User:Xyn1/ect

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Electroconvulsive therapy
ICD-10-PCSGZB
ICD-9-CM94.27
MeSHD004565
OPS-301 code8-630
MedlinePlus007474

Electroconvulsive therapy (ECT), (also known as electroshock), is a controversial psychiatric treatment where electrodes are placed on the brain to induce electrical seizures for treating psychiatric illnesses such as depression and schizophrenia.[1] The efficacy of ECT has been debated by psychiatrists as it was shown that persons even receiving placibo (or 'fake') ECT recovered at an almost equal rate. Therefore, ECT is usually used as a last line of intervention for major depressive disorder, schizophrenia, mania and catatonia.[2] A standard ECT involves administrations across weeks, months and years and ECT in itself doesn't usually have a sustained benefit, thus, drug therapy is continued during and after ECT.[3] It was first introduced in 1938 by Italian neuropsychiatrists Ugo Cerletti and Lucio Bini, and gained widespread popularity among psychiatrists as a form of treatment in the 1940s and 1950s.[4][5]

Although it is depicted as a painful procedure in western fiction, a majority of ECT is administered under general anestesia.[6]

Due to various side effects associated with the treatment such as short term and long term memory loss, The World Health Organization discourages its use on children and advises that it should only be given after informed consent is taken from the patient. But, in exceptional circumstance, such as in emergencies, it permits the patient's guardian to offer consent for the procedure.[7][8][9]

History[edit]

A Bergonic chair "for giving general electric treatment for psychological effect, in psycho-neurotic cases", according to original photo description. World War I era.

As early as the 16th century, agents to induce seizures were used to treat mental illness. In 1785, this was documented in the London Medical Journal.[1] Convulsive therapy was introduced in 1934 by Hungarian neuropsychiatrist Ladislas J. Meduna who incorrectly believed that schizophrenia and epilepsy were disorders which couldn't co-occur, He first induced seizures first with camphor and then metrazol (cardiazol).[10][11] During this time It was known that inducing convulsions aided in helping those with schizophrenia like symptoms. Ladislas Meduna is considered to be the father of convulsive therapy.[12] The first international meeting on convulsive therapy was held in 1937, in Switzerland by the Swiss psychiatrist Muller. The proceedings were published in the American Journal of Psychiatry and, within three years, cardiazol convulsive therapy was being used worldwide.[11] Italian neuropsychiatrist Ugo Cerletti and Lucio Bini used electric shocks to produce seizures in animal experiments, and developed the idea of using electricity as a substitute for metrazol in convulsive therapy in humans. In 1937 they experimented for the first time on a human. Cerletti had noted a shock to the head produced convulsions in dogs. To use the same idea on humans came to Cerletti when he saw pigs were given an electric shock to put them in an anesthetized state, before being slaughtered.[13] Cerletti and Bini practiced until they felt they had the right parameters needed to have a successful human trial. Once they started trials on humans they found that after 10 to 20 treatments, the results were positive. Although they noted that the reason that their patients were more receptive to ECT (compared to other means of seasure induction) was due to the side effect of autobiographical memory loss or retrograde amnesia.[13] ECT soon replaced metrazol therapy all over the world because it was cheaper, less frightening and more convenient.[14] Cerletti and Bini were even nominated for a Nobel Prize. By 1940, it was introduced to both England and the US. In Germany and Austria it was promoted by Friedrich Meggendorfer. Through the 1940s and 1950s, the use of ECT became widespread to treat various forms of mental illness.

In the early 1940s, in an attempt to reduce the memory disturbance and confusion also known as retrograde amnesia, two modifications were introduced: the use of unilateral electrode placement and the replacement of sinusoidal current with brief pulse. It took many years for brief-pulse equipment to be widely adopted.[15] In the 1940s and early 1950s ECT was usually given in "unmodified" form, without muscle relaxants, and the seizure resulted in a full-scale convulsion. A rare but serious complication of unmodified ECT was fracture or dislocation of the long bones. In the 1940s psychiatrists began to experiment with curare, the muscle-paralysing South American poison, in order to modify the convulsions. The introduction of suxamethonium (succinylcholine), a safer synthetic alternative to curare, in 1951 led to the more widespread use of "modified" ECT. Thus, a short-acting anesthetic was usually given along with a muscle relaxant to prevent feelings of suffocation that can be experienced with muscle relaxants.[15]

