Handbook of ECT: A Guide to Electroconvulsive Therapy for Practitioners 110840328X, 9781108403283

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Handbook of ECT: A Guide to Electroconvulsive Therapy for Practitioners
 110840328X, 9781108403283

Table of contents :
Cover
Handbook of ECT:
A Guide to Electroconvulsive Therapy
for Practitioners
Copyright
Dedication
Contents
Preface
Abbreviations
1 Basic Concepts of ECT
2 ECT: Patient Selection
and Preparation
3 ECT Technique
4 ECT Treatment Course
5 Common Adverse Effects
6 The ECT Service
7 Special Issues
Index

Citation preview

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 One Liberty Plaza, 20th Floor, New York, NY 10006, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia 314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India 79 Anson Road, #06-04/06, Singapore 079906 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 Basic Concepts  1 Overview  1 Theories of Mechanism of Action  3 Basics of Electricity  7 Medical Physiology  9

2

ECT Treatment Course  87

5

Common Adverse Effects  95

ECT: Patient Selection and Preparation  19

Indications  19 The ECT Consultation  21 The ECT Consultation Note  23 The Pre-ECT Evaluation  25 ECT in Specific Medical Conditions  27 Concurrent Medications  31 Informed Consent  36

3

4

ECT Technique  49

Electrode Placement  49 Stimulus Dosing  53 Practical Advice on Choosing the Stimulus Dose  57 Electrode Site Preparation  57 Physiological Monitoring  61 Anesthetics and Muscular Relaxation  67 Cardiovascular Agents  73 Missed, Short, and Prolonged Seizures  75 Treatment Procedure  79

6

7

Treatment Schedule  87 Clinical Monitoring  88 Continuation/Maintenance ECT  89 Cognition  95 Headache, Muscle Aches, and Nausea  98

The ECT Service  101

Staffing and Administration  101 The ECT Suite  102 Record Keeping  102

Special Issues  105

Stigma  105 Patient-Centered ECT  105 Malpractice Litigation and Insurance  106 Research  106

Index  109

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 stimulation 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 scientific 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 indications 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 practitioners and trainees who need a quick, up-to-date source about most aspects of clinical 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 efficacy 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 therapeutic 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

1

Basic Concepts of ECT

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, including 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 circumscribed and not overly complex. Of course, as in any clinical endeavor, situations 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, commonsense attitude to approaching the patient who needs ECT. At all times, technical 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 treatment 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

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Chapter 1: Basic Concepts of ECT

renewed clinical interest in ECT has led to the growth of professional societies dedicated 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 annually in the United States is almost certainly greater, although, surprisingly, precise 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 epidemiological 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 antidepressant 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 expertise should be required of all psychiatric residents, there can be little disagreement 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 practitioners 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 cardiopulmonary 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 accurate 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 information 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

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Chapter 1: Basic Concepts of ECT

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 cognitive 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 characteristics) 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 dentate gyrus of the hippocampus (Bolwig & Madsen, 2007; Lamont et al., 2005; Madsen et al., 2000). This line of research continues rapidly, with frequent additions 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 neurotrophic 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 subcortical 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 hippocampal 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 evidence 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

Chapter 1: Basic Concepts of ECT

5

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 hippocampal 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 restorative 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 responsible 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 modulatory role for monoamine systems, rather than a simple deficit-­adequacy model (Heninger et al., 1996). Specifically, ECT is known to enhance dopaminergic, serotonergic, and adrenergic neurotransmission. Animal studies 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 monoaminergic 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 tomography (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

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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 preclinical, as well as clinical studies have yielded complex, sometimes contradictory 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 transmission 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 hippocampus, 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 anticonvulsant 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 isolated. ECT results in release of prolactin, thyroid-­stimulating hormone (TSH), adrenocorticotropic hormone (ACTH), and endorphins, among other neurohumoral substances (Kamil & Joffe, 1991). A putative antidepressant neuropeptide, “antidepressin” or “euthymesin,” has been theorized to be released from the hypothalamus during the ECT seizure, exerting beneficial effects on mood disorders 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).

Chapter 1: Basic Concepts of ECT

7

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, possibly 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 significance 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 stimulus is more efficient at inducing seizures and consequently can produce seizures 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).

8

Chapter 1: Basic Concepts of ECT

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 predetermined 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 (assuming fixed impedance of 220 Ω and current of 0.8 A). Impedance may be highly variable between individual patients. The primary 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 psychiatrist to check impedance before delivering the stimulus (see section “Electrode Site Preparation” in Chapter 3). The person delivering the stimulus is at no risk

Chapter 1: Basic Concepts of ECT

9

for getting shocked unless he or she actually touches the metal or the conducting 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, consisting of patterns of low-­voltage fast activity and polyspike rhythms. These patterns correlate with tonic or irregular clonic motor movements. With seizure progression, 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.

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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 cerebral metabolism. The brief rise in intracranial pressure is rarely of clinical consequence, but it is the reason for the historical proscription of ECT in patients with space-­occupying mass lesions. Postictally, cerebral blood flow and metabolism 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 stimulus; 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 sympathetic 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 tachycardia 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 anesthesia, 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

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of demand myocardial ischemia (Messina et al., 1992). Kadoi et al. (2001), using transthoracic echocardiography, showed transient left ventricular dysfunction after the ECT stimulus; the clinical significance of these findings remains unknown.

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Shorter, E., & Healy, D. (2007). Shock therapy: a history of electroconvulsive treatment in mental illness. New Brunswick, NJ: Rutgers University Press. Sienaert, P., Vansteelandt, K., Demyttenaere, K., & Peuskens, J. (2009). Randomized comparison of ultra-­brief bifrontal and unilateral electroconvulsive therapy for major depression: clinical efficacy. J Affect Disord, 116(1–2), 106–112. doi:10.1016/j.jad.2008.11.001.   (2010). Randomized comparison of ultra-­brief bifrontal and unilateral electroconvulsive therapy for major depression: cognitive side-effects. J Affect Disord, 122(1–2), 60–67. doi:10.1016/j.jad.2009.06.011. Slade, E. P., Jahn, D. R., Regenold, W. T., & Case, B. G. (2017). Association of electroconvulsive therapy with psychiatric readmissions in US hospitals. JAMA Psychiatry, 74(8), 798–804. doi:10.1001/jamapsychiatry.2017.1378. Smitha, J. S., Roopa, R., Sagar, B. K., Kutty, B. M., & Andrade, C. (2014). Images in electroconvulsive therapy: ECS dose-­dependently increases cell proliferation in the subgranular region of the rat hippocampus. J ECT, 30(3), 193–194. doi:10.1097/ YCT.0000000000000076. Staton, R. D., Hass, P. J., & Brumback, R. A. (1981). Electroencephalographic recording during bitemporal and unilateral non-­dominant hemisphere (Lancaster Position) electroconvulsive therapy. J Clin Psychiatry, 42(7), 264–269. Svensson, M., Grahm, M., Ekstrand, J., Hoglund, P., Johansson, M., & Tingstrom, A. (2016). Effect of electroconvulsive seizures on cognitive flexibility. Hippocampus, 26(7), 899–910. doi:10.1002/hipo.22573. Swartz, C. (2009). Electroconvulsive and neuromodulation therapies. Cambridge; New York: Cambridge University Press. Thompson, J. W., Weiner, R. D., & Myers, C. P. (1994). Use of ECT in the United States in 1975, 1980, and 1986. Am J Psychiatry, 151(11), 1657–1661. doi:10.1176/ ajp.151.11.1657. Tor, P. C., Bautovich, A., Wang, M. J., Martin, D., Harvey, S. B., & Loo, C. (2015). A systematic review and meta-­analysis of brief versus ultrabrief right unilateral electroconvulsive therapy for depression. J Clin Psychiatry, 76(9), e1092–1098. doi:10.4088/JCP.14r09145. van Oostrom, I., van Eijndhoven, P., Butterbrod, E., van Beek, M. H., Janzing, J., Donders, R., . . . Tendolkar, I. (2018). Decreased cognitive functioning after electroconvulsive therapy is related to increased hippocampal volume: exploring the role of brain plasticity. J ECT. doi:10.1097/YCT.0000000000000483. Verwijk, E., Comijs, H. C., Kok, R. M., Spaans, H. P., Stek, M. L., & Scherder, E. J. (2012). Neurocognitive effects after brief pulse and ultrabrief pulse unilateral electroconvulsive therapy for major depression: a review. J Affect Disord, 140(3), 233–243. doi:10.1016/j.jad.2012.02.024. Wade, B. S., Joshi, S. H., Njau, S., Leaver, A. M., Vasavada, M., Woods, R. P., . . . Narr, K. L. (2016). Effect of electroconvulsive therapy on striatal morphometry in major depressive disorder. Neuropsychopharmacology, 41(10), 2481–2491. doi:10.1038/npp.2016.48. Weiner, R. D., Coffey, C. E., & Krystal, A. D. (1991). The monitoring and management of electrically induced seizures. Psychiatr Clin North Am, 14(4), 845–869.

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Welch, C. A., & Drop, L. J. (1989). Cardiovascular effects of ECT. Convuls Ther, 5(1), 35–43. Wilkinson, S. T., Sanacora, G., & Bloch, M. H. (2017). Hippocampal volume changes following electroconvulsive therapy: a systematic review and meta-analysis. Biol Psychiatry Cogn Neurosci Neuroimaging, 2(4), 327–335. doi:10.1016/j. bpsc.2017.01.011. Yatham, L. N., Liddle, P. F., Lam, R. W., Zis, A. P., Stoessl, A. J., Sossi, V., . . . Ruth, T. J. (2010). Effect of electroconvulsive therapy on brain 5-HT(2) receptors in major depression. Br J Psychiatry, 196(6), 474–479. doi:10.1192/bjp.bp.109.069567.

Chapter

2

ECT: Patient Selection and Preparation

Indications

The primary indications for electroconvulsive therapy (ECT) are major depression (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 situation; 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 unipolar 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 catatonia 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

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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 outcome; 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 bilateral 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 presence 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 clinical 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

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disease when patients have become refractory to or intolerant of antiparkinsonian medication. Because it may be a viable alternative to deep brain stimulation (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 particularly 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 controlled 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 provide 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 consultation. For outpatients, this is usually a single 45- to 90-­minute session; for inpatients, 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 information 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 questioning during the consultation interview.

Does the Patient Have an ECT-­Responsive Illness?

While the overall format of the consultation interview follows that of the standard 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

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Chapter 2: ECT: Patient Selection and Preparation

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 special 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, including 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 likelihood 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 anesthesia. 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.

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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 discontinued, 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 differences 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 situation 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 psychiatric 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 particular 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).

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Chapter 2: ECT: Patient Selection and Preparation 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 intrusive 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 abstinent 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 communications, 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 current suicidal ideation, insight, and judgment good. Impression: Major depression, single episode, severe. Because of the severity of the patient’s current illness, and his failure to respond to multiple medication 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

Chapter 2: ECT: Patient Selection and Preparation

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told of the requirements of pre-­procedural medical and laboratory evaluation. We discussed the differences between bilateral and right unilateral electrode placements; 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 monoamine 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 symptom 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 during 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 cognitive impairment or patients who are deemed likely to report subjective memory dysfunction). Both objective and subjective cognitive assessments are considered 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 examination, psychiatric history, mental status examination, and limited laboratory

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Chapter 2: ECT: Patient Selection and Preparation

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 policies 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 electroencephalogram (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 benefits is critical when the clinician encounters a patient with serious medical illness 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

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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 illnesses. 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 depression (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

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Chapter 2: ECT: Patient Selection and Preparation

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 definition 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 surprising 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 depression, cognitive function may improve after treatment of the depression. Patients with preexisting dementia who are given ECT may experience transient cognitive 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 anticholinergic premedications. Also, elderly patients may be particularly sensitive to ECT–drug interactions. ECT to treat the agitation that is often part of the clinical picture of advanced dementia is clearly helpful and becoming more widespread, 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 seizures, 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 absolute 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 problematic (Maltbie et  al., 1980). Large edematous tumors causing mass effect are clearly extremely dangerous. However, small calcified meningiomas without associated edema probably pose little risk (Abrams, 2002; Goldstein  & Richardson, 1988; Kellner et al., 1991; McKinney et al., 1998; Teraishi et al.,

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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 hypotension, 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 anticonvulsant 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 catecholamine surge and subsequent hypertension and tachycardia that accompany 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 attention 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 tachycardia if there is concern about their ability to tolerate the hemodynamic effects

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of ECT safely (Boere et al., 2014). An alternative strategy is to treat patients with coronary artery disease with nitroglycerin, either before the procedure (transdermally 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 tachyarrhythmias may be treated with intravenous beta-­blockers, as previously discussed. Transient benign hypertension, tachycardia, and premature ventricular contractions 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 bronchodilators 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 preferred 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 recommended 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).

