How Can We Best Use Electroconvulsive Therapy?

Abstract: The first half of this 2-part series summarized the use of electroconvulsive therapy (ECT) in the treatment of several psychiatric and medical conditions. However, despite its efficacy, ECT is not often used within the United States. The second part of this series will discuss the various methods of ECT administration, adverse effects, and treatment options. 

Electroconvulsive therapy (ECT) is now considered a safe and effective treatment for several psychiatric and medical conditions. Published guidelines have helped implement high standards for modern ECT administration.

However, ECT remains a controversial treatment and many clinicians consider it a last resort treatment for patients with ineffective or poorly tolerated response to psychiatric medications. 

ECT can lead to a substantial, effective, and rapid clinical improvement, particularly in the severely ill, elderly, and physically debilitated populations. Modern ECT techniques are performed under general anesthesia and use muscle relaxation, and the selective passage of an electrical current through the brain, which induces modified seizures to achieve the intended therapeutic purposes. 

The second part in this ECT series will address the administration of ECT, its contraindications and the needed documentation prior to the procedure, the equipment and techniques throughout, the possible complications, and the recommended maintenance and follow-up care. 
_____________________________________________________________________________________________________________________________________________________________________

RELATED CONTENT
What Do We Know About Electroconvulsive Therapy?
Electroconvulsive Therapy in a Geriatric Heart Transplant Patient
_____________________________________________________________________________________________________________________________________________________________________

Preparing the Patient for ECT Contraindications 

Although there are no absolute contraindications for ECT treatment, it is pertinent to weigh the relative risk with the potential benefits of treatment; certain medical conditions that are substantially associated with increased risk need to be evaluated on a case-by-case basis by the attending physician and treating psychiatrist.^1,2 The mortality rates associated with modern ECT are no greater than those associated with minor operative procedures involving a general anesthetic; some have suggested that patients who received ECT may experience an improved survival rate.^2-5

Relative contraindications include:^1,4,5 

• Unstable or severe cardiovascular conditions, such as recent myocardial infarction, unstable angina, poorly compensated heart failure, and severe valvular cardiac disease, including critical aortic stenosis

• Aneurysm or vascular malformation that might be susceptible to rupture with increased blood pressure

• Increased intracranial pressure, as may occur with some brain tumors or other space-occupying cerebral lesions

• Recent cerebral infarction

• Pulmonary conditions, such as severe chronic obstructive pulmonary disease, asthma, or pneumonia

• Patients with anaesthesia risks

• Certain conditions, such as pheochromocytoma, retinal detachment, and acute narrow angle glaucoma^1,4

Pregnancy by itself is not a contraindication to the use of ECT.^1,6 The presence of seizure disorder or co-occurring psychiatric condition does not represent a significant risk factor for ECT as long as it is being accurately diagnosed and treated.⁷ 

Once the decision has been made for a patient to have ECT there is usually a pretreatment evaluation that determines what factors will allow for maximum benefits and minimum risk.

Pre-ECT Documentation and Referral

The following should be documented before ECT administration:^1,7-10 

• Indication for use of ECT

• Comorbid psychiatric diagnoses

• Concurrent medical conditions highlighting those that can substantially enhance the risk of ECT

• Current medications

• If a physical examination, including a baseline blood pressure and pulse rate, has been completed within the recommended time frame and the pertinent findings

• If consent was obtained and who signed the consent (eg, patient, patient’s designated substitute decision-maker, public trustee, or medical director)

• If sample information about ECT was given to the patient and/or family

• If an anesthesiologist was consulted and the American Society of Anesthesiologists classification in the physical health category is available

• Copies of pertinent consultations by other specialists during the pre-ECT workup

• If the patient has a cardiac pacemaker or implanted automatic defibrillator

• Dentition and the presence of dentures

• Allergies

• Baseline cognitive functioning

• Any prior history of ECT and its outcome

• The referring physician’s or patient’s preference for bilateral or unilateral ECT, if requested, and at what frequency. (Note: ECT technique and frequency should be at the discretion of the ECT practitioner while considering these preferences and the clinical situation.)

