LETTERS TO THE EDITOR

Postictal Agitation Syndrome or Anxiety Symptoms To the Editor: he study described as “postictal agitation after electroconvulsive therapy”1 primarily concerns symptoms of postictal anxiety not the syndrome of postictal agitation. The syndrome typically persists for hours unless medicated. The behavioral disturbance the authors call severe lasted under 10 minutes. This is simply not typical postictal agitation. Their data indicate this disturbance occurred in 5%. Statistical hypothesis testing based on 5% occurrence in a group of 13 patients (seemingly 1 patient) is dubious. Moreover, the incidence of postictal agitation syndrome among men and women was observed as 2/37, 5%.2 Finding 6 patients with this syndrome should involve recruiting approximately 120, not 13. Apparently, this study included 1 patient with no more than unusually mild postictal agitation. This ECT protocol resembles a study demonstrating that propofol decreases cognitive adverse effects to negligible, except propofol was infused 15 seconds poststimulus after bitemporal electrode placement.3 Of course, the outcome measures differed. For preventing postictal agitation syndrome in clinical practice, I continue to find that 1.1-mg/kg succinylcholine4 with prompt postictal methohexital infusion (30–40 mg)5 is reliable. Propofol instead of methohexital should work similarly. With prevention, the support staff also remains calmer than when treating only after agitation appears.

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Conrad M. Swartz, PhD, MD Oregon Health & Science University Portland, OR [email protected]

The author has ownership interests in Medtronic Inc, IntelGenx Technologies Corp, Abbott Laboratories, Somatics LLC, CVS Caremark Corp., GlaxoSmithKline Corp, and the Vanguard Healthcare Fund, and I am a paid director of Somatics LLC. REFERENCES 1. Tzabazis A, Schmitt HJ, Ihmsen H, et al. Postictal agitation after electroconvulsive therapy. J ECT. 2013;29:189–195. 2. Auriacombe M, Reneric JP, Usandizaga D, et al. Post-ECT agitation and plasma lactate concentrations. J ECT. 2000;16:263–267. 3. Warnell RL, Swartz CM, Thomson A. Propofol interruption of ECT seizure to

reduce side-effects. Psychiatry Res. 2010;175:184–185. 4. Swartz CM. Electroconvulsive therapy emergence agitation and succinylcholine dose. J Nerv Mental Dis. 1990;178:455–457. 5. Swartz CM. ECT emergence agitation and methohexital-succinylcholine interaction. Gen Hosp Psychiatry. 1993;15: 339–341.

Postictal Agitation After Electroconvulsive Therapy To the Editor: e have read with great interest the letter of Dr Conrad M. Swartz regarding our recently published article “Postictal agitation after electroconvulsive therapy: incidence, severity, and propofol as a treatment option” and would like to comment on some of his remarks. Dr Swartz states that we have not investigated postictal agitation but rather postictal anxiety because, according to his experience, postictal agitation “typically persists for hours.” There certainly is some ambiguity with regard to terminology of adverse effects typically occurring after ECT. As a matter of fact, the scientific community should make efforts to standardize nomenclature. Commonly used terms used in conjunction with “electroconvulsive therapy” adverse events are “postictal delirium” (yielding 4 PubMed results) and “postictal agitation” (yielding 11 PubMed results). “Postictal anxiety” as suggested by Dr Swartz yields no PubMed results and has not specifically been mentioned in articles reviewing common adverse effects after ECT.1,2 Furthermore, these review articles report the length of postictal agitation from several minutes to up to 1 hour, which also is consistent with our clinical observations. Therefore, it is unclear how a clear distinction based on length as suggested by Dr Swartz can be made between these 2 and if they are at all different clinical entities. It is correct that 5 minutes after end of the seizure, incidence for severe postictal agitation (PIA) (ie, 1 or more nurses were required to physically hold down the patient) was 5% in the group that did not receive propofol compared to 0% in the group that received propofol.3 We have proposed a score for assessing PIA severity (Table 13). As we have pointed out several times in our article, it is important that we agree on a standardized way of reporting

