Journal of ECT • Volume 30, Number 4, December 2014
Letters to the Editor
5. Bundy BD, Hewer W, Andres FJ, et al. Influence of anesthetic drugs and concurrent psychiatric medication on seizure adequacy during electroconvulsive therapy. J Clin Psychiatry. 2010;71:775–777.
Depth of Anesthesia Appropriate for Electroconvulsive Therapy The Lash Reflex Need Not Be Abolished To the Editor: odern anesthetic management is an integral part of contemporary electroconvulsive therapy (ECT). General anesthesia is given to allay anxiety, to prevent pain, and to allow the administration of succinylcholine as a muscle relaxant. The patient must be rendered unconscious before the administration of succinylcholine, but too deep a plane of anesthesia raises the seizure threshold and may interfere with the production of the therapeutic seizure. The ultrashort-acting barbiturate methohexital is the induction agent of choice for ECT; it is a nearly ideal agent for many reasons, including its pharmacodynamics, low cost, and only modest anticonvulsant properties. Doses of approximately 1 mg/kg of ideal body weight typically produce an appropriate level of anesthesia in the time it takes the drug to circulate from the injection site to the active site in the brain. Alternative agents such as propofol can also be used to induce general anesthesia for ECT; however, propofol is potently anticonvulsant and may raise the seizure threshold or shorten the therapeutic seizure.1,2 Confirmation of an appropriate level of anesthesia is generally accepted as a loss of response to verbal commands. Another test of anesthesia depth, the “eyelash reflex,” first proposed by Guedel in 1937, is often used as well. This test is one of a series of physical signs that indicate the plane of ether anesthesia and does not necessarily apply to anesthesia induced by today’s intravenous anesthetics. The afferent limb of the eyelash reflex is mediated by the sensory afferents of the trigeminal nerve (cranial nerve V). The efferent limb is via the facial nerve (cranial nerve VII). The eyelash reflex can be elicited by gently brushing a gloved finger across the patient’s eyelashes and watching for reflexive blinking (contraction of the orbicularis oculi) in response to the stimulus. This “lash reflex” test is often used in the operating room setting to confirm an appropriate depth of anesthesia after administration of propofol, but this reflex is not inhibited after induction
M
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www.ectjournal.com
with methohexital even when the patient is under an appropriate level of anesthesia.3 It is important to recognize the historical context in which these tests were developed and that they do not necessarily apply to all modern anesthetics. Even attempts to determine the patient's level of anesthesia using modern devices such as the bispectral index may not be reliable in this population given the interictal changes in bispectral index values observed in conscious patients between ECT treatments.4 Ascertainment of unconsciousness is a critical part of the procedural sequence in ECT. In general, succinylcholine should only be administered after it is clear that the patient is fully unconscious from the effects of the induction agent. This is best determined by speaking to the patient as he/she falls asleep. When the patient no longer responds to questions or commands, an appropriate level of anesthesia has been achieved, despite the persistence of the eyelash reflex. Relying on the loss of the eyelash reflex may result in administration of unnecessarily high doses of methohexital, with potential reduction of efficacy of ECT. Ethan O. Bryson, MD Department of Anesthesiology Mount Sinai School of Medicine New York, NY [email protected]
Mimi C. Briggs, BA Rosa M. Pasculli, BA Dennis M. Popeo, MD Charles H. Kellner, MD Department of Psychiatry Mount Sinai School of Medicine New York, NY
The authors have no conflicts of interest or financial disclosures to report. All authors contributed equally to this article. REFERENCES 1. Vaidya PV, Anderson EL, Bobb A, et al. A within-subject comparison of propofol and methohexital anesthesia for electroconvulsive therapy. J ECT. 2012;28:14–19. 2. Luo J, Min S, Wei K, et al. Propofol interacts with stimulus intensities of electroconvulsive shock to regulate behavior and hippocampal BDNF in a rat model of depression. Psychiatry Res. 2012;198:300–306. 3. Strickland TL, Drummond GB. Comparison of pattern of breathing with other measures of induction of anaesthesia, using propofol, methohexital, and sevoflurane. Br J Anaesth. 2001;86:639–644. 4. Thimmaiah R, Thirthalli J, Ramesh VJ, et al. Effect of a course of electroconvulsive therapy on interictal bispectral index values: a prospective study. J ECT. 2012;28:20–23.
