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COMMENTARY
Year : 2020  |  Volume : 13  |  Issue : 4  |  Page : 385-388  

Electroconvulsive therapy: Boon or bane?


Department of Psychiatry, Dr. DY Patil Medical College, Hospital and Research Centre, Dr. DY Patil Vidyapeeth, Pune, Maharashtra, India

Date of Submission17-Nov-2019
Date of Decision19-Nov-2019
Date of Acceptance06-Jan-2020
Date of Web Publication20-Jul-2020

Correspondence Address:
Suprakash Chaudhury
Department of Psychiatry, Dr. DY Patil Medical College, Hospital and Research Centre, Dr. DY Patil Vidyapeeth, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mjdrdypu.mjdrdypu_312_19

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How to cite this article:
Chaudhury S, Mujawar S. Electroconvulsive therapy: Boon or bane?. Med J DY Patil Vidyapeeth 2020;13:385-8

How to cite this URL:
Chaudhury S, Mujawar S. Electroconvulsive therapy: Boon or bane?. Med J DY Patil Vidyapeeth [serial online] 2020 [cited 2020 Aug 6];13:385-8. Available from: http://www.mjdrdypv.org/text.asp?2020/13/4/385/290175



While the mechanism of action of electroconvulsive therapy (ECT) remains shrouded in mystery, this effective procedure itself remains mired in controversy. So is it a boon or bane? Let us examine the evidence.


  Historical Background Top


The therapeutic use of seizure induction was reported in the London Medical and Surgical Journal as early as 1785.[1] By 1801, Giovanni Aldini had used galvanism to manage the patients suffering from different forms of mental illnesses.[2] The Hungarian neuropsychiatrist Ladislas J. Meduna in 1934 introduced convulsive therapy using initially camphor and then metrazol (cardiazol).[3] Cerletti and Bini on April 11, 1938, used electricity for the induction of therapeutically effective convulsions.[4] ECT soon replaced metrazol therapy all over the world because it was cheaper, less frightening, and more convenient.[5] Till the introduction of effective psychopharmacological drugs in the 1950s, it remained the only effective treatment in psychiatry. Even today, it remains a safe and effective therapeutic modality in psychiatry.


  Mechanism of Action Top


The therapeutic effect of ECT depends on the induction of a bilateral generalized seizure. Electroencephalogram EEG- monitored studies of ECT have revealed that the generalized seizure is followed by postictal suppression for a period of about 60–90 s. Preseizure appearances return in about 30 min. In addition, the seizure resulted in a transient increase in cerebral blood flow, the use of glucose and oxygen, and the permeability of the blood–brain barrier. Following the seizure, blood flow and glucose metabolism decrease, most noticeably in the frontal lobes. This decrease in blood flow and glucose metabolism is strongly correlated to the therapeutic outcome of ECT.[6]

Almost all the neurotransmitter systems are affected by ECT, most commonly downregulation and desensitization of postsynaptic beta-adrenergic receptors and upregulation of postsynaptic serotonin receptors. There are also decreased serotonin turnover, reduction of acetylcholine levels in the brain and cerebrospinal fluid, and also diminished levels of dopamine. In addition, ECT affects the regulation of calcium entry into neurons, the coupling of G proteins to their receptors, and the activity of adenylyl cyclase and phospholipase C. Similar changes are reported with all antidepressant treatments.[6]

Variations in cortical thickness from magnetic resonance imaging data across time and with symptom improvement were evaluated in 29 patients at three time points during ECT treatment and in 29 controls at two time points. During the course of ECT, they observed an increased thickness in the bilateral anterior cingulate cortex (ACC), inferior and superior temporal, parahippocampal, entorhinal, and fusiform cortex, and in various prefrontal areas in patients, while no changes were observed in controls. Extensive neuroplasticity in neocortical, limbic, and paralimbic regions follows the administration of ECT, and these changes correlate to the amount of antidepressant response. Since variations in ACC thickness differentiate treatment responders and predict treatment response early in the course of ECT, it has been proposed as a biomarker of overall clinical outcome.[7]


