Electroconvulsive therapy

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Electroconvulsive therapy (ECT) is a controversial psychiatric therapy that involves inducing a seizure in a patient by passing electricity through the brain. Patients with several conditions sometimes show dramatic short-term improvement after ECT. While many psychiatrists believe that properly administered ECT is a safe and effective treatment for some conditions, a vocal minority of psychiatrists, former patients, antipsychiatry activists, and others warn that ECT might harm the patients' subsequent mental state.

ECT was introduced for treating schizophrenia in the 1930s, and became a common treatment for mood disorders. In its early days, ECT was given without anaesthesia or muscle relaxants. Patients were often injured as a side effect of the seizure. Currently, ECT is given under anaesthesia and muscle relaxants, which limit the effects of the procedure to the brain itself. ECT without anaesthesia is known as "unmodified ECT", or "direct ECT", and is illegal in most countries.

ECT was a common treatment until the late 20th century, when better drug therapies became available for more conditions. It is now reserved for severe cases of clinical depression and bipolar disorder that do not respond to other treatments. When still in common use, ECT was sometimes abused by mental health professionals to punish or control uncooperative patients. Many people came to view ECT unfavorably after negative depictions of it in several books and films, and the treatment is still controversial.

Current use

ECT is mainly used to treat severe depression, particularly if complicated by psychosis [1]. It is also used in cases of severe depression where antidepressant medication (sometimes in multiple courses), psychotherapy, or both, have been ineffective (refractory depression),when medication cannot be taken, or when other treatments would be too slow (for example, in a person with delusional depression and intense, unremitting suicidal tendencies). Specific indications include depression accompanied by a physical illness or pregnancy, which makes the use of the usually preferred antidepressants dangerous to the patient or to a developing fetus. Under such circumstances, some psychiatrists consider ECT to be the safest treatment option. It is also sometimes used to treat the manic phase of bipolar disorder and the rare condition of catatonia.

Recent epidemiological surveys in the USA show that modern use of ECT is generally limited to evidence-based indications.[2] Indeed, concern has been raised that, in some settings, particularly in the public sector and outside major metropolitan areas, ECT may be underutilized.[3] In particular, minority patients tend to be underrepresented among those receiving ECT.[4] Accurate statistics about the frequency, context and circumstances of ECT in the USA are hard to obtain as few states have laws that require this information to be given to state authorities. [5]

Overview

The aim of ECT is to induce a bilateral tonic clonic seizure (where the person loses consciousness and has convulsions) which lasts for at least 60 seconds. Before the discovery of muscle relaxants, ECT was given unmodified. Patients were rendered instantly unconscious, but the strength of the muscle contractions and the subsequent fit sometimes led to complications. Muscle relaxants allow a modified fit, where contractions are weak or nonexistent. However, the patient must first be given a general anaesthetic to prevent him or her from experiencing the very uncomfortable state of being paralysed. As a result, the patient drifts off to sleep and wakes up a short time later unable to recall the details of the procedure.

To induce the seizure, short bursts of a fixed current (typically 0.9A) are passed through electrodes applied to the scalp at particular points, using a gel, paste or saline solution to prevent burns to the skin. The ECT therapist tries to minimize the total energy by restricting the strength and duration of the current. The seizure is confirmed by observation or by EEG neuromonitoring[1].

Electrical current flows between two electrodes placed on the scalp, usually from temple to temple in the past, although now ECT is more often applied to the non-dominant brain hemisphere. Placing both electrodes on one side of the head over the nondominant (generally right) cerebral hemisphere, results in delivery of the initial stimulation away from the primary learning and memory centers. With unmodified ECT, the seizure is characteristically more severe than a naturally occurring epileptic seizure. The production of an adequate, generalized seizure is required for therapeutic efficacy.[6]. ECT is usually given three times per week for 6 to 12 treatments, on either an inpatient or outpatient basis. Studies have shown that each fit must be separated by at least a day.