Takotsubo Cardiomyopathy in a Young Man After Maintenance Electroconvulsive Therapy and Clozapine Initiation A Case Report To the Editor: lozapine and electroconvulsive therapy (ECT) represent effective treatment options for psychotic and mood disorders. Initiation of either therapy requires careful medical monitoring, and both therapies are associated with adverse cardiac effects. Stress-induced cardiomyopathy, commonly referred to as Takotsubo cardiomyopathy (TCM), has been reported in the setting of ECT; these rare cases have been limited to older female patients.1 We report the case of a young man who developed TCM in the context of clozapine initiation and maintenance ECT.
C
CASE Mr S is a 31-year-old man with hypertension, seizure disorder, schizoaffective disorder, and an unspecified pervasive developmental disorder. Approximately 3 years before presentation, Mr S was admitted to an inpatient psychiatric facility for psychotic and mood symptoms that limited his ability to care for himself. Because his symptoms were medication-resistant, he was successfully treated with ECT and had no adverse effects. Electroconvulsive therapy was tapered in frequency to discontinuation after a 6-month course, with a total of 30 sessions. Thereafter, Mr S was transferred to a chronic recovery unit, which permitted intensive psychiatric follow-up in anticipation of transition to the community; he resided in this facility for 33 months before the reported presentation. Two years before the presentation, after several unsuccessful antipsychotic medication trials and decompensated psychiatric symptoms, Mr S was started on clozapine. Although his psychiatric symptoms responded favorably, Mr S experienced seizures that responded preferentially to carbamazepine. Clozapine was discontinued to minimize the risk for neutropenia; when Mr S experienced worsened psychotic and mood symptoms, ECT was reinitiated. After 17 sessions, the frequency of ECT was decreased to once-a-week maintenance. The decision was made to reinitiate clozapine, provided seizures could be adequately controlled off of carbamazepine. The anticonvulsant regimen was switched successfully to zonisamide, and clozapine was retitrated to a final dose of 350 mg daily. © 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Journal of ECT • Volume 30, Number 4, December 2014
During the clozapine titration, Mr S did not experience any adverse effects. Throughout this process, he continued to receive weekly ECT treatments, with more than 50 treatments received in total. Several hours after his final ECT treatment, Mr S became symptomatically hypotensive to 72/41 mm Hg, with a pulse of 98 beats per minute. The patient denied any subjective symptoms, including chest pain, shortness of breath, diaphoresis, or nausea. Despite aggressive fluid resuscitation, systolic blood pressure remained below 80 mm Hg. An electrocardiogram was obtained the following morning, which showed sinus tachycardia (pulse, 113 beats per minute) with a stable right bundle branch block, unchanged from prior studies, and new nonspecific Twave abnormalities in the inferior leads. Echocardiogram revealed hypokinesis in the left ventricular walls in addition to anterior and inferior septa. Left ventricular function was described as low-normal with an estimated ejection fraction of 50% to 55%. A consulting cardiologist found these findings to be consistent with Takotsubo (stress-induced) cardiomyopathy. Furthermore, Mr S underwent cardiac magnetic resonance, which showed no evidence of inflammation, dilation, hypertrophy, or infarction. Mr S was treated supportively and placed on a βblocker, and clozapine was discontinued. Within a few weeks, the patient’s cardiac function recovered fully.