  Advantages Top


It was estimated in 2001 that around one million people received ECT annually.[8] Approximately 70% of patients receiving ECT are females.[1] It might be due to the fact that females are more likely to be diagnosed with depression.[9] ECT can be used in a number of different conditions. A course of ECT was found to be effective in approximately half of the patients with treatment-resistant major depressive disorder, whether it is unipolar or bipolar.[10] Thus, ECT is usually reserved for cases when other treatments have failed or in emergency situations such as an imminent suicide.[11] ECT has safely been used in specific cases of depression occurring along with medical conditions such as Huntington's chorea, multiple sclerosis, Parkinson's disease, arteriovenous malformations in the brain, and hydrocephalus.[12] A meta-analytic review paper published in 2004 reported that in terms of efficacy, ECT had a significant superiority versus simulated ECT, versus placebo, versus antidepressants in general, versus tricyclics, and versus monoamine oxidase inhibitors.[13] The UK ECT review group undertook a systematic review and meta-analysis which compared ECT to placebo and antidepressant drugs and found a large effect size for ECT in both comparisons.[14] When ECT was compared with transcranial magnetic stimulation (TMS) for people with treatment-resistant major depressive disorder, it was shown to alleviate depression about two times as well and showed a reduction in the Hamilton Rating Scale for Depression score by 15 points, while TMS reduced it by about 9 points.[15] When looking at treatment options for severely depressed pregnant women, ECT was found to be one of the options, which was least harmful to the gestating fetus.[16] ECT is frequently used as a second-line treatment for patients with catatonia who do not respond to other treatments. However, it can be used as a first-line management option in cases of severe or life-threatening catatonia.[17] In patients with bipolar mania, it is generally used as a second-line treatment.[18] In schizophrenia, ECT is used in treatment-resistant illness when a patient's symptoms show little response to antipsychotics alone. A Cochrane review concluded that ECT, combined with antipsychotic drugs, is an option for schizophrenia patients, especially when rapid global improvement and reduction of symptoms is desired, and in those patients who show limited response to medication alone.[19]


  Disadvantages Top


In adolescents, it is very effective for many psychiatric illnesses, with few and relatively benign adverse effects.[20] Research suggests that administration of either low doses of benzodiazepines or low doses of general anesthetics, to induce sedation but not anesthesia, to such patients reduces the side effects of ECT.[21] Even though there are no absolute contraindications for ECT, care should be taken in patients who suffer from unstable or severe cardiovascular conditions or aneurysms, who have in recent times had a stroke, who have raised intracranial pressure (e.g. brain tumor or any space-occupying lesion), or who have compromised lung functions, or who are generally at high risk for receiving anesthesia.[22]

Cognitive impairment is sometimes noticed after ECT.[23],[24] Its adverse effects have been found to be both retrograde and anterograde amnesia.[25] Approximately 75% of ECT patients say that memory impairment is the worst adverse effect. Studies based on neuropsychological testing of ECT patients show that anterograde amnesia can persist for at least 3 months after a course of ECT. However, follow-up data indicate that almost all patients are back to their cognitive baseline after 6 months.[6]

However, no cognitive impairment was observed in eight patients after more than 100 lifetime ECT sessions.[26] ECT is relatively safe during all trimesters of pregnancy, particularly when compared to pharmacological treatments if care is taken to reduce the potential risks.[27] It may also lead to the absence of blood flow and oxygen supply to the heart, arrhythmias of the heart, and “persistent asystole.”[28] Even though heart failure is very uncommon as a complication of ECT, it may occur, and mortality during ECT is often as a result of cardiovascular complications.[29] Hase et al. reported that asystole lasting for 2 or more seconds was found in < 50% of subjects, but in all these patients, the heartbeat returned without any intervention.[30] Another study found that 65.8% of geriatric patients had developed brief asystole; however, no significant complications were seen after it.[31]


  Misconceptions Top


Despite numerous claims otherwise, there has been no evidence of structural brain damage caused by ECT. Several studies using various brain imaging techniques have confirmed this fact. Similarly, in animal electroconvulsive shock studies, histopathologic studies revealed no structural neuronal damage. Finally, autopsy studies of patients who received ECT have failed to show a pattern of central nervous system damage caused by ECT.[6]