•Name and signature of the attending physician

• Medications for each ECT treatment—which medications should be given on the morning of ECT and which ones should be continued post-ECT

Pretreatment Evaluation 

Although the specific components of the evaluation of patients identified for ECT vary based on each patient’s individual characteristics, each facility should identify a minimal set of evaluations to be undertaken in all cases. The ECT evaluation should be performed by both an individual privileged to administer ECT as well as the anesthesia provider. 

A pre-ECT evaluation should include the following components, to be carried out within 10 days for inpatients and 30 days for outpatients:^1,7-10 

• Physical examination

• Evaluation of dentition for the presence of dentures and dental problems that could affect the use of the bite block. Temporal-mandibular joint problems can also be noted

• An electrocardiogram for those over age 45, or those with a known cardiovascular disease

• Other routine lab investigations are not mandatory and should be guided by the patient’s history and a physical exam. Common investigations include hemoglobin, electrolytes, and renal function tests

The pre-ECT evaluation may also include:

• A chest x-ray if there is a florid or unstable cardiopulmonary condition

• A cervical spine x-ray for individuals with suspected cervical spine instability (eg, rheumatoid arthritis, severe osteoporosis, Down syndrome, certain collagen vascular diseases) because the procedure would warrant full muscle relaxation during ECT and monitoring the maximum relaxation time using a nerve stimulator

• An anesthesia consult is strongly advised for individuals over age 60, individuals with significant cardiovascular or neurologic conditions, pregnant women, and those with potentially unstable cervical spine instability

• A pertinent specialty consultation from cardiology and neurology is also advised for medical conditions that would substantially increase the risk of ECT. Specialty consultation for special populations may also be indicated such as in pediatric patients. An obstetrical consult well before the ECT is also strongly advised for those who have high-risk pregnancies or are near term.

While no specific laboratory tests are routinely required as part of the pre-ECT evaluation, the results can be used to confirm the presence and severity of medical risk factors. A workup should include a complete blood count, serum chemistry, renal function, electrocardiogram, and urinalysis.^1,7-10 

(Continue to the next page for Managing Preexisting Medical Conditions, Concurrent Medications, and Informed Consent)Managing Preexisting Medical Conditions 

Those with cardiac pacemakers and implanted automatic defibrillators warrant some caution.^1,11 It is unlikely that ECT would disrupt the functioning of a modern cardiac pacemaker, but if uncertain, a cardiologist consultation would be required.¹² The monitoring leads should be well-grounded, and it is preferable not to have someone holding the patient who is grounded to the floor.^1,11

Because implanted automatic defibrillators are more susceptible to the effects of ECT during stimulation, a cardiologist and an anesthesiologist should be consulted well ahead of time.^1,12

Important concurrent treatment of cardiovascular conditions, diabetes, gastroesophageal disease, neurological conditions,¹³ and the elderly should be considered prior to ECT.^1,7,11 

Concurrent Psychiatric  Medications Assessment 

Certain medications are known to interfere with ECT so it is advised that, whenever possible, ECT be administered without concurrent medications. However, it may be necessary to use certain medications with appropriate monitoring. These include:

• Antidepressants. The routine use of adjunctive antidepressant medications to improve efficacy with acute ECT is not recommended.⁷ Despite the prediction that reintroducing antidepressants during a course of acute ECT would reduce the risk of post-ECT relapse, additional research is needed to explore the specific effects of administering antidepressants during ECT.^1,7,11,14

• Lithium. Although in certain clinical circumstances, lithium can be beneficially administered during ECT,¹⁵ there is no consensus on the safety of this practice since lithium prolongs the neuromuscular blockade of succinylcholine and has been reported to increase the risk of post-ECT delirium.⁷ It is generally advisable to withdraw lithium prior to ECT. For certain bipolar patients who are well-controlled on lithium, the risk of ECT-induced mania may outweigh the risk of delirium, in which case lithium should be continued during ECT.^16,17

