Journal of ECT • Volume 30, Number 4, December 2014
ECT was administered to only 3 patients (2 men), just 0.18% of the 1600 admissions in the same period. In the SUHC, ECT was administered to only one male patient (0.1% of the 991 hospital admissions in the same period). The condition of all patients was diagnosed as schizophrenia, and they received 6 and 10 to 12 sessions of ECT in the SUHC and OUHC, respectively. Patients in all 3 centers underwent the same pretreatment evaluation: physical examination, electroencephalogram, electrocardiogram, standard laboratory tests and CT scan, and approval by a physician and an anesthesiologist. Written informed consent for ECT given by the patient or his/her legal guardian was mandatory. Printed information leaflets for patients about ECT were available. The only contraindication to treatment was a severe medical condition such as fever, acute infection, and uncontrolled high blood pressure. No significant adverse effect was reported during the survey period. The ECT team comprised a psychiatrist, an anesthesiologist, and psychiatric and anesthesiology nurses. Before the ECT, atropine (0.01 mg/kg) was given as premedication 5 minutes before ECT to avoid parasympathetic reaction. After oxygenation with 100% O2, general anesthesia was induced with propofol (1mg/kg); in one case, sugammadex was used. Intravenous succinylcholine (0.5 mg/kg) was administered for muscle relaxation, and ventilation was assisted with a face mask and 100% oxygen. Electroconvulsive therapy was administered using Thymatron Model DGx device (Somatics Inc, 1995). Electrodes were placed bifrontally. Seizure threshold titration was not practiced; only age-based method was used in all cases. Seizure activity was monitored with visual observation and electroencephalogram. During ECT, pulse rate, blood pressure, electrocardiogram, peripheral oxygen saturation (SpO2) and endexpiratory CO2 partial pressure (end-tidal CO2) were regularly monitored. Patients were moved from the recovery room when they are fully conscious/alert. There was no fixed number of sessions of ECT, which would continue until adequate treatment response was achieved as judged by the treating psychiatrist. In contrast to most other centraleastern European countries,1 only 3 institutions offered ECT in Croatia. A similarly low number of ECT centers were reported from Bulgaria2 and Ukraine,3 indicating rather limited accessibility to ECT in these countries. As for the indications of ECT, the Croatian practice closely resembles that of some other central-eastern European countries,1 whereas with regard © 2014 Lippincott Williams & Wilkins
Letters to the Editor
to ECT delivery—brief pulse stimulation and bifrontal electrode placement—it is close to the Western European and international standards. Electroconvulsive therapy is taught as a part of the regular medical curricula in the Zagreb School of Medicine, the Osijek School of Medicine, and the Split School of Medicine, which are linked with the ZUHC, OUHC, and SUHC, respectively. Electroconvulsive therapy is part of the standard psychiatric training course run at the ZUHC. However, there are no certified courses on ECT or any formal training for mental health professionals on the theory and practice of ECT. Similar to other European countries,4 training is informally provided by senior psychiatrists experienced in ECT as mentors. There are no national guidelines on ECT in Croatia, although the overall standard of ECT practice conforms to international recommendations.5 Martina Rojnic Kuzman, MD, PhD University Hospital Centre Zagreb Zagreb, Croatia and Zagreb School of Medicine Zagreb, Croatia [email protected]
Tamara Pranjkovic Zagreb School of Medicine Zagreb, Croatia
Dunja Degmecic, MD, PhD University Hospital Centre Osijek Osijek, Croatia and Osijek School of Medicine Zagreb, Croatia
Davor Lasić, MD University Hospital Centre Split Split, Croatia
Ana Medic Zagreb School of Medicine Zagreb, Croatia
Gábor Gazdag, MD, PhD Centre for Psychiatry and Addiction Medicine Szent István and Szent Laszló Hospitals Budapest, Hungary and Department of Psychiatry and Psychotherapy Semmelweis University Faculty of Medicine Budapest, Hungary
The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Leiknes KA, Jarosh-von Schweder L, Høie B. Contemporary use and practice of electroconvulsive therapy worldwide. Brain Behav. 2012;2:283–344. 2. Hranov LG, Hranov G, Ungvari GS, et al. Electroconvulsive therapy in Bulgaria: a snapshot of past and present. J ECT. 2012;28:108–110.