Exactly how ECT exerts its effects is not known, but repeated application affects several kinds of neurotransmitters in the central nervous system. ECT seems to sensitize two subtypes of serotonin receptor (5-HT receptor), thereby strengthening signaling. ECT also affects the functioning of norepinephrine and dopamine, inhibiting auto-receptors in the locus coeruleus and substantia nigra, respectively, causing more of each to be released.[7] One study suggests that long-term ECT increases the expression of brain-derived neurotrophic factor and its receptor in limbic brain regions.[8]

Types of ECT

There are two basic forms of ECT: bilateral and unilateral, and bilateral ECT can be subdivided into bitemporal and bifrontal ECT. In bitemporal ECT, current is passed across the temporal lobes, between electrodes placed on either side of the head. With unilateral, the electrodes are only on the right side, and pass current mainly through the right temporal lobe. According to several trials, unilateral ECT is associated with almost no detectable, persistent memory loss.[9] [10] Unilateral ECT is less potent and acts more slowly than bilateral ECT, particularly in the most severe cases of depression or mania. An approach that is sometimes used is to begin with unilateral ECT and switch to bilateral ECT after about six treatments if there is no response.

The relationship of electrical dose to clinical response depends on the electrode placement; for bilateral ECT, as long as an adequate seizure is obtained, a higher dose will merely add to the cognitive toxicity, whereas for unilateral ECT, a therapeutic effect will not be achieved unless the electrical stimulus is more than just above the seizure threshold.[6]

Even a moderately high electrical dosage in unilateral ECT has fewer cognitive adverse effects than bilateral ECT. On the other hand, high-dose bilateral ECT might be an avoidable cause of severe memory impairment. Bifrontal ECT is a modified form of bitemporal ECT in which electrodes are placed 2 inches above the lateral angle of each orbit. It has fewer adverse effects on memory than bitemporal ECT, and it increases the blood flow to the prefrontal cortex.[11]

Side effects and complications

Much of the risk of ECT arises from the use of general anesthesia; there is considerable disagreement about other risks. The most common adverse effects are confusion and retrograde memory loss for events surrounding the period of ECT treatment, and generalised but mild muscle aches after waking. Some of the confusion seen on awakening after ECT clears soon after. More persistent memory problems are difficult to quantify. Most typical with standard, bilateral ECT has been a loss of memories for the time of the ECT series and extending back for an average of 6 months, combined with impairment in learning new information, which continues for perhaps 2 months after ECT.[12] No long-term studies of cognition, memory ability, and memory loss have been done in the past two decades, but some long-term studies before this reported permanent amnesia,[13] although others found problems were gone by seven months after ECT.[14] Calev (1994) concluded that patients must be warned of possible non-memory cognitive deficits, as "they are not going to function well on more tasks than they anticipate".[15]. At least a third of ECT patients have some permanent memory loss, according to a systematic review in 2003.[16] Formal neuropsychological testing has documented permanent neuropsychological deficits in ECT patients[17]. The degree of impairment and resulting impact on functioning vary between individuals.[18] Critics of ECT believe that there is enough evidence that patients' memories can be permanently and severely damaged to justify a moratorium, at least until more research has been done.

Many studies from the 1940s, 1950s, and early 1960s indicated that ECT was associated with brain abnormalities However, other authors point out that today's ECT is different, and recent work has found no evidence that the seizures cause brain damage [19] with prospective studies appearing to confirm this [20].

More recent work has found some brain abnormalities in those who have had ECT. but it is not established whether these are caused by ECT. Many schizophrenics, for instance, have abnormal brain anatomy as part of their condition and brain changes have also been found in depressive patients.

ECT may have adverse psychological effects. John Breeding, a psychologist at the University of Texas, has highlighted what he regards as psychological effects of ECT, including suppression of ability to heal by emotional release; emotional distress, with deep feelings of terror and powerlessness; promotion of human beings in the roles of victims and passive dependents of medical professionals, and confirmation of patients' belief that there is something really wrong with them (shame)." [21] Breeding regards psychiatric illness as the product of unresolved psychic conflict, often due to abuse, and feels that the correct treatment for such problems is to bring out this underlying conflict.

