Secondary Logo

Journal Logo


The Use of Electroconvulsive Therapy in Eating Disorders

A Systematic Literature Review and Case Report

Pacilio, Rachel M. BS*; Livingston, Robin K. MD; Gordon, Mollie R. MD

Author Information
doi: 10.1097/YCT.0000000000000599
  • Free


Electroconvulsive therapy (ECT) has long been used to treat mental illness, particularly in patients who require immediate resolution of severe and life-threatening symptoms.1 According to the 2001 American Psychiatric Association guidelines, ECT is considered a first-line therapy for use in major depressive disorder (MDD), mania, and schizophrenia. Notably, the guidelines specify that ECT should not be reserved solely for use in treatment-resistant patients with these conditions. There is considerable evidence supporting the safety and efficacy of ECT and withholding its use can effectively “prolong suffering”2 in patients with these conditions. Also used for refractory cases of a variety of conditions beyond those specifically indicated, ECT has shown efficacy when used across the spectrum of affective and psychotic disorders. There are no absolute contraindications to ECT,2 but it is important to note that careful and individualized consideration should be taken prior to initiating treatment with ECT for refractory conditions that lack strong supporting evidence. It is crucial to ensure that the potential benefits of treatment outweigh the risk. When used safely and appropriately, ECT has been shown to be useful in conditions as varied as obsessive-compulsive disorder (OCD), Parkinson disease, and posttraumatic stress disorder (PTSD), so there is some evidence to indicate that it can be effectively used more broadly than indicated.3

As there have been no randomized controlled trials to determine the efficacy of ECT in patients with eating disorders (EDs), the validated evidence for its use in EDs is limited. Rarely used in the treatment of anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), or associated disorders, there is scant and inconsistent literature regarding its efficacy. Eating disorders are difficult to treat, and long-term outcomes remain less than favorable.4 With published mortality rates for AN as high as 5%, EDs account for some of the highest rates of morbidity and mortality among all mental illnesses. Additionally, the rate of relapse leading to chronic illness is high.5–7 According to the American Psychiatric Association Practice Guideline for the Treatment of Patients with Eating Disorders, treatment programs take a multidisciplinary approach in order to address the medical, nutritional, psychiatric, and emotional needs of the patient, although weight restoration and medical stabilization are often the primary goal.7–9 Eating disorders are highly associated with comorbid mood, personality, or other psychiatric disorders,10,11 and a variety of treatment modalities are often needed to address the wide range of medical and psychiatric symptoms that patients can present with. It is necessary to address comorbid conditions along with the ED, so patients often receive unique combinations of medication, psychotherapy, and nutritional rehabilitation.12 Pharmacotherapy has been shown to be useful in treating comorbid psychiatric conditions in patients with EDs, but evidence for the use of psychiatric medication in treating the ED itself is limited, especially in the acute setting.13 Typically, a combination of various pharmacological and psychotherapeutic methods is utilized depending on the individual traits of each patient's ED,8,9 which can be widely variable. Overall, the treatment that is most relied upon remains psychotherapy, most often cognitive behavioral therapy (CBT).14 Although often very effective in treating EDs, psychotherapy takes time, active participation, and insight in order to produce results. The effects of malnutrition, nutritional imbalance, and extreme mood lability may prevent patients from deriving maximal benefit from psychotherapy early in their treatment when their physical condition is most critical, especially when comorbid psychiatric disorders are present.15 There exists a need for a safe and effective therapy that would allow for rapid improvement of the patient's most severe and life-threatening symptoms such as strict calorie restriction, purging behavior, self-harm, or suicidality.

The intent of this review is to determine what is known about the efficacy and risks of ECT in patients with EDs with or without co-occurring mood disturbance and to inform clinicians regarding the utility and safety of its use in practice. We will also present a case of a patient with AN and refractory MDD who benefitted from the use of ECT in her treatment course.


Our patient is a 30-year-old African American woman with AN and recurrent MDD with suicidal ideation who was treated with ECT during her hospitalization and subsequent outpatient follow-up.