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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 recommended 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, metoclopramide, 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 intubate 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 medications 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

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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 therapeutic range. The occasional patient who presents for treatment having inadvertently 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” antidepressants 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 “powerful” 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 medication, 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 combination 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 procedure. The issue of potential adverse effects of TCAs given in conjunction with

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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 concurrent 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 benzodiazepines before ECT, if possible. However, it is quite permissible to continue lowor 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 morning 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.

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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, flumazenil. 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 enhancement in patients not taking any benzodiazepine, on the theoretical assumption that reduction of endogenous GABA-­ergic tone will lead to seizure enhancement (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 indications 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 anticonvulsant 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 treatment 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 schizophrenia is likely, as it is with first-­generation drugs (Zheng et al., 2016). Numerous

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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 development 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/maintenance ECT and resume them after their ECT. Tapering/discontinuation regimens 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/antiarrhythmic 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 diuretics (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 hypoglycemics 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 ketoacidosis, 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 endocrinologist 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).

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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 echothiophate (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 essential 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 document (pp. 319–322). The ECT practitioner should ensure that the ECT consent

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conforms to all applicable laws, statutes, and hospital policies. Essential information 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, provided 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 substituted consent (with surrogate decision makers) is required, as defined by local jurisdiction.

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Allman, P., & Hawton, K. (1987). ECT for post-­stroke depression: beta blockade to modify rise in blood pressure. Convuls Ther, 3(3), 218–221. American Psychiatric Association. Committee on Electroconvulsive Therapy & Weiner, R. D. (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association (2nd edn). Washington, DC: American Psychiatric Association. Andersen, K., Balldin, J., Gottfries, C. G., Granerus, A. K., Modigh, K., Svennerholm, L., & Wallin, A. (1987). A double-­blind evaluation of electroconvulsive therapy in Parkinson’s disease with “on-­off ” phenomena. Acta Neurol Scand, 76(3), 191–199. Anderson, E. L., & Reti, I. M. (2009). ECT in pregnancy: a review of the literature from 1941 to 2007. Psychosom Med, 71(2), 235–242. doi:10.1097/PSY.0b013e318190d7ca Bailine, S. H., Safferman, A., Vital-Herne, J., & Bernstein, S. (1994). Flumazenil reversal of benzodiazepine-­induced sedation for a patient with severe pre-­ECT anxiety. Convuls Ther, 10(1), 65–68. Beck, A. T., Ward, C. H., Mendelson, M., Mock, J., & Erbaugh, J. (1961). An inventory for measuring depression. Arch Gen Psychiatry, 4, 561–571. Birkenhager, T. K., & Pluijms, E. M. (2016). Possible synergy between electroconvulsive therapy and imipramine: a case report. J Psychiatr Pract, 22(6), 478–480. doi:10.1097/PRA.0000000000000192 Boere, E., Birkenhager, T. K., Groenland, T. H., & van den Broek, W. W. (2014). Betablocking agents during electroconvulsive therapy: a review. Br J Anaesth, 113(1), 43–51. doi:10.1093/bja/aeu153 Bolwig, T. G., Hertz, M. M., Paulson, O. B., Spotoft, H., & Rafaelsen, O. J. (1977). The permeability of the blood-­brain barrier during electrically induced seizures in man. Eur J Clin Invest, 7(2), 87–93. Borisovskaya, A., Bryson, W. C., Buchholz, J., Samii, A., & Borson, S. (2016). Electroconvulsive therapy for depression in Parkinson’s disease: systematic review of evidence and recommendations. Neurodegener Dis Manag, 6(2), 161–176. doi:10.2217/nmt-2016-0002 Brown, G. L., & Wilson, W. P. (1972). Parkinsonism and depression. South Med J, 65(5), 540–545. Brown, W. A. (2007). Treatment response in melancholia. Acta Psychiatr Scand Suppl (433), 125–129. doi:10.1111/j.1600-0447.2007.00970.x Bruce, B. B., Henry, M. E., & Greer, D. M. (2006). Ischemic stroke after electroconvulsive therapy. J ECT, 22(2), 150–152. Bryson, E. O., Aloysi, A. S., Popeo, D. M., Bodian, C. A., Pasculli, R. M., Briggs, M. C., & Kellner, C. H. (2012). Methohexital and succinylcholine dosing for electroconvulsive therapy (ECT): actual versus ideal. J ECT, 28(3), e29–30. doi:10.1097/YCT.0b013e3182503bc9 Burgut, F. T., Popeo, D., & Kellner, C. H. (2010). ECT for agitation in dementia: is it appropriate? Med Hypotheses, 75(1), 5–6. doi:10.1016/j.mehy.2010.04.013 Carroll, B. J., Feinberg, M., Smouse, P. E., Rawson, S. G., & Greden, J. F. (1981). The Carroll rating scale for depression. I. Development, reliability and validation. Br J Psychiatry, 138, 194–200.

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Fink, M., Fricchione, G., Rummans, T., & Shorter, E. (2016a). Catatonia is a systemic medical syndrome. Acta Psychiatr Scand, 133(3), 250–251. doi:10.1111/acps.12510 Fink, M., Kellner, C. H., & McCall, W. V. (2016b). Optimizing ECT technique in treating Catatonia. J ECT, 32(3), 149–150. doi:10.1097/YCT.0000000000000345 Fink, M., & Taylor, M. A. (2003). Catatonia: a clinician’s guide to diagnosis and treatment. Cambridge; New York: Cambridge University Press. Fochtmann, L. (1988). A mechanism for the efficacy of ECT in Parkinson’s disease. Convuls Ther, 4(4), 321–327. Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res, 12(3), 189–198. Glass, O. M., Forester, B. P., & Hermida, A. P. (2017). Electroconvulsive therapy (ECT) for treating agitation in dementia (major neurocognitive disorder) – a promising option. Int Psychogeriatr, 29(5), 717–726. doi:10.1017/S1041610216002258 Goldstein, M. Z., & Richardson, C. (1988). Meningioma with depression: ECT risk or benefit? Psychosomatics, 29(3), 349–351. doi:10.1016/S0033-3182(88)72377-4 Good, M. S., Dolenc, T. J., & Rasmussen, K. G. (2004). Electroconvulsive therapy in a patient with glaucoma. J ECT, 20(1), 48–49. Griesemer, D. A., Kellner, C. H., Beale, M. D., & Smith, G. M. (1997). Electroconvulsive therapy for treatment of intractable seizures. Initial findings in two children. Neurology, 49(5), 1389–1392. Grinspoon, L., & Greenblatt, M. (1963). Pharmacotherapy combined with other treatment methods. Compr Psychiatry, 4, 256–262. Grover, S., Hazari, N., & Kate, N. (2015). Combined use of clozapine and ECT: a review. Acta Neuropsychiatr, 27(3), 131–142. doi:10.1017/neu.2015.8 Hamilton, M. (1960). A rating scale for depression. J Neurol Neurosurg Psychiatry, 23, 56–62. Harmandayan, M., Romanowicz, M., & Sola, C. (2012). Successful use of ECT in post-­stroke depression. Gen Hosp Psychiatry, 34(1), 102 e105–106. doi:10.1016/ j.genhosppsych.2011.08.006 Haskett, R. F., & Loo, C. (2010). Adjunctive psychotropic medications during electroconvulsive therapy in the treatment of depression, mania, and schizophrenia. J ECT, 26(3), 196–201. doi:10.1097/YCT.0b013e3181eee13f Hausner, L., Damian, M., Sartorius, A., & Frolich, L. (2011). Efficacy and cognitive side effects of electroconvulsive therapy (ECT) in depressed elderly patients with coexisting mild cognitive impairment or dementia. J Clin Psychiatry, 72(1), 91–97. doi:10.4088/JCP.10m05973gry Horn, P. J., Reti, I., & Jayaram, G. (2010). Transdermal selegiline in patients receiving electroconvulsive therapy. Psychosomatics, 51(2), 176–178. doi:10.1176/appi. psy.51.2.176 Husain, M. M., Rush, A. J., Fink, M., Knapp, R., Petrides, G., Rummans, T., . . . Kellner, C. H. (2004). Speed of response and remission in major depressive disorder with acute electroconvulsive therapy (ECT): a Consortium for Research in ECT (CORE) report. J Clin Psychiatry, 65(4), 485–491.

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Iancu, I., Pick, N., Seener-Lorsh, O., & Dannon, P. (2015). Patients with schizophrenia or schizoaffective disorder who receive multiple electroconvulsive therapy sessions: characteristics, indications, and results. Neuropsychiatr Dis Treat, 11, 853–862. doi:10.2147/NDT.S78919 Jacobowski, N. L., Heckers, S., & Bobo, W. V. (2013). Delirious mania: detection, diagnosis, and clinical management in the acute setting. J Psychiatr Pract, 19(1), 15–28. doi:10.1097/01.pra.0000426324.67322.06 Jenkins, L. C., & Graves, H. B. (1965). Potential hazards of psychoactive drugs in association with anaesthesia. Can Anaesth Soc J, 12, 121–128. Kamel, H., Cornes, S. B., Hegde, M., Hall, S. E., & Josephson, S. A. (2010). Electroconvulsive therapy for refractory status epilepticus: a case series. Neurocrit Care, 12(2), 204–210. doi:10.1007/s12028-009-9288-7 Kellner, C. H. (1995). Is ECT the treatment of choice for first-­break psychosis? Convuls Ther, 11(3), 155–157. Kellner, C. H., Ahle, G. M., & Geduldig, E. T. (2015). Electroconvulsive therapy for bipolar disorder: evidence supporting what clinicians have long known. J Clin Psychiatry, 76(9), e1151–1152. doi:10.4088/JCP.14com09498 Kellner, C. H., Beale, M. D., Pritchett, J. T., Bernstein, H. J., & Burns, C. M. (1994). Electroconvulsive therapy and Parkinson’s disease: the case for further study. Psychopharmacol Bull, 30(3), 495–500. Kellner, C. H., Burns, C. M., Bernstein, H. J., Monroe, R. R., Jr., & George, M. S. (1991). Safe administration of ECT in a patient with a calcified frontal mass. J Neuropsychiatry Clin Neurosci, 3(3), 353–354. doi:10.1176/jnp.3.3.353 Kellner, C. H., Fink, M., Knapp, R., Petrides, G., Husain, M., Rummans, T., . . . Malur, C. (2005). Relief of expressed suicidal intent by ECT: a consortium for research in ECT study. Am J Psychiatry, 162(5), 977–982. doi:10.1176/appi.ajp.162.5.977 Kellner, C. H., Husain, M. M., Knapp, R. G., McCall, W. V., Petrides, G., Rudorfer, M. V., . . . Group, C. P. W. (2016). Right unilateral ultrabrief pulse ECT in geriatric depression: phase 1 of the PRIDE study. Am J Psychiatry, 173(11), 1101–1109. doi:10.1176/appi.ajp.2016.15081101 Kellner, C. H., Knapp, R., Husain, M. M., Rasmussen, K., Sampson, S., Cullum, M., . . . Petrides, G. (2010). Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. Br J Psychiatry, 196(3), 226–234. doi:10.1192/bjp. bp.109.066183 Kellner, C. H., Knapp, R. G., Petrides, G., Rummans, T. A., Husain, M. M., Rasmussen, K., . . . Fink, M. (2006). Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE). Arch Gen Psychiatry, 63(12), 1337–1344. doi:10.1001/archpsyc.63.12.1337 Kellner, C. H., Nixon, D. W., & Bernstein, H. J. (1991). ECT–drug interactions: a review. Psychopharmacol Bull, 27(4), 595–609. Krystal, A. D., Watts, B. V., Weiner, R. D., Moore, S., Steffens, D. C., & Lindahl, V. (1998). The use of flumazenil in the anxious and benzodiazepine-­dependent ECT patient. J ECT, 14(1), 5–14.