3. Oleksev A, Ungvari GS, Gazdag G. ECT practice in Ukraine. J ECT. 2014. [Epub ahead of print]. 4. Dragasek J. Electroconvulsive therapy in Slovakia. J ECT. 2012;28:7–8. 5. Rush G, Kimmich O, Lucy JV. Electroconvulsive therapy: international guidelines, clinical governance and patient selection. Ir J Psychol Med. 2007;24:103–107.
Transient Babinski Sign After Electroconvulsive Therapy (ECT) Dear Editor: he Babinski sign, or extensor plantar response, was first described by Joseph Francois Felix Babinski, a French neurologist of Polish descent, in his monograph of 1898.1 This reflex is characterized by extension of the big toe, occasionally accompanied by fanning of the rest of the toes, in response to the stimulus of stroking the lateral aspect of the sole of the foot.2 Initially of use in distinguishing hysteria from organic disease, the Babinski sign reflects dysfunction of the pyramidal tract anywhere along its course from the cortex, subcortical white matter, or brainstem to the spinal cord.2,3 A reliable sign of upper motor neuron dysfunction, the upgoing toe, reflects release of descending inhibition on spinal motor neurons, as well as inhibition of the local segmental cutaneous reflex, which normally triggers plantar flexion.4 Neonates will also exhibit an extensor response owing to incomplete development of the pyramidal tract; however, with maturation of upper motor neuron pathways, the Babinski sign disappears, and stimulation of the sole elicits the flexor response at approximately 12 to 24 months of age.3 We report a middle-aged woman with depression and a medical history of hypothyroidism and prior thyroid resection who developed a transient Babinski response after her initial right unilateral electroconvulsive therapy (ECT) dose-titration session. Her medications included diphenhydramine, 50 mg, oral, every night at bedtime; lorazepam, 1 mg, oral, 2 times a day; aripiprazole, 5 mg, oral, daily; mirtazapine, 7.5 mg, oral, every night at bedtime; paroxetine, 40 mg, oral, daily; and levothyroxine, 100 μg oral, daily. Anesthesia was induced with 50 mg of methohexital followed by 50 mg of succinylcholine. She received a single stimulus at 5% “energy” (25 mC; pulse width, 0.25 millisecond), resulting in a motor seizure of 38 seconds and an electroencephalographic seizure of 77 seconds. The Babinski phenomenon was bilateral, was elicited immediately after cessation of the seizure, and resolved within 15 minutes.
T
www.ectjournal.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
e43
Journal of ECT • Volume 30, Number 4, December 2014
Letters to the Editor
Transient upper motor neuron signs can occur after a variety of reversible disturbances of cortical function including seizures, migraines, deep sleep, anesthesia, or metabolic abnormalities.4 In his 1952 textbook on ECT, Kalinowsky reports observing the Babinksi sign in approximately one fifth of the cases.5 Todd’s paralysis,6 a transient focal neurological deficit after a seizure, has also been reported after ECT.7,8 Our patient had no neurological complications during her course of 6 right unilateral ECT treatments at 30% energy, and her depressive illness remitted completely (Hamilton Rating Scale for Depression, 24-Item, score decreased from 28 to 9). Her Babinksi sign was not elicited in subsequent treatments, the significance of which remains to be explored. Amy S. Aloysi, MD, MPH Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY
Ethan O. Bryson, MD Departments of Psychiatry and Anesthesiology Icahn School of Medicine at Mount Sinai New York, NY
Lauren S. Liebman, BA Mimi C. Briggs, BA Charles H. Kellner, MD Department of Psychiatry Icahn School of Medicine at Mount Sinai New York, NY [email protected]
Dr. Kellner is supported by an NIMH grant U01MH055495. The other authors have no financial conflicts of interest or financial disclosures to report. REFERENCES 1. Babinski J. Du phénomène des orteils et de sa valeur sémiologique. Semaine Médicale. 1898; 18:321–322. 2. Goetz CG. History of the extensor plantar response: Babinski and Chaddock signs. Semin Neurol. 2002;22:391–398. 3. Lance JW. The Babinski sign. J Neurol Neurosurg Psychiatry. 2002;73:360–362. 4. van Gijn J. The Babinski reflex. Postgrad Med J. 1995;71:645–648. 5. Kalinowsky LB, Hoch PH. Shock Treatments, Psychosurgery and Other Somatic Treatments in Psychiatry. New York, NY: Grune and Stratton; 1952:143. 6. Todd RB. On the pathology and treatment of convulsive diseases. London Medical Gazette. 1849;8:668. 7. Liff JM, Bryson EO, Maloutas E, et al. Transient hemiparesis (Todd’s paralysis) after electroconvulsive therapy (ECT) in a patient with major depressive disorder. J ECT. 2013;29:247–248.