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PIA and, in particular, its severity to make results of different groups comparable. When combining moderate (ie, restless patient requiring a nurse standing next to the bed) and severe PIA, incidences were 21% and 8% for the nonpropofol and propofol group, respectively (Table 43). Dr Swartz’ conclusion that if 5% out of 13 patients showed PIA there must have been only 1 patient with PIA is incorrect, because most patients were observed at 6 different time points (3 with and 3 without propofol). In the nonpropofol group, 11, 6, and 2 patients showed mild (ie, restless patient, who calms down when talking to him), moderate, and severe PIA, respectively, corresponding to percentages of 30%, 16%, and 5% because 37 sessions were included. The intraindividual crossover design and the statistical analysis (generalized linear model with repeated measurements) is sound and was reviewed by a biostatistician chosen by the Journal of ECT. It is correct that Warnell et al4 have used propofol to interrupt ECT seizure and have showed a decrease in severity of cognitive adverse effects. This is, however, a different approach because we have chosen to wait for spontaneous seizure cessation before administering the propofol bolus and to focus on the effects of this propofol bolus on postictal agitation and recovery times rather than emphasizing on cognitive effects. Administering methohexital and a sufficient dose of succinylcholine (0.9– 1.2 mg/kg in our study) followed by a— presumably—second postictal (smaller) bolus of methohexital as suggested by Dr Swartz is a very acceptable approach. Although one has to keep in mind that it is usually necessary to titrate the succinylcholine dose to the individual patient’s needs over a series of electroconvulsive therapies based on clinical signs, that is, preventing muscle contractions during the seizure. Because psychiatric comedications, for example, lithium,5 can alter the required succinylcholine dose a fixed dose, as suggested by Dr Swartz, cannot be recommended as it might lead to an overdose in some patients with the possible effects of prolonged effect which can by itself cause agitation. Our study was not designed to show superiority of propofol compared to methohexital for preventing postictal agitation. However, our results have clearly shown that propofol is also a suitable drug to decrease PIA incidence and/or severity after ECT. www.ectjournal.com

Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

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Letters to the Editor

Alexander Z. Tzabazis, MD Department of Anesthesia Stanford University Stanford, CA [email protected]

Hubert J. Schmitt, MD Tino Muenster, MD Department of Anesthesia University Hospital Erlangen, Germany

The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Augoustides JG, Greenblatt E, Abbas MA, et al. Clinical approach to agitation after electroconvulsive therapy: a case report and literature review. J ECT. 2002;18:213–217. 2. Cristancho MA, Alici Y, Augoustides JG, et al. Uncommon but serious complications associated with electroconvulsive therapy: recognition and management for the clinician. Curr Psychiatry Rep. 2008;10:474–480. 3. Tzabazis A, Schmitt HJ, Ihmsen H, et al. Postictal agitation after electroconvulsive therapy: incidence, severity, and propofol as a treatment option. J ECT. 2013;29:189–195. 4. Warnell RL, Swartz CM, Thomson A. Propofol interruption of ECT seizure to reduce side-effects: a pilot-study. Psychiatry Res. 2010;175:184–185. 5. Hill GE, Wong KC, Hodges MR. Lithium carbonate and neuromuscular blocking agents. Anesthesiology. 1977;46:122–126.

Geriatric ECT at a Turkish Teaching Hospital A 5-Year Experience To the Editor: e present here our 5-year experience with the practice of electroconvulsive therapy (ECT) at the Bakirkoy Hospital in Istanbul, Turkey, in patients older than 65 years. The data were obtained by retrospective chart review of inpatients treated with ECT while hospitalized at the Bakirkoy Hospital between March 2006 and May 2010. Sociodemographic characteristics, general medical conditions, mean number of patients who received ECT, the diagnoses according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, mean number of ECT sessions, response rates, adverse reactions, and duration of hospital stay were determined. For purposes of statistical analysis, every treatment course was recorded as a separate patient. Descriptive analysis was performed using SPSS 17 Software (SPSS, Inc, Chicago, Ill) and the results are presented as mean (SD).

