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Electroconvulsive shock therapy (ECT) or Electroconvulsive therapy is a controversial psychiatric shock therapy involving the induction of a seizure in a patient by passing electricity through the brain. Researchers do not understand how ECT affects mental state, but patients with several conditions show short-term improvement after the procedure. 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 strongly criticize the procedure as extremely harmful to patients' subsequent mental state[citation needed].

ECT was introduced as a treatment for schizophrenia in the 1930s, and soon became a common treatment for mood disorders. ECT was originally administered without anaesthesia or muscle relaxants, and often resulted in injury to the patient as a result of the induced seizure. Currently, in most countries, ECT is administered under anaesthesia and muscle relaxants, which limit the effects of the procedure to the brain itself. ECT without anaesthesia is referred to as "unmodified ECT", or "direct ECT", and is illegal in most countries.

ECT was a common psychiatric treatment until the late 20th century, when it fell into disuse as 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 forms of therapy. When still in common use, ECT was sometimes abused by unethical mental health professionals as a means of punishing and controlling unruly or 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

Currently, ECT is mainly used to treat severe depression, particularly if complicated by psychosis.[1] [2] It is also used in cases of severe depression where antidepressant medication (sometimes in multiple courses), psychotherapy, or both, have been ineffective (refractory depression),[3] 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 renders the use of the usually preferred antidepressants dangerous to the patient or to a developing fetus. Under such circumstances, after carefully weighing the risks and benefits, 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 United States show that modern use of ECT is generally limited to evidence-based indications.[4] Indeed, concern has been raised that, in some settings, particularly in the public sector and outside major metropolitan areas, ECT may be underutilized.[5] In particular, minority patients tend to be underrepresented among those receiving ECT.[6]


The aim of ECT is to induce a bilateral tonic clonic seizure (a 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 by the electrical current, but the strength of the muscle contractions and the subsequent fit sometimes led to complications, such as compression fractures of the spine or damage to the teeth. Muscle relaxants allow a modified fit, where contractions are weak or nonexistent. However, before using muscle relaxants, the patient must be given a general anaesthetic to prevent the patient from experiencing the very uncomfortable state of being paralysed. The end result is that 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 0.9 A) are passed through electrodes applied to the scalp at specific points using a gel, paste or saline solution to prevent burns to the skin. Modern ECT machines regulate the current to keep it constant, and thus the voltage may vary up to a maximum, typically 450 V, but is usually about half that in most cases. The ECT therapist tries to minimize the total energy by restricting the strength and duration of the current. The existence of 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 using the proper amount of stimulation is required for therapeutic efficacy.[7] Therapeutic 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.

After the seizure, cortical electrical activity ceases for a short time, during which an EEG reading is 'flat'. After treatment, patients do not remember the seizure or the events immediately before it.

Exactly how ECT exerts its effects is not known, but repeated applications 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 decreases the functioning of norepinephrine and dopamine, inhibiting auto-receptors in the locus coeruleus and substantia nigra, respectively, causing more of each to be released.[8] One study suggests that long-term ECT increases the expression of brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, in limbic brain regions.[9]

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 controlled trials, unilateral ECT is associated with almost no detectable, persistent memory loss.[10] [11] However, most clinicians find that unilateral ECT is less potent and acts more slowly 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 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, any 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 minimally above the seizure threshold.[12]

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 unnecessarily risky and 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.[13]

Side effects and complications

  1. REDIRECT Template:Totally-disputed-section

Side-effect profile

Much of the accepted 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 and disorientation seen on awakening after ECT clears soon after.

More persistent memory problems are variable and 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[14]. No long-term (six months post-ECT or more) 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[15] [16], although others found problems were gone by seven months after ECT[17]. Calev (1994)[18] surveyed the literature and 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". At least a third of ECT patients have some permanent memory loss, according to a systematic review in 2003[19]. Formal neuropsychological testing has documented permanent neuropsychological deficits in ECT patients[20], including an IQ loss of more than 30 points in one[21]. The degree of impairment and resulting impact on functioning vary between individuals[22]. 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 into its effects on the brain.

Many early studies from the 1940's, 50's, and early 60's indicated that ECT was associated with brain abnormalities.[23] However, other authors such as Sackeim (1994) and Weiner (1984)[24] dismiss the work done in the 1940's and 1950's, pointing out that today's ECT is different. This is supported by the changes in procedure in the 1960's, by the far more effective imaging techniques used today to assess brain damage, by the fact that very few of the earlier studies were prospective, and by the fact that many [25] were post hoc accounts of single patients rather than clinical trials. Of the case studies which have not found brain changes after ECT, perhaps the most persuasive is a patient who had received more than 1250 bilateral ECT treatments and whose brain was in perfectly good health when she died at 89[26]. The recent work assessing the consequences of seizures has found no evidence that they cause brain damage[27], with prospective studies appearing to confirm this[28].