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8. Bell C, Lepping P, Clifford J, et al. A case of Todd’s Palsy following unilateral electroconvulsive therapy. Indian J Psychiatry. 2012;54:192–193.
Role of High-Frequency Repetitive Transcranial Magnetic Stimulation in Augmentation of Treatment of Bipolar Depression To the Editor: lthough patients with bipolar disorder reportedly spend more of their lifetime in depressive episodes,1 the treatment of bipolar depression (BD) has received limited attention. Whereas a recent meta-analysis2 has reported a modest to large effect size of active repetitive transcranial magnetic stimulation (rTMS) over sham treatment in major depression, there are very few clinical/controlled trials evaluating the efficacy of rTMS in BD. Given its efficacy and benign adverse effect profile in major depression, including a low risk of switch to mania,3 rTMS is a potential treatment option for BD. Studies using rTMS for BD report varied efficacy ranging from no benefit or partial response to good efficacy; however, controlled trials are far and few. There is also a lack of consensus on stimulus parameters and duration of treatment with rTMS for BD. We report a patient who was prescribed rTMS as augmentation treatment for BD. A 32-year-old male patient presented to us in 2013 with an episodic illness of 3 years’ duration, characterized by an initial prolonged manic episode of 2 years followed by a depressive episode of 1 year. His condition was diagnosed as bipolar affective disorder—current episode: moderate depression with somatic syndrome (International Statistical Classification of Diseases, 10th Revision; World Health Organization, 1992) and nicotine dependence. The manic episode responded to a combination of olanzapine plus lithium and valproate. The patient had a breakthrough depressive episode, which was characterized by pervasive low mood, lack of interest, low energy, decreased sleep, and poor social interaction with significant sociooccupational dysfunction. The depression did not improve much despite adequate treatment trials with fluoxetine and agomelatine, while the patient was being compliant on lithium and valproate. At admission, the patient scored 24 on the 21-item Hamilton Depression Rating Scale, 22 on the Beck Depression Inventory, and 4 on the Clinical Global Impression scale, indicating that
A
he was moderately ill. Initially, lithium, valproate, and agomelatine were augmented with cognitive behavior therapy and day structuring to which the patient failed to respond. After discussing with the patient about the merits and demerits of ECT and rTMS, the patient preferred rTMS in view of its benign adverse effect profile as a further augmentation strategy to the aforementioned treatment. He was prescribed rTMS after obtaining written informed consent and ruling out contraindications to rTMS. The patient received 10 sessions (5 sessions per week 2 weeks) of highfrequency rTMS to the left dorsolateral prefrontal cortex4 5.5 cm anterior to the motor cortical area corresponding to the right thumb at 100% resting-motor threshold. Ten trains were administered in each session at 15-Hz frequency for 10 seconds, with an intertrain interval of 60 seconds, for a total of 1500 pulses per session. The patient received a total of 15,000 pulses over 2 weeks. Although a few studies4 suggest that the efficacy of rTMS is better if given for more than 2 weeks, we could not extend treatment with rTMS as the patient had requested for discharge because of compelling personal reasons. After 2 weeks of rTMS, the patient reported a subjective improvement in mood from 4 to 8 on a scale of zero to 10, with zero being severely depressed mood and 10 being normal mood. There was an improvement in the 21-item Hamilton Depression Rating Scale scores from 24 to 14 and the Beck Depression Inventory scores from 22 to 12, which was approximately 40% to 45% improvement in the scores of both scales. Clinically, his mood, sleep, social