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Electroconvulsive therapy - Electroshock (ECT)
Electroconvulsive therapy, also known as electroshock or ECT, is a
controversial type of psychiatric shock therapy involving the
induction of an artificial seizure in a patient by passing electricity
through the brain. Researchers remain uncertain as to exactly how ECT
produces improvements in mental state.
ECT was first introduced as a treatment for schizophrenia in the
1930s, and quickly became adopted as a common treatment method for
mood disorders?and as a dreaded mechanism for disciplining unruly
psychiatric inpatients. While its use today has mostly been displaced
by medication, ECT (now administered under anaesthesia and muscle
relaxants) continues to be used for the treatment of several
conditions for which medication is not appropriate, occupying a narrow
but important niche in modern psychiatry.
Overview
During ECT, a grand mal seizure is induced in a patient by passing an
electrical current through the brain, and the existence of the seizure
is confirmed by means of an EEG. The patient is first placed under
general anesthesia and is unconscious. Muscle relaxants are used to
prevent the patient's muscles from moving during the treatment;
otherwise, multiple bone fractures may result from the violent muscle
spasms induced by the seizure.
Electrical current flows between two electrodes placed on the scalp,
usually from temple to temple, though sometimes electroshock may be
applied to only one hemisphere of the brain. The resultant seizure is
characteristically more severe than a naturally occurring epileptic
seizure. The production of an adequate, generalized seizure using the
proper amount of electrical stimulation is required for therapeutic
efficacy (Sackheim et al., 1993). Placement of both stimulus
electrodes on one side of the head ("unilateral" ECT), over the
nondominant (generally right) cerebral hemisphere, results in delivery
of the initial electrical stimulation away from the primary learning
and memory centers.
Following the seizure, there is a short period of time during which
cortical electrical activity in the brain ceases and an EEG reading is
flat. Opponents of the practice claim this is no different to the
state of being brain dead, and that brain cell death occurs during
this time. After treatment, patients have no memory of the seizure or
events immediately preceding it.
Therapeutic ECT is usually administered more than once over a period of
time. A typical course of ECT entails 6 to 12 treatments, administered
at a rate of three times per week, on either an inpatient or
outpatient basis.
The exact mechanisms by which ECT exerts its therapeutic effect are
not known, but studies show that repeated applications have effects on
several kinds of neurotransmitters in the central nervous system. ECT
seems to sensitize two subtypes of serotonin (5-HT) receptor, thereby
strengthening signaling. ECT also decreases the funtioning of
norepinephrine and dopamine inhibiting auto-receptors in the locus
ceruleus and substantia nigra, respectively, causing more of each to
be released (Ishihara K, Sasa M., 1999).
Current usage
ECT is currently typically used to treat bipolar disorder and severe
depression in cases where antidepressant medication, psychotherapy, or
both have proven ineffective (Potter et al., 1991; Depression
Guideline Panel, 1993), when medication cannot be taken, or when
alternative treatments would be too slow (for example, in a person
with delusional depression and intense, unremitting suicidal behavior).
It is also used in cases where ECT is known to be particularly
beneficial, such as depression or mania accompanied by psychosis or
catatonia (NIH & NIMH Consensus Conference, 1985; Depression Guideline
Panel, 1993; Potter & Rudorfer, 1993). Examples of specific
indications include depression unresponsive to multiple medication
trials, or accompanied by a physical illness or pregnancy, which
renders the use of a usually preferred antidepressant dangerous to the
patient or to a developing fetus. Under such circumstances, carefully
weighing risks and benefits, some doctors consider ECT to be the
safest treatment option for severe depression. It should be
administered under controlled conditions, with appropriate personnel (Rudorfer
et al., 1997).
Recent epidemiological surveys in the United States show that the
modern use of ECT is generally limited to evidence-based indications
(Hermann et al., 1999). Indeed, concern has been raised that in some
settings, particularly in the public sector and outside major
metropolitan areas, ECT may be underutilized due to the wide
variability in the availability of this treatment across the country
(Hermann et al., 1995). Consequently, minority patients tend to be
underrepresented among those receiving ECT (Rudorfer et al., 1997).
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Historical usage
ECT was developed in 1934 based on the mistaken belief that epilepsy
and schizophrenia could not exist at the same time in an individual.
When ECT was first instituted, the procedure was performed on fully
conscious patients, without the use of anesthesia or muscle relaxants.
The patient lost consciousness during the application of the current,
and experienced powerful and violently uncontrolled muscle movement.
Patients would often break bones, especially vertebrae, and pull
muscles from the violent convulsions induced by the seizure. Patients
grew to dread the procedure, and it was not uncommonly employed as a
means of punishment and sedation for difficult patients in psychiatric
wards.
With the development of effective medications for the treatment of
major mental disorders a half-century ago, the need for ECT lessened,
but did not disappear. Prior to that time, ECT often had been
administered for a variety of conditions for which it is not now
generally regarded effective, for example, the treatment of
schizophrenia.
