View
230
Download
0
Category
Preview:
Citation preview
8/13/2019 Everything About ECT and Ablation Neurosurgery
1/34
INTRODUCTION Electroconvulsive therapy (ECT) uses a small electric current to produce
a generalized cerebral seizure under general anesthesia. ECT is used mainly to treat severe
depression, but is also indicated for patients with other conditions, including bipolar disorder,
schizophrenia, schizoaffective disorder, delirium, and neuroleptic malignant syndrome.
There is no question about the efficacy and safety of ECT, which is practiced widely in the
United States and the rest of the world . Nevertheless, it remains controversial and stigmatizedbecause of misinformation and outmoded perceptions about how the treatment is performed.
This topic provides an overview of ECT. The indications for treating unipolar major depression
with ECT, the efficacy of ECT for treating unipolar depression, technique for performing ECT,
and medical consultation for ECT are discussed separately.
HISTORY OF ECT The use of seizures to treat psychiatric disorders has progressed over
time, and began with observations that schizophrenic patients often improved temporarily after
a spontaneous seizure. Initially, physicians induced seizures with medications. In 1938, Italianpsychiatrists used an electric current to induce seizures as a treatment for schizophrenia. ECT
quickly spread around Europe and the rest of the world, and was first used in the United States
in 1939. Patients suffered bone fractures occasionally and considerable anticipatory anxiety, but
advances in anesthesia techniques in the 1950s allowed for the use of general anesthesia and
muscle relaxation for ECT, which reduced the incidence of these problems.
The use of ECT in the United States has fluctuated. Use of ECT declined in the 1970s, and
subsequently increased, possibly as a result of greater treatment resistance to pharmacotherapy
in depressed patients, increased recognition of the limitations of pharmacotherapy, and better
public acceptance. A practice survey from 1988-89 estimated that at least 100,000 patients
received ECT annually. The typical ECT patient today is relatively affluent and receives ECT in
a private sector psychiatric facility. State hospitals rarely offer the treatment, even though many
of the patients would meet indications for ECT.
MECHANISM OF ACTION The mechanism of action for ECT is unknown, but there are a
myriad of well-documented changes in the central nervous system:
Human and animal studies show that ECT increases release of monoamine neurotransmitters,
particularly dopamine and serotonin. ECT also enhances monoamine transmission by
desensitizing presynaptic adrenergic autoreceptors.
One theory postulates that ECT exerts its beneficial effects by increasing release of central
neuropeptides, including corticotrophin releasing factor, somatostatin (STS), and neuropeptide
Y .
The neuroendocrine hypothesis is based upon the diabetes/insulin model and suggests that
mood disorders are caused by insufficiency of a hypothalamic mood-maintaining peptide.
Repeated seizures enhance the production and release of the putative hypothalamic peptide
8/13/2019 Everything About ECT and Ablation Neurosurgery
2/34
antidepression, which relieves both neuroendocrine and behavioral abnormalities.
ECT has anticonvulsant properties, which has led to the suggestion that these properties are
responsible for the therapeutic effects of the treatment.
Positron emission tomography (PET) studies demonstrate decreased metabolic activity in
frontal and cingulate cortex after ECT.
Functional magnetic resonance imaging before and after successful treatment with ECT reveals
a reduction in global connectivity within the left dorsal lateral prefrontal cortex. Quantitativeelectroencephalogram (EEG) studies demonstrate increased slow (delta) wave activity in the
prefrontal cortex after ECT, which is associated with clinical response.
Several human and animal studies indicate that ECT has trophic effects on the central nervous
system. ECT increases brain derived neurotrophic factor (BDNF) in patients and
electroconvulsive stimulation induces neurogenesis and mossy fibre sprouting from granule
cells in rat hippocampus.
PRE-ECT EVALUATION The goals of the pre-ECT evaluation are to:
Determine whether ECT is indicated.
Establish baseline psychiatric and cognitive status to serve as reference points for
evaluating response and cognitive effects.
Identify and treat any nonpsychiatric medical conditions that might be associated with an
increased risk of adverse events from ECT.
Initiate and continue the informed consent process.
A complete medical history should be taken. Medical consultation prior to ECT is
indicated for most patients 40 years or older, and is frequently obtained in youngerpatients as well. Particular attention should be paid to any history of cardiopulmonary
disease and prior surgeries (with inquiry about type of anesthesia and any complications).
A history of skull fractures should be determined, as this may affect electrode placement.
Appropriate physical examination and laboratory evaluation, guided by the relevant
history, should be performed. The patient's handedness and any dental problems should
be noted. Specific laboratory tests are not indicated for patients without known medical
comorbidities.
SPECIFIC MEDICAL CONDITIONS Inducing a seizure causes transient increases in bloodpressure, pulse, and intracranial pressure, which can have deleterious effects. Organ systems of
most concern are:
Cardiovascular
Pulmonary
Central nervous system
Seizures increase cardiac workload and oxygen demand. Thus, it is important to try to
8/13/2019 Everything About ECT and Ablation Neurosurgery
3/34
maximize the patient's cardiovascular status before ECT. Additionally, medication to
blunt increases in heart rate and blood pressure is indicated prior to ECT and during the
procedure in patients for whom these increases would be detrimental.
Coronary heart disease Cardiac complications are the most common cause of serious
morbidity and mortality during ECT.
Patients with coronary heart disease should be evaluated prior to ECT with a careful
cardiac history and ECG. Additional cardiovascular diagnostic testing and evaluation by
a cardiology consultant may be indicated for selected patients, and for any patient with
unstable disease.
History of myocardial infarction History of myocardial infarction and current unstable
angina present increased risk. Careful consideration of the risk/benefit ratio of ECT in
such cases is essential. The key factors in this assessment are the extent of myocardial
damage and subsequent healing, and the residual functional cardiac status.
In general, the longer one waits after a myocardial infarction, the safer it is to perform
ECT. For patients who have had a myocardial infarction and are not at imminent risk
from their depressive episode, we suggest waiting a minimum of three months prior to
starting a course of ECT. However, patients at high risk of death due to their depression
can be treated sooner. For severely depressed patients, treatment with ECT on an
emergent basis may be indicated.
Hypertension The patient's blood pressure should be well controlled prior to ECT. Thepatient should take his or her currently prescribed antihypertensive medications (with the
exception of diuretics) with a small sip of water, prior to each ECT treatment.
Use of prophylactic beta blockers to prevent treatment-induced hypertension is discussed
separately.
Heart failure and valvular disease The use of ECT in patients with heart failure or
valvular disease is discussed separately.
Pacemakers and implantable defibrillators The use of ECT in patients with
pacemakers or implantable defibrillators is discussed separately.
Pulmonary disease Optimizing pulmonary status before ECT is important. The
anesthesiologist manipulates the patient's airway during ECT using a bag and mask
circuit and there is a risk of inducing bronchoconstriction. All patients should receive
supplemental oxygen via nasal cannula, initiated a few minutes prior to each treatment.
8/13/2019 Everything About ECT and Ablation Neurosurgery
4/34
Elective intubation is not indicated for ECT, except in rare circumstances in which the
anesthesiologist assesses that intubation would be exceptionally difficult should the
airway become compromised.
Neurologic disease The use of ECT for patients with brain tumors, history of stroke,
dementia, and neuromuscular disease is discussed separately
CONCURRENT MEDICATIONS The patient's current medications, including prescription,
over-the-counter, and complementary or alternative drugs should be reviewed prior to ECT. The
ECT psychiatrist, anesthesiologist, or medical consultant should decide which to continue and
which to taper and discontinue.
Psychotropic drugs Many psychotropic medications may be continued during a course of
ECT for their synergistic effect without compromising safety, including antidepressants,
antipsychotics, and lithium. Morning doses on the day of ECT are given after the patient hasrecovered from that day's procedure. Anticonvulsants and benzodiazepines often interfere with
ECT and may need to be tapered and discontinued.
Antidepressants improve the efficacy of ECT. A review of 10 systematic reviews, 7 meta-
analyses, and 3 practice guidelines found that for depressed patients, a tricyclic may improve
the antidepressant effect of ECT. As an example, a randomized trial assigned 319 depressed
patients receiving an acute course of ECT to concomitant nortriptyline, venlafaxine, or placebo.
Remission occurred in more patients who received nortriptyline or venlafaxine compared with
placebo (63 and 60 versus 49 percent) with a significant difference between nortriptyline andplacebo.
Antidepressants are generally safe to use with ECT and do not affect its tolerability. As an
example, a randomized trial of depressed patients receiving an acute course of ECT with
concomitant nortriptyline, venlafaxine, or placebo found the number of adverse events did not
differ significantly between the three groups . Other types of antidepressants are also well
tolerated during ECT, including selective serotonin reuptake inhibitors, tetracyclics, and
monoamine oxidase inhibitors.