DISCUSSION Takotsubo cardiomyopathy is a transient ballooning of the cardiac apex that is associated with intense states of emotional stress.2 It is rare and has been reported to preferentially affect postmenopausal women.3 An increase in epinephrine and norepinephrine is hypothesized to underlie the onset of TCM; this hypothesis has been supported in murine models.4 A spike in epinephrine and norepinephrine within the context of a controlled seizure contributes, at least in part, to the therapeutic efficacy of ECT.5 Mann et al6 demonstrated a peak plasma norepinephrine level within 1 to 3 minutes postictally. Although this surge increases the potential for severe cardiac abnormalities, including TCM, the most commonly associated cardiac complication of ECT consists of transient electrocardiogram changes affecting individuals with preexisting heart disease.7 To our knowledge, only 7 cases of TCM have been reported in the context of ECT; in all circumstances, the patients were postmenopausal women, and cardiomyopathy developed early after ECT induction in all but 1 case.1 Similarly, although the therapeutic effect of clozapine is attributed to central © 2014 Lippincott Williams & Wilkins
Letters to the Editor
antagonism of dopamine and serotonin receptors, its structure as a tricyclic dibenzodiazepine lends it the unique property of elevating epinephrine and norepinephrine levels systemically.8,9 Despite this, clozapine has never been reported to cause TCM, although it has been associated with dilated cardiomyopathy.10 Most reported cardiac complications of clozapine occur during novel exposures; our patient tolerated clozapine well historically, without any serious adverse effects, before developing TCM during a reinitiation. The case of Mr S is unusual for various reasons, including the patient’s demographic (young male) as well as tolerance of ECT and clozapine historically without cardiac complications. The large number of ECT sessions (>50) before this incident suggests that ECT is an improbable unilateral cause of TCM. Likewise, because clozapine alone has not been reported to cause TCM and our patient has tolerated the drug without cardiac effects historically, the reinitiation of clozapine alone is unlikely to have precipitated TCM. Given the paucity of available data to guide our understanding of this particular complication in a young male patient, we presume one possible explanation is that TCM was precipitated by the simultaneous titration of clozapine in the setting of maintenance ECT. Both clozapine and ECT are thought to exert therapeutic efficacy through increasing levels of plasma catecholamines.6,9 We hypothesized that the surge of catecholamines generated by clozapine or ECT, independently, was not enough to affect our patient’s cardiac status but that their combined effects resulted in catecholamine excess sufficient to cause TCM. Mr S was only receiving ECT once weekly when clozapine therapy was initiated, and it was not until his clozapine dose was within the therapeutic range that he experienced symptomatic cardiomyopathy after ECT. Takotsubo cardiomyopathy remains a condition of which psychiatric providers should be aware. Despite early case reports that are limited to postmenopausal women, TCM may occur in any individual who is exposed to multiple mechanisms of plasma catecholamine excess, including the combination of ECT and clozapine.
Melanie Grubisha, MD, PhD Priya Gopalan, MD Western Psychiatric Institute and Clinic Pittsburgh, PA
Pierre N. Azzam, MD Western Psychiatric Institute and Clinic Pittsburgh, PA Veterans Affairs Boston Healthcare System Boston, MA
The authors declare no conflict of interest. REFERENCES 1. Sharp RP, Welch EB. Takotsubo cardiomyopathy as a complication of electroconvulsive therapy. Ann Pharmacother. 2011;45:1559–1565. 2. Bybee KA, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141:858–865. 3. Deshmukh A, Kumar G, Pant S, et al. Prevalence of Takotsubo cardiomyopathy in the United States. Am Heart J. 2012;162:22–71. 4. Ueyama T. Emotional stress-induced Tako-tsubo cardiomyopathy: animal model and molecular mechanism. Ann N Y Acad Sci. 2004; 1018:437–444. 5. Kellner CH, et al. ECT in treatment-resistant depression. Am J Psychiatry. 2012;169: 1238–1244. 6. Mann JJ, et al. Acute effects of single and repeated electroconvulsive therapy on plasma catecholamines and blood pressure in major depressive disorder. Psychiatry Res. 1990;34: 127–137. 7. Rayburn B. Electroconvulsive therapy in patients with heart failure or valvular heart disease. Convuls Ther. 1997;13:145–156. 8. Green AI, et al. Clozapine response and plasma catecholamines and their metabolites. Psychiatry Res. 1993;46:139–149. 9. Wang JF, et al. Clozapine-induced myocarditis: role of catecholamines in a murine model. Eur J Pharmacol. 2008;592:123–127. 10. Roh S, et al. Cardiomyopathy associated with clozapine. Exp Clin Psychopharmacol. 2006; 14:94–98.
Electroconvulsive Therapy (ECT) Protocols for Variations in Technique To the Editor: ecently, a commentary about medical errors appeared in the New York Times.1 It described a case in which a surgeon had operated on the wrong ankle, and then reported the mistake immediately to the appropriate hospital authorities and to the patient upon awakening. He also apologized to the patient. The discussion (and the letters that followed) centered on whether the physician should be punished for his error. This got us to thinking about potential “errors” in electroconvulsive therapy (ECT) and how they might be dealt with. The list of potential errors ranges from serious to trivial. Failure to insert a bite
R
www.ectjournal.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
e41
Letters to the Editor
5. Bundy BD, Hewer W, Andres FJ, et al. Influence of anesthetic drugs and concurrent psychiatric medication on seizure adequacy during electroconvulsive therapy. J Clin Psychiatry. 2010;71:775–777.