interaction, and involvement in ward activities improved. The Clinical Global Impression scale—Severity of Illness score improved from 4 to 2 (borderline, mentally ill). The patient reported headache on a few occasions after rTMS, which subsided spontaneously. This improvement was maintained for the next 4 days after which the patient was discharged. Our report suggests that high-frequency rTMS to the left dorsolateral prefrontal cortex is efficacious as an augmentation treatment for BD. This is in line with some of the published literature, including a randomized controlled trial of high-frequency rTMS for BD5 and a retrospective naturalistic study, where 56 patients with BD remitted with highfrequency rTMS.4 Furthermore, apart from headache, our patient did not experience any of the other reported adverse effects of rTMS. However, rTMS for BD needs to be explored further in well-designed trials before it can be routinely recommended in clinical practice. © 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
ECT was administered to only 3 patients (2 men), just 0.18% of the 1600 admissions in the same period. In the SUHC, ECT was administered to only one male patient (0.1% of the 991 hospital admissions in the same period). The condition of all patients was diagnosed as schizophrenia, and they received 6 and 10 to 12 sessions of ECT in the SUHC and OUHC, respectively. Patients in all 3 centers underwent the same pretreatment evaluation: physical examination, electroencephalogram, electrocardiogram, standard laboratory tests and CT scan, and approval by a physician and an anesthesiologist. Written informed consent for ECT given by the patient or his/her legal guardian was mandatory. Printed information leaflets for patients about ECT were available. The only contraindication to treatment was a severe medical condition such as fever, acute infection, and uncontrolled high blood pressure. No significant adverse effect was reported during the survey period. The ECT team comprised a psychiatrist, an anesthesiologist, and psychiatric and anesthesiology nurses. Before the ECT, atropine (0.01 mg/kg) was given as premedication 5 minutes before ECT to avoid parasympathetic reaction. After oxygenation with 100% O2, general anesthesia was induced with propofol (1mg/kg); in one case, sugammadex was used. Intravenous succinylcholine (0.5 mg/kg) was administered for muscle relaxation, and ventilation was assisted with a face mask and 100% oxygen. Electroconvulsive therapy was administered using Thymatron Model DGx device (Somatics Inc, 1995). Electrodes were placed bifrontally. Seizure threshold titration was not practiced; only age-based method was used in all cases. Seizure activity was monitored with visual observation and electroencephalogram. During ECT, pulse rate, blood pressure, electrocardiogram, peripheral oxygen saturation (SpO2) and endexpiratory CO2 partial pressure (end-tidal CO2) were regularly monitored. Patients were moved from the recovery room when they are fully conscious/alert. There was no fixed number of sessions of ECT, which would continue until adequate treatment response was achieved as judged by the treating psychiatrist. In contrast to most other centraleastern European countries,1 only 3 institutions offered ECT in Croatia. A similarly low number of ECT centers were reported from Bulgaria2 and Ukraine,3 indicating rather limited accessibility to ECT in these countries. As for the indications of ECT, the Croatian practice closely resembles that of some other central-eastern European countries,1 whereas with regard © 2014 Lippincott Williams & Wilkins
Letters to the Editor
