73, 74,
rating scales, 88 75, 76, 77, 78, 81, 97, 98, 103
receptors, 5 seizure duration, 4, 78
recommendation for ECT, 22 seizure generalization, 9, 70
recommendations, 3, 23, 57, 74, 103 seizure induction, 9
recovery, 33, 50, 62, 68, 81, 87, 88, 96, 97, Seizure initiation, 63
98, 99, 101, 102, 103 seizure length, 71, 75, 77
referring doctor, 25 seizure progression, 9
reflexes, 67, 70 seizure threshold, 2, 7, 8, 29, 33, 34, 52,
reflux, 31, 36, 72, 79 54, 55, 56, 57, 75, 76, 77, 78
116 Index
selegiline, 33 subgenual cortex, 4

self-adhesive electrodes, 58 subsequent treatments, 55, 57, 70, 71,
self-injury, 2, 21 75, 78, 98
self-rating scale, 25 successive treatments, 75
self-test, 8, 57, 61 succinylcholine, 31, 36, 61, 66, 67, 70, 71,
self-test features, 8 72, 80, 98
sensors, 58 sugammadex, 71
seriously ill patients, 88 suicidal intentions, 19, 22, 24, 37, 50
serotonin, 5, 32 suicidality, 20
sertraline, 24 suprathreshold stimuli, 55
settings, 3, 7, 8, 54, 55, 56, 57, 62, 67, 76, surge, 10, 29
77, 97 surgery, 2, 33, 96, 102
severity criteria, 50 sympathetic activation, 10
severity of illness, 50 sympathetic nervous system, 10
sex, 54, 56 symptom severity, 19, 25
short seizures, 75, 77, 78 symptomatic relief, 19
side effects, 25, 37, 49, 51, 55, 74, 88 symptoms, 20, 22, 24, 25, 34, 35, 69, 88, 91
Sinemet, 28
single treatments, 90 T waves, 10
site preparation, 57, 58, 59, 76 tachyarrhythmias, 30
sites, 58, 59, 62, 66, 76, 79 tachycardia, 10, 29, 30, 68, 69, 73, 74
skin, 8, 57, 59, 60, 61, 70 TCAs, 32
skin-to-electrode contact, 61 teeth, 23, 31, 72, 80
skull, 8, 52 temporomandibular joint disease, 31
SNRIs, 32 testing, 22, 25
sodium citrate, 31 theophylline, 26, 30, 35, 36, 78
spasticity, 71 therapeutic effects, 3, 6, 50
square-wave pulses, 7 thiopental, 68
SSRIs, 24, 32 thought process, 24
ST segment, 10 thrombin inhibitors, 36
status epilepticus, 7, 29, 30, 78 Thymatron devices, 55, 56, 58, 66, 80
Stick-on Electrodes, 59 thyroid-stimulating hormone (TSH), 6
stigma, 28, 95, 105 tibial nerve, 67
stimulus cable, 61 time interval between treatments, 57
stimulus characteristics, 52, 54 tissues, 8
stimulus charge, 56 toes, 66, 70, 80
stimulus delivery, 57, 61, 72 tolerability, 21, 22, 23, 95, 106
stimulus dose, 30, 50, 54, 55, 57, 75, 76, tone, 10, 34, 67, 70
77, 79, 89 tracing, 62, 63, 66, 79
choosing, 57 transthoracic echocardiography, 11
stimulus dose titration, 30, 54, 75, 76 trauma, 71
stimulus dosing, 33, 52, 55, 56, 75, 76, 96 treatment course, 20, 25, 33, 37, 69, 75,
stimulus duration, 7, 77 87, 89
stimulus electrodes, 9, 59, 60, 61, 76, treatment frequency, 28, 88, 89
79, 80 treatment modalities, 22
stimulus site preparation, 58 treatment options, 19, 96
stimulus, strength of, 52 treatment plan, 91
stroke, 21, 27, 29 treatment procedure, 62, 79
structural abnormalities, 4 treatment response, 22
subconvulsive stimuli, 30, 71 treatment scheduling, 87, 88
subgenual cingulate gyrus, 4 treatment session, 67, 76, 97
Index 117
treatment trials, 22 variability, 8, 97