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Kumar, D. R., Han, H. K., Tiller, J., Loo, C. K., & Martin, D. M. (2016). A brief measure for assessing patient perceptions of cognitive side effects after electroconvulsive therapy: the subjective assessment of memory impairment. J ECT, 32(4), 256–261. doi:10.1097/YCT.0000000000000329 Lally, J., Tully, J., Robertson, D., Stubbs, B., Gaughran, F., & MacCabe, J. H. (2016). Augmentation of clozapine with electroconvulsive therapy in treatment resistant schizophrenia: A systematic review and meta-analysis. Schizophr Res, 171(1–3), 215–224. doi:10.1016/j.schres.2016.01.024 Lauritzen, L., Odgaard, K., Clemmesen, L., Lunde, M., Ohrstrom, J., Black, C., & Bech, P. (1996). Relapse prevention by means of paroxetine in ECT-­treated patients with major depression: a comparison with imipramine and placebo in medium-­term continuation therapy. Acta Psychiatr Scand, 94(4), 241–251. Lee, K. (2006). Acute embolic stroke after electroconvulsive therapy. J ECT, 22(1), 67–69. Leiknes, K. A., Cooke, M. J., Jarosch-von Schweder, L., Harboe, I., & Hoie, B. (2015). Electroconvulsive therapy during pregnancy: a systematic review of case studies. Arch Womens Ment Health, 18(1), 1–39. doi:10.1007/s00737-013-0389-0 Li, E. H., Bryson, E. O., & Kellner, C. H. (2016). Muscle relaxation with succinylcholine in electroconvulsive therapy. Anesth Analg, 123(5), 1329. doi:10.1213/ ANE.0000000000001475 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 Lutz, A. S. F. (2014). Each day I like it better: autism, ECT and the treatment of our most impaired children. Nashville: Vanderbilt University Press. Maltbie, A. A., Wingfield, M. S., Volow, M. R., Weiner, R. D., Sullivan, J. L., & Cavenar, J. O., Jr. (1980). Electroconvulsive therapy in the presence of brain tumor. Case reports and an evaluation of risk. J Nerv Ment Dis, 168(7), 400–405. McKinney, P. A., Beale, M. D., & Kellner, C. H. (1998). Electroconvulsive therapy in a patient with a cerebellar meningioma. J ECT, 14(1), 49–52. Mehta, V., Mueller, P. S., Gonzalez-Arriaza, H. L., Pankratz, V. S., & Rummans, T. A. (2004). Safety of electroconvulsive therapy in patients receiving long-­term warfarin therapy. Mayo Clin Proc, 79(11), 1396–1401. doi:10.4065/79.11.1396 Miras Veiga, A., Moreno, D. C., Menendez, A. I., Siscart, I. M., Fernandez, M. D., Sanchez, E. G., . . . Saez, F. G. (2017). Effectiveness of electroconvulsive therapy for refractory status epilepticus in febrile infection-­related epilepsy syndrome. Neuropediatrics, 48(1), 45–48. doi:10.1055/s-0036-1584939 Mirzakhani, H., Guchelaar, H. J., Welch, C. A., Cusin, C., Doran, M. E., MacDonald, T. O., . . . Nozari, A. (2016). Minimum effective doses of succinylcholine and rocuronium during electroconvulsive therapy: a prospective, randomized, crossover trial. Anesth Analg, 123(3), 587–596. doi:10.1213/ ANE.0000000000001218

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Mizen, L., Morton, C., & Scott, A. (2015). The cardiovascular safety of the empirical measurement of the seizure threshold in electroconvulsive therapy. BJ Psych Bull, 39(1), 14–18. doi:10.1192/pb.bp.112.038695 Montgomery, S. A., & Asberg, M. (1979). A new depression scale designed to be sensitive to change. Br J Psychiatry, 134, 382–389. Mueller, P. S., Schak, K. M., Barnes, R. D., & Rasmussen, K. G. (2006). Safety of electroconvulsive therapy in patients with asthma. Neth J Med, 64(11), 417–421. Mukherjee, S., Sackeim, H. A., & Schnur, D. B. (1994). Electroconvulsive therapy of acute manic episodes: a review of 50 years’ experience. Am J Psychiatry, 151(2), 169–176. 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 Oudman, E. (2012). Is electroconvulsive therapy (ECT) effective and safe for treatment of depression in dementia? A short review. J ECT, 28(1), 34–38. doi:10.1097/ YCT.0b013e31823a0f5a Oulis, P., Florakis, A., Markatou, M., Tzanoulinos, G., & Masdrakis, V. G. (2011). Corrected QT interval changes during electroconvulsive therapy-antidepressantsatypical antipsychotics coadministration: safety issues. J ECT, 27(1), e4–6. doi:10.1097/YCT.0b013e3181d77632 Parab, A. L., Chaudhari, L. S., & Apte, J. (1992). Use of nitroglycerin ointment to prevent hypertensive response during electroconvulsive therapy – a study of 50 cases. J Postgrad Med, 38(2), 55–57. Perugi, G., Medda, P., Toni, C., Mariani, M. G., Socci, C., & Mauri, M. (2017). The role of electroconvulsive therapy (ECT) in bipolar disorder: effectiveness in 522 patients with bipolar depression, mixed-­state, mania and catatonic features. Curr Neuropharmacol, 15(3), 359–371. doi:10.2174/1570159X14666161017233642 Petrides, G., & Fink, M. (1996). Atrial fibrillation, anticoagulation, and electroconvulsive therapy. Convuls Ther, 12(2), 91–98. Petrides, G., Fink, M., Husain, M. M., Knapp, R. G., Rush, A. J., Mueller, M., . . . Kellner, C. H. (2001). ECT remission rates in psychotic versus nonpsychotic depressed patients: a report from CORE. J ECT, 17(4), 244–253. Petrides, G., Malur, C., Braga, R. J., Bailine, S. H., Schooler, N. R., Malhotra, A. K., . . . Mendelowitz, A. (2015). Electroconvulsive therapy augmentation in clozapine-­ resistant schizophrenia: a prospective, randomized study. Am J Psychiatry, 172(1), 52–58. doi:10.1176/appi.ajp.2014.13060787 Pettinati, H. M., Stephens, S. M., Willis, K. M., & Robin, S. E. (1990). Evidence for less improvement in depression in patients taking benzodiazepines during unilateral ECT. Am J Psychiatry, 147(8), 1029–1035. doi:10.1176/ajp.147.8.1029 Pier, K. S., Briggs, M. C., Pasculli, R. M., & Kellner, C. H. (2012). Successful electroconvulsive therapy for major depression misdiagnosed as Alzheimer dementia. Am J Geriatr Psychiatry, 20(10), 909–910. doi:10.1097/ JGP.0b013e318254619a

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Popeo, D., & Kellner, C. H. (2009). ECT for Parkinson’s disease. Med Hypotheses,73(4), 468–469. doi:10.1016/j.mehy.2009.06.053 Pritchett, J. T., Bernstein, H. J., & Kellner, C. H. (1993). Combined ECT and antidepressant drug therapy. Convuls Ther, 9(4), 256–261. Rakesh, G., Thirthalli, J., Kumar, C. N., Muralidharan, K., Phutane, V. H., & Gangadhar, B. N. (2017). Concomitant anticonvulsants with bitemporal electroconvulsive therapy: a randomized controlled trial with clinical and neurobiological application. J ECT, 33(1), 16–21. doi:10.1097/YCT.0000000000000357 Raskin, D. E. (1984). Cardiac irritability, tricyclic antidepressants, and electroconvulsive therapy. J Clin Psychopharmacol, 4(4), 237–238. Rasmussen, K., & Abrams, R. (1991). Treatment of Parkinson’s disease with electroconvulsive therapy. Psychiatr Clin North Am, 14(4), 925–933. Rasmussen, K. G., Ryan, D. A., & Mueller, P. S. (2006). Blood glucose before and after ECT treatments in Type 2 diabetic patients. J ECT, 22(2), 124–126. Rasmussen, K. G., & Zorumski, C. F. (1993). Electroconvulsive therapy in patients taking theophylline. J Clin Psychiatry, 54(11), 427–431. Rubner, P., Koppi, S., & Conca, A. (2009). Frequency of and rationales for the combined use of electroconvulsive therapy and antiepileptic drugs in Austria and the literature. World J Biol Psychiatry, 10(4 Pt 3), 836–845. doi:10.1080/15622970902838242 Rush, A. J., Trivedi, M. H., Ibrahim, H. M., Carmody, T. J., Arnow, B., Klein, D. N., . . . Keller, M. B. (2003). The 16-­Item Quick Inventory of Depressive Symptomatology (QIDS), clinician rating (QIDS-­C), and self-­report (QIDS-­SR): a psychometric evaluation in patients with chronic major depression. Biol Psychiatry, 54(5), 573–583. Sackeim, H. A., Decina, P., Prohovnik, I., Malitz, S., & Resor, S. R. (1983). Anticonvulsant and antidepressant properties of electroconvulsive therapy: a proposed mechanism of action. Biol Psychiatry, 18(11), 1301–1310. Sackeim, H. A., Dillingham, E. M., Prudic, J., Cooper, T., McCall, W. V., Rosenquist, P., . . . Haskett, R. F. (2009). Effect of concomitant pharmacotherapy on electroconvulsive therapy outcomes: short-­term efficacy and adverse effects. Arch Gen Psychiatry, 66(7), 729–737. doi:10.1001/archgenpsychiatry.2009.75 Sadananda, S. K., Narayanaswamy, J. C., Srinivasaraju, R., & Math, S. B. (2013). Delirium during the course of electroconvulsive therapy in a patient on lithium carbonate treatment. Gen Hosp Psychiatry, 35(6), 678 e671–672. doi:10.1016/j. genhosppsych.2013.01.011 Saito, S., Kadoi, Y., Iriuchijima, N., Obata, H., Arai, K., Morita, T., & Goto, F. (2000). Reduction of cerebral hyperemia with anti-­hypertensive medication after electroconvulsive therapy. Can J Anaesth, 47(8), 767–774. Sajedi, P. I., Mitchell, J., Herskovits, E. H., & Raghavan, P. (2016). Routine cross-­ sectional head imaging before electroconvulsive therapy: a tertiary center experience. J Am Coll Radiol, 13(4), 429–434. doi:10.1016/j.jacr.2015.11.012 Sartorius, A., Wolf, J., & Henn, F. A. (2005). Lithium and ECT – concurrent use still demands attention: three case reports. World J Biol Psychiatry, 6(2), 121–124.