to ECT delivery—brief pulse stimulation and bifrontal electrode placement—it is close to the Western European and international standards. Electroconvulsive therapy is taught as a part of the regular medical curricula in the Zagreb School of Medicine, the Osijek School of Medicine, and the Split School of Medicine, which are linked with the ZUHC, OUHC, and SUHC, respectively. Electroconvulsive therapy is part of the standard psychiatric training course run at the ZUHC. However, there are no certified courses on ECT or any formal training for mental health professionals on the theory and practice of ECT. Similar to other European countries,4 training is informally provided by senior psychiatrists experienced in ECT as mentors. There are no national guidelines on ECT in Croatia, although the overall standard of ECT practice conforms to international recommendations.5 Martina Rojnic Kuzman, MD, PhD University Hospital Centre Zagreb Zagreb, Croatia and Zagreb School of Medicine Zagreb, Croatia [email protected]
Tamara Pranjkovic Zagreb School of Medicine Zagreb, Croatia
Dunja Degmecic, MD, PhD University Hospital Centre Osijek Osijek, Croatia and Osijek School of Medicine Zagreb, Croatia
Davor Lasić, MD University Hospital Centre Split Split, Croatia
Ana Medic Zagreb School of Medicine Zagreb, Croatia
Gábor Gazdag, MD, PhD Centre for Psychiatry and Addiction Medicine Szent István and Szent Laszló Hospitals Budapest, Hungary and Department of Psychiatry and Psychotherapy Semmelweis University Faculty of Medicine Budapest, Hungary
The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Leiknes KA, Jarosh-von Schweder L, Høie B. Contemporary use and practice of electroconvulsive therapy worldwide. Brain Behav. 2012;2:283–344. 2. Hranov LG, Hranov G, Ungvari GS, et al. Electroconvulsive therapy in Bulgaria: a snapshot of past and present. J ECT. 2012;28:108–110.
3. Oleksev A, Ungvari GS, Gazdag G. ECT practice in Ukraine. J ECT. 2014. [Epub ahead of print]. 4. Dragasek J. Electroconvulsive therapy in Slovakia. J ECT. 2012;28:7–8. 5. Rush G, Kimmich O, Lucy JV. Electroconvulsive therapy: international guidelines, clinical governance and patient selection. Ir J Psychol Med. 2007;24:103–107.
Transient Babinski Sign After Electroconvulsive Therapy (ECT) Dear Editor: he Babinski sign, or extensor plantar response, was first described by Joseph Francois Felix Babinski, a French neurologist of Polish descent, in his monograph of 1898.1 This reflex is characterized by extension of the big toe, occasionally accompanied by fanning of the rest of the toes, in response to the stimulus of stroking the lateral aspect of the sole of the foot.2 Initially of use in distinguishing hysteria from organic disease, the Babinski sign reflects dysfunction of the pyramidal tract anywhere along its course from the cortex, subcortical white matter, or brainstem to the spinal cord.2,3 A reliable sign of upper motor neuron dysfunction, the upgoing toe, reflects release of descending inhibition on spinal motor neurons, as well as inhibition of the local segmental cutaneous reflex, which normally triggers plantar flexion.4 Neonates will also exhibit an extensor response owing to incomplete development of the pyramidal tract; however, with maturation of upper motor neuron pathways, the Babinski sign disappears, and stimulation of the sole elicits the flexor response at approximately 12 to 24 months of age.3 We report a middle-aged woman with depression and a medical history of hypothyroidism and prior thyroid resection who developed a transient Babinski response after her initial right unilateral electroconvulsive therapy (ECT) dose-titration session. Her medications included diphenhydramine, 50 mg, oral, every night at bedtime; lorazepam, 1 mg, oral, 2 times a day; aripiprazole, 5 mg, oral, daily; mirtazapine, 7.5 mg, oral, every night at bedtime; paroxetine, 40 mg, oral, daily; and levothyroxine, 100 μg oral, daily. Anesthesia was induced with 50 mg of methohexital followed by 50 mg of succinylcholine. She received a single stimulus at 5% “energy” (25 mC; pulse width, 0.25 millisecond), resulting in a motor seizure of 38 seconds and an electroencephalographic seizure of 77 seconds. The Babinski phenomenon was bilateral, was elicited immediately after cessation of the seizure, and resolved within 15 minutes.