Later on, due to the emergence of antidepressant medications including SSRIs such as Prozac, which was depicted in the mass media more positively compared to the negative depictions of ECT to a marked decline in its use during the 1950s to the 1970s. The Surgeon General stated there were problems with electroshock therapy in the initial years before anesthesia was routinely given, and that "these now-antiquated practices contributed to the negative portrayal of ECT in the popular media."[16] The New York Times described the public's negative perception of ECT as being caused mainly by one movie. It stated:

For Big Nurse in One Flew Over the Cuckoo's Nest, it was a tool of terror, and, in the public mind, shock therapy has retained the tarnished image given it by Ken Kesey's novel: dangerous, inhumane and overused

— The New York Times, circa 1990, Goleman, Daniel (1990-08-02). "The Quiet Comeback of Electroshock Therapy". The New York Times. p. B5. Retrieved 2008-01-01

In 1976, Dr. Blatchley developed and demonstrated the efficacy of his constant current, brief pulse ECT device. It replaced earlier devices because of the reduction in cognitive side effects such as memory loss. Although very few clinics still use sine-wave ECT devices, even to this day.[17]

In the 1970s the American Psychiatric Association (APA) published its report on ECT which were followed up by two others in 1990 and 2001. All of these endorsed the use of ECT in the treatment of depression. [18] The critics during this time pointed to shortcomings such as side effects (such as memory loss) as well as it being used as a form of abuse or being unevenly used. The use of ECT declined until the 1980s, when the New York Times, reported:

[its] use began to [again] increase amid growing awareness of its benefits and cost-effectiveness for treating severe depression"

— The New York Times, Goode, Erica (1999-10-06). "Federal Report Praising Electroshock Stirs Uproar". New York Times. Retrieved 2008-01-01.

In 1985 the government agencies, National Institute of Mental Health and National Institutes of Health staged a conference on ECT for developing a consensus. It concluded that, while ECT was the most controversial treatment in psychiatry and had significant side-effects, it has been shown to be effective for a narrow range of severe psychiatric disorders.[19]

Along with the pre-existing criticisms, national institutions also reviewed prior practices and set new standards. In 1978, The American Psychiatric Association released its first task force report in which new standards for consent were introduced which stipulated that ECT cannot be given to children and involuntary ECT can only be adminstried in emergency settings. It also recommended the use of unilateral electrode placement. The conference organized by the NIMH also confirmed the efficacy of ECT in certain circumstances. The second report on ECT released by the American Psychiatric Association in 1990 documented the specific details on the delivery, education, and training of ECT. The last report on ECT, by the APA in 2001 emphasized the importance of informed consent, and the expanded role that the procedure has in modern medicine.

Mechanism of action[edit]

There is a diversity of opinion as to the mode of action of ECT. One set of psychiatrists and scientists maintain that the mechanism of actions hasn't been found and another set claim that ECT is efficacious due to the side effects it produces such as memory loss.

The latter group point to studies which suggest the the efficacy is due to the retrograde amnesia associated with it. This can be confirmed by the varying levels of efficacy seen with differing electrode placement and electronic modulation. It has been suggested that bilateral electrode placement (where the two electrodes are placed on both sides of the temple) and sine wave stimulation (where the rate of electricity is constant or higher) results in greater memory loss compared to unilateral electrode placement (where one electrode is placed on either temple and the other is placed above the forehead) and brief pulse stimulation (where the electricity is given by brief pulses). Thus, some psychiatrists suggest its efficacy it due to the side effect of amnesia that ECT is used for depression (where old memory is lost). [20][21][22][23]

Other scientists maintain that the mechanism of action is more contentious. Ladislas J. Meduna believed that chemically induced seizures, brought on by drugs, could change the chemical makeup of the brain of a patient with schizophrenia. It is known that the central nervous system is regulated by small electrical current; disrupting or "restarting" that current by induced seizure (colloquially, "jumpstarting the brain"), has shown positive effects in patients with severe depression or schizophrenia.[12]

Peter Breggin, a critic of ECT and evidence-based psychiatry, claims that it induces "a closed-head injury caused by an overwhelming current of electricity sufficient to cause a grand mal seizure" and that the improvements in mood seen in patients receiving ECT are resultant from brain damage.[24] Such claims are rejected as wholly unsubstantiated by the consensus of the scientific and medical community.[25][26][27]

There is a vast body of literature on the effects of ECT in animals; however, though human and animal brains are very similar, animal models of depression are widely acknowledged to parallel only limited aspects of depressive illness, a uniquely human disease. Some suggest pruning of normally dense synaptic connections in the hippocampus, a richly connected area deep in the temporal lobe vital in controlling both mood and memory, seen in animal studies may play a role in its effectiveness.[28]

Selection of patients[edit]

The American Psychiatric Association's guidelines state that ECT can be benificial for multiple conditions. These include depression, schinopherenia, catatonia and mania.