Antipsychotic medications are often continued during ECT and may provide a synergistic
antipsychotic effect, especially second generation antipsychotics. In addition, antipsychotics
generally do not appear to affect the tolerability of ECT. Second generation antipsychotics and
high potency first generation antipsychotics are thought to be safe. A review found that early
reports warned of hypotension and cardiac complications from combining chlorpromazine and
ECT, but later reports did not substantiate these problems . Nonetheless, combining of low
potency, first generation antipsychotics with ECT should be done cautiously.
8/13/2019 Everything About ECT and Ablation Neurosurgery
5/34
Lithium has the potential to increase the adverse cognitive effects of ECT and to prolong the
effects of succinylcholine (which is typically used during ECT to reduce tonic-clonic
movements), but these problems are rare . However, a review of several case series found that
concomitant lithium and ECT is safe [33]. We suggest reducing lithium levels below the full
therapeutic range at the time of each ECT treatment by withholding one or two doses of lithium
prior to each treatment.
Benzodiazepines should be tapered and discontinued whenever possible during ECT because of
their anticonvulsant properties, which can increase seizure threshold, shorten seizure duration,
and decrease the intensity of the ECT seizure [34]. These effects may decrease the clinical
efficacy of ECT.
For patients who need to continue their benzodiazepine during ECT, some authorities
recommend switching from drugs with a long half-life to one with a short half-life, and
withholding the evening dose before each ECT treatment. Small doses of benzodiazepines,
however, may not be a problem. Patients who are very anxious about the ECT procedure itself
may take a dose of benzodiazepine (eg, 1 mg of lorazepam sublingual) 30 to 60 minutes before
the treatment.
Anticonvulsants may interfere with the efficacy of ECT, similar to benzodiazepines [35]. When
anticonvulsants are used for mood stabilization, they generally should be tapered and
discontinued prior to ECT.
Patients with epilepsy should continue their anticonvulsants during a course of ECT. Clinicians
should consider reducing the dose if seizures are difficult to elicit, or withholding a dose the
evening or night before the ECT treatment.
Other drugs
Cardiovascular medications Patients should receive their routine antihypertensive (other than
diuretics) and antianginal medications with a small sip of water approximately two hours before
ECT. Diuretics should not be given because it is better to minimize the amount of urine in the
bladder during the procedure, to prevent the patient from wetting himself as a result of the
seizure.
Asthma medications Glucocorticoids and beta-adrenergic agonists may be given before ECT,
as needed, to prevent bronchoconstriction. Patients who routinely use a fast-acting inhaler
should do so immediately before the treatment. Theophylline should be avoided or maintained
at the lowest effective blood level because it has been associated with prolonged seizures and
status epilepticus [36].
Gastrointestinal medications Patients with gastroesophageal reflux disease (GERD) should
8/13/2019 Everything About ECT and Ablation Neurosurgery
6/34
receive their H2 blocker, proton pump inhibitor, or metoclopramide with a sip of water two
hours before ECT to prevent reflux and possible aspiration. Sodium citrate (30 cc po) may be
given immediately before treatment to neutralize any acid remaining in the stomach [29].
INFORMED CONSENT The psychiatrist should ensure that the consent process conforms
to all state and local laws and statutes, and hospital policies. Informed consent requires that the
patient [29]:
Receive adequate information about depression and ECT
Is capable of understanding and acting reasonably on this information
Is given the opportunity to consent in the absence of coercion
ECT consent forms are more detailed compared with those for most other medical
procedures because ECT is closely scrutinized.
Informational material written for the layperson is typically provided to patients and family
members as part of obtaining informed consent. In addition, patients and family members maywatch video to augment the written material and discussion with the psychiatrist recommending
ECT.
The vast majority of ECT is done with fully informed consent given by the patient. In
circumstances when the patient is too ill (eg, catatonic or psychotic) and lacks capacity to
provide consent, and the need for ECT is urgent or emergent, the psychiatrist should seek
substitute consent by a court.
The patient should be cautioned not to make major personal or financial decisions during orimmediately after a course of ECT. In addition, the patient should not drive until the cognitive
effects of ECT have resolved. Patients who are receiving continuation or maintenance ECT
should not drive until 24 hours after each treatment [37].
TREATMENT COURSE
Number of treatments There is no standard number of treatments for an acute ECT course
and no way to predict how many treatments a particular patient will need. Most patients remit
with 6 to 12 treatments, but some require only three while others require 20 or more [29].
In a study of 184 patients with unipolar major depression, the mean number of treatments
needed to reach remission was 7 (standard deviation 3) [38]. A second study of 230 patients
with unipolar or bipolar major depression found that 90 percent or more of the remissions
occurred with nine or fewer seizures, depending upon the type of electrode placement [39].
Acute ECT should last until the patient remits, reaches an improvement plateau, or develops
limiting adverse effects. It is becoming more common to taper the frequency of ECT treatments
8/13/2019 Everything About ECT and Ablation Neurosurgery
7/34
rather than abruptly stop a course.
Once remission is achieved, however, ongoing continuation and maintenance treatments are
frequently indicated.
Treatment frequency The frequency of treatments varies by country and the clinical urgency.
Standard practice in the United States is to give ECT three times per week on a Monday-Wednesday-Friday schedule. The routine in many other countries is twice a week, particularly
for elderly patients. Urgently ill patients (eg, catatonic or severely malnourished) may be given
daily bilateral ECT until some improvement is evident [37].
Meta-analyses of five randomized trials (169 patients with unipolar major depression) found
that symptomatic improvement, remission, and number of ECT treatments were comparable for
twice-weekly and thrice-weekly ECT; however, duration of treatment was significantly longer
for twice-weekly ECT (by nearly five days) [40]. The data were insufficient to analyze
differences in cognitive impairment.
Clinical monitoring Depressive symptoms and cognition should both be monitored. Several
depression rating scales are available; the most common is the Hamilton Rating Scale for
Depression (HRSD or "HAM-D") [41]. The scale should be administered at baseline, weekly
during the course of ECT, and when the ECT course is completed.
Many scales are also available for monitoring cognition; the most common is the Mini Mental
State Examination [42]. It is easy to use and adequate for routine clinical use, although its
sensitivity may be limited [43]. More comprehensive neuropsychologic testing may be
indicated for selected patients (eg, those with known cognitive deficits at baseline).
ADVERSE EFFECTS The adverse effects of ECT may be divided into medical or cognitive
effects.
Adverse medical effects The mortality rate of ECT is 2 to 4 deaths per 100,000 treatments,
making it one of the safest procedures performed under general anesthesia [44,45]. A review of
10 systematic reviews, 7 meta-analyses, and 3 practice guidelines found that the mortality
associated with ECT was comparable to the mortality associated with minor procedures
involving general anesthesia [27]. Concerns that ECT causes structural brain damage have been
dispelled by multiple human and nonhuman primate studies [1,27].
Mortality is mostly related to cardiopulmonary events. Patients with coronary heart disease may
be at risk for cardiac ischemic events because the seizure increases cardiac workload and
oxygen demand. The cardiovascular effects of ECT are discussed separately.
Other adverse medical effects include:
8/13/2019 Everything About ECT and Ablation Neurosurgery
8/34
Aspiration pneumonia Risk is increased in patients who do not have an empty stomach
Fracture Patients with severe osteoporosis are at increased risk of fracture, and extra
care should be taken to insure excellent muscle relaxation [46].
Dental and tongue injuries These may occur when the oral bite block is not fully
protective [47]. Loose teeth are at risk for dislodgement during the procedure and
possible aspiration, and should be stabilized or extracted before ECT. Headache This is the most common, nonserious adverse medical effect of ECT [48-50].
Patients should be told to expect some headache after each treatment. It is typically
managed with acetaminophen or ibuprofen given after the treatment. Prophylaxis with IV
ketorolac 30 mg may be considered for patients with significant post-ECT headache [51].
Nausea Transient, postprocedure nausea is common and is the result of the anesthesia
and airway manipulation, which may introduce air into the stomach. Prophylaxis with IV
ondansetron 4 mg should be given to patients with significant post-ECT nausea.
Other somatic symptoms Patients may complain of other somatic symptoms such asmyalgias. However, one study assessed a group of depressed patients pre-ECT and during
an acute course of ECT, and found the frequency of somatic symptoms other than
headache did not increase [52]. The authors suggested that these other somatic symptoms
may have been due to the depressive illness, the use of psychotropic medications, or
withdrawal from such medications.
Adverse cognitive effects Most patients report some adverse cognitive effects during
and after a course of ECT. The incidence depends upon electrode placement, stimulustype and dose, anesthesia, and the patient's pretreatment cognitive status. A systematic
review found four studies in which the proportion of patients who reported any memory
loss ranged from 51 to 79 percent [53].
ECT causes three types of cognitive impairment:
Acute confusion
Anterograde amnesia
Retrograde amnesia
The acute confusional state is the result of both the seizure and the anesthesia. It typically
resolves 10 to 30 minutes after the procedure.