• Other mood stabilizers and anticonvulsants. Although anticonvulsants increase seizure threshold, it may be appropriate to continue these medications during ECT if they are used for mood stabilization.¹⁸ Patients with seizure disorder should continue to receive their anticonvulsant medications, however a temporary dose reduction may be needed and a neurology consultation is recommended.¹⁸

• Antipsychotics. There is no contraindication for the coadminstration of ECT and antipsychotic medications, especially in patients whose symptoms are refractory to conventional treatments.^19,20

• Benzodiazepines and sedative hypnotics. This class of medications—even those with shorter half-lives—are not recommended for routine use due to their anticonvulsant properties. It is important to decrease their total dosage or discontinue these medications either before or early in the course of ECT.^7,18,21

_____________________________________________________________________________________________________________________________________________________________________
RELATED CONTENT
Electroconvulsive Therapy: When Stigma Delays Use
Dabigatran-Induced Hemorrhage in an Elderly Man
_____________________________________________________________________________________________________________________________________________________________________

Informed Consent

Informed consent is an important part of the process for ECT and is sought before treatment, even though the capacity to provide voluntary consent for ECT was traditionally determined by the attending psychiatrist. The capacity to consent has generally been interpreted as evidence that the patient can understand information about the procedure and can act responsibly on the basis of this information.^1,11,22 

 Unless evidence to the contrary is compelling and determined by a court, individuals with mental illness are considered to have capacity to consent to ECT. No patient with a capacity to give voluntary consent should be treated with ECT without his or her written, informed consent. The use of involuntary ECT is rare and should only be reserved for patients who need emergency treatment and who have a legally appointed guardian who has agreed to the use of ECT.^1,8,11 

Clinicians must be familiar with local, state,^1,7,23 and national laws about the use of ECT.^1,8,11 The informed consent process should be documented in the patient’s medical record and should include the following information:^8,23

• The clinician recommending ECT and the indication for pursuing it 

• A description and summary of other treatment alternatives

• A detailed description of the technique, timing, and location of the ECT treatment

• A clarification of the various options regarding the electrode placement

• The recommended range for the number of treatments

• A statement that the treatment is not guaranteed to be fully successful

• A statement concerning the need for continuation or maintenance treatment

• Discussion of the possible risks, including death, cardiovascular complications, delirium, and cognitive sequela, especially memory impairment

• A statement that the consent also applies to emergency treatment that may be clinically necessary during periods when the patient is unconscious 

• A listing of patient requirements during the ECT course, such as fasting after midnight 

• A statement that the patient has had an opportunity to ask questions and an indication of who can be contacted with further questions

• A statement that consent is voluntary and can be withdrawn at any time

• Printed literature and videotapes about ECT may be useful.^1,8,11,23 The family of the patient should be included in this discussion.²⁴

• Whenever possible documents should be written in the primary language of the patient 

Second Opinion 

Although a second opinion is not required for ECT, a patient may choose to undergo an independent evaluation from a psychiatrist who is knowledgeable about ECT and not directly responsible for the individual’s treatment. The psychiatrist providing the second opinion should review the diagnosis, confirm illness severity and treatment resistance, corroborate the advisability of ECT, and review the adequacy of the pre-ECT evaluation.^3,21,23

Cultural Considerations 

It is important to understand the cultural context by which patients consent or refuse ECT. For example, there may be specific cultural beliefs on electricity and touching of the head that may prevent a patient from accepting ECT as a form of treatment.^24,25 Refugees and immigrants who may have experienced incarceration for political reasons in psychiatric institutions and who have been subjected to ECT involuntarily without psychiatric indication and/or survivors of torture may refuse such treatments.²⁶ 

In these circumstances, the reluctance to proceed with ECT is unfortunate since the individuals would likely benefit significantly with the procedure for the treatment of depression and psychotic disorders that have developed as a complication of trauma.^24-26

(Continue to next page for Administration of ECT)Administering an ECT

Equipment 

ECT equipment includes sufficient medical supplies and pharmacological agents for inducing anesthesia, providing ventilation, monitoring physiologic functions including seizure activity, and performing resuscitation.

