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.


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).

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.


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.


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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