Advances in treatment technique over the past generation have enabled
a reduction of adverse cognitive effects of ECT (NIH & NIMH Consensus
Conference, 1985; Rudorfer et al., 1997). Nearly all ECT devices
deliver a lower current, brief-pulse electrical stimulation, rather
than the original sine wave output; with a brief pulse electrical
wave, a therapeutic seizure may be induced with as little as one-third
the electrical power as with the older method, thereby reducing the
potential for confusion and memory disturbance (Andrade et al., 1998).
Side effects
The major risks of ECT are those of brief general anesthesia. There
are virtually no absolute health contraindications precluding its use
where warranted (Potter & Rudorfer, 1993; Rudorfer et al., 1997).
The most common adverse effects are confusion and memory loss for
events surrounding the period of ECT treatment. The confusion and
disorientation seen upon awakening after ECT typically clear within an
hour.
More persistent memory problems are variable. Most typical with
standard, bilateral electrode placement (one electrode on each side of
the head) has been associated with a pattern of memory loss from the time of the ECT series and extending back an average of 6 months, combined with
impairment of learning new information, which continues for perhaps
2 months following ECT (NIH & NIMH Consensus Conference, 1985). Some
neuropsychological studies have shown that by several months after
completion of ECT, the ability to learn and remember are normal (Calev,
1994). Although most patients return to full functioning following
successful ECT, the degree of post-treatment memory impairment and
resulting impact on functioning are highly variable across individuals
(NIH & NIMH Consensus Conference, 1985; CMHS, 1998). While clearly the
exception rather than the rule, a number of rather vocal former
psychiatric patients opposed to ECT anecdotally claim that their
memories were permanently and severely damaged by the procedure. No
reliable data on the incidence of severe post-ECT memory impairment
are available.
Fears that ECT causes gross structural brain pathology have not been
supported by decades of research in both humans and animals (NIH &
NIMH Consensus Conference, 1985; Devanand et al., 1994; Weiner &
Krystal, 1994; Greenberg, 1997; CMHS, 1998). Recent studies suggest
the opposite; long term ECT treatment, like antidepressant treatment,
seems to protect the brain from the damaging effects of depression.
ECT increases the expression of brain-derived neurotrophic factor (BDNF)
in the limbic system, stimulating growth and protecting neurons from
the atrophy that long term depression can otherwise cause (Duman RS,
Vaidya VA., 1998). Still, the decision to use ECT must be evaluated
for each individual, weighing the potential benefits and known risks
of all available and appropriate treatments in the context of informed
consent (NIH & NIMH Consensus Conference, 1985).
After the course of ECT ends, memory gradually improves, though
whether it ever returns to pre-ECT levels is highly variable. Some
patients anecdotally claim their memory is permanently impaired
following ECT, while a few even report better memory afterwards.
Unilateral ECT
According to several controlled trials, unilateral ECT is associated
with virtually no detectable, persistent memory loss (Horne et al.,
1985; NIH Consensus Conference, 1985; Rudorfer et al., 1997). However,
most clinicians find unilateral ECT less potent and more slowly acting
an intervention than conventional bilateral ECT, particularly in the
most severe cases of depression or mania. One approach that is
sometimes used is to begin a trial of ECT with unilateral electrode
placement and switch to bilateral treatment after about six treatments
if there has been no response.
Research has demonstrated that the relationship of electrical dose to
clinical response differs depending on electrode placement; for
bilateral ECT, as long as an adequate seizure is obtained, any
additional dosage will merely add to the cognitive toxicity, whereas
for unilateral electrode placement, a therapeutic effect will not be
achieved unless the electrical stimulus is more than minimally above
the seizure threshold (Sackeim et al., 1993).
Even a moderately high electrical dosage in unilateral ECT still has
fewer cognitive adverse effects than bilateral ECT. On the other hand,
high-dose bilateral ECT may be unnecessarily risky and may be a
preventable cause of severe memory impairment.
Use in combination with other medications
Some types of medication, such as lithium, also add to confusion and
cognitive impairment when given during a course of ECT and are best
avoided. Medications that raise the seizure threshold and make it
harder to obtain a therapeutic effect from ECT, including
anticonvulsants and some minor tranquilizers, may also need to be
tapered or discontinued.
Effectiveness
Accumulated clinical experience -- later confirmed in controlled
clinical trials, which included the use of simulated or "sham" ECT as
a control (Janicak et al., 1985), determined ECT to be highly
effective against severe depression, some acute psychotic states, and
mania (Small et al., 1988).
No controlled study has shown any other treatment to have superior
efficacy to ECT in the treatment of depression (Janicak et al., 1985;
Rudorfer et al., 1997). ECT has not been demonstrated to be effective
in dysthymia, substance abuse, anxiety, or personality disorders. The
foregoing conclusions, and many of those discussed below, are the
products of review of extensive research conducted over several
decades (Depression Guideline Panel, 1993; Rudorfer et al., 1997) as
well as by an independent panel of scientists, practitioners, and
consumers (NIH & NIMH Consensus Conference, 1985).