However, critics argue that the differences might make the procedure more damaging, not less. Anesthesia and muscle-paralyzing drugs increase the risks of the procedure and thus its mortality rate.[29] The claim that oxygenation prevents brain damage and thus makes some earlier studies irrelevant is disputed, for example, Sackheim[30] does not always oxygenate his patients: "They don't turn blue", so earlier studies in which animals are not oxygenated might still be relevant. Against this is evidence from more sensitive modern imaging studies, and the evidence from those suffering from epileptic fits of comparable duration to those provoked by ECT, who do not suffer hypoxic brain injury. In addition, while early ECT devices were less powerful than those of today[31], causing opponents of ECT to suggest that today's machines might be more likely to cause brain damage than those used in the early studies, research has shown that the amount of electricity which reaches the brain tissue is significantly below the intensity and duration which would cause damage[32].

There is more recent work noting brain abnormalities in those who have had ECT. Colon & Notermans found changes in nuclear volume in the cortex, but without loss of neurons[33]. Calloway et al. found an association with frontal lobe atrophy and ECT on a retrospective review of scans[34], and accordingly did not claim these were caused by ECT (many schizophrenics, for instance, have abnormal brain anatomy as part of their condition[35], and brain changes have also been found in depressive patients[36]). Diehl et al. in a study of six patients found significant post-ECT T2 increases in the right and left thalamus consistent with a post-ECT increase in brain water content[37]. Dolan et al. found that a past history of treatment by electroconvulsive therapy was associated with greater sulcal widening in the parietal and occipital areas, although again they did not suggest this was due to ECT [38]. Accordingly, while some practitioners may fail to adhere to accepted guidelines for administering ECT, no studies since anesthesia and oxygenation were introduced as standard practice have shown that they cause any damage, despite the much better imaging currently available.

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,[39] 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[40].


Some psychiatric researchers contend that there are virtually no absolute health contraindications that preclude the use of ECT where warranted,[41] i.e. where the treating psychiatrist, often at his sole discretion but frequently 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 known space-occupying lesion such as meningioma, because of the danger of herniation due to transient further increase in intracranial pressure during the procedure.

Device Risk

ECT should be administered under controlled conditions, with appropriate personnel[42] and some mental health laws mandate this.

The United States Food and Drug Administration has classified the devices used to administer ECT as Class III medical devices.[43] Class III is the highest-risk class of medical devices. The risks of ECT, according to the FDA, include brain damage and memory loss.[44]


Some studies  — later confirmed in controlled clinical trials which included the use of simulated (placebo) ECT as a control,[45] have shown that ECT is very effective against severe depression, some acute psychotic states, and mania.[46]. No controlled study has shown that any other treatment for depression is more effective than ECT.[47] ECT has not been shown to be effective in dysthymia, substance abuse, anxiety, or personality disorders. These conclusions, and many of those discussed below, are the product of review of extensive research over several decades[48] as well as by a panel of scientists, practitioners, and consumers.[49]

Although the average 60-70% response rate[50] 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.[51] 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.[52] "Maintenance ECT" refers to indefinite periods of repeated ECT, usually scheduled a few weeks apart. Critics of ECT assert that maintenance ECT is needed because the brain requires approximately four weeks to recover from each closed head injury caused by ECT; thus, when the brain has healed, the temporary euphoric effects are lost and ECT must be given again to attain the previous mood gain. Individuals who repeatedly relapse after 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.[53]

Informed consent

Informed consent is an integral part of the ECT process.[54] 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. Active discussion with the treatment team, possibly supplemented by the growing amount of printed and videotaped information for consumers, is thought by some to be advisable in the decision-making process both prior to and throughout a course of ECT. Theoretically, 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.

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 in grave danger because of lack of food or fluid intake caused by catatonia.

Australian states take the other approach and the law regards 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 two ECTs in a life-threatening situation, at the discretion of the treating psychiatrist. This is most commonly invoked in the case of a patient who has stopped drinking fluids whilst suffering from a severe depressive illness. Further ECT, or involuntary ECT in less urgent circumstances, must be authorised by an independent psychiatrist, who, if in agreement, will usually give consent for a total of twelve ECT.