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Schak, K. M., Mueller, P. S., Barnes, R. D., & Rasmussen, K. G. (2008). The safety of ECT in patients with chronic obstructive pulmonary disease. Psychosomatics, 49(3), 208–211. doi:10.1176/appi.psy.49.3.208 Schmidt, S. T., Lapid, M. I., Sundsted, K. K., Cunningham, J. L., Ryan, D. A., & Burton, M. C. (2014). Safety of electroconvulsive therapy in patients receiving dabigatran therapy. Psychosomatics, 55(4), 400–403. doi:10.1016/j.psym.2013.06.010 Schnur, D. B., Mukherjee, S., Silver, J., Degreef, G., & Lee, C. (1989). Electroconvulsive therapy in the treatment of episodic aggressive dyscontrol in psychotic patients. Convuls Ther, 5(4), 353–361. Shao, E., Moore, R., & Linnane, J. (2017). Rivaroxaban for treatment of pulmonary embolism while receiving electroconvulsive therapy. J ECT, 33(3), e25–e26. doi:10.1097/YCT.0000000000000396 Shuman, M., Hieber, R., Moss, L., & Patel, D. (2015). Rivaroxaban for thromboprophylaxis in a patient receiving electroconvulsive therapy. J ECT, 31(1), e19–20. doi:10.1097/YCT.0000000000000206 Sienaert, P., & Peuskens, J. (2007). Anticonvulsants during electroconvulsive therapy: review and recommendations. J ECT, 23(2), 120–123. doi:10.1097/ YCT.0b013e3180330059 Sinha, P., Goyal, P., & Andrade, C. (2017). A meta-­review of the safety of electroconvulsive therapy in pregnancy. J ECT, 33(2), 81–88. doi:10.1097/ YCT.0000000000000362 Small, J. G., Klapper, M. H., Kellams, J. J., Miller, M. J., Milstein, V., Sharpley, P. H., & Small, I. F. (1988). Electroconvulsive treatment compared with lithium in the management of manic states. Arch Gen Psychiatry, 45(8), 727–732. Spodniakova, B., Halmo, M., & Nosalova, P. (2015). Electroconvulsive therapy in pregnancy – a review. J Obstet Gynaecol, 35(7), 659–662. doi:10.3109/01443615. 2014.990427 Stromgren, L. S. (1997). ECT in acute delirium and related clinical states. Convuls Ther, 13(1), 10–17. Stromgren, L. S., Dahl, J., Fjeldborg, N., & Thomsen, A. (1980). Factors influencing seizure duration and number of seizures applied in unilateral electroconvulsive therapy. Anaesthetics and benzodiazepines. Acta Psychiatr Scand, 62(2), 158–165. Sundsted, K. K., Burton, M. C., Shah, R., & Lapid, M. I. (2014). Preanesthesia medical evaluation for electroconvulsive therapy: a review of the literature. J ECT, 30(1), 35–42. doi:10.1097/YCT.0b013e3182a3546f Tancer, M. E., & Evans, D. L. (1989). Electroconvulsive therapy in geriatric patients undergoing anticoagulation therapy. Convuls Ther, 5(1), 102–109. Tang, V. M., Pasricha, A. N., Blumberger, D. M., Voineskos, D., Pasricha, S., Mulsant, B. H., & Daskalakis, Z. J. (2017). Should benzodiazepines and anticonvulsants be used during electroconvulsive therapy?: A case study and literature review. J ECT, 33(4), 237–242. doi:10.1097/YCT.0000000000000441 Teraishi, T., Nakatake, M., Hirano, J., Ide, M., Kuwahara, T., & Nomura, S. (2012). Electroconvulsive therapy and meningioma: a brief review. Nihon Shinkei Seishin Yakurigaku Zasshi, 32(2), 57–61.

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Tess, A. V., & Smetana, G. W. (2009). Medical evaluation of patients undergoing electroconvulsive therapy. N Engl J Med, 360(14), 1437–1444. doi:10.1056/ NEJMra0707755 Thirthalli, J., Harish, T., & Gangadhar, B. N. (2011). A prospective comparative study of interaction between lithium and modified electroconvulsive therapy. World J Biol Psychiatry, 12(2), 149–155. doi:10.3109/15622975.2010.504860 Trollor, J. N., & Sachdev, P. S. (1999). Electroconvulsive treatment of neuroleptic malignant syndrome: a review and report of cases. Aust N Z J Psychiatry, 33(5), 650–659. doi:10.1080/j.1440-1614.1999.00630.x van den Broek, W. W., Birkenhager, T. K., Mulder, P. G., Bruijn, J. A., & Moleman, P. (2006). Imipramine is effective in preventing relapse in electroconvulsive therapy-­ responsive depressed inpatients with prior pharmacotherapy treatment failure: a randomized, placebo-­controlled trial. J Clin Psychiatry, 67(2), 263–268. Verdura Vizcaino, E. J., Ballesteros Sanz, D., & Sanz-Fuentenebro, J. (2011). Electroconvulsive therapy as treatment for malignant neuroleptic syndrome. Rev Psiquiatr Salud Ment, 4(3), 169–176. doi:10.1016/j.rpsm.2011.04.005 Villalonga, A., Planella, T., Castillo, J., Hernandez, C., Cabrer, C., Manalich, M., . . . Nalda, M. A. (1989). [Nitroglycerin spray in the prevention of hypertension induced by electroconvulsive therapy]. Rev Esp Anestesiol Reanim, 36(5), 264–266. Virupaksha, H. S., Shashidhara, B., Thirthalli, J., Kumar, C. N., & Gangadhar, B. N. (2010). Comparison of electroconvulsive therapy (ECT) with or without anti-­ epileptic drugs in bipolar disorder. J Affect Disord, 127(1–3), 66–70. doi:10.1016/ j.jad.2010.05.008 Volpe, F. M., & Tavares, A. R. (2012). Lithium plus ECT for mania in 90 cases: safety issues. J Neuropsychiatry Clin Neurosci, 24(4), E33. doi:10.1176/appi. neuropsych.11110321 Wachtel, L. E., Jaffe, R., & Kellner, C. H. (2011). Electroconvulsive therapy for psychotropic-­refractory bipolar affective disorder and severe self-­injury and aggression in an 11-year-old autistic boy. Eur Child Adolesc Psychiatry, 20(3), 147–152. doi:10.1007/s00787-010-0155-z Wachtel, L. E., Shorter, E., & Fink, M. (2018). Electroconvulsive therapy for self-­ injurious behaviour in autism spectrum disorders: recognizing catatonia is key. Curr Opin Psychiatry, 31(2), 116–122. doi:10.1097/YCO.0000000000000393 Weiner, R. D., Whanger, A. D., Erwin, C. W., & Wilson, W. P. (1980). Prolonged confusional state and EEG seizure activity following concurrent ECT and lithium use. Am J Psychiatry, 137(11), 1452–1453. doi:10.1176/ajp.137.11.1452 Xiang, Y. T., Ungvari, G. S., Correll, C. U., Chiu, H. F., Lai, K. Y., Wang, C. Y., . . . Shinfuku, N. (2015). Use of electroconvulsive therapy for Asian patients with schizophrenia (2001–2009): Trends and correlates. Psychiatry Clin Neurosci, 69(8), 489–496. doi:10.1111/pcn.12283 Yi, J., Torres, J., Azner, Y., Vaidya, P., Schiavi, A., & Reti, I. M. (2012). Flumazenil pretreatment in benzodiazepine-­free patients: a novel method for managing declining ECT seizure quality. J ECT, 28(3), 185–189. doi:10.1097/ YCT.0b013e3182507752

Chapter 2: ECT: Patient Selection and Preparation Zeiler, F. A., Matuszczak, M., Teitelbaum, J., Gillman, L. M., & Kazina, C. J. (2016). Electroconvulsive therapy for refractory status epilepticus: a systematic review. Seizure, 35, 23–32. doi:10.1016/j.seizure.2015.12.015 Zheng, W., Cao, X. L., Ungvari, G. S., Xiang, Y. Q., Guo, T., Liu, Z. R., . . . Xiang, Y. T. (2016). Electroconvulsive therapy added to non-­clozapine antipsychotic medication for treatment resistant schizophrenia: meta-­analysis of randomized controlled trials. PLoS One, 11(6), e0156510. doi:10.1371/journal.pone.0156510 Zielinski, R. J., Roose, S. P., Devanand, D. P., Woodring, S., & Sackeim, H. A. (1993). Cardiovascular complications of ECT in depressed patients with cardiac disease. Am J Psychiatry, 150(6), 904–909. doi:10.1176/ajp.150.6.904 Zolezzi, M. (2016). Medication management during electroconvulsant therapy. Neuropsychiatr Dis Treat, 12, 931–939. doi:10.2147/NDT.S100908

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ECT Technique

Electrode Placement

There are three commonly used electrode placements in current ECT practice: 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 advantages and disadvantages of each. In clinical practice, it should be relatively easy to decide whether to use bilateral or unilateral electrode placement. The decision should be based primarily on the severity and urgency of the patient’s condition. 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 agitation places them at risk for dehydration and physical exhaustion. Catatonia, in any diagnostic category, is generally considered an indication for bilateral 49

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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 rating 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 unilateral ECT. Finally, patients with severe medical conditions that might increase the risks of repeated anesthesia sessions should be considered for bilateral electrode 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 impairment, 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 confusion or memory impairment after the first treatment, consideration should be given to switching to left unilateral electrode placement for the second treatment 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

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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 combine the efficacy of BT placement, with a cognitive effect profile similar to that of RUL placement. Several moderate-­sized studies support these contentions (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

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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 bilateral 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 vertex. 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

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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 anatomical 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 possible 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 practitioner 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 generalized ECT seizures, if induced with a stimulus very close to seizure threshold (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 impairment. Several options are available to the ECT practitioner in attempting to deal with this clinical dilemma. Despite its having been widely adopted in clinical 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)

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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 minimum 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 indicate the “energy” setting in joules, they are constant-­current devices, and, therefore, 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.

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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 condition, 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 without 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 stimulus charge. Unless there are extenuating circumstances, adolescents and young adults (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 remembered 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 seizures (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

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elderly patient with a very high seizure threshold or in a patient taking anticonvulsants. 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.

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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 duration 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 benzoate), 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

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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 continue to use caffeine as an adjunctive medication in ECT, we no longer recommend 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 epilepticus 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

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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.

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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.

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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.

References Abrams, R. (2002). Electroconvulsive therapy (4th edn). Oxford; New York: Oxford University Press. Abrams, R., & Swartz, C. M. (2016). Thymatron® System IV Instruction Manual (Nineteenth edn): Somatics, LLC. 21–22. Abrams, R., Swartz, C. M., & Vedak, C. (1991). Antidepressant effects of high-­dose right unilateral electroconvulsive therapy. Arch Gen Psychiatry, 48(8), 746–748. Aksay, S. S., Bumb, J. M., Janke, C., Hoyer, C., Kranaster, L., & Sartorius, A. (2014). New evidence for seizure quality improvement by hyperoxia and mild hypocapnia. J ECT, 30(4), 287–291. doi:10.1097/YCT.0000000000000109 American Psychiatric Association. Committee on Electroconvulsive Therapy., & Weiner, R. D. (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association (2nd edn). Washington, DC: American Psychiatric Association. Bailine, S. H., Petrides, G., Doft, M., & Lui, G. (2003). Indications for the use of propofol in electroconvulsive therapy. J ECT, 19(3), 129–132. Bailine, S. H., Rifkin, A., Kayne, E., Selzer, J. A., Vital-Herne, J., Blieka, M., & Pollack, S. (2000). Comparison of bifrontal and bitemporal ECT for major depression. Am J Psychiatry, 157(1), 121–123. doi:10.1176/ajp.157.1.121 Bansod, A., Sonavane, S. S., Shah, N. B., De Sousa, A. A., & Andrade, C. (2017). A randomized, nonblind, naturalistic comparison of efficacy and cognitive outcomes with right unilateral, bifrontal, and bitemporal electroconvulsive therapy in schizophrenia. J ECT. doi:10.1097/YCT.0000000000000454 Beale, M. D., Kellner, C. H., Lemert, R., Pritchett, J. T., Bernstein, H. J., Burns, C. M., & Roy, R. (1994). Skeletal muscle relaxation in patients undergoing electroconvulsive therapy. Anesthesiology, 80(4), 957. Beale, M. D., Kellner, C. H., Pritchett, J. T., Bernstein, H. J., Burns, C. M., & Knapp, R. (1994). Stimulus dose-­titration in ECT: a 2-­year clinical experience. Convuls Ther, 10(2), 171–176. Boere, E., Birkenhager, T. K., Groenland, T. H., & van den Broek, W. W. (2014). Betablocking agents during electroconvulsive therapy: a review. Br J Anaesth, 113(1), 43–51. doi:10.1093/bja/aeu153