Anterograde amnesia is the decreased ability to retain newly acquired information. It occurs
during a course of ECT and typically resolves within two weeks after completing the course.
We thus suggest that patients refrain from driving for 24 hours after an ECT treatment or from
making important business or personal decisions one to two weeks after completing an acute
8/13/2019 Everything About ECT and Ablation Neurosurgery
9/34
course of ECT [54].
Retrograde amnesia involves forgetting recent memories and is the most anxiety-producing
cognitive effect of ECT. The memories are for events that occur during the course of ECT and a
period of weeks to a few months prior to that. The deficits are greatest and most persistent for
knowledge about public or world events (impersonal memory) compared with knowledge about
the self (personal memory) [55]. Bilateral ECT causes more retrograde amnesia than rightunilateral. Retrograde amnesia recovers more slowly than anterograde amnesia [55-57].
Some of the lost memories of events prior to the course of ECT may be expected to return,
while others may not. A systematic review found four studies in which the proportion of
patients who reported persistent or permanent memory loss ranged from 29 to 55 percent [53].
The etiology of these more severe memory impairments is controversial [58,59]. Regardless,
the typical ECT patient is profoundly depressed and accepts some degree of memory loss as a
reasonable tradeoff for resolution of the depressive episode.
Impaired cognition due to depression often improves after a course of ECT [60]. A review of
ECT in elderly patients with impaired cognition due to depression ("pseudodementia")
examined six studies that tested cognition before and after ECT in patients mostly 55 years or
older [61]. Patients were assessed with a cognitive screening instrument, either the Mini Mental
State Examination [42] or the Mattis Dementia Rating Scale [62]. Global cognitive functioning
in patients with cognitive impairment improved in all studies.
CONTINUATION AND MAINTENANCE ECT Continuation ECT is the practice of
providing a single ECT treatment, at an interval of one to eight weeks, during the first six
months after remission. The purpose is to prevent relapse of the mood or psychotic episode that
prompted the acute course of ECT. Maintenance ECT refers to ECT given beyond continuation
ECT, to patients who have recovered from the acute mood or psychotic episode but require
treatment to prevent recurrence of a new episode. Continuation and maintenance ECT are
usually outpatient procedures.
Mood and psychotic disorders are chronically recurring illnesses. Therefore, continuation and
maintenance treatment (with pharmacotherapy, ECT, psychotherapy, or a combination) are
required for most patients who recover from an initial episode. As an example, in a prospective,
observational study of 154 patients with major depression who remitted after successful
treatment with ECT in community hospitals, 64 percent relapsed during 24 weeks of follow-up
[63].
We suggest continuation and maintenance ECT for depressed patients who have successfully
completed a course of acute ECT and:
Relapse without continuation and maintenance treatment (either pharmacotherapy or ECT), and
8/13/2019 Everything About ECT and Ablation Neurosurgery
10/34
require a second a course of acute ECT
Fail one or more courses of continuation and maintenance pharmacotherapy
Prefer continuation and maintenance ECT
The electrode placement used for continuation and maintenance ECT should be the same as that
used for acute ECT.
Pharmacotherapy is often combined with continuation and maintenance ECT, with improved
outcomes [64].
The schedule for continuation and maintenance ECT generally starts with weekly treatments for
several weeks, and gradually tapers to the maximal interval that allows the patient to remain
euthymic. Following an acute course of ECT three times per week, we suggest treatments be
administered [38]:
Weekly for four weeks
Biweekly for eight weeks
Monthly for two months
Some patients continue to taper down to one treatment every three months, depending upon
their clinical status and preference. Patients who benefit from maintenance ECT can receive it
indefinitely. Use of self report and clinician administered rating scales to monitor the patients
clinical status is discussed separately.
Following acute ECT, continuation ECT alone appears to be comparable to continuation
pharmacotherapy alone. A randomized trial compared continuation treatment with either ECT
or pharmacotherapy in 184 patients who remitted from unipolar major depression after an acute
course of bilateral ECT [38]. Patients were assigned to a fixed schedule of continuation ECT or
combination pharmacotherapy with lithium plus venlafaxine. In both groups, 46 percent of
patients remained euthymic for the six months of the study. In addition, the two continuation
treatments did not differ in memory effects [65].
Cognitive effects of continuation and maintenance ECT are generally minor or nonexistent:
A controlled trial randomly assigned depressed patients who remitted with an acute course of
ECT to continuation ECT or continuation pharmacotherapy, and evaluated them with an
extensive battery of memory tests at baseline and after 24 weeks of treatment [65]. There were
no significant differences between groups on any of the memory tests.
An observational study evaluated 20 patients (multiple diagnoses) receiving maintenance ECT
with a comprehensive neuropsychologic battery and retested them one year later [66]. There
were no significant differences in test scores over time. In addition, test scores for the patients
receiving maintenance ECT did not differ significantly from a control group of patients not
receiving ECT.
8/13/2019 Everything About ECT and Ablation Neurosurgery
11/34
STIGMA, ACCESS, AND TRAINING
Stigma Stigma remains the biggest impediment to the appropriate use of ECT. The level of
knowledge about modern ECT among patients and medical practitioners is low [67]. The
portrayal of ECT in the media as a crude and coercive treatment remains problematic,
frightening off patients who might benefit from it. Improved education about ECT among
health care professionals will lead to more favorable perceptions about its use [68].
Access Access to ECT in the United States is variable and very limited in some rural areas.
It is rarely available to patients in state psychiatric hospitals. Patients with no or limited
insurance coverage may be unable to pay for ECT, leading to a situation in which ECT is
preferentially available to more affluent patients with better insurance [69].
Training ECT is a standard part of training in general psychiatry residency programs in the
United States, and many programs offer in-depth hands-on training. Guidelines for curriculum
are suggested by the American Psychiatric Association [29]. Several post-residency hands-on
training courses are offered throughout the United States.
Individual United States hospitals issue privileges to psychiatrists to perform ECT, but there is
no board certification for ECT in the United States [1].
A typical course of ECT consists of 6 to 12 treatments, individualized for each patient.
Treatment should usually continue until remission of mood or psychotic symptoms
Standard practice in the United States is to give ECT three times per week. The routine in many
other countries is twice a week.
Continuation ECT is the practice of providing a single ECT treatment, at an interval of one to
eight weeks, during the first six months after remission. Maintenance ECT refers to ECT given
beyond continuation ECT. Continuation and maintenance ECT are usually provided on an
outpatient basis to prevent relapse or recurrence of the mood or psychotic episode that prompted
the acute course of ECT.
The mortality rate of ECT is 2 to 4 deaths per 100,000 treatments, making it one of the safest
procedures performed under general anesthesia. Mortality is mostly related to cardiopulmonary
events. Other adverse medical effects include aspiration pneumonia, fracture, dental and tongue
injuries, headache, and nausea. Most patients report some adverse cognitive effects during and
after a course of ECT, including acute confusion (delirium), anterograde amnesia, and
retrograde amnesia.
SETTING ECT is performed in a dedicated ECT treatment suite, a hospital post-anesthesia
care unit, or an ambulatory surgery suite.
8/13/2019 Everything About ECT and Ablation Neurosurgery
12/34
ECT may be performed on an inpatient or outpatient basis, and there is an increasing trend
toward outpatient ECT. Patients with severe medical or psychiatric illness may start ECT on an
inpatient basis and as they improve, switch to outpatient treatment. Continuation and
maintenance ECT are almost always given on an outpatient basis.
PRE-ECT ORDERS The orders for each ECT treatment include:
No food or drink (NPO) after midnight
Intravenous line
The patient receives general anesthesia as part of ECT and thus should not eat solid food
for six to eight hours prior to the procedure, and not drink clear liquids for two hours,
except for necessary medications with a small sip of water [2,3]. The patient should
empty his or her bladder before the treatment.
TREATMENT PROTOCOL ECT is administered by a team that typically includes a
psychiatrist, anesthesiologist, and nurse. Most patients are treated according to a protocol thataddresses the following issues [3]:
Patient safety Confirm the identity of the patient, that the patient is NPO, has taken
necessary medications, and signed the informed consent form. In addition, the patient is
monitored after the seizure for approximately 30 to 60 minutes.
Equipment ECT device, device to monitor vital signs and pulse oximetry, anesthesia
equipment, nasal cannula to provide oxygen, nerve stimulator to assess degree of motor
relaxation, electromyograph, blood pressure cuffs (arm and ankle)
Medications Anesthetic, neuromuscular blocker. Anticholinergic and cardiovascular
medication as indicated
Documentation Record vital signs, ECT device settings, and duration of seizure
PHYSIOLOGIC MONITORING Physiologic functions monitored during ECT include:
Vital signs
Blood oxygen saturationCardiac rhythms (ECG)
Electrical activity of the brain (EEG)
In addition, electromyography (EMG) may be performed to evaluate the electrical activity of
the muscles and a nerve stimulator may be used to monitor the effects of succinylcholine (used
to reduce tonic-clonic contractions).