• Anesthesia. This should be administered by trained specialists familiar with the various psychiatric conditions that require ECT treatment, an anesthesia-trained nurse practitioner, or a trainee anesthesiologist who has received adequate training and who has access to appropriate supervision may administer anesthesia.^1,11 

The procedure is performed under general anesthesia using short-acting intravenous agents, most commonly methohexital or propofol. Methohexital is the preferred anesthetic because of its established safety record, effectiveness, and low cost.^1,11 The inhalational anesthetic sevoflurane can also be used. 

The goals of anesthesia are to induce rapid unconsciousness and early recovery. Excessive anesthesia may prolong unconsciousness and may cause cardiovascular complications; inadequate anesthesia may lead to an incomplete unconsciousness and autonomic arousal.^1,8,11 Although anesthesia usually has no clinical significant effect on the seizure duration and amplitude, the anesthetic agent may affect ECT cognitive outcome.²⁷ 

If a generalized seizure can be induced with a lower current, it could increase the patient’s overall quality of life by decreasing the effects on cognitive function. If this remains consistent, it would be the determining factor in choosing the ideal agent for anesthesia. The appropriate anesthetic dose should be established at each treatment and adjustments made with each subsequent treatments.^1,11 Standard precautions for infection control must be adopted for all anaesthetic practice.

• Anticholinergics. Although not all clinicians routinely use anticholinergics, some would administer these agents (eg, atropine, glycopyrrolate) prior to anesthesia due to their effect on reducing the risk of vagally mediated bradyarrhythmias or asystole, and on decreasing oral and respiratory secretions ^1,11 However, anticholinergics can increase preexisting tachycardia and can cause constipation, fecal impaction, and urinary retention.^1,11

• Neuromuscular blockers. Neuromuscular blockers are administered to prevent bone fractures and physical injury related to motor activity during the seizure.^1,11,27,28 This is especially important if the patient has osteoporosis or a history of spinal injury; in these cases, complete relaxation may be indicated.^27,28 

The preferred depolarizing neuromuscular blocker is succinylcholine.^1,11 Atracurium, mivacurium, rocuronium, and rapacuronium are alternatives to succinylcholine.^1,11 A nondepolarizing muscle relaxant may be indicated in patients with pseudocholinesterase deficiency, hypercalcemia, severe neuromuscular disease, severe osteoporosis, or a personal or family history of malignant hyperthermia.^1,11 

Airway control is usually maintained with a bite block and mask ventilation. Prior to the electrical stimulation, the sufficiency of muscle relaxation is determined by the reduction or loss of knee, ankle, or plantar withdrawal reflexes, loss of muscle tone, the reduction or failure to respond to a nerve stimulator, or any combination of these factors.^1,11 

Stimulus Intensity and Dosing 

A brief pulse waveform is used to produce a sufficient electrical stimulus to induce a seizure in modern ECT machines.⁸ The dose is measured in millicoulombs of charge delivered.²⁸ There are 3 methods that are used to determine the dosing and the intensity of the stimulus.^1,7,11,29 

1. Empirical titration method: The most precise method for determining seizure threshold by gradually and progressively administrating higher doses during the first ECT session until seizure threshold is reached. 

2. Formula-based titration method: The dose is based on factors such as age, gender, and electrode placement.

3. Fixed-dose method: A fixed dose is given independent of patient personal characteristics or demographic factors.

Note: Historically, the glissando method—where the stimulus intensity was progressively increased during delivery from a subconvulsive to a convulsive level—was preferred. There in no clinical justification for the continued use of this method.^1,11

Stimulus Electrode Placement 

Common electrode positions include the bifrontotemporal, right unilateral, and bifrontal positions.^1,11,30,31

• Bifrontotemporal. Commonly referred to as bilateral, electrodes are placed bifrontotemporally, with the center of each electrode about 1 in above the midpoint of an imaginary line drawn from the tragus to the external canthus.^1,11,30

• Right unilateral. One electrode is typically placed over the nondominant frontotemporal area, and the other electrode is placed on the nondominant centroparietal scalp, just lateral to the midline vertex.^7,14 Because the left hemisphere is dominant in most people, unilateral electrode placement is almost always over the right hemisphere.^1,11

• Bifrontal. The placement of an electrode on each side of the head is more frontal than in standard bifrontotemporal placement.^1,11 

• Asymmetric bilateral.³¹ The left electrode is moved about 6 cm anterior from the standard frontotemporal position and its lateral edge is medial to the bony intersection ridge between the temple and the forehead while the right electrode is in the standard frontotemporal position. Note: This position still requires additional research.