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Bryden, M. P. (1982). Laterality: functional asymmetry in the intact brain. New York: Academic Press. Bryson, E. O., Aloysi, A. S., Farber, K. G., & Kellner, C. H. (2017). Individualized anesthetic management for patients undergoing electroconvulsive therapy: a review of current practice. AnesthAnalg, 124(6), 1943–1956. doi:10.1213/ ANE.0000000000001873 Bryson, E. O., Aloysi, A. S., Popeo, D. M., Bodian, C. A., Pasculli, R. M., Briggs, M. C., & Kellner, C. H. (2012). Methohexital and succinylcholine dosing for electroconvulsive therapy (ECT): actual versus ideal. J ECT, 28(3), e29–30. doi:10.1097/YCT.0b013e3182503bc9 Coffey, C. E., Lucke, J., Weiner, R. D., Krystal, A. D., & Aque, M. (1995). Seizure threshold in electroconvulsive therapy (ECT) II. The anticonvulsant effect of ECT. Biol Psychiatry, 37(11), 777–788. doi:10.1016/0006-3223(95)00053-J Coffey, C. E., Weiner, R. D., Hinkle, P. E., Cress, M., Daughtry, G., & Wilson, W. H. (1987). Augmentation of ECT seizures with caffeine. Biol Psychiatry, 22(5), 637–649. d’Elia, G. (1970). Unilateral electroconvulsive therapy. Acta Psychiatr Scand Suppl, 215, 1–98. deArriba-Arnau, A., Dalmau, A., Soria, V., Salvat-Pujol, N., Ribes, C., Sanchez-Allueva, A., & Urretavizcaya, M. (2017). Protocolized hyperventilation enhances electroconvulsive therapy. J Affect Disord, 217, 225–232. doi:10.1016/ j.jad.2017.04.007 Farzan, F., Boutros, N. N., Blumberger, D. M., & Daskalakis, Z. J. (2014). What does the electroencephalogram tell us about the mechanisms of action of ECT in major depressive disorders? J ECT, 30(2), 98–106. doi:10.1097/YCT.0000000000000144 Gomez-Arnau, J., de Arriba-Arnau, A., Correas-Lauffer, J., & Urretavizcaya, M. (2018). Hyperventilation and electroconvulsive therapy: a literature review. Gen Hosp Psychiatry, 50, 54–62. doi:10.1016/j.genhosppsych.2017.09.003 Hamilton, M. (1960). A rating scale for depression. J Neurol Neurosurg Psychiatry, 23, 56–62. Howsepian, A. A. (2011). On describing “seizure length” in electroconvulsive therapy. J ECT, 27(1), 93–94; author reply94. doi:10.1097/YCT.0b013e3181d7766c Kadoi, Y., Nishida, A., & Saito, S. (2013). Recovery time after sugammadex reversal of rocuronium-­induced muscle relaxation for electroconvulsive therapy is independent of cardiac output in both young and elderly patients. J ECT, 29(1), 33–36. doi:10.1097/YCT.0b013e31826cf348 Kellner, C. H. (2011). Muscle relaxation in electroconvulsive therapy. J ECT, 27(1), 93; author reply93.doi:10.1097/YCT.0b013e3181d7a976 Kellner, C. H., & Bryson, E. O. (2013). Electroconvulsive therapy anesthesia technique: minimalist versus maximally managed. J ECT, 29(3), 153–155. doi:10.1097/ YCT.0b013e31827a7aef Kellner, C. H., Farber, K. G., Chen, X. R., Mehrotra, A., & Zipursky, G. D. N. (2017). A systematic review of left unilateral electroconvulsive therapy. Acta Psychiatr Scand, 136(2), 166–176. doi:10.1111/acps.12740

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Kellner, C. H., Husain, M. M., Knapp, R. G., McCall, W. V., Petrides, G., Rudorfer, M. V., & Group, C. P. W. (2016). Right unilateral ultrabrief pulse ECT in geriatric depression: phase 1 of the PRIDE study. Am J Psychiatry, 173(11), 1101–1109. doi:10.1176/appi.ajp.2016.15081101 Kellner, C. H., & Iosifescu, D. V. (2017). Ketamine and ECT: better alone than together? Lancet Psychiatry, 4(5), 348–349. doi:10.1016/S2215-0366(17)30099-8 Kellner, C. H., Knapp, R., Husain, M. M., Rasmussen, K., Sampson, S., Cullum, M., & Petrides, G. (2010a). Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. Br J Psychiatry, 196(3), 226–234. doi:10.1192/bjp. bp.109.066183 Kellner, C. H., Tobias, K. G., & Wiegand, J. (2010b). Electrode placement in electroconvulsive therapy (ECT): a review of the literature. J ECT, 26(3), 175–180. doi:10.1097/YCT.0b013e3181e48154 Lapidus, K. A., & Kellner, C. H. (2011). When to switch from unilateral to bilateral electroconvulsive therapy. J ECT, 27(3), 244–246. doi:10.1097/ YCT.0b013e31820059e1 Letemendia, F. J., Delva, N. J., Rodenburg, M., Lawson, J. S., Inglis, J., Waldron, J. J., & Lywood, D. W. (1993). Therapeutic advantage of bifrontal electrode placement in ECT. Psychol Med, 23(2), 349–360. MacPherson, R. D., Lawford, J., Simpson, B., Mahon, M., Scott, D., & Loo, C. (2010). Low dose lignocaine added to propofol does not attenuate the response to electroconvulsive therapy. J Affect Disord, 126(1–2), 330–333. doi:10.1016/ j.jad.2010.02.134 McCall, W. V., Reboussin, D. M., Weiner, R. D., & Sackeim, H. A. (2000). Titrated moderately suprathreshold vs fixed high-­dose right unilateral electroconvulsive therapy: acute antidepressant and cognitive effects. Arch Gen Psychiatry, 57(5), 438–444. McCall, W. V., Reid, S., Rosenquist, P., Foreman, A., & Kiesow-Webb, N. (1993). A reappraisal of the role of caffeine in ECT. Am J Psychiatry, 150(10), 1543–1545. doi:10.1176/ajp.150.10.1543 McGirr, A., Berlim, M. T., Bond, D. J., Chan, P. Y., Yatham, L. N., & Lam, R. W. (2017). Adjunctive ketamine in electroconvulsive therapy: updated systematic review and meta-analysis. Br J Psychiatry, 210(6), 403–407. doi:10.1192/bjp.bp.116.195826 Minelli, A., Abate, M., Zampieri, E., Gainelli, G., Trabucchi, L., Segala, M., & Bortolomasi, M. (2016). Seizure adequacy markers and the prediction of electroconvulsive therapy response. J ECT, 32(2), 88–92. doi:10.1097/ YCT.0000000000000274 O’Neill-Kerr, A., Yassin, A., Rogers, S., & Cornish, J. (2017). Switching from age-­based stimulus dosing to dose titration protocols in electroconvulsive therapy: empirical evidence for better patient outcomes with lower peak and cumulative energy doses. J ECT, 33(3), 181–184. doi:10.1097/YCT.0000000000000391 Okamoto, N., Nakai, T., Sakamoto, K., Nagafusa, Y., Higuchi, T., & Nishikawa, T. (2010). Rapid antidepressant effect of ketamine anesthesia during electroconvulsive therapy of treatment-­resistant depression: comparing ketamine and propofolanesthesia. J ECT, 26(3), 223–227. doi:10.1097/YCT.0b013e3181c3b0aa

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Petrides, G., Braga, R. J., Fink, M., Mueller, M., Knapp, R., Husain, M., & Group, C. (2009). Seizure threshold in a large sample: implications for stimulus dosing strategies in bilateral electroconvulsive therapy: a report from CORE. J ECT, 25(4), 232–237. Petrides, G., & Fink, M. (1996). The “half-­age” stimulation strategy for ECT dosing. Convuls Ther, 12(3), 138–146. Pinkhasov, A., Biglow, M., Chandra, S., & Pica, T. (2016). Pretreatment with caffeine citrate to increase seizure duration during electroconvulsive therapy: a case series. J Pharm Pract, 29(2), 177–180. doi:10.1177/0897190014549838 Pitts, F. N., Desmarais, G. M., Stewart, W., & Schaberg, K. (1965). Induction of anesthesia with methohexital and thiopental in electroconvulsive therapy. The effect on the electrocardiogram and clinical observations in 500 consecutive treatments with each agent. N Engl J Med, 273(7), 353–360. Pratt, R. T., Warrington, E. K., & Halliday, A. M. (1971). Unilateral ECT as a test for cerebral dominance, with a strategy for treating left-handers. Br J Psychiatry, 119(548), 79–83. Rasmussen, K. G., Jarvis, M. R., & Zorumski, C. F. (1996). Ketamine anesthesia in electroconvulsive therapy. Convuls Ther, 12(4), 217–223. Recart, A., Rawal, S., White, P. F., Byerly, S., & Thornton, L. (2003). The effect of remifentanil on seizure duration and acute hemodynamic responses to electroconvulsive therapy. Anesth Analg, 96(4), 1047–1050, table of contents. Rosenman, S. J. (2017). Electroconvulsive therapy stimulus titration: not all it seems. Aust N Z J Psychiatry, 4867417743793.doi:10.1177/0004867417743793 Sackeim, H. A., Dillingham, E. M., Prudic, J., Cooper, T., McCall, W. V., Rosenquist, P., & Haskett, R. F. (2009). Effect of concomitant pharmacotherapy on electroconvulsive therapy outcomes: short-­term efficacy and adverse effects. Arch Gen Psychiatry, 66(7), 729–737. doi:10.1001/archgenpsychiatry.2009.75 Sackeim, H. A., Long, J., Luber, B., Moeller, J. R., Prohovnik, I., Devanand, D. P., & Nobler, M. S. (1994). Physical properties and quantification of the ECT stimulus: I. Basic principles. Convuls Ther, 10(2), 93–123. Sackeim, H. A., Prudic, J., Devanand, D. P., Kiersky, J. E., Fitzsimons, L., Moody, & B. J., Settembrino, J. M. (1993). Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med, 328(12), 839–846. doi:10.1056/NEJM199303253281204 Sackeim, H. A., Prudic, J., Nobler, M. S., Fitzsimons, L., Lisanby, S. H., Payne, N., & Devanand, D. P. (2008). Effects of pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimul, 1(2), 71–83. doi:10.1016/j.brs.2008.03.001 Shrestha, S., Shrestha, B. R., Thapa, C., Pradhan, S. N., Thapa, R., & Adhikari, S. (2007). Comparative study of esmolol and labetalol to attenuate haemodynamic responses after electroconvulsive therapy. Kathmandu Univ Med J (KUMJ), 5(3), 318–323. Sienaert, P., Vansteelandt, K., Demyttenaere, K., & Peuskens, J. (2009). Randomized comparison of ultra-­brief bifrontal and unilateral electroconvulsive therapy for major depression: clinical efficacy. J Affect Disord, 116(1–2), 106–112. doi:10.1016/j.jad.2008.11.001