Ms X. presented to the emergency room with suicidal ideation in the context of multiple psychosocial stressors. She reported a history of AN, depression, anxiety, PTSD, and multiple suicide attempts. After the death of her husband 8 months prior to admission, her depression returned following roughly a decade-long remission with a several-year period of time without any use of psychotropic medications. In the emergency room, she reported depressed mood, anhedonia, insomnia, hopelessness, worthlessness, and guilt, as well as a 30-lb weight loss over the last 4 months. She had been deliberately heavily restricting her caloric intake, abusing laxatives, and exercising excessively and noted that she “enjoys” starving herself and felt proud of her weight loss. She had a body mass index (BMI) of 15.2 kg/m2, considerably lower than her baseline of 19.4 kg/m2. She reported anxiety about gaining weight and nearly constant preoccupation with thoughts about her weight and food. She started feeling suicidal about 6 weeks prior to presentation and had a plan to overdose with sleeping pills. At that time, she was admitted to an outside psychiatric hospital for 5 days and discharged on fluoxetine and mirtazapine. She did not follow up after discharge and stopped taking the medications because they stimulated her appetite. Her suicidal ideation, ED, and depressive symptoms continued to worsen and were exacerbated by homelessness, unemployment, and grief, so she voluntarily presented to our hospital requesting treatment.

Upon admission, Ms X. was noted to be thin, but medically stable without notable abnormalities on laboratory studies or physical examination. Her medical history included asthma as well as Wolff-Parkinson-White syndrome with ablation at age 10 years. She reported 3 prior suicide attempts with subsequent psychiatric hospitalizations and had been prescribed multiple antidepressant medications in the past including escitalopram, paroxetine, duloxetine, fluoxetine, and mirtazapine. She has no significant history of tobacco, alcohol, or drug use. She had a history of sexual trauma at ages 4 and 17 years and was previously diagnosed with PTSD. She reported a long history of MDD as well as AN that was present in the absence of depressive symptoms, but worsened during periods of depression. At her time of presentation, she lacked social support, had little contact with any family members, and interacted only occasionally with friends from her church. She was recently fired from her job and asked to leave her home by a roommate because of her ED behaviors. She reported feeling that “no one would miss me if I were dead.” She denied physical symptoms beyond mild abdominal pain and constipation and was noted to be guarded and dysphoric on presentation.

As it had worked for her in the past, Ms X. was started on paroxetine 10 mg daily. She did not think it would increase her appetite, so she was amenable to taking this medication. She was also prescribed trazodone 50 mg for sleep. On the unit, she was noticed to be severely restricting her food intake and reported that she was allowing herself only 300 calories per day and would exercise for 10 minutes for every 100 calories eaten. One week into her admission, she had no improvement in mood or suicidal ideation, so she agreed to an increase in dose of paroxetine to 40 mg daily augmented with aripiprazole 2.5 mg daily. Her low mood and suicidality persisted, and she reported that she had little appetite. She continued to eat only minimal amounts of food and refused to drink anything other than coffee and tea. She was mildly bradycardic and hypotensive and reported headaches, lightheadedness, and dizziness. Electroconvulsive therapy was recommended because of the urgency of her condition and need for immediate intervention for her suicidality and restricting behavior.

Ms X. was medically cleared for ECT and underwent a total of 11 ultrabrief-pulse right unilateral treatments 3 times a week using the Somatics Thymatron System IV (Somatics, LLC, Venice, FL) at 6 times seizure threshold with anesthesia of methohexital, succinylcholine, and glycopyrrolate pretreatment. Her initial Montgomery-Åsberg Depression Rating Scale (MADRS) score was 33. After the third treatment, the patient's mood improved considerably, and MADRS score was 18. At this time, she began to eat more for the first time during her admission, and her thoughts of self-harm began to decrease. After her seventh inpatient ECT treatment, her MADRS score was 12, and she was eating most of her meals. Notably, though, she still felt considerably guilty about eating and was conflicted about whether she would continue to maintain her caloric intake after discharge. As her mood had improved significantly, and she was no longer reporting a desire to self-harm, she was discharged from the unit at a weight of 97 lb, a BMI of 15.7 kg/m2. It was determined that further inpatient stay was not warranted because it was unlikely to alter the course of her illness. She had an additional 4 treatments after discharge with a final MADRS score of 10. She continued to report that she was maintaining her weight and food intake but still felt guilty after eating and was anxious about gaining weight. Follow-up for medication management was arranged, but maintenance treatment was not sought because of patient preference. Her social situation (homelessness) and lack of stable transportation prevented her participation in the intensive outpatient treatment program. Unfortunately, her ability to receive ED-specific therapy was extremely limited as there are no treatment programs available to the uninsured in our area.