Continuation phase therapy

Successful acute phase antidepressant pharmacotherapy or ECT is generally followed by at least 6 months of continued treatment.[55] During this phase, the 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%.[56] Relapse despite continuation pharmacotherapy might suggest either nonadherence[57] or loss of a placebo response.[58]

A second goal of continuation pharmacotherapy is to consolidate a response into complete remission(i.e. a 'complete resolution of affective symptoms to a level similar to healthy people').[59] Residual symptoms are associated with increased risk of relapse[60]. 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.[61]

Historical usage

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.

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 sometimes break bones, especially vertebrae, and pull muscles from the violent convulsions induced by the seizure. Patients came to dread the procedure, and it was sometimes used to punish or sedate difficult patients in psychiatric hospitals.

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. 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 over the past generation have led to fewer adverse cognitive effects of ECT.[62] 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.[63] Ultra-brief pulse, higher frequency and longer stimulus duration also contribute to ECT effectiveness while minimizing adverse cognitive effects.


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; although its effectiveness has been demonstrated by many controlled trials, many people regard it as inhumane and primitive — even barbaric. 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 their ECT did more harm than good, and some campaign to have the treatment banned.

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 complete truth about the risks and benefits of ECT.[64] To demonstrate what would be required to fully satisfy the legal obligation for 'informed consent', one psychiatrist has formulated his own 'consent form'[65] using the Texas Legislature[66] as a model. It should be noted that printed or videotaped materials regarding ECT might be commissioned by the manufacturers of the equipment used, and so the possibility of this information leaning towards confirmation bias should be considered. Some question the effects of drugs on the ability to give informed consent.

The use of ECT has been banned in the Republic of Slovenia.

Cultural Depictions of ECT

Electroconvulsive therapy has been depicted in several 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 1960's. It is implied in the film that the hospital staff use ECT to punish uncooperative patients.

In the film Girl, Interrupted, Angelina Jolie's character runs away from a mental hospital because she is being given what she calls "shocks." Other negative depictions can be found in the books Zen and the Art of Motorcycle Maintenance and The Bell Jar, and in the films Requiem for a Dream and "The Sleep Room" (a movie based on MK Ultra and Ewan Cameron). An episode of Quantum Leap depicts ECT in which the main character, Sam, receives ECT as punishment by a nurse, and the ordeal makes it unable for him to leap. The episode is concluded when he receives another shock of high voltage, enabling him to complete his leap. An episode of the NBC TV drama Law & Order entitled "Cruel and Unusual" also featured negative depictions of ECT. In an episode of The Simpsons entitled Don't Fear the Roofer, Homer is subjected to ECT after his family mistakingly believes that his friend Ray Magini is imaginary.

The U2 song "Electric Co." from the album Boy is an anti-ECT anthem. It is about the widespread use of ECT in Ireland's state hospitals in the 1970s, and was reportedly written in response to the treatment's use on one of their close friends.

It has occasionally been portrayed in a positive light, however. Martha Manning's autobiographical 'Undercurrents' acknowledges the downside of treatment: "I felt like I'd been hit by a truck for a while, but that was, comparatively speaking, not so bad", while acknowledging that it worked for her: "Afterwards, I thought, do regular people feel this way all the time? It's like you've not been in on a great joke for the whole of your life".

Research into treatments

There is current research in using Magnetic stimulation therapy (MST) as an alternative to ECT although presently it seems to be somewhat less effective. Dietary omega-3 fatty acids and sleep deprivation are also being researched. Vagus nerve stimulation therapy is another alternative to ECT.