The decision to use ECT must be evaluated by each individual, weighing the potential benefits and known risks of all available, appropriate treatments in the context of informed consent [22] free of coercion and veiled threats. Studies in 2004 and 2005 showed that half of ECT patients did not feel that they could refuse the treatment.[23]

Some psychiatric researchers contend that there are virtually no absolute health contraindications that preclude the use of ECT where warranted [24] i.e. where the treating psychiatrist, sometimes in consultation with a multidisciplinary team, decides that the likely benefits outweigh the possible risks. The only major contraindication is increased intracranial pressure, as in cases of recent cerebrovascular accident or meningioma, because of the danger of herniation due to transient further increase in intracranial pressure during the procedure.

ECT should be given under controlled conditions, with appropriate personnel.[25]. The United States Food and Drug Administration has classified the devices used to administer ECT as Class III medical devices. [26] Class III is the highest-risk class of medical devices. The risks of ECT, according to the FDA, include brain damage and memory loss.[27]

Effectiveness

Some studies, including some that used simulated (placebo) ECT as a control, [28] show that ECT is effective against severe depression, some acute psychotic states, and mania.[29]. These conclusions, and many of those discussed below, are the product of review of extensive research [30] as well as by a panel of scientists, practitioners, and consumers.[31]

Although the average 60-70% response rate seen with ECT is similar to that seen with pharmacotherapy, there is evidence that the antidepressant effect of ECT occurs faster than with medication, which supports the use of ECT when depression is accompanied by potentially uncontrollable suicidal ideas and actions. However, ECT does not provide long-term protection against suicide; it is now recognized that a single course of ECT should be regarded as a short-term treatment for acute illness. To sustain the response to ECT, continuation treatment, often in the form of antidepressant and/or mood stabilizer medication, is needed. [32] "Maintenance ECT" refers to indefinite periods of repeated ECT, usually scheduled a few weeks apart. Individuals who repeatedly relapse after ECT despite continuation medication may be candidates for maintenance ECT [33]

Informed consent

Informed consent is an integral part of the ECT process. [34]. The potential benefits and risks, and those of available alternative interventions, are reviewed carefully, and discussed with patients and, where appropriate, family or friends. Candidates for ECT should be informed that its benefits are short-lived without continuation treatment, and that there is some risk of permanent severe memory loss. Active discussion with the treatment team, possibly supplemented by the growing amount of printed and videotaped information for consumers, is advisable in the decision-making process before and during a course of ECT. Care should be taken that the informed consent materials come from objective sources and not, for example, from the manufacturer of ECT devices. In most jurisdictions, consent may be revoked at any time during a series of ECT sessions.

Involuntary ECT

Procedures for involuntary ECT vary from country to country depending on local mental health laws. Legal proceedings are required in some countries, while in others ECT is seen as another form of treatment that may be given involuntarily as long as legal conditions are observed. The World Health Organization, in its 2005 publication "Human Rights and Legislation WHO Resource Book on Mental Health," specifically states, "ECT should be administered only after obtaining informed consent."

In nearly all states in the USA, involuntary ECT may not be initiated by a physician or family member without a judicial proceeding. In nearly 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, the law requires that such petitions are granted only where the prompt institution of ECT is regarded as potentially lifesaving, as in the case of a person in grave danger because of lack of food or fluid intake caused by catatonia. In Oregon, an institution may administer involuntary ECT without any judicial proceeding at all through the use of an administrative override that requires, among other things, the review of the case by a physician unaffiliated with the treating facility.

Australian states regard involuntary treatment with ECT in the same light as any other involuntary treatment. There is an appeal process available for patients and relatives. This position facilitates the expedited use of ECT in emergencies.