Less than 2 weeks after her final ECT treatment, Ms X. returned to the emergency room with worsening suicidal ideation, although she was not admitted to the unit. She stated that her worsening mood was again due to her social stressors, but she reported continuing to maintain adequate caloric intake, although she was still classified as underweight at this time.


We conducted a review of available literature on the use of ECT in patients with EDs. PubMed, PsycINFO, and MEDLINE were searched independently by 2 of the authors (R.P. and R.K.L.). Search terms included “Electroconvulsive Therapy,” “ECT,” and “Electroshock” each combined with “Anorexia Nervosa,” “Bulimia Nervosa,” “Binge Eating Disorder,” “OSFED,” “EDNOS,” and “Eating Disorder.” These searches were performed between September and October 2018 and included literature published from 1946 onward. A total of 89 results were returned. Titles and abstracts of each returned article were reviewed by all of the authors. The full texts of English language articles meeting inclusion criteria were reviewed. Details extracted from each case report included the patient's psychiatric diagnoses, age, details of ECT treatment, outcome of treatment and reported outcome measures, medical comorbidities, adverse outcomes of treatment, BMI before and after treatment, and presence of comorbid personality pathology.

Inclusion/Exclusion Criteria

Texts included were those that described administration of ECT to patients with active symptoms of a diagnosed ED with or without additional comorbidities. Only articles available in English language were included. Texts excluded were those that did not pertain to the use of ECT in patients with EDs and those that were not relevant to ED behaviors or common medical comorbidities encountered in patients with EDs. Articles detailing other neuromodulation techniques such as transcranial direct current stimulation, transcranial magnetic stimulation, or deep brain stimulation in place of ECT were also excluded. Reviews that included cases already identified in the literature search were also excluded (Fig. 1).

Study inclusion and exclusion methodology. Of the 89 articles returned during a search of available literature on ECT in patients with EDs, 77 were thoroughly reviewed based on their titles and abstracts. Eleven articles ultimately met inclusion criteria. Data from included studies were extracted, and details are described in the Results section. This figure demonstrates the methodology utilized in selecting studies for inclusion.


After excluding 78 articles that did not meet criteria, 11 relevant articles16–26 were included in our review. Through this review, we identified 14 patients aged 12 to 94 years old with EDs who underwent ECT as part of their treatment. Extracted data are summarized in Table 1. Of those patients, 13 were diagnosed with AN, and 1 patient was diagnosed with BED. No patients with BN were reported; however, at least 4 patients engaged in some form of bulimic behavior including binge eating, purging, laxative abuse, or diuretic abuse. Patients underwent between 5 and 45 treatments, with a mean of 19 treatments. Laterality was reported as bitemporal/bilateral in 8 cases, right unilateral with a switch to bilateral in 1 case, and not specified in the remaining 5 cases. Psychiatric comorbidities included MDD, OCD, schizophrenia, generalized anxiety disorder, suicidal ideation, and nonsuicidal self-harm. Notably, only 3 of 14 patients were diagnosed with solely an ED in the absence of additional psychiatric comorbidities, all of whom showed improvement in their ED following ECT. Twelve of 14 patients were female; of the 2 reported male patients, one was diagnosed with AN and the other with BED.

