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Mechanism of action

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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.

Some studies 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). [1][2][3][4]

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.[5]

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.[6] Such claims are rejected as wholly unsubstantiated by the consensus of the scientific and medical community.[7][8][9]

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.[10]

Selection of patients

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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.[11] 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.[12]

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"[7]: 5–6  and those recommendations were unchanged in the 2010 update.[13]: 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.[14]

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.[15]

Efficacy

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Patient characteristics

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About 70 percent of ECT patients are women.[16] This is due to women being more likely to be diagnosed with depression.[16][17] Patients who are older and higher in socie-economic status also receive ECT at higher rate compared to use in ethinic minorities.[17][18]

Degree of effectiveness and risks

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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.[19]

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.[20]

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.[21]

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."[22]

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".[23]

A 2011 paper in the Journal of Psychiatric Nurses Association reported that ECT was effective.[24]

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.[25][26][27][28][29][30] 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.[31][32][33] In justifying their position, panelists referred to the memory loss associated with ECT and the lack of long-term data.[34]

Duration of effect

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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.[35] The relapse rate in the first six months continues to be high despite the use of psuchotropic medications or further ECT.[36][37]

Likelihood of remission

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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.[38]

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.[39] 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%.[39]

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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. ^ Ottosson, J-O. (1960). Experimental studies of memory impairment after electroconvulsive therapy, Acta Psychiatrica Scandinavica, 35(S145), 103-131. doi:10.1111/j.1600-0447.1960.tb08352.x
  2. ^ Donahue, A. B. (2000). Electroconvulsive therapy and memory loss: A personal journey, Journal of ECT, 16(2), 133-143
  3. ^ Squire, L. R. (1986). Memory functions as affected by electroconvulsive therapy, Annals of the New York Academy of Science, 462, 307-314. doi:10.1111/j.1749-6632.1986.tb51265.x
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  6. ^ Dr. Peter Breggin for Huffington Post. February 9, 2008. Brain-Disabling Treatments in Psychiatry: Drugs, Electroshock and the Psychopharmaceutical Complex
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  11. ^ Lisanby, S.H. (2007) Electroconvulsive Therapy for Depression Volume 357, No. 19, pp. 1939–1945
  12. ^ Cite error: The named reference APA2001guideline was invoked but never defined (see the help page).
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  14. ^ Tharyan, P. Adams, C.E. (2005). Tharyan, Prathap (ed.). "Electroconvulsive therapy for schizophrenia". The Cochrane Database of Systematic Reviews (2): CD000076. doi:10.1002/14651858.CD000076.pub2. PMID 15846598.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Murray ED, Buttner N, Price BH (2012). "Depression and Psychosis in Neurological Practice". In Bradley WG, Daroff RB, Fenichel GM, Jankovic J (ed.). Bradley's Neurology in Clinical Practice: Expert Consult - Online and Print, 6e (Bradley, Neurology in Clinical Practice e-dition 2v Set). Vol. 1 (6th ed.). Philadelphia, PA: Elsevier/Saunders. pp. 114–115. ISBN 978-1-4377-0434-1.{{cite book}}: CS1 maint: multiple names: authors list (link)
  16. ^ a b Cite error: The named reference Rudorfer was invoked but never defined (see the help page).
  17. ^ a b Cite error: The named reference Reid was invoked but never defined (see the help page).
  18. ^ Euba R, Saiz A (2006). "A comparison of the ethnic distribution in the depressed inpatient population and in the electroconvulsive therapy clinic". J ECT. 22 (4): 235–6. doi:10.1097/01.yct.0000235928.39279.52. PMID 17143151.
  19. ^ Dierckx, B. (2012). "Efficacy of electroconvulsive therapy in bipolar versus unipolar major depression: A meta-analysis". Bipolar Disorders. 12 (2): 146–150. doi:10.1111/j.1399-5618.2012.00997.x. PMID 22420590. {{cite journal}}: |first2= missing |last2= (help); |first3= missing |last3= (help); |first4= missing |last4= (help)
  20. ^ 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.
  21. ^ 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.
  22. ^ 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)
  23. ^ Cite error: The named reference Read 333–47 was invoked but never defined (see the help page).
  24. ^ http://jap.sagepub.com/content/17/3/217.short
  25. ^ 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)
  26. ^ 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.
  27. ^ 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.
  28. ^ Committee on Mental Health (March 2002). "Report on Electroconvulsive Therapy". New York State Assembly. Retrieved 8 March 2011.
  29. ^ Melding, P (2006-07-07). "Electroconvulsive therapy in New Zealand: terrifying or electrifying?". The New Zealand Medical Journal. 119 (1237): U2051. PMID 16862197.
  30. ^ Cite error: The named reference Teh was invoked but never defined (see the help page).
  31. ^ 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.
  32. ^ Duff Wilson for the New York Times. January 28, 2011 F.D.A. Panel Is Split on Electroshock Risks
  33. ^ "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.
  34. ^ Mechcatie, Elizabeth. "FDA Regulation of ECT Devices in Transition". Clinical Psychiatry News. Retrieved 8 March 2011.
  35. ^ 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.
  36. ^ 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)
  37. ^ 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)
  38. ^ Surgeon General (1999). Mental Health: A Report of the Surgeon General, chapter 4.
  39. ^ 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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