Depth of Anesthesia Appropriate for Electroconvulsive Therapy The Lash Reflex Need Not Be Abolished To the Editor: odern anesthetic management is an integral part of contemporary electroconvulsive therapy (ECT). General anesthesia is given to allay anxiety, to prevent pain, and to allow the administration of succinylcholine as a muscle relaxant. The patient must be rendered unconscious before the administration of succinylcholine, but too deep a plane of anesthesia raises the seizure threshold and may interfere with the production of the therapeutic seizure. The ultrashort-acting barbiturate methohexital is the induction agent of choice for ECT; it is a nearly ideal agent for many reasons, including its pharmacodynamics, low cost, and only modest anticonvulsant properties. Doses of approximately 1 mg/kg of ideal body weight typically produce an appropriate level of anesthesia in the time it takes the drug to circulate from the injection site to the active site in the brain. Alternative agents such as propofol can also be used to induce general anesthesia for ECT; however, propofol is potently anticonvulsant and may raise the seizure threshold or shorten the therapeutic seizure.1,2 Confirmation of an appropriate level of anesthesia is generally accepted as a loss of response to verbal commands. Another test of anesthesia depth, the “eyelash reflex,” first proposed by Guedel in 1937, is often used as well. This test is one of a series of physical signs that indicate the plane of ether anesthesia and does not necessarily apply to anesthesia induced by today’s intravenous anesthetics. The afferent limb of the eyelash reflex is mediated by the sensory afferents of the trigeminal nerve (cranial nerve V). The efferent limb is via the facial nerve (cranial nerve VII). The eyelash reflex can be elicited by gently brushing a gloved finger across the patient’s eyelashes and watching for reflexive blinking (contraction of the orbicularis oculi) in response to the stimulus. This “lash reflex” test is often used in the operating room setting to confirm an appropriate depth of anesthesia after administration of propofol, but this reflex is not inhibited after induction
M
e40
www.ectjournal.com
with methohexital even when the patient is under an appropriate level of anesthesia.3 It is important to recognize the historical context in which these tests were developed and that they do not necessarily apply to all modern anesthetics. Even attempts to determine the patient's level of anesthesia using modern devices such as the bispectral index may not be reliable in this population given the interictal changes in bispectral index values observed in conscious patients between ECT treatments.4 Ascertainment of unconsciousness is a critical part of the procedural sequence in ECT. In general, succinylcholine should only be administered after it is clear that the patient is fully unconscious from the effects of the induction agent. This is best determined by speaking to the patient as he/she falls asleep. When the patient no longer responds to questions or commands, an appropriate level of anesthesia has been achieved, despite the persistence of the eyelash reflex. Relying on the loss of the eyelash reflex may result in administration of unnecessarily high doses of methohexital, with potential reduction of efficacy of ECT. Ethan O. Bryson, MD Department of Anesthesiology Mount Sinai School of Medicine New York, NY [email protected]
Mimi C. Briggs, BA Rosa M. Pasculli, BA Dennis M. Popeo, MD Charles H. Kellner, MD Department of Psychiatry Mount Sinai School of Medicine New York, NY
The authors have no conflicts of interest or financial disclosures to report. All authors contributed equally to this article. REFERENCES 1. Vaidya PV, Anderson EL, Bobb A, et al. A within-subject comparison of propofol and methohexital anesthesia for electroconvulsive therapy. J ECT. 2012;28:14–19. 2. Luo J, Min S, Wei K, et al. Propofol interacts with stimulus intensities of electroconvulsive shock to regulate behavior and hippocampal BDNF in a rat model of depression. Psychiatry Res. 2012;198:300–306. 3. Strickland TL, Drummond GB. Comparison of pattern of breathing with other measures of induction of anaesthesia, using propofol, methohexital, and sevoflurane. Br J Anaesth. 2001;86:639–644. 4. Thimmaiah R, Thirthalli J, Ramesh VJ, et al. Effect of a course of electroconvulsive therapy on interictal bispectral index values: a prospective study. J ECT. 2012;28:20–23.