A 2007 questionnaire survey in Australia, consisting of 379 members of the general public, indicated that more than 60% of respondents had some knowledge about the main aspects of ECT. Subjects were mostly against to the use of ECT on depressed patients with psychosocial issues, on children, and on patients against their wishes. Public opinions on ECT were found to be generally negative.[32] The use of ECT remains controversial, as has been indicated by a number of surveys which included public opinions, also the testimony of patients, the legal restrictions, and disagreements regarding the efficacy and adverse effects of ECT within the psychiatric community.[33],[34],[35],[36]


  Conclusion Top


Despite continuous advances in psychopharmacology, psychiatric disorders are often refractory to medications. ECT has been administered worldwide for 80 years, even in patients with significant concurrent medical or neurologic illness. Despite its proven safety and efficacy, ECT does have disadvantages. The American Psychiatric Association recently has launched a petition to reclassify ECT as a low-risk treatment.[37] At this time, ECT remains a highly potent modality for the treatment of severe and refractory psychiatric disorders. Education of patients, families, and even medical professionals is essential for removal of misconceptions and stigma of ECT. Further research is needed to help identify those psychiatric patients who are likely to have a better outcome with ECT and give them a better quality of life. For some patients with psychiatric disorders, ECT is certainly a boon.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Pompili M, Dominici G, Giordano G, Longo L, Serafini G, Lester D, et al. Electroconvulsive treatment during pregnancy: A systematic review. Expert Rev Neurother 2014;14:1377-90.  Back to cited text no. 16
    
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Leroy A, Naudet F, Vaiva G, Francis A, Thomas P, Amad A, et al. Is electroconvulsive therapy an evidence-based treatment for catatonia? A systematic review and meta-analysis. Eur Arch Psychiatry Clin Neurosci 2018;268:675-87.  Back to cited text no. 17
    
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Gallegos J, Vaidya P, D'Agati D, Jayaram G, Nguyen T, Tripathi A, et al. Decreasing adverse outcomes of unmodified electroconvulsive therapy: Suggestions and possibilities. J ECT 2012;28:77-81.  Back to cited text no. 21
    
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McClintock SM, Choi J, Deng ZD, Appelbaum LG, Krystal AD, Lisanby SH, et al. Multifactorial determinants of the neurocognitive effects of electroconvulsive therapy. J ECT 2014;30:165-76.  Back to cited text no. 23
    
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Loo CK, Katalinic N, Smith DJ, Ingram A, Dowling N, Martin D, et al. Arandomized controlled trial of brief and ultrabrief pulse right unilateral electroconvulsive therapy. Int J Neuropsychopharmacol 2014;18. pii: pyu045.  Back to cited text no. 24
    
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26.
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Hirachan A, Maskey A. Acute myocardial infarction following electroconvulsive therapy in a schizophrenic patient. Egypt Heart J 2017;69:71-3.  Back to cited text no. 28
    
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Bhat SK, Acosta D, Swartz CM. Postictal asystole during ECT. J ECT 2002;18:103-6.  Back to cited text no. 29
    
30.
Hase K, Yoshioka H, Nakamura T, Kamei T, Isse K, Nakamura M, et al. Asystole during electroconvulsive therapy. Masui 2005;54:1268-72.  Back to cited text no. 30
    
31.
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32.
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33.
Fisher P. Psychological factors related to the experience of and reaction to electroconvulsive therapy. J Ment Health 2012;21:589-99.  Back to cited text no. 33
    
34.
Philpot M, Treloar A, Gormley N, Gustafson L. Barriers to the use of electroconvulsive therapy in the elderly: A European survey. Eur Psychiatry 2002;17:41-5.  Back to cited text no. 34
    
35.
Whitaker R. Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill (Rev. pbk. ed.). New York, NY: Basic Books; 2010. p. 102-6.  Back to cited text no. 35
    
36.
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37.
Levin S, Binder R. Time is now to Support the ECT Reclassification Effort. Arlington, VA: American Psychiatric Association Blog; 2016. Available from: https://www.psychiatry.org/news-room/apa-blogs/apa-blog/2016/01/time-is-now-to-support-the-ect-reclassification-effort. [Last accessed on 2019 Nov 17].  Back to cited text no. 37
    




 

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  Mechanism of Action
  Advantages
  Disadvantages
  Misconceptions
  Conclusion
   References

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