In England and Wales, the Mental Health Act 1983 allows the use of ECT on detained patients (with and without capacity), if the treatment is authorised by a psychiatrist from the Mental Health Act Commission's panel. If the treating psychiatrist thinks the need for treatment is urgent they may start a course of ECT before authorisation. About 2,000 people a year are treated without their consent under the Mental Health Act.[35] A small number of informal patients are treated without their consent under common law. In Scotland the Mental Health (Care and Treatment) (Scotland) Act 2003 gives patients with capacity the right to refuse ECT.

In 2006, the organization Mental Disability Rights International published the results of a two-year investigation in Turkey that found what MDRI termed "widespread" involuntary ECT administered without anesthesia.Template:Fact

Continuation phase therapy

Successful acute phase antidepressant pharmacotherapy or ECT is generally followed by at least 6 months of continued treatment.[36] During this continuation phase, most patients are seen biweekly or monthly. The main goal of continuation pharmacotherapy is to prevent relapse (i.e. exacerbation of symptoms). Continuation pharmacotherapy reduces the risk of relapse from 40-60% to 10-20%.[37] Relapse despite continuation pharmacotherapy might suggest either nonadherence or loss of a placebo response.

A second goal of continuation pharmacotherapy is to consolidate a response into complete remission of symptoms, as residual symptoms are associated with increased risk of relapse. Many psychotherapists taper a successful course of treatment by scheduling several sessions (every other week or monthly) before termination. There is evidence that relapse is less common following successful treatment with one type of psychotherapy—cognitive-behavioral therapy—than with antidepressants.[38]

History

ECT was developed in the 1930s by Italian neurologist Ugo Cerletti. Cerletti saw electric shocks given to hogs before slaughter. This rendered them unconscious but did not kill them. Cerletti found that such electric shocks caused his obsessive and difficult mental patients to become meek and manageable. At first, ECT 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 sometimes break bones, especially vertebrae, and pull muscles from the violent convulsions induced by the seizure. Patients came to fear the procedure, and it was sometimes used to punish or sedate difficult patients in psychiatric hospitals.

With the development of effective medications for major mental disorders, the need for ECT lessened, but did not disappear. Until then, ECT often had been administered for several conditions for which it is now generally regarded as ineffective, for example, for treating schizophrenia. Advances in treatment technique have led to fewer adverse effects of ECT.[39] 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 can be induced with as little as one-third of the electrical power used by the older method, reducing the risk of confusion and memory disturbance.[40] Ultra-brief pulse, higher frequency and longer stimulus duration also contribute to ECT effectiveness while minimizing adverse cognitive effects.

Controversy

As of 2006, most psychiatrists believe that ECT can be beneficial in some circumstances. However, ECT remains controversial, and a vocal minority of psychiatrists oppose it; some regard it as inhumane and primitive. Opponents claim that the mechanism through which ECT changes mental state is nothing more than the destruction of brain cells, and even proponents are unsure how it works. Many patients who have had ECT claim it caused their mental state to improve; many others think it did more harm than good, and some campaign to have the treatment banned, as it is in the Republic of Slovenia. Antipsychiatry believes that, for the most part, there are no real mental illnesses, and that ECT is used to suppress certain behaviors which, although perhaps uncommon, are still within the normal range. Anti-ECT activists allege that patients are rarely told the full truth about the risks and benefits of ECT.[41].

Fictional and semi-fictional depictions of ECT

ECT has been depicted in several fictional and semi-fictional films, books, and songs, almost always in an extremely negative light. A great deal of anti-ECT sentiment was generated by its depiction in the 1975 movie One Flew Over the Cuckoo's Nest, based on a novel by Ken Kesey, which in turn was based loosely on the author's experiences in various mental hospitals during the 1960s. It is implied in the film that the hospital staff use ECT to punish uncooperative patients. ECT has occasionally been portrayed in a positive light, however. In Elizabeth Flock's novel But Inside I'm Screaming, the main character, Isabel, is initally reluctant to undergo ECT for her severe depression, but the ECT is a major factor in her recovery.