EEG monitoring is crucial because it enables the practitioner to confirm that a cerebral seizure
has occurred and has ended in a timely fashion. The EEG is typically recorded with one or two
8/13/2019 Everything About ECT and Ablation Neurosurgery
13/34
channels, from right and left frontal and mastoid positions (figure 1). ECT devices display the
EEG tracing on a paper record and/or computer screen, and may also provide information about
the adequacy of the recorded seizure by means of automated indices. Despite the device
interpretation, interpretation of the EEG remains an important skill for the ECT practitioner.
EMG is generally recorded from the right foot in order to measure the length of the motor
component of the seizure. This corresponds with the possible use of right unilateral electrodeplacement. A blood pressure cuff is placed and inflated on the right ankle to prevent
succinylcholine from entering the foot. An alternative to using the EMG is to simply place a
blood pressure cuff on the ankle and have a member of the treatment team watch the foot after
the electric stimulus is administered and record the duration of tonic-clonic contractions.
ELECTRODE PLACEMENT The electric current used to induce the seizure passes briefly
through the brain via two electrodes applied to the scalp (using either the adhesive type of
electrode or hand-held type). Psychiatrists typically position the stimulating electrodes in one of
three ways (figure 2):
Bilateral
Right unilateral
Bifrontal
Bilateral, also known as bitemporal, is the original, "gold standard" placement. One electrode is
placed on each temple, with the center of the electrode placed 2 to 3 cm above the midpoint of
the line connecting the outer canthus of the eye and the external auditory meatus on each side of
the head. Bilateral placement has the greatest antidepressant efficacy and quickest speed of
response, but may cause the most memory impairment.
Right unilateral electrode placement consists of placing one electrode on the right temple and
one on the scalp, just to the right of the vertex (d'Elia placement). Specifically, one electrode is
positioned as in bilateral on the right side, and the center of the other electrode is placed 2 to 3
cm to the right side of the vertex of the skull. This technique avoids initial stimulation of the left
cerebral hemisphere, which is usually dominant for language functions. Right unilateral may be
slightly less effective for some patients, but generally causes fewer adverse cognitive effects
such as memory impairment.
Bifrontal consists of placing each electrode on the forehead above the outer canthus of each eye
The center of each stimulating electrode is placed 4 to 5 cm above the outer canthus of the eye
along a vertical line perpendicular to a line connecting the pupils. Some clinicians believe that
bifrontal is as effective as bilateral with the same cognitive impairment as right unilateral,
although there is a much smaller evidence base for this technique. Nonetheless, it is used widely
in clinical practice.
A meta-analysis of 22 randomized trials (1408 patients) found that although bilateral ECT was
8/13/2019 Everything About ECT and Ablation Neurosurgery
14/34
8/13/2019 Everything About ECT and Ablation Neurosurgery
15/34
unilateral is 6 times seizure threshold, based upon data showing that seizures need to be elicited
with stimuli that are several times greater than seizure threshold for unilateral placement to be
maximally effective [7,12].
The higher dose required for right unilateral occasionally becomes a problem because ECT
devices manufactured in the United States are limited to a charge output of 600 millicoulombs
by Food and Drug Administration regulations. This prevents a small number of patients with arelatively high seizure threshold from being treated at fully six times seizure threshold [13].
It is common for seizure threshold to increase during an acute course of ECT. This may
necessitate incrementally increasing the dose of the electric stimulus periodically.
Clinicians should follow the specific instructions of the ECT device as specified by the
manufacturer.
ANESTHESIA TECHNIQUE The goal of anesthesia for ECT is to provide the patient with
a safe, comfortable experience. The anesthesiologist preoxygenates the patient and administers
medications to induce unconsciousness and to relax or paralyze skeletal muscles. In addition, an
anticholinergic drug may be given prior to ECT to prevent bradycardia or asystole.
Preoxygenation The patient is preoxygenated with supplemental oxygen (2 L/min) via nasal
cannula while the procedure is being set up, with the goal of maintaining oxygen saturation at
or near 100 percent. This makes ECT safer with fewer adverse effects than either a spontaneous
(epileptic) seizure or ECT in the past. In addition, the patient is often hyperventilated
immediately prior to delivering the electrical stimulus. This induces cerebral hypocarbia, which
increases seizure intensity [14].
Anticholinergic medication Premedication with an anticholinergic agent, either
glycopyrrolate (0.2 mg, IV) or atropine (0.4 mg, IV), is often used to prevent vagally-mediated
bradycardia and excess oral and respiratory secretions. Bradycardia is most common at the first
treatment, when there is a greater chance of administering a subconvulsive stimulus that leads
to vagal outflow unopposed by subsequent sympathetic activity from a seizure. Anticholinergics
may cause or exacerbate tachycardia.
Anesthetic medication The anesthesia should not interfere with inducing an effective grand
mal seizure. The induction agent of choice is methohexital, generally given at a dose of 0.75 to
1 mg/kg. Propofol is a commonly used alternative, but it is more potently anticonvulsant than
methohexital and may reduce seizure duration in some circumstances. Other induction agents
include thiopental, etomidate, and ketamine [15]. There has been interest in the use of
ultrashort-acting narcotics such as remifentanil to replace at least some of the standard
induction agent, but this has not been widely adopted [16].
8/13/2019 Everything About ECT and Ablation Neurosurgery
16/34
Muscle relaxation medication Skeletal muscle relaxation is used during ECT to minimize the
motor seizure and prevent musculoskeletal injury. This is particularly important for patients
with osteoporosis. The standard agent for muscle relaxation is succinylcholine, a depolarizing
neuromuscular blocker, given at a dose of 0.75 to 1 mg/kg via intravenous infusion. Muscle
relaxation subsides promptly with discontinuing the infusion.
Nondepolarizing muscle relaxants such as atracurium, mivacurium, or rocuronium are usedonly in special circumstances when succinylcholine cannot be used. Such circumstances include
pseudocholinesterase deficiency, severe neuromuscular disease or injury (quadriplegia,
amyotrophic lateral sclerosis, or muscular dystrophy), severe muscular rigidity, or recent severe
and widespread burns [2,15].
Pseudocholinesterase is needed to metabolize succinylcholine, and its absence will lead to
prolonged apnea and muscle relaxation. A pseudocholinesterase level (also referred to as
dibucaine number) is measured only in patients with a personal or family history of prolonged
apnea following exposure to muscle relaxants.
It is important to ascertain that the patient is unconscious before proceeding with the muscle
relaxant, to avoid unnecessary patient distress. The patient is rendered apneic by the muscle
relaxant, at which point the anesthesiologist provides ventilation by bag and mask with 100
percent oxygen.
The sufficiency of muscle relaxation is determined using a nerve stimulator and observing the
decrement and eventual disappearance of response. In addition, the clinician can assess knee
and plantar withdrawal reflexes, and can simultaneously observe for fasciculations in the calves
and left foot and wait until they subside, usually within one to two minutes of administering the
muscle relaxant. Perfusion of the right foot with the muscle relaxant is prevented by an inflated
blood pressure cuff on the right ankle.
Muscle contractions often occur despite the use of a muscle relaxant. As an example, masseter
muscles may contract, and thus it is important to remove dentures, if present, prior to
administering the electric stimulus. In addition, a member of the treatment team should insert a
bite block to protect the teeth, making sure that the tongue is pushed inferiorly and posteriorly
in the mouth, and that the chin is held firmly against the bite block.
Cardiovascular medication Prophylactic cardiac medications immediately before or during
ECT may be administered for the purpose of blunting the hypertensive, tachycardic response to
the seizure and reducing the risk of myocardial ischemia. The most commonly used drugs in
this situation are beta blockers. The use of beta blockers for this purpose is discussed separately.
SEIZURE DURATION The minimal duration for a therapeutic ECT seizure is 15 seconds.
Beyond this, the efficacy of ECT is not related to seizure duration [2].
8/13/2019 Everything About ECT and Ablation Neurosurgery
17/34
Most therapeutic ECT seizures last 15 to 70 seconds on EEG recording. The recording typically
lasts 10 to 30 percent longer than the motor seizure [17].
Problems with ECT include [2]:
Missed seizures the electrical stimulus does not induce a seizureShort seizures last less than 15 seconds
Prolonged seizures last longer than two to three minutes
Short seizures may be subtherapeutic, and prolonged seizures may be associated with increased
cognitive impairment.
Missed seizures should be followed by a brief (eg, 20 seconds) period of hyperventilation and
restimulation at an incrementally higher stimulus dose. Short seizures should be followed by a
longer period of hyperventilation (eg, 60 seconds) and restimulation at an incrementally higher
stimulus dose.