Literature Review of the Use of ECT in ED Patients

The most common medical comorbidity was malnutrition and very low body weight as was seen in 13 of 14 patients. Of articles reporting BMI, the median increase in BMI following treatment was 3.36, and in articles reporting weights, the weight gain after completion of treatment ranged from 4.4 to 39 lb, with an average gain of 17.7 lb. After treatment, 50% of patients had “normal” BMIs as compared with 0% prior to treatment, including 1 patient with BED and an initial BMI of 97 kg/m2. However, this is limited because of only 6 patients having pretreatment and posttreatment BMIs reported. Adverse outcomes were rarely reported. Only 2 of 14 patients experienced mild memory or cognitive disturbance following treatment with ECT.20,22 Most patients showed considerable improvement following their course of ECT, with only 1 patient diagnosed with AN and MDD reporting no change.22 Notably, all of these patients were critically ill at the time of treatment with ECT, and most had failed numerous treatments prior to consideration and initiation of ECT.

In addition to the case reports detailed above, 2 review articles27,28 were found that described cases not otherwise obtained during our search. These articles were not included in our data because of primary sources being in other languages; however, they described a total of 56 patients with AN who were treated with ECT. Specific details about these patients and their outcomes following ECT were not reported, but ECT was noted to have been successful achieving remission in many of these cases.


A review of the pertinent literature in addition to the case presented indicates that ECT can be considered for use in patients with EDs, specifically in severe AN and in patients who are refusing to eat or drink or who continue to compulsively engage in high-risk behaviors. While only the first step in ED treatment, weight restoration and medical stabilization are crucial in determining a patient's likelihood for mortality and relapse, and early weight gain is a strong predictor of remission.29,30 Compulsory feeding and psychotropic medications with increased appetite and weight gain profiles are most often used to facilitate this first stage in treatment, although these strategies lack solid evidence and consensus.31 Because of the egosyntonic nature of EDs, patients often resist refeeding attempts and medications that they believe will lead to weight gain.32 Electroconvulsive therapy might be a favorable alternative for patients and could be preferable to forced caloric intake or medication administration in cases that require immediate intervention due to medical instability or limited access to care. Although detailing patients without diagnosed EDs, some studies have indicated that increased appetite and return of spontaneous eating behavior were an early outcome of treatment with ECT.33,34 Often thought of as a “last resort” in patients with EDs, it is reasonable to consider ECT earlier in order to prevent a protracted hospital course, further extreme weight loss, or the later need for invasive interventions such as nasogastric feeding or percutaneous endoscopic gastrostomy placement.35 It is important to note, however, that relative outcomes between these 2 strategies are unknown as there are no studies available for direct comparison.

As patients with EDs may be medically unstable, extra consideration should be taken to ensure patient safety during ECT treatment. With a thorough medical workup in addition to preventive stabilization measures prior to the initiation of therapy, including but not limited to intravenous hydration, electrolyte repletion, and careful anesthesia administration, clinicians can minimize the risk of adverse outcomes in these medically complex psychiatric patients. Notably, our patient was treated with glycopyrrolate prior to ECT in order to prevent worsening bradycardia or asystole and ultimately had a safe and successful course of ECT. There have been no reported cases of adverse medical outcomes resulting from the use of ECT in patients with EDs, so there is no evidence to suggest that the use of ECT should be specifically limited in this patient population.

Although potentially effective in expediting early treatment and weight restoration efforts, ECT should not be expected to affect a patient's attitude toward eating and is not a substitute for ED-focused psychotherapy and related interventions. It is possible that ECT enhances the response to ED-specific treatment, but may be insufficient when used in the absence of standard therapy. As was seen in our patient, ECT was considerably more effective in treating her comorbid conditions than her ED itself. The improvement in her depressive symptoms was accompanied by a concurrent reduction in ED behaviors, which may indicate that her progress toward ED recovery was positively influenced by ECT. Eating disorders are highly correlated with comorbid conditions, so it is important to note that ECT was effective in treating her depression despite the presence of an ED and that presence of an ED does not preclude the use of ECT when a comorbid indicated condition is present. More studies, including a randomized controlled trial in patients with and without comorbid psychiatric illness, would aid in determining if ECT is an effective treatment option specifically for EDs.