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  (2010). Randomized comparison of ultra-­brief bifrontal and unilateral electroconvulsive therapy for major depression: cognitive side-effects. J Affect Disord, 122(1–2), 60–67. doi:10.1016/j.jad.2009.06.011 Small, J. G., Small, I. F., Milstein, V., Kellams, J. J., & Klapper, M. H. (1985). Manic symptoms: an indication for bilateral ECT. Biol Psychiatry, 20(2), 125–134. Swartz, C. M., & Michael, N. (2013). Age-based seizure threshold determination. J ECT, 29(1), 18–20. doi:10.1097/YCT.0b013e3182656e5d Takekita, Y., Suwa, T., Sunada, N., Kawashima, H., Fabbri, C., Kato, M., . . . Serretti, A. (2016). Remifentanil in electroconvulsive therapy: a systematic review and meta-­ analysis of randomized controlled trials. Eur Arch Psychiatry ClinNeurosci, 266(8), 703–717. doi:10.1007/s00406-016-0670-0 Tiller, J. W., & Ingram, N. (2006). Seizure threshold determination for electroconvulsive therapy: stimulus dose titration versus age-­based estimations. Aust N Z J Psychiatry, 40(2), 188–192. doi:10.1080/j.1440-1614.2006.01773.x Verwijk, E., Comijs, H. C., Kok, R. M., Spaans, H. P., Stek, M. L., & Scherder, E. J. (2012). Neurocognitive effects after brief pulse and ultrabrief pulse unilateral electroconvulsive therapy for major depression: a review. J Affect Disord, 140(3), 233–243. doi:10.1016/j.jad.2012.02.024 Wajima, Z., Yoshikawa, T., Ogura, A., Imanaga, K., Shiga, T., Inoue, T., & Ogawa, R. (2001). The effects of diltiazem on hemodynamics and seizure duration during electroconvulsive therapy. Anesth Analg, 92(5), 1327–1330.   (2002). Intravenous verapamil blunts hyperdynamic responses during electroconvulsive therapy without altering seizure activity. Anesth Analg, 95(2), 400–402, table of contents. Wan, L. B., Levitch, C. F., Perez, A. M., Brallier, J. W., Iosifescu, D. V., Chang, L. C., & Murrough, J. W. (2015). Ketamine safety and tolerability in clinical trials for treatment-­resistant depression. J Clin Psychiatry, 76(3), 247–252. doi:10.4088/ JCP.13m08852 Zhang, Y., White, P. F., Thornton, L., Perdue, L., & Downing, M. (2005). The use of nicardipine for electroconvulsive therapy: a dose-­ranging study. Anesth Analg, 100(2), 378–381. doi:10.1213/01.ANE.0000144419.44481.59

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ECT Treatment Course

Treatment Schedule Number of Treatments

There is no standard number of ECT treatments in a course, and a patient cannot 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 recoveries, 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.

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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 cognitive 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 frequently 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, catatonic, 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 treatment, 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 psychotic 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 supplemented by objective rating scales. Many excellent depression rating scales are available, including the Hamilton Rating Scale for Depression (HRSD or

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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 completion 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 acceptable, 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 functioning, 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 consideration 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 adjunctive 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, medication (either monotherapy or combination therapy) clearly reduces relapse

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rates of unipolar depression (Frank et al., 1990; Sackeim et al., 2001). The CORE continuation ECT versus pharmacotherapy study demonstrated that continuation 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 history of relapse on medication following response to ECT. Continuation or maintenance 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 concomitant 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 applicable 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 treatments at long intervals are not expected to cause significant cognitive impairment, 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 overnight 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.

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For a full review of issues related to ambulatory ECT, the reader should consult 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 appropriate 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 treatment 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.

References Abrams, R. (1967). Daily administration of unilateral ECT. Am J Psychiatry, 124(3), 384–386. doi:10.1176/ajp.124.3.384 Bailine, S., Fink, M., Knapp, R., Petrides, G., Husain, M. M., Rasmussen, K., . . . Kellner, C. H. (2010). Electroconvulsive therapy is equally effective in unipolar and bipolar depression. Acta Psychiatr Scand, 121(6), 431–436. doi:10.1111/j.16000447.2009.01493.x Biedermann, S. V., Bumb, J. M., Demirakca, T., Ende, G., & Sartorius, A. (2016). Improvement in verbal memory performance in depressed in-­patients after treatment with electroconvulsive therapy. Acta Psychiatr Scand, 134(6), 461–468. doi:10.1111/acps.12652 Fink, M., Abrams, R., Bailine, S., & Jaffe, R. (1996). Ambulatory electroconvulsive therapy: report of a task force of the association for convulsive therapy. Association for Convulsive Therapy. Convuls Ther, 12(1), 42–55. Fligelman, B., Pham, T., Bryson, E. O., Majeske, M., & Kellner, C. H. (2016). Resolution of acute suicidality after a single right unilateral electroconvulsive therapy. J ECT, 32(1), 71–72. doi:10.1097/YCT.0000000000000258 Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res, 12(3), 189–198. 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.

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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. Kellner, C. H., Husain, M. M., Knapp, R. G., McCall, W. V., Petrides, G., Rudorfer, M. V., . . . Group, C. P. W. (2016). A novel strategy for continuation ECT in geriatric depression: phase 2 of the PRIDE study. Am J Psychiatry, 173(11), 1110–1118. doi:10.1176/appi.ajp.2016.16010118 Kellner, C. H., Knapp, R. G., Petrides, G., Rummans, T. A., Husain, M. M., Rasmussen, K., . . . Fink, M. (2006). Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE). Arch 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., . . . Keller, M. B. (2003). The 16-­Item Quick Inventory of Depressive Symptomatology (QIDS), clinician rating (QIDS-­C), and self-­report (QIDS-­SR): a psychometric evaluation in patients with chronic major depression. Biol Psychiatry, 54(5), 573–583.

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Sackeim, H. A., Haskett, R. F., Mulsant, B. H., Thase, M. E., Mann, J. J., Pettinati, H. M., . . . Prudic, J. (2001). Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA, 285(10), 1299–1307. Sackeim, H. A., Prudic, J., Devanand, D. P., Decina, P., Kerr, B., & Malitz, S. (1990). The impact of medication resistance and continuation pharmacotherapy on relapse following response to electroconvulsive therapy in major depression. J Clin Psychopharmacol, 10(2), 96–104. Sienaert, P., Vansteelandt, K., Demyttenaere, K., & Peuskens, J. (2009). Ultra-brief pulse ECT in bipolar and unipolar depressive disorder: differences in speed of response. Bipolar Disord, 11(4), 418–424. doi:10.1111/j.1399-5618.2009.00702.x Stromgren, L. S. (1990). Frequency of ECT treatments. Convuls Ther, 6(4), 317–318. Thomas, S. G., & Kellner, C. H. (2003). Remission of major depression and obsessive-­ compulsive disorder after a single unilateral ECT. J ECT, 19(1), 50–51. Tran, D. V., Meyer, J. P., Farber, K. G., Chen, X. R., Rosenthal, B. D., & Kellner, C. H. (2017). Rapid response to electroconvulsive therapy: a case report and literature review. J ECT, 33(3), e20–e21. doi:10.1097/YCT.0000000000000408 Wilkinson, S. T., Ostroff, R. B., & Sanacora, G. (2017). Computer-assisted cognitive behavior therapy to prevent relapse following electroconvulsive therapy. J ECT, 33(1), 52–57. doi:10.1097/YCT.0000000000000348

Chapter

5

Common Adverse Effects

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 95

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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 cognition 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 confusion generally subside within 10–20 min and typically are resolved within an hour. With ultrabrief pulse right unilateral ECT, reorientation may occur in several 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 usually easily managed with a short-­acting, rapid-­onset benzodiazepine such as

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midazolam (typically 2 mg, range: 1–4 mg) administered intravenously. If a patient has become agitated at a previous treatment session, at the next session, 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 olanzapine (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 management 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 individuality, 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 tremendous variability in this regard: most patients report that the amount of memory

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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 confused 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 contemporary 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 muscles 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 intravenous 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 acetaminophen 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 myalgias persist after subsequent treatments and the patient’s muscular block is adequate, 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 ventilation. When it is a regular occurrence, nausea may be treated with intravenous

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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 Abrams, R. (2002). Electroconvulsive therapy (4th edn). Oxford; New York: Oxford 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). Treatmentresistant 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

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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

6

The ECT Service

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 development of a mutually respectful, trusting relationship is as important as a good intravenous line! Such a relationship takes some time to develop and is facilitated 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 supervise 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 assessment, 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 maintaining 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 colleagues 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 101

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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 available 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 frightening to patients. A location on the psychiatry unit or a separate area in an outpatient 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.

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The Medical Record

The patient’s medical record should contain the ECT consultation sheet, detailing the indications for treatment, pertinent medical issues, and recommendations 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 medications, electrode placement, treatment number, stimulus parameters and dose, motor and EEG seizure durations, and any complications noted and their management. 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 recommendations for continuation therapy. Such separate ECT records facilitate retrieval of ECT information that may be needed for future patient care, for transmittal 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., & Weiner, R. D. (2001). The practice of electroconvulsive therapy: recommendations for treatment, training, and privileging: a task force report of the American Psychiatric Association (2nd edn). Washington, DC: American Psychiatric Association.

Chapter

7

Special Issues

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 exaggerated 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 psychiatrist 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 appropriate 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 105

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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 Abrams, R. (2002). Electroconvulsive therapy (4th edn). Oxford; New York: Oxford 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

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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 Therapy (ACT) ACTH. See adrenocorticotropic hormone (ACTH) acute-phase ECT, 35 additional treatments, 76, 77 adolescents, 21, 55, 69 adrenocorticotropic hormone (ACTH), 6 advantages, 49, 51, 69 adverse effects, 25, 32, 69, 78, 88, 95, 96 adverse events, 37 affect restricted, 24 affective features, 20 age, 24, 54, 55, 56, 57 age-based dosing, 54, 55 agitation, 20, 28, 49, 69, 96 airway, 70, 71, 72 airway management, 70, 72 airway secretions, 71 alcohol, 24 alfentanil, 68, 69 algorithms, 54, 76 allergies, 23 AMD. See anterograde memory dysfunction (AMD) amygdala, 4 analgesics, 70 anatomical factors, 52, 58, 66 anesthesia, 3, 9, 10, 22, 23, 24, 26, 33, 34, 35, 50, 55, 61, 67, 69, 71, 72, 74, 96, 101, 102, 103 anesthetic agents, 79 anesthetics, 67, 68 aneurysm, 27 angina, 74 animal studies, 4, 5 ankle, 54, 70, 79, 80, 81 antecubital vein, 79 anterograde memory dysfunction (AMD), 96, 97 antianginals, 36 antiarrhythmics, 30, 36, 73

antiarrythmics, 35 antiasthmatics, 35 anticholinergic agent, 71 anticholinergics, 28, 30, 71 anticoagulants, 36 anticonvulsant effect, 7 anticonvulsant theory, 7 anticonvulsants, 6, 7, 24, 29, 34, 35, 55, 68, 69, 74, 76, 77, 78 antidepressants, 1, 2, 3, 5, 6, 7, 9, 31, 32, 35, 55, 56, 69, 90, 95 antihypertensive agents, 29, 61, 73 antihypertensives, 29, 30, 36, 73, 75 antipsychotic effects, 5, 20, 34 antipsychotics, 31, 34 anxiety, 24, 33, 67 APA Task Force on Electroconvulsive Therapy, 3 apnea, 36, 68 appropriate dose, 56 arousal, 10 arrhythmias, 30, 73, 74 artifact, 58, 62, 66, 67 aspiration, 31, 72 assessment, 23, 25, 67, 89, 101 Association for Convulsive Therapy (ACT), 2 asthma, 27, 30, 73 asystole, 10 Ativan, 78 atropine, 30, 71 auditory meatus, 51 augmentation, 69 autism, 21, 106 availability, 3, 5, 30 awakening, 31, 96 barbiturates, 68 basal ganglia, 4 basics of the treatment, 1 Beck Depression Inventory, 25 benefits, 21, 23, 26, 28, 105 109