A prolonged seizure is a potentially serious complication that needs to be recognized and
treated promptly. We suggest terminating seizures that last longer than 180 seconds. The
standard procedure is to administer one-half the induction dose of the anesthetic (when it is
either methohexital or propofol). Alternatively, a dose of benzodiazepine (eg, diazepam 5 mg
IV) may be given [2].
Managing missed or short seizures There are several procedures to use for persistent missed
or short seizures [2,3,18,19]:
Decreasing or discontinuing anticonvulsant mood stabilizers and benzodiazepines, if possible
Hyperventilating the patient before and during the seizure
Decreasing the anesthetic dose to the minimum compatible with full unconsciousness
Switching anesthetic to etomidate (0.15 to 0.30 mg/kg IV) or ketamine (1 to 2 mg/kg IV),
which are less anticonvulsant than methohexital
Intravenous caffeine has been used to prolong seizures, but is no longer recommended because
its clinical benefits are uncertain.
PREGNANCY Many aspects of administering ECT to pregnant patients are comparable to
the technique used for patients who are not pregnant. As an example, the electrical stimulus
dose is not adjusted for pregnancy because it is not clear that pregnancy changes seizure
threshold during ECT [20,21]. Electrical stimulus dosing is discussed elsewhere in this topic.
(See 'Stimulus' above.)
However, ECT technique for pregnant patients should be modified as follows [21-23]:
8/13/2019 Everything About ECT and Ablation Neurosurgery
18/34
Avoid hyperventilating the patient (hyperventilation can diminish fetal oxygenation by
decreasing placental blood flow and reducing the dissociation of oxygen from hemoglobin)
Hydrate patients with intravenous fluids prior to each ECT treatment to minimize the risk of
premature contractions
For pregnancies between 12 and 23 weeks of gestation, document the fetal heart rate before andafter each ECT treatment
When the gestational age exceeds 20 weeks, place a wedge beneath the patients right hip
during each ECT treatment to displace the uterus from the aorta and vena cava and thus
optimize maternal venous return, cardiac output, blood pressure, and uterine blood flow.
For pregnancies 24 weeks of gestation (the fetus is considered viable if born at this gestation
age), continuously monitor the fetal heart rate and uterine activity for 30 to 60 minutes before
and after each ECT treatment. A clinician with experience placing monitoring devices and
interpreting these tracings should be available.
Administer ECT at facilities with resources for treating obstetric and neonatal emergencies
Pregnant patients are at increased risk for gastric reflux and aspiration pneumonitis, which can
be minimized with one or more of the following measures during each ECT treatment [20-
22,24]:
Withhold anticholinergic drugs Glycopyrrolate or atropine may decrease lower esophageal
sphincter tone and thus increase reflux. However, for pregnant patients who require an
anticholinergic drug to prevent excessive bradycardia, we suggest glycopyrrolate, which does
not cross the placenta as readily as atropine. Use of anticholinergic medication during ECT is
discussed elsewhere in this topic. (See 'Anticholinergic medication' above.)
Administer one or two of the following drugs 40 to 60 minutes prior to the procedure to
mitigate the effects of aspiration if it occurs: a nonparticulate antacid (eg, sodium citrate 30 mL
orally), a histamine-2 receptor antagonist (eg, ranitidine 50 mg intravenously), a proton pump
inhibitor (eg, omeprazole 20 mg orally), or prokinetic drug (eg, metoclopramide 10 mg
intravenously)
Intubate the patient, especially at week 25 of gestation and beyond Intubation is the least
preferred option for managing aspiration risk because of its associated morbidity, especially
during pregnancy due to weight gain, edema, and hypervascularity; even minor trauma can lead
to profuse bleeding. Intubation of pregnant patients is discussed separately.
The teratogenic risks and postnatal effects of ECT are discussed separately.
8/13/2019 Everything About ECT and Ablation Neurosurgery
19/34
EEG recording leads in ECT
Electroencephalogram (EEG) electrode placement.
Reprinted with permission from: Handbook of ECT (Copyright 1997). American PsychiatricPublishing, Inc.
Electrode placement for electroconvulsive therapy (ECT)
8/13/2019 Everything About ECT and Ablation Neurosurgery
20/34
INDICATIONS FOR ECT The primary indication for ECT is for the treatment of major
depression that is refractory to antidepressant medications [1]. Indications listed in the
American Psychiatric Association guideline for the treatment of patients with major depressive
disorder include psychotic depression, catatonic stupor, severe suicidality, food refusal leading
to nutritional compromise, and pregnancy and other situations where a rapid antidepressant
response is required (table 1) [2]. The report also recommends ECT for patients who have
8/13/2019 Everything About ECT and Ablation Neurosurgery
21/34
previously shown a positive response to it and for those who have medical conditions that
prevent the use of antidepressant medications. The Canadian Psychiatric Association clinical
guidelines for the treatment of depressive disorders suggest similar indications [3].
Other psychiatric conditions for which ECT is effective include bipolar disorder, mania, and
atypical psychosis [5]. ECT also may be effective or have application in patients with organic
delusional disorder, organic mood disorder, obsessive compulsive disorder, catatonia secondaryto medical conditions, neuroleptic malignant syndrome, neuroleptic-induced Parkinsonism, and
neuroleptic-induced tardive dyskinesia [5,6].
TECHNIQUE AND ANESTHESIA ECT is usually administered two or three times per
week for a total of 6 to 12 treatments. The treatment typically causes a 30 to 60 second
generalized tonic clonic seizure, an effect that is essential to the success of ECT. The patient is
preoxygenated with supplemental oxygen (2 L/min) via nasal cannula while the procedure is
being set up. Prophylactic beta blockers may be administered immediately before or during
ECT to blunt the hypertensive, tachycardic response to the seizure. The anesthesia of choice is
methohexital. Other induction agents include propofol, thiopental, etomidate, and ketamine.
Skeletal muscle relaxation is used during ECT to minimize the motor seizure and prevent
musculoskeletal injury. The standard agent is succinylcholine via intravenous infusion.
MORBIDITY AND MORTALITY Clinicians should be aware of certain potential side
effects or complications of ECT. (See "Overview of electroconvulsive therapy (ECT) for
adults", section on 'Adverse effects'.)
The American Psychiatric Association lists the following conditions as associated with
increased risk [7]:
Unstable or severe cardiovascular disease
Space-occupying intracranial lesion with evidence of elevated intracranial pressure
Recent cerebral hemorrhage or stroke
Bleeding or otherwise unstable vascular aneurysm
Severe pulmonary condition
ASA (American Society of Anesthesiologists) Class 4 or 5 (table 2)
Mortality ECT is one of the safest procedures performed under general anesthesia.With modern anesthetic technique, the rate is sufficiently low and the potential life saving
benefit is compelling enough that absolute contraindications to treatment no longer exist.
Cardiovascular effects A 15- to 20-second parasympathetic discharge occurs during the
procedure as the patient enters the tonic phase of seizure. This can lead to arrhythmias including
bradycardia with or without hypotension, atrial arrhythmias, premature atrial and ventricular
contractions, atrioventricular block, and asystole. Asystole can occur with the first treatment or
at any time later in a patient's course [8]; patients are at higher risk with longer periods of
8/13/2019 Everything About ECT and Ablation Neurosurgery
22/34
subconvulsive seizures [9]. In one study of older adult patients, 66 percent had asystole lasting
greater than 5 seconds with no lasting complications [10]. A history of hypertension or evidence
of ischemia on electrocardiogram (ECG) did not predict asystole, nor did current use of calcium
channel blockers, nitroglycerin, angiotensin converting enzyme (ACE) inhibitors, diuretics, or
psychiatric medications (beta blockers were not included). Interestingly, patients with heart
block and/or rhythm abnormalities were less likely to develop asystole (54 versus 16 percent).
The clonic phase of the seizure then leads to a catecholamine surge that causes tachycardia and
hypertension. The duration of tachycardia usually correlates with the length of the seizure itself
[11]. These hemodynamic responses continue into the postictal period and usually resolve
within 10 to 20 minutes of the seizure [12]. Occasionally patients have persistent hypertension
that requires treatment.
All patients are followed with ECG during the procedure; even healthy patients can have
transient ECG changes. However, these changes are rarely significant, as illustrated by a study
of 29 patients comprising a total of 80 treatments, in which no one had persistent T wave
inversion, pathologic Q waves, or a demonstrable rise in cardiac enzymes at four and six hours
(although some had a mild increase in creatine kinase [CPK], presumably from skeletal muscle)
[13].
ECT can also cause a transient depression in the ejection fraction of healthy patients [14]. A
study in 53 adults undergoing ECT found that seven developed new global left ventricular (LV)
systolic dysfunction and eight developed regional wall motion abnormalities [15]. Among the
14 patients who developed global or regional abnormalities after the first ECT treatment, 13 had
resolution of these abnormalities after the fourth ECT treatment (generally about one week
later), and there were no short-term adverse events in any of the patients with LV dysfunction.