Beyond the use of ECT and not included in this review were several articles that detail successful use of noninvasive neuromodulation techniques including transcranial direct current stimulation,36 transcranial magnetic stimulation,37 and deep brain stimulation38 in treating EDs. Transcranial direct current stimulation specifically has shown promising results in treating EDs, particularly BN39 and BED,40,41 and may help these patients reduce impulsivity. These techniques warrant further study in patients with EDs alongside ECT.


1. Folkerts HW. Electroconvulsive therapy: indications, procedure and treatment results. Nervenarzt. 2011;82:93–102.
2. American Psychiatric Association. Committee on Electroconvulsive Therapy. The Practice of Electroconvulsive Therapy: Recommendations for Treatment, Training, and Privileging: A Task Force Report of the American Psychiatric Association. 2nd ed. Washington, DC: American Psychiatric Association; 2001.
3. Rosenquist PB. When all else fails: the use of electroconvulsive therapy for conditions other than major depressive episode. Psychiatr Clin North Am. 2018;41:355–371.
4. Harrington BC, Jimerson M, Haxton C, et al. Initial evaluation, diagnosis, and treatment of anorexia nervosa and bulimia nervosa. Am Fam Physician. 2015;91:46–52.
5. Arcelus J, Mitchell AJ, Wales J, et al. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch Gen Psychiatry. 2011;68:724–731.
6. Steinhausen H. The outcome of anorexia nervosa in the 20th century. Am J Psychiatry. 2002;159:1284–1293.
7. Steinhausen HC. Outcome of eating disorders. Child Adolesc Psychiatr Clin N Am. 2009;18:225–242.
8. American Psychiatric Association. Practice guideline for the treatment of patients with eating disorders (revision). American Psychiatric Association Work Group on Eating Disorders. Am J Psychiatry. 2000;157:1–39.
9. Yager J, Devlin MJ, Halmi KA, et al. Guideline Watch (August 2012): practice guideline for the treatment of patients with eating disorders, 3rd edition. Focus. 2014;12:416–431.
10. Herzog DB, Keller MB, Sacks NR, et al. Psychiatric comorbidity in treatment-seeking anorexics and bulimics. J Am Acad Child Adolesc Psychiatry. 1992;31:810–818.
11. O'Brien KM, Vincent NK. Psychiatric comorbidity in anorexia and bulimia nervosa: nature, prevalence, and causal relationships. Clin Psychol Rev. 2003;23:57–74.
12. Woodside BD, Staab R. Management of psychiatric comorbidity in anorexia nervosa and bulimia nervosa. CNS Drugs. 2006;8:655–663.
13. Marvanova M, Gramith K. Role of antidepressants in the treatment of adults with anorexia nervosa. Ment Health Clin. 2018;8:127–137.
14. Hay P. A systematic review of evidence for psychological treatments in eating disorders: 2005–2012. Int J Eat Disord. 2013;46:462–469.
15. Bodell LP, Keel PK, Brumm MC, et al. Longitudinal examination of decision-making performance in anorexia nervosa: before and after weight restoration. J Psychiatr Res. 2014;56:150–157.
16. Sağlam T, Aksoy Poyraz C, Poyraz BÇ, et al. Successful use of electroconvulsive therapy in a patient with anorexia nervosa and severe acute-onset obsessive-compulsive disorder. Int J Eat Disord. 2018;51:1026–1028.
17. Andersen L, LaRosa C, Gih D. Reexamining the role of electroconvulsive therapy in anorexia nervosa in adolescents. J ECT. 2017;33:294–296.
18. Andrews JT, Seide M, Guarda AS, et al. Electroconvulsive therapy in an adolescent with severe major depression and anorexia nervosa. J Child Adolesc Psychopharmacol. 2014;24:94–98.
19. Rapinesi C, del Casale A, Serata D, et al. Electroconvulsive therapy in a man with comorbid severe obesity, binge eating disorder, and bipolar disorder. J ECT. 2013;29:142–144.