Takotsubo Cardiomyopathy in a Young Man After Maintenance Electroconvulsive Therapy and Clozapine Initiation A Case Report To the Editor: lozapine and electroconvulsive therapy (ECT) represent effective treatment options for psychotic and mood disorders. Initiation of either therapy requires careful medical monitoring, and both therapies are associated with adverse cardiac effects. Stress-induced cardiomyopathy, commonly referred to as Takotsubo cardiomyopathy (TCM), has been reported in the setting of ECT; these rare cases have been limited to older female patients.1 We report the case of a young man who developed TCM in the context of clozapine initiation and maintenance ECT.
C
CASE Mr S is a 31-year-old man with hypertension, seizure disorder, schizoaffective disorder, and an unspecified pervasive developmental disorder. Approximately 3 years before presentation, Mr S was admitted to an inpatient psychiatric facility for psychotic and mood symptoms that limited his ability to care for himself. Because his symptoms were medication-resistant, he was successfully treated with ECT and had no adverse effects. Electroconvulsive therapy was tapered in frequency to discontinuation after a 6-month course, with a total of 30 sessions. Thereafter, Mr S was transferred to a chronic recovery unit, which permitted intensive psychiatric follow-up in anticipation of transition to the community; he resided in this facility for 33 months before the reported presentation. Two years before the presentation, after several unsuccessful antipsychotic medication trials and decompensated psychiatric symptoms, Mr S was started on clozapine. Although his psychiatric symptoms responded favorably, Mr S experienced seizures that responded preferentially to carbamazepine. Clozapine was discontinued to minimize the risk for neutropenia; when Mr S experienced worsened psychotic and mood symptoms, ECT was reinitiated. After 17 sessions, the frequency of ECT was decreased to once-a-week maintenance. The decision was made to reinitiate clozapine, provided seizures could be adequately controlled off of carbamazepine. The anticonvulsant regimen was switched successfully to zonisamide, and clozapine was retitrated to a final dose of 350 mg daily. © 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Journal of ECT • Volume 30, Number 4, December 2014
During the clozapine titration, Mr S did not experience any adverse effects. Throughout this process, he continued to receive weekly ECT treatments, with more than 50 treatments received in total. Several hours after his final ECT treatment, Mr S became symptomatically hypotensive to 72/41 mm Hg, with a pulse of 98 beats per minute. The patient denied any subjective symptoms, including chest pain, shortness of breath, diaphoresis, or nausea. Despite aggressive fluid resuscitation, systolic blood pressure remained below 80 mm Hg. An electrocardiogram was obtained the following morning, which showed sinus tachycardia (pulse, 113 beats per minute) with a stable right bundle branch block, unchanged from prior studies, and new nonspecific Twave abnormalities in the inferior leads. Echocardiogram revealed hypokinesis in the left ventricular walls in addition to anterior and inferior septa. Left ventricular function was described as low-normal with an estimated ejection fraction of 50% to 55%. A consulting cardiologist found these findings to be consistent with Takotsubo (stress-induced) cardiomyopathy. Furthermore, Mr S underwent cardiac magnetic resonance, which showed no evidence of inflammation, dilation, hypertrophy, or infarction. Mr S was treated supportively and placed on a βblocker, and clozapine was discontinued. Within a few weeks, the patient’s cardiac function recovered fully.