110

Index

benzodiazepine, 33, 34, 35, 77, 78, 96, 97 beta-blockers, 29, 30, 73 bifrontal ECT, 51 bifrontal electrode placement, 53 bilateral ECT, 20, 49, 50, 51, 52, 59, 88, 96, 97 bilateral electrode placement, 50, 51, 53, 57, 90 bipolar patients, 4, 19, 20, 28, 87, 88 bite block, 54, 71, 72, 76, 77, 80, 81, 101 bladder, 35, 73 bleeding, 27, 29 blood flow, 10, 28 blood oxygen saturation, 61 blood pressure, 10, 29, 59, 61, 62, 70, 71, 73, 74, 79, 80, 81, 102 blood volume, 10 blood–brain barrier, 5, 10, 32, 71 bolus, 68, 70, 73, 74, 78 bradyarrhythmia, 30 bradycardia, 10, 30, 71 brain, 3, 4, 5, 7, 8, 9, 10, 24, 26, 28, 32, 71, 78 brain disease, 26, 78 brain electrical activity, 26 brain herniation, 28 brain tumor, 28, 29 breathing, 62, 102 brief pulse stimuli, 7, 56 bronchodilators, 30, 36 burns, 68, 71 caffeine, 77 calcium channel blockers, 73, 74 calves, 80 cancer, 95 canthus, 51, 52 carbamazepine, 77 Cardene, 74 cardiac arrhythmia, 27, 69 cardiac disease, 29 cardiac enzymes, 10 cardiac function, 27 cardiac repolarization, 10 cardioactive agents, 73, 74 cardiovascular agents, 30, 73 cardiovascular depression, 68 cardiovascular disease, 29 cardiovascular medications, 30, 35 cardiovascular system, 9, 10, 32, 61, 68, 73, 77, 78, 79

Cardizem, 74 carotid artery, 58 Carroll Rating Scale for Depression, 25 catatonia, 2, 19, 20, 21, 49, 50, 88, 95 central nervous system, 9, 27 cerebral neurons, 9 cerebrospinal fluid, 5, 7 charge, 7, 8, 52, 54, 55, 77, 101 chemotherapy, 96 childhood, 24 children, 21, 69 chin, 72, 80 cholinesterase inhibitor, 36 chronic obstructive pulmonary disease, 27 cigarettes, 24 cisatracurium, 70 classical monoamine depletion theory, 5 clinical monitoring, 88 clonic motor phase, 9 cognitive assessments, 25 cognitive dysfunction, 89 cognitive effects, 4, 5, 6, 9, 25, 37, 51, 55, 56, 57, 87, 95, 106 cognitive functioning, 25, 28, 89 cognitive impairment, 7, 25, 50, 51, 53, 56, 75, 78, 88, 90 cognitive risks, 23 combination therapy, 20 comfort, 1, 67 comorbidities, 95 complete blood count, 26 complications, 22, 29, 37, 50, 77, 87, 95, 103 concurrent medications, 31 conduction, 61, 71, 73 confusion, 50, 68, 96 connection, 61 connectivity theory, 7 Consortium for Research in Electroconvulsive Therapy (CORE), 51, 89 constant-current, 8, 54 consultation, 1, 21, 22, 23, 24, 26, 29, 31, 37, 103 consultation note, 21, 23 continuation, 20, 35, 89, 90, 91 continuation treatment, 2, 6, 21, 25, 35, 37, 78, 89, 90, 91, 97, 103, 106 controversy, 3, 49, 62, 74

Index CORE. See Consortium for Research in Electroconvulsive Therapy (CORE) coronary artery disease, 27 cortical structures, 4, 6 crying, 24 CT, 24, 26 cuff technique, 70 cuffed-limb method, 31 current density, 5, 9 current flow, 61 d’Elia placement, 52, 53 DBS. See deep brain stimulation (DBS) death, 35, 95 deep brain stimulation (DBS), 21 delirium, 28, 32, 96 delivery, 8, 9, 33, 54, 59, 60, 61, 71, 72, 75, 76, 101, 105 delta activity, 9 dementia, 28, 50, 89 dentate gyrus, 4 depolarizing agent, 70 depressive symptoms, 19, 22, 24, 25, 32, 89, 91, 95, 96 deterioration, 89 dexamethasone suppression test (DST), 6 dexmedetomidine, 97 diabetes, 6, 35 diagnostic psychiatric interview, 21 diaphragm, 70 digoxin, 36 Dilantin, 77 Diltiazem, 74 disadvantages, 49 discomfort, 34, 67, 68 disorientation, 96 distress, 22 diuretics, 35, 36, 73 dopamine, 5, 6, 28 dopaminergic tissue transplantation, 21 dorsum, 58, 66, 67, 79 dose titration, 53, 54, 55, 57, 71, 75 dose titration procedure, 57, 71, 75 dose titration sequence, 54, 55 dosing estimates, 54, 56 dosing strategies, 57, 97 dosing tables, 56 driving, 3, 23, 25 drugs, 5, 6, 24, 31, 34, 70, 73, 74, 102, 106 DST. See dexamethasone suppression test (DST)

111

duration, 4, 7, 22, 28, 33, 54, 56, 68, 69, 70, 73, 74, 81 dyskinesias, 28 dysrhythmias, 10 ear, 58 ECG, 10, 26, 60, 61, 62, 66, 79, 91, 102 echothiophate, 36 ECS. See electroconvulsive shock (ECS) ECT cerebral physiology of, 9 Consultation, 21, 23 course, 9, 24, 33, 56, 73, 76, 89, 96, 97, 103 device, 7, 8, 37, 54, 55, 56, 57, 58, 59, 60, 61, 62, 76, 77, 78, 79, 80, 102 as a First-Line Treatment, 20 ECT Treatment Course, 87 ECT–drug interactions, 28 ectopic beats, 10 Ect-Responsive Illness, 21 education, 23, 101 EEG, 4, 9, 24, 26, 54, 57, 58, 60, 61, 62, 64, 65, 66, 75, 78, 79, 81, 103 EEG Recording Electrodes, 57 EFFECT. See European Forum for ECT (EFFECT) efficacy, 1, 3, 5, 7, 9, 20, 21, 23, 28, 31, 33, 34, 35, 51, 56, 57 elderly, 20, 28, 55, 68, 76, 77, 96 electrical circuit, 8, 61 electrical dose-titration, 2 electrical safety, 8 electricity, 7 basics of, 7 electroconvulsive shock (ECS), 4, 5, 6, 7 Electroconvulsive Therapy basic concepts of, 1 electrode edge, 52 electrode paddles, 59 electrode placement, 5, 9, 21, 22, 23, 25, 28, 49, 50, 51, 52, 55, 56, 57, 58, 62, 89, 90, 96, 103, 106 electrode site preparation, 57 electrode sites, 8, 51, 52, 79 electrolytes, 26, 91 emergencies, 3, 37 EMG, 58, 60, 61, 66, 79 EMG electrodes, 58, 79 EMG Recording Electrodes, 58 EMG tracing, 66

112

Index

endorphins, 6 energy, 7, 8, 54, 55, 88 environment, 2, 81, 96, 102 epilepsy, 7, 29, 34 escitalopram, 24 esmolol, 29, 61, 73, 74, 75 Etomidate, 68, 69 European Forum for ECT (EFFECT), 2 euthymesin, 6 eye, 36, 51, 52 eyebrow, 58 family, 3, 22, 36, 37, 88, 91, 98, 102, 105 fasciculations, 70, 80, 98 FDA, 25 fever, 33 first treatment, 50, 57, 67, 70, 71, 74, 75, 96, 98 fixed high charge, 56 fixed high-dose therapy, 54, 56 flumazenil, 34 fluphenazine, 34 foot, 58, 59, 66, 67, 70 forearm, 70, 79 forehead, 9, 51, 52, 58, 62 frequency of treatments, 90 frontal leads, 58 frontomastoid, 58, 62, 66 frontotemporal electrode, 59 GABA, 6, 7, 34 gastroesophageal reflux, 36, 72 gastroesophageal reflux disease (GERD), 36 gastrointestinal disorders, 31, 36 gauze pad, 59 gel, 59, 61 GERD. See gastroesophageal reflux disease (GERD) glaucoma, 36 glutamate, 6 glycopyrrolate, 30, 71 gooseflesh, 10 gray matter, 4 guidelines, 35, 50, 57 H2 blocker, 36, 72 hairline, 58 hallucinations, 68 haloperidol, 34

Hamilton Rating Scale for Depression (HRSD), 25, 50, 88 handedness, 23 handheld electrode, 59 headache, 55, 98 headband, 59 heart, 10, 22, 62, 69, 71, 73, 74 heart rate, 10, 62, 71, 73, 74 hemispheres, 58, 70 hemodynamic responses, 69 hepatotoxicity, 33 heritability, 22 high impedance, 61 high stimulus doses, 56 hippocampus, 4, 6 history, 20, 21, 22, 23, 25, 26, 29, 31, 35, 71, 74, 77, 89, 90, 105, 106 hobbies, 24 hormones, 6 hospital ECT, 21 hospitalization, 3, 90 hospitals, 2, 3, 21, 23, 37, 88, 90, 102, 103 HPA. See hypothalamic-pituitaryadrenal (HPA) HRSD. See Hamilton Rating Scale for Depression (HRSD) hydralazine, 73, 74 hyperreflexia, 33 hypersynchronous polyspikes, 9 hypertension, 10, 27, 29, 30, 33, 55, 68, 69, 73, 74, 77 hyperventilation, 71, 76, 77 hypnotic dose, 68, 69 hypoglycemics, 35 hypomania, 24, 87 hypotension, 29, 33, 35, 73, 74 hypothalamic-pituitary-adrenal (HPA), 6 imipramine, 33 impedance, 8, 54, 61, 76, 77, 80, 81 improvement, 20, 87, 89 incontinence, 35 indications, 19, 20, 34, 103, 106 individualization, 90 induction agent, 67, 69, 72, 74, 79, 80, 97 informed consent, 21, 23, 25, 36, 37, 79 initial stimuli, 57 insight, 24 insurances, 3 intensity, 4, 33, 52, 76 interelectrode distance, 62

Index International Society for ECT and Neurostimulation (ISEN), 2 intervention, 10, 75 intracerebral hemorrhage, 27 intracranial pressure, 10, 26, 27, 28 intubation, 30, 72 involuntary ECT, 37 irritant, 68 ischemia, 11, 73, 77 ISEN. See International Society for ECT and Neurostimulation (ISEN) Isoptin, 74 jaw, 72 joules, 8, 54 judgment, 1, 24, 74, 90 ketamine, 22, 68, 69 ketoacidosis, 35 ketorolac, 98 labetalol, 29, 61, 73, 74, 75 laboratory evaluation, 23, 25, 26 language function, 50 laterality, 50, 56 left hemisphere, 50, 62 left-handedness, 50 leg, 67, 70 length of ECT course, 88 lesions, 10, 26, 27, 28 lidocaine, 3, 35, 36, 74, 77 limitations, 23 lips, 72 lithium, 20, 26, 32, 35, 90 liver, 26 location of electrodes, 51 long seizures, 75 lorazepam, 33, 78 low impedance, 61 lung, 22 maintenance, 35, 89, 91 maintenance treatment, 2, 20, 21, 28, 35, 37, 89, 90, 91, 97, 106 major depression, 19, 27 major depressive episode, 19 major psychiatric illnesses, 3 malnutrition, 20 mania, 19, 20, 49, 87 mania, delerious, 20 mania, severe, 20, 49