Although the average 60 to 70 percent response rate seen with ECT is
comparable to that obtained with pharmacotherapy, there is evidence
that the antidepressant effect of ECT occurs faster than that seen
with medication, encouraging the use of ECT where depression is
accompanied by potentially uncontrollable suicidal ideas and actions (Rudorfer
et al., 1997). However, ECT does not exert a long-term protection
against suicide. Indeed, it is now recognized that a single course of
ECT should be regarded as a short-term treatment for an acute episode
of illness. To sustain the response to ECT, continuation treatment,
often in the form of antidepressant and/or mood stabilizer medication,
must be instituted (Sackeim, 1994).
Individuals who repeatedly relapse following ECT despite continuation
medication may be candidates for maintenance ECT, delivered on an
outpatient basis at a rate of one treatment weekly to as infrequently
as monthly (Sackeim, 1994; Rudorfer et al., 1997).
Informed consent
Informed consent is an integral part of the ECT process (NIH & NIMH
Consensus Conference, 1985). The potential benefits and risks of this
treatment, and of available alternative interventions, should be
carefully reviewed and discussed with patients and, where appropriate,
family or friends. Prospective candidates for ECT should be informed,
for example, that its benefits are short-lived without active
continuation treatment, and that there may be some risk of permanent
severe memory loss after ECT.
In most cases of depression, the benefit-to-risk ratio will favor the
use of medication and/or psychotherapy as the preferred course of
action (Depression Guideline Panel, 1993). Where medication has not
succeeded, or is fraught with unusual risk, or where the potential
benefits of ECT are great, such as in delusional depression, the
balance of potential benefits to risks may tilt in favor of ECT.
Active discussion with the treatment team, supplemented by the growing
amount of printed and videotaped information packages for consumers,
is necessary in the decision-making process, both prior to and
throughout a course of ECT. Consent may be revoked at any time during
a series of ECT sessions.
Involuntary ECT
In the United States, involuntary ECT may not be initiated by a
physician or family member without a judicial proceeding. In every
state, the administration of ECT on an involuntary basis requires such
a judicial proceeding at which patients may be represented by legal
counsel. As a rule, such petitions are granted only where the prompt
institution of ECT is regarded as potentially lifesaving, as in the
case of a person who is in grave danger because of lack of food or
fluid intake caused by catatonia.
Continuation phase therapy
Successful acute phase antidepressant pharmacotherapy or ECT should
almost always be followed by at least 6 months of continued treatment
(Prien & Kupfer, 1986; Depression Guideline Panel, 1993; Rudorfer et
al., 1997). During this phase, known as the continuation phase, most
patients are seen biweekly or monthly.
The primary goal of continuation pharmacotherapy is to prevent relapse
(i.e., an exacerbation of symptoms sufficient to meet syndromal
criteria). Continuation pharmacotherapy reduces the risk of relapse
from 40-60 percent to 10-20 percent (Prien & Kupfer, 1986; Thase,
1993). Relapse despite continuation pharmacotherapy might suggest
either nonadherence (Myers & Branthwaithe, 1992) or loss of a placebo
response (Quitkin et al., 1993a).
A second goal of continuation pharmacotherapy is consolidation of a
response into a complete remission and subsequent recovery (i.e., 6
months of sustained remission). A remission is defined as a complete
resolution of affective symptoms to a level similar to healthy people
(Frank et al., 1991a). As residual symptoms are associated with
increased relapse risk (Keller et al., 1992; Thase et al., 1992),
recovery should be achieved before withdrawing antidepressant
pharmacotherapy.
Many psychotherapists similarly taper a successful course of treatment
by scheduling several sessions (every other week or monthly) prior to
termination. There is some evidence, albeit weak, that relapse is less
common following successful treatment with one type of
psychotherapy?cognitive-behavioral therapy?than with antidepressants
(Kovacs et al., 1981; Blackburn et al., 1986; Simons et al., 1986;
Evans et al., 1992). If confirmed, this advantage may offset the
greater short-term costs of psychotherapy.
Controversy
There is much debate both within the field of psychiatry and among the
general public as to the utility of electroconvulsive therapy.
Opponents claim that the mechanism through which electroshock creates
changes in mental state is nothing more than the destruction of brain
cells, and even proponents are not quite sure how it works. Many
patients who have undergone ECT claim it caused their subsequent
mental state to improve; many others think their ECT treatments did
more harm than good, and some actively campaign to have the treatment
legally banned. Controversy also stems from the fact that many leading
proponents of the treatment hold financial interests in the companies
which manufacture ECT equipment.
Alternative treatments
There is current research in using transcranial magnetic stimulation
(TMS) as an alternative to ECT. Omega-3 fatty acids and sleep
deprivation are also being researched.
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