DISCUSSION Takotsubo cardiomyopathy is a transient ballooning of the cardiac apex that is associated with intense states of emotional stress.2 It is rare and has been reported to preferentially affect postmenopausal women.3 An increase in epinephrine and norepinephrine is hypothesized to underlie the onset of TCM; this hypothesis has been supported in murine models.4 A spike in epinephrine and norepinephrine within the context of a controlled seizure contributes, at least in part, to the therapeutic efficacy of ECT.5 Mann et al6 demonstrated a peak plasma norepinephrine level within 1 to 3 minutes postictally. Although this surge increases the potential for severe cardiac abnormalities, including TCM, the most commonly associated cardiac complication of ECT consists of transient electrocardiogram changes affecting individuals with preexisting heart disease.7 To our knowledge, only 7 cases of TCM have been reported in the context of ECT; in all circumstances, the patients were postmenopausal women, and cardiomyopathy developed early after ECT induction in all but 1 case.1 Similarly, although the therapeutic effect of clozapine is attributed to central © 2014 Lippincott Williams & Wilkins
Letters to the Editor
antagonism of dopamine and serotonin receptors, its structure as a tricyclic dibenzodiazepine lends it the unique property of elevating epinephrine and norepinephrine levels systemically.8,9 Despite this, clozapine has never been reported to cause TCM, although it has been associated with dilated cardiomyopathy.10 Most reported cardiac complications of clozapine occur during novel exposures; our patient tolerated clozapine well historically, without any serious adverse effects, before developing TCM during a reinitiation. The case of Mr S is unusual for various reasons, including the patient’s demographic (young male) as well as tolerance of ECT and clozapine historically without cardiac complications. The large number of ECT sessions (>50) before this incident suggests that ECT is an improbable unilateral cause of TCM. Likewise, because clozapine alone has not been reported to cause TCM and our patient has tolerated the drug without cardiac effects historically, the reinitiation of clozapine alone is unlikely to have precipitated TCM. Given the paucity of available data to guide our understanding of this particular complication in a young male patient, we presume one possible explanation is that TCM was precipitated by the simultaneous titration of clozapine in the setting of maintenance ECT. Both clozapine and ECT are thought to exert therapeutic efficacy through increasing levels of plasma catecholamines.6,9 We hypothesized that the surge of catecholamines generated by clozapine or ECT, independently, was not enough to affect our patient’s cardiac status but that their combined effects resulted in catecholamine excess sufficient to cause TCM. Mr S was only receiving ECT once weekly when clozapine therapy was initiated, and it was not until his clozapine dose was within the therapeutic range that he experienced symptomatic cardiomyopathy after ECT. Takotsubo cardiomyopathy remains a condition of which psychiatric providers should be aware. Despite early case reports that are limited to postmenopausal women, TCM may occur in any individual who is exposed to multiple mechanisms of plasma catecholamine excess, including the combination of ECT and clozapine.
Melanie Grubisha, MD, PhD Priya Gopalan, MD Western Psychiatric Institute and Clinic Pittsburgh, PA
Pierre N. Azzam, MD Western Psychiatric Institute and Clinic Pittsburgh, PA Veterans Affairs Boston Healthcare System Boston, MA
The authors declare no conflict of interest. REFERENCES 1. Sharp RP, Welch EB. Takotsubo cardiomyopathy as a complication of electroconvulsive therapy. Ann Pharmacother. 2011;45:1559–1565. 2. Bybee KA, et al. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141:858–865. 3. Deshmukh A, Kumar G, Pant S, et al. Prevalence of Takotsubo cardiomyopathy in the United States. Am Heart J. 2012;162:22–71. 4. Ueyama T. Emotional stress-induced Tako-tsubo cardiomyopathy: animal model and molecular mechanism. Ann N Y Acad Sci. 2004; 1018:437–444. 5. Kellner CH, et al. ECT in treatment-resistant depression. Am J Psychiatry. 2012;169: 1238–1244. 6. Mann JJ, et al. Acute effects of single and repeated electroconvulsive therapy on plasma catecholamines and blood pressure in major depressive disorder. Psychiatry Res. 1990;34: 127–137. 7. Rayburn B. Electroconvulsive therapy in patients with heart failure or valvular heart disease. Convuls Ther. 1997;13:145–156. 8. Green AI, et al. Clozapine response and plasma catecholamines and their metabolites. Psychiatry Res. 1993;46:139–149. 9. Wang JF, et al. Clozapine-induced myocarditis: role of catecholamines in a murine model. Eur J Pharmacol. 2008;592:123–127. 10. Roh S, et al. Cardiomyopathy associated with clozapine. Exp Clin Psychopharmacol. 2006; 14:94–98.
Electroconvulsive Therapy (ECT) Protocols for Variations in Technique To the Editor: ecently, a commentary about medical errors appeared in the New York Times.1 It described a case in which a surgeon had operated on the wrong ankle, and then reported the mistake immediately to the appropriate hospital authorities and to the patient upon awakening. He also apologized to the patient. The discussion (and the letters that followed) centered on whether the physician should be punished for his error. This got us to thinking about potential “errors” in electroconvulsive therapy (ECT) and how they might be dealt with. The list of potential errors ranges from serious to trivial. Failure to insert a bite
R
www.ectjournal.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
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![[Takotsubo cardiomyopathy after electroconvulsive therapy: A case report].](/assets/img/hold.png)