113

manic episode, 20 MAOI, 25, 33 mastoid bone, 58 mastoid process, 58 mechanism of action, 3, 4, 6, 7 MECTA, 56, 58, 66, 80 MECTA devices, 56 medical condition, 26, 27, 30, 50, 55 medical factors, 25 medical issues, 23, 103 medical physiology, 9 medical problems, 21, 22 medical risks, 23 medical status, 23, 26, 91 Medicare, 3 medication, 20, 21, 22, 24, 29, 30, 31, 32, 36, 55, 61, 72, 73, 74, 78, 89, 90, 106 medication management, 25 medication–ECT strategies, 35 medications, 1, 2, 3, 5, 23, 24, 29, 30, 31, 32, 34, 35, 36, 74, 79, 89, 90, 91, 101, 103 memory dysfunction, 25 memory function, 88, 95, 97 memory loss, 95, 96, 97, 98, 105 meningiomas, 28 mental status examination, 25, 26 metabolic panel, 26 metabolism, 10 metal electrodes, 59 metal stimulus electrodes, 59 methohexital, 68, 69, 74, 78, 79 metoclopramide, 31, 36 midazolam, 34, 78, 97 Mini-Mental State Exam (MMSE), 25, 89 missed seizures, 75 mivacurium, 70 mixed affective state, 19 MMSE. See Mini-Mental State Exam (MMSE) MoCA, 25, 89 modifications, 9, 21, 22, 27, 28, 77 monitoring, 30, 57, 58, 61, 62, 66, 88, 91, 103 monoamine systems, 5 Montgomery-Asberg Depression Rating Scale, 25, 89 Montreal Cognitive Assessment (MoCA), 25, 89 mood, 2, 6, 20, 21, 22, 24, 35, 88, 89, 90, 95

114

Index

mood disorders, 2, 6, 22, 89, 95 motivation, 24 motor systems, 28 mouth, 72, 73, 80, 90 MRI, 4, 5, 24, 26 MRS, 4 Muscle Aches, 98 muscle relaxant, 66, 67, 70, 80, 98 muscle relaxant effect, 66 muscle relaxation, 31 muscles, 66, 72, 98 muscular relaxation, 67, 70 assessment of, 70 musculoskeletal disorders, 31 musculoskeletal injury, 70 myalgias, 98 myocardial infarction, 27, 29, 74 myocardial ischemia, 10, 29, 71, 73, 74 myoclonic jerks, 69 myoclonus, 68 narcotics, 69 National Institute of Mental Health (NIMH), 2 nausea, 55, 98 near-threshold dosing, 56 neostigmine, 71 nerve stimulator, 59, 61, 66, 70, 80, 102 neural networks, 7 neurobiology, 3 neuroendocrine theory, 6 neurogenesis, 4 neurohormones, 7 neurohumoral substances, 6 neuroleptic malignant syndrome (NMS), 20, 21, 31 neuroleptics, 31 neurological aspects, 9 neuromuscular junction, 70 neuropeptide, 6 neurophysiologic effects, 10 neuropsychological assessment, 25 neurotransmission, 5, 6 neurotransmitters, 6 neurotrophic effects, 4 neurotrophic theory, 4 nicardepine, 74 nicardipine, 74 NIMH. See National Institute of Mental Health (NIMH) nitrates, 29, 35, 74

nitroglycerin, 30, 73, 74 NMDA antagonist, 69 NMS. See neuroleptic malignant syndrome (NMS) nondepolarizing muscle relaxants, 70 nortriptyline, 90 nothing by mouth, 72 nothing by mouth status (NPO), 3, 23, 25, 72, 79 NPO. See nothing by mouth status (NPO) number of treatments, 22, 87, 90 nutritional status, 49 OCD, 24 olanzapine, 97 older patients, 57, 67 ondansetron, 99 opiates, 98 opioids, 7 osteoporosis, 27, 31, 70 outcomes, 4, 25, 98 outpatient ECT, 3, 25, 102 oversleeping, 24 oxygen demand, 10, 73, 74 oxygen saturation, 62 oxygenation, 29, 71 pallidotomy, 21 paralysis, 70, 71 Parkinson’s disease, 20, 27, 106 patient care, 3, 101, 102, 103 patient characteristics, 54, 56 patient selection, 19 patterns, 9, 66 PCP. See phencyclidine (PCP) peptic ulcer disease, 36 perspiration, 61 PET, 5 pharmacological interventions, 78 pharmacotherapy, 19, 90 phencyclidine (PCP), 69 phenytoin, 77 pheochromocytoma, 27 physical examination, 25, 26 physiological effects, 9 physiological monitoring, 61 piloerection, 10 placement, 49, 50, 51, 58, 60, 61, 67 poor electrical connections, 76

Index

115

post-ECT, 28, 34, 62, 73, 74, 96 postictal agitation, 96, 97 postictal confusional state, 96 postsynaptic effects, 6 pre-ECT evaluation, 25, 26, 103 pregnancy, 20, 30, 72 premedication, 28, 30, 71, 79 preparation, 8, 19, 52, 76 pre-procedural evulations, 23, 25 pretreatment, 34, 61, 70, 72, 98 PRIDE study, 90 prior treatment, 22 proconvulsant, 68, 69, 78 prolactin, 6 prolonged seizure, 75, 78 prophylaxis, 31, 72 propofol, 68, 69, 74, 78, 79, 97 proton pump inhibitor, 36, 72 pseudocholinesterase, 71 psychiatric history, 22, 25, 26 Psychiatry Consultation-Liaison service, 21 psychosis, 20, 49 psychotherapy, 22, 24, 89, 91 psychotic symptoms, 22, 24, 32, 34, 69, 88, 95 psychotropics, 31, 32, 35 public, 2, 102 pulmonary aspiration, 30 pulmonary disease, 30 pulse, 56, 61, 102 pulse oximetry, 61 pulse width, 7, 52, 54, 56, 89

relapse prevention, 32 relapse rates, 89, 90 relapses, 35 remifentanil, 68, 69 remission, 19, 32, 89, 90 renal failure, 27 reserpine, 35, 73 resistance, 8, 89 respiration, 71, 97 response, 1, 4, 9, 19, 20, 22, 25, 29, 50, 56, 67, 68, 69, 73, 80, 90, 103 response rate, 19 restimulation, 75 restlessness, 96 retinal detachment, 27 retrograde memory dysfunction (RMD), 96, 97 reversal agents, 71 rhythms, 9 right unilateral ECT, 50, 53, 88, 96 right unilateral electrode placement, 52, 57 risk, 8, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 34, 35, 36, 37, 49, 71, 73, 74, 78, 91, 95, 106 risk–benefit ratio, 91, 95 risks, 21, 22, 23, 25, 26, 28, 29, 30, 50, 74, 91, 95, 96 rituals, 24 RMD. See retrograde memory dysfunction (RMD) rocuronium, 70 rTMS, 22

QIDS-SR. See Quick Inventory of Depressive Symptomatology-Self report (QIDS-SR) Quick Inventory of Depressive Symptomatology-Self report (QIDS-SR), 25

safety, 23, 31, 33, 35, 55, 67, 95, 106 saline, 59 scalp, 8, 9, 57, 59 Schizoaffective disorder, 19 schizophrenia, 7, 19, 20, 34, 88 seizure, 2, 3, 4, 5, 6, 7, 8, 9, 10, 28, 29, 30, 32, 33, 34, 35, 52, 54, 55, 56, 57, 58, 62, 64, 65, 66, 68, 69, 70, 71, 73, 74, 75, 76, 77, 78, 81, 97, 98, 103 seizure duration, 4, 78 seizure generalization, 9, 70 seizure induction, 9 Seizure initiation, 63 seizure length, 71, 75, 77 seizure progression, 9 seizure threshold, 2, 7, 8, 29, 33, 34, 52, 54, 55, 56, 57, 75, 76, 77, 78

rapid and sustained response, 56 rating scales, 88 receptors, 5 recommendation for ECT, 22 recommendations, 3, 23, 57, 74, 103 recovery, 33, 50, 62, 68, 81, 87, 88, 96, 97, 98, 99, 101, 102, 103 referring doctor, 25 reflexes, 67, 70 reflux, 31, 36, 72, 79

116

Index

selegiline, 33 self-adhesive electrodes, 58 self-injury, 2, 21 self-rating scale, 25 self-test, 8, 57, 61 self-test features, 8 sensors, 58 seriously ill patients, 88 serotonin, 5, 32 sertraline, 24 settings, 3, 7, 8, 54, 55, 56, 57, 62, 67, 76, 77, 97 severity criteria, 50 severity of illness, 50 sex, 54, 56 short seizures, 75, 77, 78 side effects, 25, 37, 49, 51, 55, 74, 88 Sinemet, 28 single treatments, 90 site preparation, 57, 58, 59, 76 sites, 58, 59, 62, 66, 76, 79 skin, 8, 57, 59, 60, 61, 70 skin-to-electrode contact, 61 skull, 8, 52 SNRIs, 32 sodium citrate, 31 spasticity, 71 square-wave pulses, 7 SSRIs, 24, 32 ST segment, 10 status epilepticus, 7, 29, 30, 78 Stick-on Electrodes, 59 stigma, 28, 95, 105 stimulus cable, 61 stimulus characteristics, 52, 54 stimulus charge, 56 stimulus delivery, 57, 61, 72 stimulus dose, 30, 50, 54, 55, 57, 75, 76, 77, 79, 89 choosing, 57 stimulus dose titration, 30, 54, 75, 76 stimulus dosing, 33, 52, 55, 56, 75, 76, 96 stimulus duration, 7, 77 stimulus electrodes, 9, 59, 60, 61, 76, 79, 80 stimulus site preparation, 58 stimulus, strength of, 52 stroke, 21, 27, 29 structural abnormalities, 4 subconvulsive stimuli, 30, 71 subgenual cingulate gyrus, 4

subgenual cortex, 4 subsequent treatments, 55, 57, 70, 71, 75, 78, 98 successive treatments, 75 succinylcholine, 31, 36, 61, 66, 67, 70, 71, 72, 80, 98 sugammadex, 71 suicidal intentions, 19, 22, 24, 37, 50 suicidality, 20 suprathreshold stimuli, 55 surge, 10, 29 surgery, 2, 33, 96, 102 sympathetic activation, 10 sympathetic nervous system, 10 symptom severity, 19, 25 symptomatic relief, 19 symptoms, 20, 22, 24, 25, 34, 35, 69, 88, 91 T waves, 10 tachyarrhythmias, 30 tachycardia, 10, 29, 30, 68, 69, 73, 74 TCAs, 32 teeth, 23, 31, 72, 80 temporomandibular joint disease, 31 testing, 22, 25 theophylline, 26, 30, 35, 36, 78 therapeutic effects, 3, 6, 50 thiopental, 68 thought process, 24 thrombin inhibitors, 36 Thymatron devices, 55, 56, 58, 66, 80 thyroid-stimulating hormone (TSH), 6 tibial nerve, 67 time interval between treatments, 57 tissues, 8 toes, 66, 70, 80 tolerability, 21, 22, 23, 95, 106 tone, 10, 34, 67, 70 tracing, 62, 63, 66, 79 transthoracic echocardiography, 11 trauma, 71 treatment course, 20, 25, 33, 37, 69, 75, 87, 89 treatment frequency, 28, 88, 89 treatment modalities, 22 treatment options, 19, 96 treatment plan, 91 treatment procedure, 62, 79 treatment response, 22 treatment scheduling, 87, 88 treatment session, 67, 76, 97

Index treatment trials, 22 triptans, 98 TSH. See thyroid-stimulating hormone (TSH) tumors, 28 ultra-brief pulse, 7 ultrabrief pulse stimuli, 2, 54, 56, 57 unconsciousness, 68, 71 unilateral ECT, 3, 4, 9, 20, 23, 25, 28, 33, 49, 50, 52, 53, 55, 57, 58, 59, 60, 62, 70, 88, 96, 97, 106 unilateral electrode placement, 49, 50, 55 unipolar patients, 4, 19, 88, 89 urgency, 19, 22, 49, 55 vagal bradyarrhythmias, 71 vagal tone, 10

variability, 8, 97 vecuronium, 70 vegetative signs, 22 ventilation, 71, 72, 80, 81, 98 ventricular contractions, 30 ventricular dysfunction, 11 verapamil, 74 Versed, 78 vertex, 52, 59, 60 vital signs, 61, 79, 81, 101, 103 voltage, 8, 9 weight loss, 22 young adults, 21, 55 young patients, 55, 57, 70, 78 Zofran, 99

117