triptans, 98 vecuronium, 70
TSH. See thyroid-stimulating hormone vegetative signs, 22
(TSH) ventilation, 71, 72, 80, 81, 98
tumors, 28 ventricular contractions, 30
ventricular dysfunction, 11
ultra-brief pulse, 7 verapamil, 74
ultrabrief pulse stimuli, 2, 54, 56, 57 Versed, 78
unconsciousness, 68, 71 vertex, 52, 59, 60
unilateral ECT, 3, 4, 9, 20, 23, 25, 28, 33, vital signs, 61, 79, 81, 101, 103
49, 50, 52, 53, 55, 57, 58, 59, 60, 62, voltage, 8, 9
70, 88, 96, 97, 106
unilateral electrode placement, 49, 50, 55 weight loss, 22
unipolar patients, 4, 19, 88, 89
urgency, 19, 22, 49, 55 young adults, 21, 55
young patients, 55, 57, 70, 78
vagal bradyarrhythmias, 71
vagal tone, 10 Zofran, 99

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1 Basic Concepts of ECT 1 4 ECT Treatment Course 87

This book is a revision of Brain Stimulation in Psychiatry (Kellner, 2012), but

United States was recently well summarized in an editorial in JAMA Psychiatry,

ACT Association for Convulsive Therapy

medically ill as to require hospitalization. Many, however, with adequate family

Theories of Mechanism of Action

ECT may produce suboptimal clinical outcomes despite adequate seizure

studies, n = 174) that ECT is associated with volume increases of hippocampus

Classical (Monoamine) Neurotransmitter Theory

Cerebral Physiology of ECT

Other Neurophysiological Effects of ECT

Fink, M., & Taylor, M. A. (2003). Catatonia: a clinician’s guide to diagnosis and

(2016). Right unilateral ultrabrief pulse ECT in geriatric depression: phase 1

Shorter, E., & Healy, D. (2007). Shock therapy: a history of electroconvulsive treatment in

Major Depressive Episode

Table 2.1 Major indications for ECT

Table 2.2 Indications for ECT as a first-­line treatment

disease when patients have become refractory to or intolerant of antiparkin-

The ECT Consultation

Does the Patient Have an ECT-­Responsive Illness?

Does the Patient Have Any Medical Problems That

The patient’s handedness (relevant for electrode placement), height and

Has Appropriate Informed Consent Been Obtained?

The ECT Consultation Note

told of the requirements of pre-­procedural medical and laboratory evaluation. We

The Pre-­ECT Evaluation

Table 2.3 Pre-ECT Evaluation

evaluation (in selected cases, an electrocardiogram [ECG], a complete blood

Table 2.4 Situations of increased risk

Table 2.5 Common medical conditions that may necessitate modifications in ECT

ECT in Specific Medical Conditions

Central Nervous System (CNS) Disease

2012). Neurosurgical consultation should be considered in patients with brain

Other Medical Conditions

Neuroleptic Malignant Syndrome

Psychotropic Medications During Continuation/Maintenance ECT

Table 2.6 Morning medications that should be given (and those that

Consent for the Depressed Patient

Tess, A. V., & Smetana, G. W. (2009). Medical evaluation of patients undergoing

Right Unilateral ECT

immediate cognitive impairment. It should also be remembered that another

Figure 3.1 Bilateral electrode placement

Figure 3.2 Right unilateral electrode placement

Figure 3.4 Bifrontal electrode placement

Stimulus Dose Titration

strategy can, of course, be used on MECTA devices, with appropriate calcula-

Fixed High-­Dose Therapy

Dosing Estimates Based on Patient Characteristics

Ultrabrief Pulse Stimuli

Practical Advice on Choosing the Stimulus Dose

Electrode Site Preparation

EEG Recording Electrodes

Frontal EEG lead placement Mastoid EEG lead placement

Figure 3.5 Electroencephalogram (EEG) placement

Electromyogram (EMG) Recording Electrodes

Stimulus Site Preparation

Right Unilateral Considerations

Metal Stimulus Electrodes

Disposable, Stick-­on Electrodes

4 channel setup – 2 EEG, 1 EMG, 1 ECG channel *

Table 2.2 Indications for ECT as a first-line treatment

Does the Patient Have an ECT-Responsive Illness?

told of the requirements of pre-procedural medical and laboratory evaluation. We

The Pre-ECT Evaluation

Fixed High-Dose Therapy

Disposable, Stick-on Electrodes

The Self-Test Procedure

post-ECT recovery period. This simple, noninvasive monitoring procedure

(2010). Randomized comparison of ultra-brief bifrontal and unilateral

“HAM-D”) (Hamilton, 1960) the Montgomery-Asberg Depression Rating Scale

chemotherapy. Many cancers are lethal, life-threatening illnesses for which