See also

Notes and references

  1. NIH & NIMH Consensus Conference, 1985; Depression Guideline Panel (1993)
  2. Potter WZ, Rudorfer MV. Electroconvulsive therapy--a modern medical procedure. N Engl J Med. 1993 Mar 25;328(12):882-3. [PMID 8441434]
  3. Potter et al. (1991); Depression Guideline Panel (1993)
  4. Hermann et al. Diagnoses of patients treated with ECT: a comparison of evidence-based standards with reported use. Psychiatr Serv. 1999 Aug;50(8):1059-65. [PMID 10445655]
  5. Hermann et al. Variation in ECT use in the United States. Am J Psychiatry. 1995 Jun;152(6):869-75. [PMID 7755116]
  6. Rudorfer et al. (1997)
  7. Sackeim et al. Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. N Engl J Med. 1993 Mar 25;328(12):839-46. [PMID 8441428]
  8. Ishihara & Sasa (1999)
  9. Duman RS & Vaidya VA. Molecular and cellular actions of chronic electroconvulsive seizures. J ECT. 1998 Sep;14(3):181-93. [PMID 9773357]
  10. Horne et al. Comparing bilateral to unilateral electroconvulsive therapy in a randomized study with EEG monitoring. Arch Gen Psychiatry. 1985 Nov;42(11):1087-92. [PMID 3901956]
  11. NIH Consensus Conference (1985); Rudorfer et al. (1997)
  12. Sackeim et al. (1993) [PMID 8441428]
  13. Blumenfeld et al. (2003)
  14. NIH & NIMH Consensus Conference, 1985
  15. Janis IL, Astrachan M. The effects of electroconvulsive treatments on memory efficiency. J Abnorm Soc Psychol. 1951 Oct;46(4):501-11 [PMID 14880367]
  16. Squire LR, Slater PC. Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. Br J Psychiatry. 1983 Jan;142:1-8. [PMID 6831121]
  17. Squire LR, Slater PC, Miller PL. Retrograde amnesia and bilateral electroconvulsive therapy. Long-term follow-up. Arch Gen Psychiatry. 1981 Jan;38(1):89-95. [PMID 7458573]
  18. [PMID 7878183]
  19. Rose (2003)
  20. FDA, Docket #82P-0316
  21. Donahue (1999); Andre (2001); Cott (2004)
  22. NIH & NIMH Consensus Conference (1985); CMHS (1998)
  23. Alpers,1942; Ebaugh et al., 1942; Faurbye, 1942; Neuberger, 1942; Heilbrun, 1941; Heilbrunn, 1942, 1943; Bjerner, 1944; Gralnick, 1944; Jetter, 1944; Lidbeck, 1944; Meyer et al., 1945; Ferraro et al., 1946; Ferraro et al., 1949; Sprague and Taylor, 1948; Will and Rehfeldt, 1948; Martin, 1949; Riese and Fultz, 1949; Liban E, Halpern L, Rozanski J. Vascular changes in the brain in a fatality following electroshock. J Neuropathol Exp Neurol 1951; 10:309-18 [PMID 14861666]; Maclay WS. Death due to treatment. Proc R Soc Med 1953;46:13-20 [PMID 13027286]; Corsellis JA & Meyer A. Histological changes in the brain after uncomplicated electro-convulsant treatment. J Ment Sci. 1954 Apr;100(419):375-83. [PMID 13175001]; Clemedson CJ, Hartelius H, Holmberg G. The effect of high explosive blast on the cerebral vascular permeability. Acta Pathol Microbiol Scand 1957; 40:89-95 [PMID 13424280]; Mckegney FP, Panzetta AF. An unusual fatal outcome of electro-convulsive therapy. Am J Psychiatry 1963; 120:398-400 [PMID 14069472]
  24. See Sackeim's 2004 deposition, Weiner's deposition and testimony in the same case, the testimony of Mecta owners and employees, and the credits given to each in the Mecta manuals
  25. Liban et al. (1951) [PMID 14861666], Maclay (1953) [PMID 13027286], McKegney & Panzetta (1963) [PMID 14069472]
  26. Abrams R. 'Electroconvulsive Therapy'. 2nd ed. New York: Oxford University Press, 1992
  27. Meldrum BS. Neuropathological consequences of chemically and electrically induced seizures. Ann N Y Acad Sci 1986; 462:186-93 [PMID 3085568]; Dwork AJ et al. Absence of histological lesions in primate models of ECT and magnetic seizure therapy. Am J Psychiatry. 2004; 161:576-8 [PMID 14992989]
  28. Coffey CE et al. Brain anatomic effects of ECT: A prospective magnetic resonance imaging study. Arch Gen Psychiatry 1991; 115:1013-21 [PMID 1747016]
  29. Barker JC, Baker AA. Deaths associated with electroplexy. J Ment Sci 1959;105:339-48 [PMID 13665295], Impastato DJ, Berg S, Gabriel AR. Practical elimination of fractures in electroshock therapy by succinylcholine. NY State J Med 1957; 57:2513-7 [PMID 13452099]
  30. Sackeim (2004)
  31. Cameron (1994)
  32. Weiner RD. Does ECT cause brain damage? Brain Behav Sci 1984; 7:153
  33. Colon EJ, Notermans SLH (1975) A long-term study of the effects of electro-convulsions on the structure of the cerebral cortex. Acta Neuropathologica (Berlin) 32:21-5 [PMID 1146505]
  34. Calloway SP et al.(1981). ECT and cerebral atrophy. A computed tomographic study. Acta Psychiatrica Scandinavica 64:442 5 [PMID 7347109]
  35. Turner et al. Imaging phenotypes and genotypes in schizophrenia. Neuroinformatics. 2006;4(1):21-49. [PMID 16595857]; Honea et al. Regional deficits in brain volume in schizophrenia: a meta-analysis of voxel-based morphometry studies. Am J Psychiatry. 2005 Dec;162(12):2233-45. [PMID 16330585]; Keshavan et al. Premorbid indicators and risk for schizophrenia: a selective review and update. Schizophr Res. 2005 Nov 1;79(1):45-57. [PMID 16139479]; Tanskanen et al. Hippocampus and amygdala volumes in schizophrenia and other psychoses in the Northern Finland 1966 birth cohort. Schizophr Res. 2005 Jun 15;75(2-3):283-94. Epub 2004 Nov 14. [PMID 15885519]
  36. Dolan et al. The cerebral cortical appearance in depressed subjects. Psychol Med. 1986 Nov;16(4):775-9. [PMID 3823294]
  37. Diehl DJ, et al. (1994) Post-ECT increases in MRI regional T2 relaxation times and their relationship to cognitive side effects: a pilot study. Psychiatry Res 54:177-84 [PMID 7761551]
  38. Dolan RJ et al. (1986) The cerebral cortical appearance in depressed subjects. Psychol Med 16:775-9 [PMID 3823294]
  39. NIH & NIMH Consensus Conference, 1985
  40. Philpot (2004); Rose (2005)
  41. Potter & Rudorfer (1993); Rudorfer et al. (1997)
  42. Rudorfer et al. (1997)
  43. Federal Register (1979), p. 51776
  44. Federal Register (1978), p. 55729
  45. Janicak et al. (1985)
  46. Small et al. (1988)
  47. Janicak et al. (1985); Rudorfer et al. (1997)
  48. Depression Guideline Panel (1993); Rudorfer et al. (1997)
  49. NIH & NIMH Consensus Conference (1985)
  50. Higher response rates have been reported, e.g. 85-90% in Whybrow PC. 'A Mood Apart: Depression, Mania, and Other Afflictions of the Self'. New York: Basic Books, 1997. and in excess of 90% in Mondimore FM 'Depression: The Mood Disease'. Baltimore: Johns Hopkins University Press, 1995.
  51. Rudorfer et al. (1997)
  52. Sackeim (1994)
  53. Sackeim (1994); Rudorfer et al. (1997)
  54. NIH & NIMH Consensus Conference (1985)
  55. Prien & Kupfer (1986); Depression Guideline Panel (1993); Rudorfer et al. (1997)
  56. Prien & Kupfer (1986); Thase (1993)
  57. Myers & Branthwaithe (1992)
  58. Quitkin et al. (1993a)
  59. Frank et al. (1991a)
  60. Keller et al. (1992); Thase et al. (1992)
  61. Kovacs et al. (1981); Blackburn et al. (1986); Simons et al. (1986); Evans et al. (1992)
  62. NIH & NIMH Consensus Conference (1985); Rudorfer et al. (1997)
  63. Andrade et al., 1998
  64. Rose 2005
  65. Johnson, 2003
  66. Texas Legislature, 2004