Several studies have investigated the incidence of serious cardiac complications from ECT:
In a retrospective study of 42 patients who had undergone ECT, 12 of the 17 patients with
underlying cardiac disease had cardiac complications [16]. Most of these were benign and self-
limited, including atrial and ventricular ectopy and nonsustained ventricular tachycardia. There
was evidence of ischemia in two patients and one cardiac arrest of unknown etiology. Seventy
percent of all complications, self-limited or not, occurred in patients with cardiovascular disease
identified on the history, physical examination, or ECG, and all occurred in patients greater than
50 years of age. This study did not, however, systematically document the degree of preexisting
cardiac disease.
A prospective study of 40 patients with cardiac disease found that 55 percent had at least one
complication with ECT [17]. These included minor complications, such as transient arrhythmias
or ST segment changes, and major complications, such as persistent ECG changes accompanied
by chest pain, asystole, or persistent arrhythmias. Only 7.5 percent in the control group without
cardiac disease had a cardiac complication, and all were transient and minor.
8/13/2019 Everything About ECT and Ablation Neurosurgery
23/34
A case-control study of 80 patients over the age of 50 found that the risk of major complications
was 11.5 percent in patients at high risk for cardiovascular disease [18]. The patients were able
to complete their course of therapy once the complications were treated.
These findings suggest that the incidence of important cardiac complications are relatively rare
and almost always occur in older patients and those with underlying cardiovascular disease.
Furthermore, even patients at high risk for cardiac complications tolerate ECT well and, if
complications occur and are treated, the vast majority can complete the treatment course.
As an example, one study treated 80 patients, one-half of whom had preexisting cardiac disease
(depressed ejection fraction, conduction disease, or frequent premature ventricular contractions)
[17]. Among those with cardiac disease, eight had major complications including chest pain,
arrhythmia, ischemia, and one myocardial infarction. Anesthesiologists and cardiologists treated
the complications as they occurred and 36 of 38 patients went on to complete treatment,
including the patient with the myocardial infarction. Similarly, a second study treated 53
patients and, of the 27 patients at risk, 31 percent required changes in medication or
pretreatment with subsequent treatments because of complications [18]. Twenty-five out of 27
patients completed the course of ECT; there were no deaths. Despite these successful outcomes,
it is not known how many of the patients in these studies were on beta blockers or other
antihypertensive medication prior to treatment.
Central nervous system and other effects Several cerebral effects occur with ECT, including
increases in cerebral blood flow and intracranial pressure. Memory loss, disorientation, and
delirium are the primary clinical manifestations. (See "Overview of electroconvulsive therapy
(ECT) for adults", section on 'Adverse effects'.)
ROLE OF THE MEDICAL CONSULTANT The preprocedure evaluation of patients before
ECT is similar to the approach to a patient undergoing any procedure that requires general
anesthesia: to identify medical issues that place the patient at risk, to propose strategies to
reduce risk, and to treat complications after the procedure.
Preprocedure evaluation A complete history and physical examination will help to identify
pertinent risk factors [19]. We agree with the recommendation from the American Psychiatric
Association that no specific laboratory tests are required in the pre-ECT evaluation. We
recommend measurement of serum electrolytes only for patients taking diuretics or other
medications that increase the likelihood of an abnormality and for patients with established
renal disease or congestive heart failure. We suggest an electrocardiogram in patients over the
age of 50 years, since most cardiac complications occur in older patients. There are no
indications for other routine laboratory studies.
The history should include a review of previous difficulties with anesthesia or ECT. As
mentioned above, there are no absolute contraindications to ECT and most patients can have the
procedure without serious complication, but clinicians should seek risk factors that may require
8/13/2019 Everything About ECT and Ablation Neurosurgery
24/34
intervention or management. Important considerations include risk factors for cardiac ischemia
or arrhythmia, heart failure, and the presence of brain tumors or other neurosurgical issues. A
history of skull fractures should be determined, as this may affect electrode placement.
The history should also include a medication history, to specifically inquire about use of herbal
medications. In one study, 54 percent of outpatients with psychiatric conditions used alternative
medication in addition to routine pharmacotherapy [20]. Common alternative medications,including Ginkgo biloba, ginseng, St. John's wort, valerian, and kava kava, have CNS effects
which might interfere with ECT. The treating psychiatrist should be made aware of a patient's
herbal supplement use, to determine if the herbal products should be tapered prior to initiating
ECT [21].
In addition, theophylline has been reported to cause status epilepticus after ECT and so should
be tapered prior to treatment [22]. The treating psychiatrist may also choose to taper or
discontinue antidepressants and/or other psychotropics prior to treatment.
A summary of management strategies for preexisting medical conditions is shown in a table
(table 3).
Strategies to reduce the risk of cardiac complications The 2007 American Heart
Association /American College of Cardiology (AHA-ACC) guideline update for noncardiac
surgery assigns procedure-related risk to several types of surgery [23]. Though not explicitly
mentioned in the AHA-ACC guidelines, ECT can be treated like a low-risk procedure because
it is usually well tolerated even in those at risk, the duration of hemodynamic changes is brief,
and the mortality rate is low [17,18,24]. As a result, it is difficult to prove a beneficial effect of
any intervention to reduce cardiovascular risk. Nevertheless, a cardiac risk assessment is
warranted preoperatively.
Barring major clinical predictors of coronary risk (unstable angina, decompensated heart
failure, severe valvular disease, malignant arrhythmias), most patients can undergo ECT with
appropriate medical management [25]. Some have suggested that sedentary patients with
intermediate risk factors should undergo further noninvasive risk stratification [26]. However,
we feel that this population can proceed without further evaluation given the low morbidity of
ECT and the potential use of prophylactic beta blockers.
Postprocedure hemodynamic changes Short acting beta blockers are used to quickly treat
persistent or severe tachycardia and hypertension after ECT. Other agents that have been useful
for the treatment of postprocedure hypertension are intravenous nitroglycerin [27], nicardipine
[28], and clonidine [12,25].
Prophylactic beta blockers Short acting beta blockers, such as intravenous esmolol or
labetalol, can be used to prevent transient and persistent hypertension and tachycardia [27-33];
8/13/2019 Everything About ECT and Ablation Neurosurgery
25/34
glycopyrrolate is administered to prevent bradycardia in these individuals. Several authors have
raised concern regarding widespread use of beta blockers because these drugs have been
implicated in cases of prolonged asystole [9,34,35]. However, in these reported cases, atropine
was not used and in some cases patients had subconvulsive treatments that can also cause
bradycardia.
While it is clear that treatment of postprocedure hemodynamic changes is indicated, use ofprophylactic beta blockers to reduce risk for patients undergoing ECT is controversial. The
overall risk of cardiovascular complications due to ECT is low and no studies have documented
reduced cardiac complications with the use of short acting beta blockers before ECT.
The 2001 American Psychiatric Association guidelines list three considerations for the use of
prophylactic short acting beta blockers, that also are relevant in patients taking long acting beta
blockers [7]:
Beta blockers may increase the risk of asystole (though this appears to be less of a risk ifatropine is used [10]).
The absolute rise in the heart rate and blood pressure with ECT is no greater in those with
baseline elevated blood pressure or heart rate [36,37].
There is a theoretical risk that excessive blunting of the hemodynamic response with beta
blockers may reduce the necessary supply of oxygen to the brain to protect against
decreased seizure length and cognitive side effects.
In addition, there is some evidence that beta blockers might result in a decrease in seizure
length and potentially decrease the efficacy of ECT [33,38], although this is not found in
all studies [39,40].
The American Psychiatric Association chose not to make a specific recommendation with
regard to using prophylactic beta blockers but does recommend that patients with unstable
hypertension be stabilized prior to starting ECT [7]. We do not recommend routine use of beta
blocker in low risk patients, given the theoretical risks and unclear benefit. We suggest the use
of prophylactic short-acting intravenous beta blockers for patients at very high risk of
complications from transient hypertension (eg, intracranial aneurysm, unstable angina or recent
myocardial infarction) [19]. Collaboration with the treating psychiatrist, anesthesiologist, and
cardiology consultation is beneficial in such patients.
Typical bolus doses of labetalol are 5 to 20 mg IV, and for esmolol, 10 to 50 mg IV. The most
authoritative study of the use of beta blockers during ECT found that labetalol produced dose-
dependent reduction in HR and rate pressure product (RPP) using 5 and 10 mg doses, compared
to placebo [41]. It is not necessary to prevent the transient hypertension and tachycardia
associated with the seizure in most patients; the main goal of the use of these agents is to reduce
the risk of myocardial ischemia (a possible result of the increased oxygen demand associated
with tachycardia) in patients with coronary artery disease. Other agents, such as calcium
8/13/2019 Everything About ECT and Ablation Neurosurgery
26/34
channel blockers or nitroglycerine, are sometimes given during ECT [42].