Seizure Quality 

In modern ECT equipments, a brief pulse waveform is used to generate an electrical stimulus that is sufficient to induce a seizure.^7,14 The dose is measured in millicoulombs of charge delivered.³⁰ When determining stimulus intensity and dosing, the seizure threshold may increase and vary between 25% and 200% over the course of treatment. These changes need to be considered while administrating the stimuli.^1,11

Seizure threshold varies greatly among patients and may need to be determined at the initiation of treatment for each individual patient. Electrical dosing in excess of seizure threshold may result in more severe cognitive effects than near threshold treatment.^30-32 The seizure duration is not directly related to the ECT efficacy and has a complex association with stimulus intensity. 

Monitoring of the electroencephalogram (EEG) during ECT is used to confirm seizure activity and document duration.³⁰ Nevertheless, if the seizure duration is <15 seconds in motor and EEG manifestations, the seizure was very likely limited by insufficient electrical stimulation.^1,11 Seizure motor activity is monitored using the “cuff” procedure, in which distribution of a muscle relaxant is blocked to the hand or foot via a tourniquet in order to maintain the potential for muscle contraction.^1,11,31 Oxygen saturation and cardiac rhythm are also monitored.³³

(Continue to next page for Post-ECT Follow-Up)Post-ECT Follow-Up

Patient Monitoring 

Close monitoring, supervised by an anesthetist, should be provided during and after treatment, until the patient is fully recovered from anesthesia.^1,11 During treatment, monitoring should include observation of seizure duration, airway patency, agitation, vital signs, and adverse effects. After treatment, observation should be provided in a designated recovery area with provisions including expert nursing care.^1,7,11 

Complications

• Medical effects. While a wide range of mortality rates are reported in the literature, 1 to 2 per 100,000 individual ECT treatments is the number widely quoted—yielding a figure of 1.6 deaths per 10,000 in a (typical) course of 8 ECTs. Note: These statistics approximate the mortality figure of 1 in 10,000, which is associated with general anaesthesia in minor surgery.^1,2,11 

Immediate side effects from ECT may include headaches, muscle aches or soreness, nausea, and confusion that usually disappear during the first few hours following the procedure.⁷ These may be secondary to the anesthetic or the ECT treatment itself and should be conservatively managed.^1,11 

Physical complications, such as spinal or other fractures, that are reported in the early days of ECT are almost never reported in present practice because of the administration of anesthesia and muscle relaxants in a controlled environment.⁸ Poor health status, rather than advancing age, increases the risk for the rare but potentially severe physical complications associated with general anesthesia and ECT—such as in cases of space-occupying cerebral lesions or other conditions that increase intracranial pressure, recent myocardial infarction associated with unstable cardiac function, recent intracerebral hemorrhage, unstable vascular aneurysm or malformation, retinal detachment, pheochromocytoma, cardiac arrhythmias, aspiration pneumonia, prolonged apnea, spinal compression fractures, or mouth injury.^1,11,34,35

• Neurological effects. Despite the increased intracranial pressure, cerebrovascular events are extremely rare among patients receiving ECT. Other sources of morbidity are prolonged and tardive seizures. The risk of prolonged seizures or status epilepticus is increased by some concomitant pharmacological treatments. These include use of adenosine antagonists (eg, theophylline), high dosage of some antipsychotics, and lithium.^8,36 This risk may also be increased among patients with a preexisting electrolyte imbalance and when >1 seizure is induced in the same treatment session.³⁷

• Cognitive effects. Individual patients vary significantly in the extent and severity of cognitive adverse effects they experience following ECT.^1,11 Cognitive impairment can be minimized with the use of the proper ECT techniques and it seems that advancing age, lower premorbid intellectual function, and female gender may be associated with greater cognitive deficits; the use of sine wave stimulation and bilateral electrode placement may result in more severe and persistent deficits. 

