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.
T
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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Journal of ECT • Volume 30, Number 3, September 2014
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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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.
T
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
W
Journal of ECT • Volume 30, Number 3, September 2014
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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