In depression it is recommended in cases where multiple courses of antidepressants fail, prior response to ECT which was favorable, and in emergency situations where where the risk of suicide or levels of psychosis is more serious than the treatment's side effects. It is also decided in relation to other factors such as the patient's preference and capacity to consent, and a weighing of the risks and benefits.[29] The guidelines also favour early ECT treatment and relapse prevention where it believes there is consensus for major depression with psychotic features, manic delirium, or catatonia. Some psychiatrists and other clinicians maintain that ECT can be used as a first line of treatment.[8]

The APA guidelines also recommend ECT when other options has been exhausted, such as unsuccessful antipsychotic medications for treatments relating to schizophrenia, schizoaffective or schizphreniforn disorder. It also stated that ECT is rarely used as a first-line treatment.

Some guidelines[which?] recommend cognitive behavioral therapy or other psychotherapy before ECT is used. However, treatment resistance is usually defined as lack of response to at least two antidepressants at adequate doses for an adequate duration and with good compliance. The APA, although, states that patients will choose alternative treatments over ECT whenever the decision arises.

The UK's National Institute for Health and Clinical Excellence (NICE) guidelines recommended ECT for patients with severe depression, catatonia, or prolonged or severe mania. It did not recommend the use of ECT as a maintenance therapy in depressive illness as "the long-term benefits and risks [...] had not been clearly established"[25]: 5–6  and those recommendations were unchanged in the 2010 update.[30]: 526 

The 2003 NICE ECT guidelines do not recommend ECT for schizophrenia, and this has been supported by meta-analysis showing no or little benefit versus placebo, or in combination with antipsychotic drugs, including Clozapine.[31]

The NICE 2003 guidelines state that doctors should be particularly cautious when considering ECT treatment for women who are pregnant and for older or younger people, because they may be at higher risk of complications with ECT. The 2001 APA ECT guidelines say that ECT may be safer than alternative treatments in the infirm elderly and during pregnancy. The APA guidelines stated that the literature supports the safety for mother and fetus during pregnency.

ECT has been used in some cases of depression occurring in the setting of multiple sclerosis, Parkinson's disease, Huntington's chorea, developmental delay, brain arteriovenous malformations and hydrocephalus.[32]

Efficacy[edit]

Patient characteristics[edit]

About 70 percent of ECT patients are women.[1] This is due to women being more likely to be diagnosed with depression.[1][33] Patients who are older and higher in socie-economic status also receive ECT at higher rate compared to use in ethinic minorities.[33][34]

Degree of effectiveness and risks[edit]

Scientific papers and articles reviewing studies of ECT effectiveness have reached conflicting conclusions.

A meta-analysis done on the effectiveness of ECT in unipolar and bipolar depression was conducted in 2012. Findings showed that although patients with unipolar depression and bipolar depression responded very differently to other medical treatments both groups responded equally as well to ECT. Overall remission rate for patients with unipolar depression was 51.5% and 50.9% in those with bipolar depression. The severity of each patient’s depression was assessed at the same baseline in each group.[35]

In 2003, The UK ECT Review group published a systematic review and meta-analysis comparing ECT to placebo and antidepressant drugs. This meta-analysis demonstrated a large effect size (high efficacy relative to the mean in terms of the standard deviation) for ECT versus placebo, and versus antidepressant drugs.[36]

In 2006, a research article by Dr. Colin A. Ross found that no studies had ever shown that ECT was more effective than a placebo (sham ECT) treatment as of 1 month posttreatment.[37]

In 2008, a meta-analytic review paper found in terms of efficacy, "a significant superiority of ECT in all comparisons: ECT versus simulated ECT, ECT versus placebo, ECT versus antidepressants in general, ECT versus TCAs and ECT versus MAOIs."[38]