A recent review in older adults found mixed results regarding the impact of ECT on cognitive domains, aside from interictal slowing of information processing speed.^30,31 ECT does not appear to impair the ability to learn and retain new information and the procedure is usually associated with subjective cognitive improvement, especially in those patients with major depression that is associated with cognitive difficulties.^1,8,11,36 

However, ECT may cause some objective cognitive impairment which consists of a transient inability to retrieve some memories, anterograde amnesia in particular for events occurring during the days, weeks, and few months preceding ECT; however, most of these memories typically return and anterograde amnesia usually resolves.^1,11 Transient inability to retrieve some memories following the ECT course retrograde amnesia could also occur and many patients also experience permanent memory loss for events occurring during the course of treatment, particularly events on treatment days.^10,17 

Some factors may impact the cognitive side effects of ECT—including the anatomic positioning of electrodes, the type of electrical waveform used, the intensity of the electrical stimulus, and the spacing of treatments.^1,11,30 Compared to application of electrodes over the right hemisphere (eg, right unilateral ECT), the traditional bifrontotemporal placement of electrodes (eg, bilateral ECT) results in prolonged recovery of orientation during the postictal period, a greater probability of developing delirium, and more extensive and severe amnesic effects.^5,27-30,37 When left and right unilateral ECT differ in the extent of amnesia they produce for verbal rather than nonverbal material, it indicates lateralized neurophysiological effects.^27-32 

Electrical waveforms that are inefficient in seizure-eliciting properties (eg, sine wave) produce greater cognitive disturbance than more efficient waveforms (brief and ultrabrief pulse).^6,27-32,37 Similarly, there is evidence that, within a waveform, the extent to which electrical dosage exceeds seizure threshold contributes to the magnitude of short-term cognitive side effects.^34,35

Post-seizure (postictal) delirium may occur in a minority of patients and is usually manifested by a brief period of disorientation, profound confusion, and impairments in attention, praxis, memory, and hallucinations.^1,11,31 These effects reverse over time and the delirium usually disappear within weeks of completing the ECT course.³⁸ 

Elderly patients are at greater risks for prolonged confusion and even delirium, particularly when they suffer from a degenerative or vascular dementia.³⁹ However, as mentioned earlier, elderly patients presenting with a dementia syndrome associated with depression may experience a dramatic improvement in cognition when they are treated with ECT.^39-42

There have been few attempts to use pharmacological strategies to reduce the cognitive side effects of ECT—including opioid antagonists, calcium-channel blockers, cholinesterase inhibitors, acetylcholine precursors, corticosteroids, thyroid hormone, vasopressin analogs, somatostatin, melanocyte-stimulating hormone, atrial natriuretic peptide, substance P, nootropics, ergoloid mesylates, and psychostimulants. 

However, none of these seems to be beneficial with the exception of the opioid antagonists naloxone.³⁴ Naloxone in low doses of 1 mg/kg to 4 mg/kg reversed ECT-induced retrograde and anterograde amnesia with a possible risk of increased retrograde amnesia with higher doses of 1.6 mg/kg. 