Famous people who have had ECT

Source note

Sections of this article were adapted from Mental Health: a report of the Surgeon General.

Footnotes

  1. NIH & NIMH Consensus Conference, 1985; Depression Guideline Panel (1993)
  2. Hermann R et al. (1999). "Diagnoses of patients treated with ECT: a comparison of evidence-based standards with reported use.". Psychiatr Serv 50: 1059-65. PMID 10445655.
  3. Hermann R, et al. (1995). "Variation in ECT use in the United States.". Am J Psychiatry 152: 869-75. PMID 7755116.
  4. Rudorfer et al. (1997)
  5. Cauchon, Dennis. "Controversy and Questions Shock Therapy: Patients often aren't informed of full danger", USA Today, 1995-12-06. (in English)
  6. 6.0 6.1 Sackeim H et al. (1993). "Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy.". N Engl J Med 328: 839-46. PMID 8441428.
  7. Ishihara & Sasa (1999)
  8. Duman R, Vaidya V (1998). "Molecular and cellular actions of chronic electroconvulsive seizures.". J ECT 14: 181-93. PMID 9773357.
  9. Horne R, et al. (1985). "Comparing bilateral to unilateral electroconvulsive therapy in a randomized study with EEG monitoring.". Arch Gen Psychiatry 42: 1087-92. PMID 3901956.
  10. NIH Consensus Conference (1985); Rudorfer et al. (1997)
  11. Blumenfeld et al. (2003)
  12. NIH & NIMH Consensus Conference, 1985
  13. Squire L, Slater P (1993). "Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study.". Br J Psychiatry 142: 1-8. PMID 6831121.
  14. Squire L, Slater P, Miller P (1981). "Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up.". Arch Gen Psychiatry 38: 89-95. PMID 7458573.
  15. Calev A (1994). "Neuropsychology and ECT: past and future research trends.". Psychopharmacol Bull 30: 461-9. PMID 7878183.
  16. Rose (2003)
  17. FDA, Docket #82P-0316
  18. NIH & NIMH Consensus Conference (1985); CMHS (1998)
  19. Dwork A et al. (2004). "Absence of histological lesions in primate models of ECT and magnetic seizure therapy.". Am J Psychiatry 161 (3): 576-8. PMID 14992989.
  20. Coffey C, et al. (1991). "Brain anatomic effects of electroconvulsive therapy. A prospective magnetic resonance imaging study.". Arch Gen Psychiatry 48: 1013-21. PMID 1747016.
  21. Breeding, John (2003). The Necessity of Madness: Explaining How Psychiatry Is a Clinical Construct and Madness Is a Metaphor. Chipmunkapublishing, 460. DOI:2003-01-03. 0954221877. 
  22. NIH & NIMH Consensus Conference, 1985
  23. Philpot (2004); Rose (2005)
  24. Potter & Rudorfer (1993); Rudorfer et al. (1997)
  25. Rudorfer et al. (1997)
  26. Federal Register (1979) p 51776
  27. Federal Register (1978), p. 55729
  28. Janicak et al. (1985)
  29. Small et al. (1988)
  30. Depression Guideline Panel (1993); Rudorfer et al. (1997)
  31. NIH & NIMH Consensus Conference (1985)
  32. Sackeim (1994)
  33. Rudorfer et al. (1997)
  34. NIH & NIMH Consensus Conference (1985)
  35. The Mental Health Act Commission: "In Place of Fear? eleventh biennial report, 2003-2005.", page 236. The Stationery Office, 2005
  36. Depression Guideline Panel (1993)
  37. Prien & Kupfer (1986); Thase (1993)
  38. Evans et al. (1992)
  39. NIH & NIMH Consensus Conference (1985)
  40. Andrade et al. (1998)
  41. Rose (2005)

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External links

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