Other prophylactic medications Medications other than beta blockers have been used to try
to prevent postprocedure hemodynamic changes. As an example, a small randomized trial found
that prophylactic intravenous nicardipine was effective in a dose-dependent fashion at
minimizing the acute hemodynamic response to ECT without shortening the duration of seizure
[43].
Coexisting cardiac disease
Hypertension Patients should receive their routine antihypertensive (other than diuretics)
with a small sip of water approximately two hours before ECT. Diuretics should not be given,
because it is better for the bladder to be empty during the procedure to prevent the patient from
soiling himself as a result of the seizure.
Coronary heart disease Antianginals such as nitrates and beta blockers should be continued
in patients with documented coronary heart disease who are already taking them. Patients taking
long acting beta blockers should receive atropine or glycopyrrolate with induction given the
potential increase in the risk of bradycardia and a small study that showed that atropine may be
protective [10].
If ECG changes or chest pain occur during the treatment period, treatments should be postponed
until the patient is evaluated and treated for potential ischemia [25,44].
Heart failure and valvular disease ECT should be delayed in patients with decompensated
heart failure or significant valvular disease, pending cardiology consultation and completion of
a thorough evaluation and optimization of cardiac status. One report of ten patients who
completed ECT (total of 144 ECT sessions) with severe aortic stenosis (valve area 0.7 to 1.0
cm2) noted good control of blood pressure and heart rate with continuation of chronic
antihypertensive medications and/or addition of a short-acting beta blocker [45]. All patients
were asymptomatic and tolerated ECT. There were no deaths attributable to ECT or aortic
stenosis. Two patients had drops in blood pressure requiring intervention, and seven patients
required intravenous medication to control systolic blood pressure >180 mm Hg. In patients
with severe aortic stenosis, clinicians should strive for tight control of blood pressure and heart
rate with attention to avoiding excessive preload or afterload reduction. Little data are available
for management of patients with less severe valvular disease, though ECT can be performed
safely, with appropriate precautions, in most patients with underlying cardiac conditions [46].
In patients with a remote history of heart failure or compensated disease, we recommend a
baseline echocardiogram, if not recently performed, to assist with periprocedure management.
In those with compensated systolic dysfunction, one may simply continue diuretics and
vasodilator therapy and minimize volume overload. In patients with diastolic dysfunction,
8/13/2019 Everything About ECT and Ablation Neurosurgery
27/34
control of blood pressure should limit the occurrence of flash pulmonary edema. This group
will benefit from prompt treatment of post-seizure hypertension if it develops.
Pacemakers and implantable defibrillators Patients with pacemakers and automatic
implantable cardiac defibrillators (AICDs) can safely undergo ECT. As an example, in a case
series of ECT in 26 patients with pacemakers and three patients with AICDs there was only one
serious cardiac event, an episode of supraventricular tachycardia [47].
The clinical team should be prepared to deactivate pacemakers with a magnet if any aberrant
signals occur [25]. A cardiologist should deactivate AICDs before induction and reactivate the
device after the seizure is complete to avoid excessive charge. The patient should have
continuous ECG monitoring while the defibrillator is deactivated [48].
Coexisting neurologic and neurosurgical disease
Brain tumors Early recommendations considered brain tumors and other space occupying
lesions to be absolute contraindications to ECT [49]. This concern was based upon the
observation that ECT raises cerebral blood flow, which in the presence of a brain tumor could
translate into an increase in intracranial pressure (ICP) and neurologic deterioration.
These concerns were illustrated in a review of 35 patients with brain tumors undergoing ECT,
74 percent of whom had major adverse neurologic and cognitive side effects, with a one-month
mortality of 28 percent [50]. Notable characteristics of patients who suffered neurologic
deterioration included the presence of a depressive illness, no previous psychiatric illness or
ECT, headache, and the presence of even soft neurologic findings on exam. However, this study
may have had a selection bias given that only one patient was known to have a tumor before
treatment.
Subsequently, one group reviewed 10 cases of successful treatment [51-54]. Eight patients had
meningiomas in differing locations, and two patients had metastatic breast cancer. No one had
abnormal neurologic examinations or evidence of increased ICP at baseline, and four had
normal spinal fluid measurements. There were no adverse events other than a prolonged seizure
after one treatment. Most recently a case report described successful treatment of a patient with
primary brain cancer and documented elevated ICP [55]. He was treated with steroids and short
acting beta blockers to minimize edema and elevations in blood pressure during the clonic
phase of seizure.
Based on this information, ECT is probably safe in patients with brain tumors as long as there is
no evidence of elevated ICP. Given that the available safety data are in the form of case series
or reports, we agree with the American Psychiatric Association that the decision should be
made on a case by case basis with the involvement of neurologic and possibly neurosurgical
consultants [7]. Evaluation should consist of a detailed history and physical examination to seek
8/13/2019 Everything About ECT and Ablation Neurosurgery
28/34
evidence suggestive of elevated ICP, such as headache, papilledema, or abnormal neurologic
examination. Any such evidence should prompt further investigation such as head CT or MRI.
Although data are limited, providers have successfully used steroids to minimize edema
[54,55], and neurologic consultants may consider using them in patients in whom elevated ICP
cannot be ruled out [56,57].
Stroke Patients who have suffered a stroke have a high rate of depression. In a study of 14patients with completed strokes undergoing ECT one month or more after the event, none had
deleterious neurologic sequelae [58]. Similarly, a second study of 24 patients with a history of
stroke found no difference in the efficacy or cardiac complication rate compared with controls
[59]. Rates of delirium were similar in both groups, although within the study group all patients
with delirium had their strokes within the preceding year. Adequate blood pressure control is
important for such patients.
Dementia Reports exist of successful ECT in depressed patients with dementia and organic
brain disease, with efficacy rates similar to that of nondemented patients [60,61]. In a review of
135 patients with organic and depressive dementia, 21 percent developed delirium or cognitive
and memory deficits; all but one had cleared by time of discharge from the hospital [60].
The severity of delirium correlates with the degree of underlying dementia or organic brain
syndrome, but is transient and does not interfere with treatment [61]. The clinical staff should
be aware that delirium is a potential side effect in demented patients. These patients can often
be managed with reassurance and alterations in level of supervision [62].
Neuromuscular disease In patients with neuromuscular disease, particularly post-polio
syndrome, depolarizing muscle relaxants such as succinylcholine may lead to severe
hyperkalemia and circulatory collapse [63,64]. Thus, depolarizing muscle relaxants should be
avoided. Patients with neuromuscular disease may receive short-acting, non-depolarizing agents
for neuromuscular blockade [65].
Epilepsy Use of ECT and anticonvulsants in patients with epilepsy is discussed separately.
Diabetes There is no clear evidence of an effect of ECT on blood sugar control in diabetic
patients. In a study of 19 patients with insulin-requiring type II DM, ECT itself did not lead to
significant acute changes in blood sugar [66]. Individual patients who developed hyperglycemia
or hypoglycemia after ECT were found to have changed their behaviors (eating or activity) in
response to resolving depression, and these behavioral changes were felt to be responsible for
the change in blood sugar control.
Patients generally do not take anything by mouth on the morning of ECT. As a general rule, we
recommend holding oral hypoglycemic agents on the morning of the procedure. For insulin-
requiring diabetics, on the morning of the procedure we recommend giving half the usual long-
8/13/2019 Everything About ECT and Ablation Neurosurgery
29/34
acting insulin dose and withholding short-acting insulin. A more detailed discussion of these
issues can be found elsewhere. (See "Perioperative management of diabetes mellitus".)
Anticoagulation The safety of ECT in patients who are anticoagulated is controversial
because of concerns about a possible increase in the risk of intracerebral hemorrhage [67]. In a
case series of 35 patients receiving long-term anticoagulation with warfarin who underwent 284
ECT treatments, no major adverse effects occurred [68]. The INR on the day of ECT was belowsubtherapeutic (below 2.0) 36 percent of the time and supratherapeutic (above 3.5) only 3
percent of the time. These data suggest that if there is an increased risk of ECT in patients
appropriately anticoagulated with warfarin, that risk is small.
Pregnancy The treatment of psychiatric conditions in pregnancy poses challenges, as
psychotropic medications may have significant side effects in both mother and fetus. However,
ECT is generally thought be safe in pregnant patients by the American Psychiatric Association
and the American College of Obstetricians and Gynecologists [7,69]. The safety of ECT and
modifications in technique for treating pregnant patients are discussed separately.
As a pregnant patient considers ECT, the informed consent and evaluation should be performed
with an obstetrician and an anesthesiologist.