Frequency of ECT Treatments

ECT is administered as a single treatment, 2 or 3 times weekly, on alternate days.^1,11 The number of treatments needed to achieve a full clinical response in patients varies widely. The course of therapy typically ranges between 6 to 12 treatments^26,33 and patients may respond after only a few or up to 10 tries. However, the total number should be a function of the patient’s degree and rate of clinical improvement, as well as the severity of cognitive adverse effects; in most cases, treatment is stopped when maximal improvement is reached.^1,11

Continuation and Maintenance ECT 

Despite its high efficacy, the relapse rate during the 6- to 12-month period after completion of an acute course of ECT exceeds 50% in patients who do not respond to pharmacological treatment. Providing additional ECT treatments referred to as continuation ECT (C-ECT) and maintenance ECT (M-ECT) would be needed to maintain remission and to reduce the risk of relapse.³⁵ 

• C-ECT. This involves the administration of additional ECT treatments during the 6-month period after remission. Indications for C-ECT include a history of ECT-responsive illness, patient preference, resistance or intolerance to medications alone, and ability of the patient (or surrogate consenter) to provide informed consent and adhere to the treatment plan.³⁴ The indications for use and patient selection for C-ECT are predominately similar to those for a short-term ECT course. The treatment guidelines and parameters for C-ECT are recommended to be consistent with the parameters used to achieve remission, with the exception of greater intertreatment intervals during C-ECT.^1,11 Although adverse cognitive effects can occur during C-ECT, the risk and severity of cognitive impairment are generally low, possibly because of the greater intertreatment intervals.^35,41 

• M-ECT. This intervention is for prevention of recurrence and its indications are the same as those for C-ECT. Since most patients who were referred for ECT have disorders that are associated with a 1-year high recurrence risk rate of 50% or more, it is important to provide M-ECT for these patients.³⁵ Typical scheduling of M-ECT involves gradually shifting frequency after remission (eg, weekly to monthly treatments over a period of 6 to 12 months). 

Decisions regarding scheduling should be made on an ongoing basis, based on patients’ history and present response. Cautious use of concomitant psychotropic agents should be considered for patients who are unable to be managed with M-ECT alone. Although M-ECT may slow down the process of cognitive recovery, it is believed that the development or worsening of cognitive impairment is unlikely with monthly treatments. 

Although there is no lifetime maximum⁴² number of treatments with ECT, the need for M-ECT should be reviewed by the practitioner and patient at least twice a year, consent should be re-obtained at least every 6 months, and anesthetic/medical and cognitive reevaluation should be performed at regular intervals. For patients requiring relatively frequent M-ECT (ie, weekly to biweekly) over a period of months to years, the presence of persistent deficits should be weighed against the anticipated benefits of continuing the treatments.^1,11,40-42

Acknowledgements: The author would like to thank the committee members of the electroconvulsive treatment program at the Veterans Affairs Central California Health Care System, including Director Avak A. Howsepian, MD, PhD, Chair Robert Emes, NP-C, and members Michael Gatley, MD, and Neil Smith, DO, as well as Sylvia Galvez, FNP, PMHNP, Nestor Manzano, MD, chief of mental health, Wessel H. Meyer, chief of staff, Robert W. Hierholzer, associate chief of staff for education and research, and the staff of the Cottage and Faleola services at the Matariki Community Mental Health Centre in Auckland, New Zealand.

Disclaimer: The views expressed in this article are those of the presenter and do not reflect the official policy of the VACCHCS or the Department of Veterans Affairs.

References:

1.Jaffe R. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging. 2nd ed. Washington, DC: American Psychiatric Association; 2001.

2.Abrams R. The mortality rate with ECT. Convuls Ther. 1997;13(3):125-127. 

3.American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013:265-290.

4.Levin L, Wambold D, Viguera A, et al. Hemodynamic responses to ECT in a patient with critical aortic stenosis. J ECT. 2000;16(1):52-61. 

5.Pandya M, Pozuelo L, Malone D. Electroconvulsive therapy: what the internist needs to know. Cleve Clin J Med. 2007;74(9):679-685.

6.Greenberg RM, Kellner CH. Electroconvulsive therapy: a selected review. Am J Geriatr Psychiatry. 2005;13(4):268-281.

7.Fink M. Convulsive therapy: a review of the first 55 years. J Affect Disord. 2001;63(1-3):1-15.

8.Bocchio-Chiavetto L, Zanardini R, Bortolomasi M, et al. Electroconvulsive therapy (ECT) increases serum brain derived neurotrophic factor (BDNF) in drug resistant depressed patients. Eur Neuropsychopharmacol. 2006;16(8):620-624. 