Further reading



  • Abrams, R., Taylor, M., Faber, R., Ts'o, T., Williams, R. and Almy, G. (1983) Bilateral vs unilateral electroconvulsive therapy: efficacy and melancholia, American Journal of Psychiatry 140: 463-5.
  • Abrams R, Taylor MA (1973). Anterior bifrontal ECT: a clinical trial. Br J Psychiatry 122: 587–90. PMID 4717031.
  • Andre L (2001). Testimony at the public hearing of the New York State (U.S.) Assembly Standing Committee on Mental Health on electroconvulsive therapy.
  • Andreasen et al. (1990). MRI of the brain in schizophrenia. Arch Gen Psychiatry 47: 35–41. PMID 2294854.
  • Barker J, Baker A (1959). Deaths associated with electroplexy. J Mental Sci 105: 339–48.
  • Blumenfeld H et al. (2003). Targeted prefrontal cortical activation with bifrontal ECT. Psychiatry Res 123: 165–70. PMID 12928104.
  • Calloway SP et al. (1981). ECT and cerebral atrophy. Acta Psychiatrica Scand 64: 442–5. PMID 7347109.
  • Calev A (1994). Neuropsychology and ECT: past and future research trends. Psychopharmacol Bull 30: 461–4. PMID 7878183.
  • Cameron DG (1994). ECT: sham statistics, the myth of convulsive therapy, and the case for consumer misinformation. J Mind Behav 15: 177–98.
  • Cerletti U, Bini L (1938). L'Elettroshock. Arch Gen Neurol Psychiat Psycoanal 19: 266–8.
  • Colon EJ, Notermans SLH (1975). A long-term study of the effects of electro-convulsions on the structure of the cerebral cortex. Acta Neuropathologica (Berlin) 32: 21–25. PMID 1146505.
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The Surgeon General's Report has been criticized: see for instance

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