Ablation Neurosurgery
INTRODUCTION Many patients with unipolar major depression do not respond to standard
treatment with pharmacotherapy and psychotherapy [1,2], and are thus candidates for
neuromodulation procedures [3-8]. Electroconvulsive therapy (ECT) is the oldest
neurostimulation procedure (it also predates all antidepressant drugs), and is the most effective
intervention for unipolar major depression [3,4,7]. In addition to ECT, other noninvasive
neurostimulatory therapies include magnetic seizure therapy, focal electrically administered
seizure therapy, transcranial magnetic stimulation (TMS), transcranial direct current
stimulation, transcranial low voltage pulsed electromagnetic fields, and cranial electrical
stimulation [9]. Invasive neuromodulation interventions (which require surgery and have
generally been studied in more treatment-refractory patients) include vagus nerve stimulation
(VNS), deep brain stimulation, direct cortical stimulation, and ablative neurosurgery.
This topic provides an overview of noninvasive and invasive neuromodulation therapies for
unipolar major depression. The initial treatment of depression and management of treatment
resistant depression are discussed separately. (See "Initial treatment of depression in adults".)
NONINVASIVE NEUROMODULATION THERAPIES Noninvasive neuromodulation
8/13/2019 Everything About ECT and Ablation Neurosurgery
30/34
procedures use an electric current or magnetic field to stimulate the central nervous system [8].
Convulsive therapies Noninvasive neurostimulation treatments for major depression include
convulsive therapies:
Electroconvulsive therapy (ECT)
Magnetic seizure therapyFocal electrically administered seizure therapy
Electroconvulsive therapy (ECT) Electroconvulsive therapy (ECT) is a clinically available
approach that uses an electric current that passes between two electrodes placed against the
scalp to induce a generalized cerebral seizure while the patient is under general anesthesia.
A course of ECT involves a series of treatments that are delivered over several days to weeks.
ECT is superior to pharmacotherapy for unipolar major depression based upon meta-analyses of
randomized trials [10,11], and is generally considered the most efficacious treatment for
depression [12]. However, ECT is associated with safety risks, adverse effects, logistical
constraints, and patient refusal, and relapse rates following remission are high, especially in
patients with treatment resistant depression [13,14].
INVASIVE/SURGICAL NEUROMODULATION THERAPIES Invasive neuromodulation
therapies for treating unipolar major depression include:
Vagus nerve stimulation
Deep brain stimulation
Direct cortical stimulation Ablative neurosurgery
Invasive neuromodulation interventions require surgery and have generally been studied in
patients with chronic, treatment-refractory, debilitating depression, because most clinicians
view invasive interventions as riskier than the noninvasive techniques described above.
Among the surgical approaches, vagus nerve stimulation, deep brain stimulation, and direct
cortical stimulation are generally:
Reversible Hardware can be removed
Revisable Stimulating electrodes can be moved to optimize response
Adjustable Stimulation parameters can be modified to optimize response
However, ablative surgery does not involve:
In dwelling metal hardware and contraindications to magnetic resonance imaging and
metal detectors
8/13/2019 Everything About ECT and Ablation Neurosurgery
31/34
Surgical follow-up to replace batteries or pulse generators every few years or to revise
dysfunctional systems
Ablative neurosurgery Ablative neurosurgery for intractable major depression is a clinically
available but rarely used approach in which a lesion is made in limbic or paralimbic structures.
Early ablative procedures for psychiatric illness, such as the prefrontal leucotomy [59], havebeen supplanted by stereotactic neurosurgical techniques that allow for more focal lesions with
fewer side effects, including [60-62]:
Anterior capsulotomy Lesion in the anterior limb of the internal capsule
Anterior cingulotomy Lesion in the dorsal anterior cingulate
Subcaudate tractotomy Lesion in thalamocortical white matter tracts inferior to the
anterior striatum
Limbic leucotomy Combines cingulotomy with subcaudate tractotomy
Unipolar major depression often does not respond to standard treatment with pharmacotherapy,
psychotherapy, and noninvasive neuromodulation interventions such as electroconvulsive
therapy (ECT) and transcranial magnetic stimulation (TMS). This has led to investigation of
invasive treatments that include:
Most studies of surgical neurostimulation interventions have maintained patients on theirpresurgical antidepressant medications and psychotherapies after surgery [3,4].
Assessment Candidates for surgical treatment of refractory unipolar major depression should
be evaluated to confirm the diagnosis and whether surgery can be performed safely. The
assessment includes a psychiatric history and mental status examination, with emphasis upon
current depressive (table 1) and psychotic symptoms, comorbid disorders (eg, substance use and
personality disorders), neuropsychological functioning, length of the current depressive episode,
types and number of failed treatments during the present episode, psychosocial functioning, and
ability to provide informed consent, as well as the number, length, and treatment history of priordepressive episodes.
In addition, a general medical history and physical examination is performed, as well as
laboratory tests and neuroimaging studies that are guided by the history, examination, and
possibility of surgery [5-7]. The medical work-up should emphasize preexisting neurologic
disease (eg, epilepsy, intracranial masses, and vascular abnormalities).
Craniotomy is typically used to perform these procedures, although a gamma knife can be used
8/13/2019 Everything About ECT and Ablation Neurosurgery
32/34
for capsulotomy because of its particularly small lesion volume [55].
Cingulotomy has been used most often, with over 500 reported cases [36].
Indication There are no established criteria (including number and type of failed treatments)
that need to be met before a patient with unipolar major depression is considered appropriate for
ablative surgery; this largely depends upon the clinical judgment of the evaluating psychiatristand neurosurgeon. Candidates include patients with chronic, severe, and incapacitating
symptoms that are refractory to [1,2,56,57]:
Pharmacotherapy
Monotherapy with several (eg, four) different antidepressant classes at therapeutic doses
for several weeks (eg, four to eight)
Multiple (eg, three) trials of an antidepressant plus an established adjunctive drug (eg,
second-generation antipsychotic, lithium, and triiodothyronine)
Adjunctive psychotherapy such as cognitive-behavioral therapy or interpersonalpsychotherapy
Electroconvulsive therapy (ECT)
Contraindications to ablative surgery for unipolar major depression include [1,56,57]:
Severe personality disorders
Comorbid substance use disorders
Suicidal ideation or behavior
Chronic, poorly controlled general medical conditions
Previously diagnosed intracranial masses
Intracerebral vascular abnormalities
Pregnancy
Institutions offering ablative neurosurgery for treatment refractory depression often have
a multidisciplinary committee to review referrals and ensure that the procedure is
indicated [1,2]. In many countries, use of the procedure is controlled by legislation and
overseen by public agencies [2,51,56].
Before undertaking ablative neurosurgery, clinicians and patients with major depression should
note that the course of illness is such that recovery can occur after lengthy periods of illness.
Response There are no randomized trials for ablative procedures in treatment refractory
depression. Based upon prospective observational studies, response (improvement from
baseline on the depression rating scale 50 percent) occurs in approximately 30 to 60 percent
of patients; the evidence includes a study of:
33 patients treated with anterior cingulotomy or limbic leucotomy (mean duration of
8/13/2019 Everything About ECT and Ablation Neurosurgery
33/34
follow-up 30 months); response occurred in 33 percent [1]
8 patients treated with anterior cingulotomy (duration of follow-up 12 months); response
occurred in 63 percent [57]
20 patients treated with anterior capsulotomy (mean duration of follow-up 7 years);
response occurred in 50 percent [2]
In a retrospective study, 23 patients treated for major depression with subcaudate
tractotomy or limbic leucotomy were interviewed, with a mean duration of follow-up of14 years; recovery occurred in 22 percent and significant improvement in 48 percent [56]
However, 29 other patients were alive and lost to follow-up, and among 24 patients who
were deceased at follow-up, 25 percent had committed suicide.
Improvement of major depression with ablative surgery generally occurs within days to weeks
of the procedure [56], but the effect may be delayed for months [1,58]. Insufficient or
impersistent improvement may lead patients to undergo a second operation to extend the lesions
created in the first operation or to make lesions in an additional site [1,2,56].
Risks and side effects For patients with treatment refractory depression, observational
studies suggest that ablative surgery is associated with:
Nonspecific neurosurgical risks [1,56]:
Intracranial bleeding
Infection
Anesthesia complications
Delirium
Risks specific to the lesion [1,2,19,56]: Epilepsy
Impaired cognition (including executive functioning, memory, set shifting, and verbal
fluency)
Personality changes (eg, impulsivity, disinhibition, and amotivation)
Weight gain
Urinary incontinence (typically transient)
However, some studies found that neurosurgery did not adversely affect
neuropsychological function [2,57].
Mechanism of action The rationale for using ablative procedures is based upon a model that
conceptualizes refractory major depression as a problem in neural networks (circuits) that
regulate mood, rather than an abnormality in a single neuroanatomical structure or
neurotransmitter system [1,46]. It is hypothesized that abnormal communication between grey
matter brain regions involved in the pathophysiology of major depression can be interrupted by
severing their white matter connections.
8/13/2019 Everything About ECT and A
Recommended