In 2010, a paper by Dr. John Reed and Dr. Richard Bentall found that ECT was only minimally more effective than a placebo during the treatment period, and that there was no difference in effect after the treatment period. In light of this finding, and the risk of side-effects, the authors concluded that the use of ECT "cannot be scientifically justified".[9]

A 2011 paper in the Journal of Psychiatric Nurses Association reported that ECT was effective.[39]

Surveys of public opinion, the testimony of former patients, legal restrictions on its use and disputes as to the efficacy, ethics and adverse effects of ECT within the psychiatric and wider medical community indicate that the use of ECT remains controversial.[40][41][42][43][44][45] This is reflected in the recent vote by the United States Food and Drug Administration's (FDA's) Neurological Devices Advisory Panel to recommend that FDA maintain ECT devices in the Class III device category for high risk devices except for patients suffering from catatonia. This may result in the manufacturers of such devices having to do controlled trials on their safety and efficacy for the first time.[46][47][48] In justifying their position, panelists referred to the memory loss associated with ECT and the lack of long-term data.[49]

Duration of effect[edit]

Half those who receive ECT successfully then relapse within six months. This is similar to the rate of relapse after discontinuing antidepressant medication, and it has been suggested that it is due to the severity and chronicity of pre-existing illness for which ECT is generally used.[50] The relapse rate in the first six months continues to be high despite the use of psuchotropic medications or further ECT.[51][52]

Likelihood of remission[edit]

The 1999 U.S. Surgeon General's Report on Mental Health summarized psychiatric opinion at the time about the effectiveness of ECT. It stated that both clinical experience and published studies had determined ECT to be effective (with an average 60 to 70 percent remission rate) in the treatment of severe depression, some acute psychotic states, and mania. Its effectiveness had not been demonstrated in dysthymia, substance abuse, anxiety, or personality disorder. The report stated that ECT does not have a long-term protective effect against suicide and should be regarded as a short-term treatment for an acute episode of illness, to be followed by continuation therapy in the form of drug treatment or further ECT at weekly to monthly intervals.[53]

A 2004 large multicentre clinical follow-up study of ECT patients in New York — describing itself as the first systematic documentation of the effectiveness of ECT in community practice in the 65 years of its use — found remission rates of only 30 to 47 percent, with 64 percent of those relapsing within six months.[54] However, when patients with co-morbid personality disorders or who were suffering from schizoaffective disorder were removed from the analysis, the remission rates climbed to 60-70%.[54]

Related experimental treatments[edit]

Recent research has investigated whether implantable devices such as those used in DBS (deep brain stimulation) could result in clinical improvements for patients with treatment-resistant depression. Althought DBS has not been authorized or approved by regulatory agencies for treatment-resistant depression.