20. Poutanen O, Huuhka K, Perko K. Severe anorexia nervosa, co-occurring major depressive disorder and electroconvulsive therapy as maintenance treatment: a case report. Cases J. 2009;2:9362.
21. Hill R, Haslett C, Kumar S. Anorexia nervosa in an elderly woman. Aust N Z J Psychiatry. 2001;35:246–248.
22. Ferguson JM. The use of electroconvulsive therapy in patients with intractable anorexia nervosa. Int J Eat Disord. 1993;13:195–201.
23. Bek R, Hotujak L. Clinical characteristics of female patients suffering from anorexia nervosa. Soc Psihijat. 1996;24:159–161.
24. Bernstein IC. Anorexia nervosa, 94-year-old woman treated with electroshock. Minn Med. 1972;55:552–553.
25. Bernstein IC. Anorexia nervosa treated successfully with electroshock therapy and subsequently followed by pregnancy. Am J Psychiatry. 1964;120:1023–1024.
26. Davis HK. Anorexia nervosa: treatment with hypnosis and ECT. Dis Nerv Syst. 1961;22:627–631.
27. Túry F, Babusa B, Varga M. History of eating disorders in Hungary. Psihijat Dan. 2010;42:73–84.
28. Thomä H. Anorexia: treatment. Adv Psychosom Med. 1972;7:300–315.
29. Madden S, Miskovic-Wheatley J, Wallis A, et al. Early weight gain in family-based treatment predicts greater weight gain and remission at the end of treatment and remission at 12-month follow-up in adolescent anorexia nervosa. Int J Eat Disord. 2015;48:919–922.
30. Lund BC, Hernandez ER, Yates WR, et al. Rate of inpatient weight restoration predicts outcome in anorexia nervosa. Int J Eat Disord. 2009;42:301–305.
31. Kishi T, Kafantaris V, Sunday S, et al. Are antipsychotics effective for the treatment of anorexia nervosa? Results from a systematic review and meta-analysis. J Clin Psychiatry. 2012;73:766.
32. Guarda AS. Treatment of anorexia nervosa: insights and obstacles. Physiol Behav. 2007;94:113–120.
33. Browning SM, Cowen PJ. Changes in mood, appetite and psychomotor retardation in depressed patients given ECT. Br J Psychiatry. 1986;149:371–373.
34. Esmaili T, Malek A. Electroconvulsive therapy (ECT) in a six-year-old girl suffering from major depressive disorder with catatonic features. Eur Child Adolesc Psychiatry. 2007;16:58–60.
35. Hussain A, Cox JG, Proctor SE. Percutaneous endoscopic gastrostomy and severe endogenous depression. Br J Psychiatry. 1993;163:699–700.
36. Khedr EM, Elfetoh NA, Ali AM, et al. Anodal transcranial direct current stimulation over the dorsolateral prefrontal cortex improves anorexia nervosa: a pilot study. Restor Neurol Neurosci. 2014;32:789–797.
37. Bartholdy S, McClelland J, Kekic M, et al. Clinical outcomes and neural correlates of 20 sessions of repetitive transcranial magnetic stimulation in severe and enduring anorexia nervosa (the TIARA study): study protocol for a randomised controlled feasibility trial. Trials. 2015;16:548.
38. Israël M, Steiger H, Kolivakis T, et al. Deep brain stimulation in the subgenual cingulate cortex for an intractable eating disorder. Biol Psychiatry. 2010;67:e53–e54.
39. Kekic M, McClelland J, Bartholdy S, et al. Single-session transcranial direct current stimulation temporarily improves symptoms, mood, and self-regulatory control in bulimia nervosa: a randomised controlled trial. PLoS One. 2017;12:e0167606.
40. Burgess EE, Sylvester MD, Amthor FR, et al. Effects of transcranial direct current stimulation (tDCS) on binge eating disorder. Int J Eat Disord. 2016;10:930–936.
41. Kekic M, McClelland J, Campbell I, et al. The effects of prefrontal cortex transcranial direct current stimulation (tDCS) on food craving and temporal discounting in women with frequent food cravings. Appetite. 2014;78:55–62.

anorexia nervosa; binge eating disorder; eating disorder; electroconvulsive therapy

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved