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Case ReportFull Access

Electroconvulsive Therapy Intolerance

Case

"Ms. Z" is a 35-year-old woman with recurrent major depression, generalized anxiety disorder, and a history of childhood trauma who was initially referred for psychiatric treatment after she endorsed suicidal ideation to her primary care provider in the context of marital and work-related stressors. At the time, she was on a regimen of escitalopram 10 mg, bupropion 300 mg, clonazepam 0.5 mg, and alprazolam 0.5 mg, all scheduled once daily, as prescribed by her primary care provider. Other than those listed, she had not been treated with other psychotropic medications. Following presentation to our clinic, because she was taking two benzodiazepines, clonazepam was discontinued shortly following referral. Escitalopram was also discontinued because of emotional blunting. Duloxetine was trialed as an antidepressant in place of escitalopram, which led to an improvement in mood, as well as remission of suicidal ideation.

However, 2 months after her initial improvement, Ms. Z experienced a relapse into depression. Brief periods of remission followed by additional episodes of depression occurred over the following year. She also reported binge eating and self-harm behaviors during this period and was diagnosed as having bulimia nervosa, as well as cluster B and C personality traits. Multiple medication trials during this period of relapse aimed to treat her depressive symptoms, as well as her difficulties with self-harm and bulimia nervosa. Treatments included topiramate, naltrexone, paroxetine, sertraline, venlafaxine, duloxetine, amitriptyline, trazodone, vilazodone, and lisdexamfetamine. However, many of these medications were either ineffective following adequate trials or discontinued as a result of adverse effects.

One year after her initial referral, the patient presented to a psychiatric facility with her husband given his concern that she was researching methods to attempt suicide. ECT was elected for treatment because of her suicidal ideation and because her condition had been resistant to pharmacotherapy. Informed consent was provided, and she voiced an understanding and willingness to start treatment. Later, however, she admitted feeling pressured into treatments by the urgency portrayed by both her husband and psychiatrist. Consequently, she reported that she consented to ECT treatments without a firm understanding of the potential risks and benefits of and alternatives to the intervention.

No remission of her depression was evident after an acute series of seven unilateral ECT treatments delivered over 2 weeks. At that time, the patient expressed to her counselor (but not her ECT provider) that treatments were causing intolerable effects. She told her counselor that she developed worsened binge eating, insomnia, avolition, anxiety, anhedonia, emotional lability, tearfulness, mixed retro- and anterograde amnesia, chills, and unsteadiness on her feet. Even while these adverse effects progressed in intensity, she received six additional bilateral treatments over another 2 weeks without any improvement. Throughout her treatment she continued to share concerns with her counselor about the side effects that she was experiencing, but she assured her ECT provider that the sessions were well tolerated.

Ultimately, ECT was discontinued per the patient’s request, and she elected to enter a partial hospitalization program. The adverse effects, aside from lingering memory concerns, resolved within a week of stopping treatment. After 1 month in the partial hospitalization program, her depression and suicidal ideation remitted, and she returned to outpatient management on a regimen of aripiprazole 5 mg, amphetamine/dextroamphetamine 20 mg, clonazepam 1 mg, desvenlafaxine 50 mg, and bupropion 300 mg, all scheduled once daily.

Two years later, a severe episode of major depression prompted reconsideration of ECT treatments, although the patient initially expressed hesitation because of her previous negative experiences with ECT. Over the course of several clinical visits, her treatment team continued to discuss the risks and benefits of and alternatives to treatment, including the use of ketamine as an augmenting therapy. Following these discussions, she elected to undergo ECT with ketamine augmentation. At this time, she reported a much more robust understanding of the context and purpose of the treatment.

A series of five bilateral ECT treatments was performed over 2 weeks with a 20-mg subanesthetic dose of ketamine given only during the first session. Within 1 week, the patient noted an improvement in her energy and motivation. She experienced none of the adverse effects associated with her previous ECT treatments aside from mixed retro- and anterograde amnesia after the third treatment. She began to receive maintenance ECT treatments with ketamine augmentation during each session. She did well in outpatient treatment with maintenance treatments alongside pharmacologic management and therapy, although she continued to report memory problems from the first ECT series.

Discussion

The literature indicates that ECT is an efficacious treatment, with adverse effects mostly limited to transient cognitive impairment (1, 2). Despite this favorable side-effect profile, the public at large tends to perceive ECT as potentially harmful (15). In one study, younger age, cultural factors (e.g., language), and exposure to individuals with mental illness were predictors of less favorable perceptions (2). In addition, patient intolerance of ECT, such as seen in the above case, may also partly drive the public’s negative perception of this therapy (6). Intolerance of ECT has been well described in the literature (1, 6, 7). For example, a 1999 study (limited in methodology to interviews based on experiences in the distant past) found that ECT led to the amplification of preexisting psychological disorders that manifested as feelings of shame, failure, and unworthiness and a sense of being abused (8).