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The characteristics of the hospital, catchment area, patients, ECT unit, and practice of ECT administration were described in detail elsewhere.1 A total of 41,295 (25,299 [61.26%] men and 15,996 [38.73%] women) acute psychiatric patients were hospitalized between March 2006 and May 2010, and 1118 (643 [57.51%] men and 475 [42.48%] women) of these patients were older than 65 years. Electroconvulsive therapy was administered to 5977 (3511 [58.74%] men and 2466 [41.25%] women) of all acute patients (14.47%). A total of 96 patients (56 [58.33%] women and 40 [41.66%] men) older than 65 years were treated with ECT, who constituted 1.6% of all patients treated with ECT. The psychiatric diagnoses of the patients were as follows: 74 (77.08%) patients had affective disorders and 22 (22.92%) patients had psychotic disorders. A total of 803 sessions of ECT were administered in 96 courses of ECT. The mean number of ECT sessions per patient was 8.36 (2.51) (range, 1–16). Ten (10.41%) patients had a history of hypothyroidism; 5 (5.2%) central nervous system malignancy; 2 (2.08%) breast cancer; 1 (1.04%) hematologic malignancy; and 1 (1.04%) skin cancer. Three (3.12%) patients had a history of hepatitis C or D. The clinical responses on discharge were classified as “total improvement,” “partial improvement,” and “non-responsiveness”, according to discharge summary, medical chart, and computer data. Total improvement was observed in 52 (54.2%) patients, and partial improvement was observed in 39 (40.6%) patients. Global clinical response rate was 94.8%, whereas 5 (5.2%) patients were discharged without any apparent change in their clinical features. There were no life-threatening complications and/or deaths. The types of acute adverse events that were reported in 8.3% of the 96 patients treated with ECT were confusion (n = 3), headache (n = 1), prolonged seizure (n = 2), and prolonged recovery (n = 2). A second or third restimulation was required in 37 sessions. Although controversy continues about psychiatric treatment algorithms for elderly patients, various studies have shown successful results with ECT. Results suggesting that elderly patients respond well to ECT were reviewed by Mitchell and Subramaniam.2 Advanced age is not by itself a contraindication to this treatment.3 We found ECT to be effective and safe, too, in the elderly patient subgroup in this study: the rate of response to treatment was 94.8%, which is similar to results of other studies.4,5 In our study, there were more female elderly patients treated with ECT. The

sex distribution is similar to studies from Western countries and differs from the findings of our other recent report.1 The distribution of diagnoses is also different. Affective disorders (77.08%) and depression (58.33%) are the leading diagnoses in the subgroup of ECT patients older than 65 years. The most frequently diagnosed disorders were depression (58.33%), followed by mania (16.70%). Although depression is a leading diagnosis, the presence of manic and psychotic (nonaffective psychosis) patients shows that ECT is not used solely for depressed patients. The mean number of ECT treatments was 8.36 (2.51) in our study, similar to many studies.4 The rate of medical comorbidities was 60% in the present study, compared with 33.66% in an Indian study and 20% in another Turkish study.4,5 The slightly younger mean age in those studies may explain the lower rate of comorbidities. Absence of any life-threatening adverse effects or death, and the occurence of relatively few adverse effects of any kind, suggest that ECT is a safe treatment modality in this patient population. It is also an indication of conformity with current practice guidelines. The most important limitation of the present study is its retrospective design. Response to treatment, adverse effects (especially cognitive effects), and complications were determined by relying on clinical records and patient charts, rather than the use of standardized measures. Also, only the short-term response to ECT was evaluated, which makes it harder to reach conclusions about long-term efficacy. Several studies have reported on the efficacy of ECT in the elderly. Its adverse effect profile may compare favorably to pharmacological treatments in this age group. We hope that clinicians will become more comfortable prescribing ECT to geriatric patients, as more experience with ECT in the elderly is documented in the medical literature. Ozge Canbek, MD Bakirkoy Teaching Hospital for Psychiatric and Neurological Diseases ECT Center Istanbul, Turkey [email protected] Goksen Yuksel, MD Bakirkoy Teaching Hospital for Psychiatric and Neurological Diseases Istanbul, Turkey Murat Ilhan Atagun, MD Department of Psychiatry Yildirim Beyazit University Medical School Ankara, Turkey © 2014 Lippincott Williams & Wilkins

Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Postictal agitation after electroconvulsive therapy.

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