  1. ^ a b c d Cite error: The named reference Rudorfer was invoked but never defined (see the help page).
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  5. ^ Psychology Frontiers and Applications – Second Canadian Edition (Passer, Smith, Atkinson, Mitchell, Muir)
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  18. ^ See Friedberg, J (1977). "Shock treatment, brain damage, and memory loss: a neurological perspective". American Journal of Psychiatry 134:1010–1014; and Breggin, PR (1979) Electroshock: its brain-disabling effects. New York: Springer
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  24. ^ Dr. Peter Breggin for Huffington Post. February 9, 2008. Brain-Disabling Treatments in Psychiatry: Drugs, Electroshock and the Psychopharmaceutical Complex
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  26. ^ Department of Health (September 2009). Electroconvulsive therapy - About your rights. Melbourne, Victoria: Mental Health and Drugs Division, Victorian Government, Department of Health. 090806.
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  28. ^ Krishnan; Nestler, EJ; et al. (October 2008). "The molecular neurobiology of depression". Nature. 455 (1): 894–902. Bibcode:2008Natur.455..894K. doi:10.1038/nature07455. PMC 2721780. PMID 18923511. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: date and year (link)
  29. ^ Lisanby, S.H. (2007) Electroconvulsive Therapy for Depression Volume 357, No. 19, pp. 1939–1945
  30. ^ "Depression in adults (update)" (PDF). National Institute for Clinical Excellence. 2010. p. 526. Retrieved 2010-05-24.
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  33. ^ a b Cite error: The named reference Reid was invoked but never defined (see the help page).
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  36. ^ UK ECT Review Group (2003). "Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis". The Lancet. 361 (9360): 799–808. doi:10.1016/S0140-6736(03)12705-5. PMID 12642045.
  37. ^ Ross CA (2006). "The sham ECT literature: implications for consent to ECT". Ethical Human Psychiatry and Psychology. 8 (1): 17–28. doi:10.1891/ehpp.8.1.17. PMID 16856307.
  38. ^ Daniel Pagnin, M.D., M.Sc.; Valéria de Queiroz, M.D., M.Sc.; Stefano Pini, M.D.; Giovanni Battista Cassano, M.D. "Efficacy of ECT in Depression: A Meta-Analytic Review". Focus.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  39. ^ http://jap.sagepub.com/content/17/3/217.short
  40. ^ Philpot, M; Treloar, A; Gormley, N; Gustafson, L (NaN undefined NaN). "Barriers to the use of electroconvulsive therapy in the elderly: a European survey". European Psychiatry. 17 (1): 41–45. doi:10.1016/S0924-9338(02)00620-X. PMID 11918992. {{cite journal}}: Check date values in: |date= (help)
  41. ^ Whitaker, Robert (2010). Mad in America : bad science, bad medicine, and the enduring mistreatment of the mentally ill (Rev. pbk. ed.). New York, NY: Basic Books. pp. 102–106. ISBN 978-0-465-02014-0.
  42. ^ Golenkov, Andrei; Ungvari, Gabor S.; Gazdag, Gábor (21 February 2011). "Public attitudes towards electroconvulsive therapy in the Chuvash Republic". International Journal of Social Psychiatry. 58 (3): 289–94. doi:10.1177/0020764010394282. PMID 21339235.
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  46. ^ Kellner, Charles H. (2012-07-05). "The FDA Advisory Panel on the Reclassification of ECT Devices: Unjustified Ambivalence". Psychiatric Times. UBM Medica. Archived from the original on 2012-10-25. Retrieved 2012-10-25.
  47. ^ Duff Wilson for the New York Times. January 28, 2011 F.D.A. Panel Is Split on Electroshock Risks
  48. ^ "FDA Executive Summary Prepared for the January 27-28, 2011 meeting of the Neurological Devices Panel Meeting to Discuss the Classification of Electroconvulsive Therapy Devices (ECT)". United States Food and Drug Administration. Archived from the original (PDF) on 2012-10-25. Retrieved 2012-10-25.
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  50. ^ Sackeim HA, Haskett RF, Mulsant BH, Thase ME, Mann JJ, Pettinati HM, Greenberg RM, Crowe RR, Cooper TB, Prudic J.(2001) Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA. 2001 Mar 14; 285(10):1299–307.
  51. ^ Tew Jr, JD; Mulsant, BH; Haskett, RF; Joan, P; Begley, AE; Sackeim, HA (2007). "Relapse during continuation pharmacotherapy after acute response to ECT: a comparison of usual care versus protocolized treatment". Annals of Clinical Psychiatry. 19 (1): 1–4. doi:10.1080/10401230601163360. PMID 17453654. {{cite journal}}: Unknown parameter |author-separator= ignored (help)
  52. ^ Kellner, CH; Knapp, RG; Petrides, G; Rummans, TA; Husain, MM; Rasmussen, K; Mueller, M; Bernstein, HJ; O'Connor, K; Smith, G; Biggs, M; Bailine, SH; Malur, C; Yim, E; McClintock, S; Sampson, S; Fink, M (December 2006). "Continuation electroconvulsive therapy vs pharmacotherapy for relapse prevention in major depression: a multisite study from the Consortium for Research in Electroconvulsive Therapy (CORE)". Archives of General Psychiatry. 63 (12): 1337–44. doi:10.1001/archpsyc.63.12.1337. PMC 3708140. PMID 17146008. {{cite journal}}: Unknown parameter |author-separator= ignored (help)CS1 maint: date and year (link)
  53. ^ Surgeon General (1999). Mental Health: A Report of the Surgeon General, chapter 4.
  54. ^ a b Prudic J, Olfson M, Marcus SC, Fuller RB, Sackeim HA (2004). "Effectiveness of electroconvulsive therapy in community settings". Biol. Psychiatry. 55 (3): 301–12. doi:10.1016/j.biopsych.2003.09.015. PMID 14744473.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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