In recent years, fewer patients have elected to undergo ECT, as reflected by the number of inpatient ECT hospital treatments in the United States dropping from 12.6 per 100,000 people annually in 1993 to 7.2 per 100,000 in 2009 (5). ECT is generally performed in the inpatient unit, and thus this decline does not simply represent a transition to outpatient treatment (5). It may, however, reflect advances in pharmacologic and nonpharmacologic treatments for depression developed over the past 30 years. As the utilization of ECT has decreased, the percentage of U.S. hospitals conducting ECT also fell from 14.8 to 10.6 during the same time period (5).

A 2012 literature review identified two risk factors for patients’ intolerance of ECT: an inadequate consent process and psychological reactions (9). As demonstrated in the above case, the informed consent process (or lack thereof) may have influenced how our patient responded to treatment. Even after providing consent, up to a third of patients believed that they were coerced to receive ECT, especially when providers used the term "last resort" (4, 9, 10). In other cases, inadequate preprocedural information caused patients to become dissatisfied with the consent process (4, 9). Our patient recalled feeling pressured by the urgency of the initial series into believing ECT was her only remaining viable option, preventing her from achieving full understanding of the treatment process, risks, and benefits. In the second series, time was taken to provide a more satisfying consent process.

Psychological reactions—the second major risk factor for ECT intolerance—include fear, feelings of powerlessness, and identity loss due to prolonged amnesia (6), which are similar to emotions recalled by our patient. Up to 50% of patients fear undergoing ECT, a reaction that stems largely from preconceived notions of its harmful nature (4, 11, 12). Fear has, in a minority of cases, been traumatic enough to impart lasting consequences (4, 11, 12). For some patients, feelings of powerlessness persist from the consent process through treatment (8, 11, 13). Finally, it has been proposed that prolonged amnesia may lead some patients to identify as "someone with memory problems," as seen in the case reported here (9).

The limited number of reports on ECT’s adverse psychological effects may be related to the vulnerability of this patient population and the desire of patients undergoing ECT to maintain a nonconfrontational relationship with their health care providers (8). In our case report, this hypothesis is supported by the patient’s unwillingness to share her concerns with her ECT provider. In later discussions, the patient stated she was reluctant to be open with her ECT provider for fear the treatment would be terminated. However, she freely expressed concerns to her counselor because the counselor was not part of the ECT process.

Our patient did not tolerate the first round of ECT because of exacerbation of her depression and binge eating, as well as the onset of chills and postural instability. Orthostatic hypotension, with accompanying dizziness and nausea, is a relatively common experience following anesthesia and may explain the postural findings (14). During the second ECT series, our patient experienced adverse effects limited to mild amnesia. Aside from the consent process, differences between the two series included anesthetic technique and ECT parameters (Table 1), as well as augmentation with ketamine. Average seizure duration was 35 seconds and 22 seconds for the first and second series, respectively, and total seizure duration was over three times longer in the first series. Longer seizure duration is correlated with cognitive impairment following ECT and may have played a role in the patient’s memory problems (7). Finally, although our patient had a robust response with ketamine augmentation, the evidence base for this practice is mixed. Ketamine has been found to accelerate ECT’s antidepressant effects only within the first 2 weeks of treatment, and other studies have reported negative results with ECT and ketamine augmentation (1, 15). Although research suggests that ketamine alleviates the cognitive effects of ECT (7), our patient continued to report some deficits related to ECT treatments.

TABLE 1. Duration of seizures across two series of ECT

Session and duration of seizure (seconds)
SeriesaTotal duration(seconds)12345678910111213
Firstb45037412927352534213865383129
Secondc129221942171217

aThe first series occurred over 28 days. The second series occurred over 11 days, up to session 5; session 6 of the second series occurred a week after session 5. During the first series, mixed-grade amnesia began after session 3 and persisted through session 4; worsening depression and binge eating began after session 5 and persisted through session 6; and chills and instability began after session 7 and persisted through the end of treatment.

bAnesthetic drugs, 80 mg methohexital, 80 mg succinylcholine, 5 mg rocuronium, and 0.2 mg glycopyrrolate.

cSubanesthetic 20 mg ketamine administered with sessions 1 and 6 only. Anesthetic drugs, 120 mg methohexital and 120 mg succinylcholine. During the second series, mixed-grade amnesia began after session 4 and persisted through the end of treatment.

TABLE 1. Duration of seizures across two series of ECT

Enlarge table

The declining use of ECT and the negative perceptions of ECT in the public eye are noteworthy (and potentially related) phenomena. Improving the consent process, addressing preexisting psychopathologies, and augmenting treatments with pharmacotherapies are all options worth investigating to improve patient tolerance. This case report highlights the need for further research on the factors contributing to patient intolerance of ECT and potential means to ameliorate it.

Key Points/Clinical Pearls

  • The number of patients electing to undergo ECT has declined over the past 20 years.

  • Negative public perception, driven in part by reports from patients who did not tolerate ECT, is likely a contributing factor for the decline.

  • Therapeutic alliance, informed consent practices, and variations in treatment protocol may mitigate patient intolerance of ECT.

Caleb Heiberger is a fourth-year medical student at the University of South Dakota Sanford School of Medicine, Sioux Falls, S.D.

The author has confirmed that details of the case have been disguised to protect patient privacy.

The author thanks Dr. Rajesh Singh, practicing psychiatrist at the University of South Dakota Sanford Health and attending faculty at the University of South Dakota, for assistance with this case report.

The author also thanks the staff at the University of South Dakota Sanford Health Psychiatry and Psychology Clinic, Sioux Falls, S.D., the University of South Dakota Sanford School of Medicine Seldinger Society, and Matthew C. Fadus, M.D., Deputy Editor of the Residents’ Journal.

References

1. Anderson IM, Blamire A, Branton T, et al.: Ketamine augmentation of electroconvulsive therapy to improve neuropsychological and clinical outcomes in depression (ketamine-ECT): a multicentre, double-blind, randomised, parallel-group, superiority trial. Lancet Psychiatry 2017; 4:365–377 CrossrefGoogle Scholar

2. Lauber C, Nordt C, Falcato L, et al.: Can a seizure help? The public’s attitude toward electroconvulsive therapy. Psychiatry Res 2005; 134:205–209 CrossrefGoogle Scholar

3. Teh SP, Helmes E, Drake DG: A Western Australian survey on public attitudes toward and knowledge of electroconvulsive therapy. Int J Soc Psychiatry 2007; 53:247–273 CrossrefGoogle Scholar

4. Chakrabarti S, Grover S, Rajagopal R: Perceptions and awareness of electroconvulsive therapy among patients and their families: a review of the research from developing countries. J ECT 2010; 26:317–322 CrossrefGoogle Scholar

5. Case B, Bertollo D, Laska E, et al.: Declining use of electroconvulsive therapy in US general hospitals. Biol Psychiatry 2013; 73:119–126 CrossrefGoogle Scholar

6. Fisher P: Psychological factors related to the experience of and reaction to electroconvulsive therapy. J Ment Health 2012; 21:589–599 CrossrefGoogle Scholar

7. Zhong X, He H, Zhang C, et al.: Mood and neuropsychological effects of different doses of ketamine in electroconvulsive therapy for treatment-resistant depression. J Affect Disord 2016; 201:124–130 CrossrefGoogle Scholar

8. Johnstone L: Adverse psychological effects of ECT. J Ment Health 1999; 8:69–85 CrossrefGoogle Scholar

9. Fisher P, Johnstone L, Williamson K: Patients’ perceptions of the process of consenting to electroconvulsive therapy. J Ment Health 2011; 20:347–354 CrossrefGoogle Scholar

10. Rose D, Wykes T, Bindmann J, et al.: Information, consent and perceived coercion: patients’ perspectives on electroconvulsive therapy. Br J Psychiatry 2005; 186:54–59 CrossrefGoogle Scholar

11. McDiarmid J: Scrambled eggs for brains. Psychiatr Serv 2005; 56:34–35 CrossrefGoogle Scholar

12. Fisher P: ECT as a traumatic experience, in Trauma Psychology in Context: International Vignettes and Applications From A Lifespan Clinical-Community Psychology Perspective. Edited by Morgan RF. Albuquerque, NM, Morgan Foundation Publishers, 2011 Google Scholar

13. Donahue A: Electroconvulsive therapy and memory loss: a personal journey. J ECT 2000; 16:133–143 CrossrefGoogle Scholar

14. Cowie D, Shoemaker J, Gelb A: Orthostatic hypotension occurs frequently in the first hours after anesthesia. Anesth Analg 2004; 98:40–45 CrossrefGoogle Scholar

15. Kishimoto T, Chawla J, Hagi K, et al.: Single-dose infusion ketamine and non-ketamine N-methyl-d-aspartate receptor antagonists for unipolar and bipolar depression: a meta-analysis of efficacy, safety and time trajectories. Psychol Med 2016; 46:1459–1472 CrossrefGoogle Scholar