9.Husain MM, McClintock SM, Rush AJ, et al. The efficacy of acute electroconvulsive therapy in atypical depression. J Clin Psychiatry. 2008;69(3):
406-411.

10.Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252.

11.Ottosson JO, Fink M. Ethics in Electroconvulsive Therapy. New York, NY: Routledge; 2004.

12.Chanpattana W, Andrade C. ECT for treatment-resistant schizophrenia: a response from the far East to the UK. NICE report. J ECT. 2006;22(1):4-12. 

13.Kushner SA, Prudic J, Louis ED. Transient improvement of essential tremor during electroconvulsive therapy. J ECT. 2007;23(2):99-102.

14.Lisanby SH. Electroconvulsive therapy for depression. N Engl J Med. 2007;357(19):1939-1945.

15.Dolenc TJ, Rasmussen KG. The safety of electroconvulsive therapy and lithium in combination: a case series and review of the literature. J ECT. 2005;21(3):165-170. 

16.Medda P, Perugi G, Zanello S, et al. Comparative response to electroconvulsive therapy in medication-resistant bipolar I patients with depression and mixed state. J ECT. 2010;26(2):82-86. 

17.Sienaert P, Peuskens J. Anticonvulsants during electroconvulsive therapy: review and recommendations. J ECT. 2007;23(2):120-123.

18.Havaki-Kontaxaki BJ, Ferentinos PP, Kontaxakis VP, et al. Concurrent administration of clozapine and electroconvulsive therapy in clozapine-resistant schizophrenia. Clin Neuropharmacol. 2006;29(1):52-56. 

19.Braga RJ, Petrides G. The combined use of electroconvulsive therapy and antipsychotics in patients with schizophrenia. J ECT. 2005;21(2):75-83.

20.Rabheru K. The use of electroconvulsive therapy in special patient populations. Can J Psychiatry. 2001;46(8):710-719.

21.Weiner RD, Krystal AD. Electroconvulsive Therapy. In: Blazer DG, Steffens DC, Busse EW, eds. Textbook of Geriatric Psychiatry. 3rd ed. Washington, DC: American Psychiatric Publishing; 2004:413-426. 

22.Harris V. Electroconvulsive therapy: administrative codes, legislation, and professional recommendations. J Am Acad Psychiatry Law. 2006;34(3):406-411.

23.McCall WV. Electroconvulsive therapy: all in the family. J ECT. 2007;23(4):213-214. 

24.Rose D, Wykes T, Leese M, et al. Patients’ perspectived on electroconvulsive therapy: systematic review. BMJ. 2003;326(7403):1363.

25.Lauber C, Rössler W. Involuntary admission and the attitude of the general population, and mental health professionals. Psychiatr Prax. 2007;34 Suppl 2:S181-185. 

26.MacPherson RD, Loo CK. Cognitive impairment following electroconvulsive therapy—does the choice of anesthetic agent make a difference? J ECT. 2008;24(1):52-56.

27.Nobler MS, Sackeim HA. Neurobiological correlates of the cognitive side effects of electroconvulsive therapy. J ECT. 2008;24(1):40-45.

28.Taylor S. Electroconvulsive therapy: a review of history, patient selection, technique, and medication management. South Med J. 2007;100(5):494-498. 

29.Lisanby SH. Electroconvulsive therapy for depression. N Engl J Med. 2007;357:1939-1945.

30.Lapidus KA, Shin JS, Pasculli RM, et al. Low-dose right unilateral electroconvulsive therapy (ECT): effectiveness of the first treatment. J ECT. 2013;29(2):83-85.

31.Perera TD, Luber B, Nobler MS, et al. Seizure expression during electroconvulsive therapy: relationships with clinical outcome and cognitive side effects. Neuropsychopharmacology. 2004;29(4):813-825. 

32.Pigot M, Andrade C, Loo C. Pharmacological attenuation of electroconvulsive therapy—induced cognitive deficits: theoretical background and clinical findings. J ECT. 2008;24(1):57-67.