T
www.ectjournal.com
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
e43
Journal of ECT • Volume 30, Number 4, December 2014
Letters to the Editor
Transient upper motor neuron signs can occur after a variety of reversible disturbances of cortical function including seizures, migraines, deep sleep, anesthesia, or metabolic abnormalities.4 In his 1952 textbook on ECT, Kalinowsky reports observing the Babinksi sign in approximately one fifth of the cases.5 Todd’s paralysis,6 a transient focal neurological deficit after a seizure, has also been reported after ECT.7,8 Our patient had no neurological complications during her course of 6 right unilateral ECT treatments at 30% energy, and her depressive illness remitted completely (Hamilton Rating Scale for Depression, 24-Item, score decreased from 28 to 9). Her Babinksi sign was not elicited in subsequent treatments, the significance of which remains to be explored. Amy S. Aloysi, MD, MPH Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, NY
Ethan O. Bryson, MD Departments of Psychiatry and Anesthesiology Icahn School of Medicine at Mount Sinai New York, NY
Lauren S. Liebman, BA Mimi C. Briggs, BA Charles H. Kellner, MD Department of Psychiatry Icahn School of Medicine at Mount Sinai New York, NY [email protected]
Dr. Kellner is supported by an NIMH grant U01MH055495. The other authors have no financial conflicts of interest or financial disclosures to report. REFERENCES 1. Babinski J. Du phénomène des orteils et de sa valeur sémiologique. Semaine Médicale. 1898; 18:321–322. 2. Goetz CG. History of the extensor plantar response: Babinski and Chaddock signs. Semin Neurol. 2002;22:391–398. 3. Lance JW. The Babinski sign. J Neurol Neurosurg Psychiatry. 2002;73:360–362. 4. van Gijn J. The Babinski reflex. Postgrad Med J. 1995;71:645–648. 5. Kalinowsky LB, Hoch PH. Shock Treatments, Psychosurgery and Other Somatic Treatments in Psychiatry. New York, NY: Grune and Stratton; 1952:143. 6. Todd RB. On the pathology and treatment of convulsive diseases. London Medical Gazette. 1849;8:668. 7. Liff JM, Bryson EO, Maloutas E, et al. Transient hemiparesis (Todd’s paralysis) after electroconvulsive therapy (ECT) in a patient with major depressive disorder. J ECT. 2013;29:247–248.
e44
www.ectjournal.com
8. Bell C, Lepping P, Clifford J, et al. A case of Todd’s Palsy following unilateral electroconvulsive therapy. Indian J Psychiatry. 2012;54:192–193.
Role of High-Frequency Repetitive Transcranial Magnetic Stimulation in Augmentation of Treatment of Bipolar Depression To the Editor: lthough patients with bipolar disorder reportedly spend more of their lifetime in depressive episodes,1 the treatment of bipolar depression (BD) has received limited attention. Whereas a recent meta-analysis2 has reported a modest to large effect size of active repetitive transcranial magnetic stimulation (rTMS) over sham treatment in major depression, there are very few clinical/controlled trials evaluating the efficacy of rTMS in BD. Given its efficacy and benign adverse effect profile in major depression, including a low risk of switch to mania,3 rTMS is a potential treatment option for BD. Studies using rTMS for BD report varied efficacy ranging from no benefit or partial response to good efficacy; however, controlled trials are far and few. There is also a lack of consensus on stimulus parameters and duration of treatment with rTMS for BD. We report a patient who was prescribed rTMS as augmentation treatment for BD. A 32-year-old male patient presented to us in 2013 with an episodic illness of 3 years’ duration, characterized by an initial prolonged manic episode of 2 years followed by a depressive episode of 1 year. His condition was diagnosed as bipolar affective disorder—current episode: moderate depression with somatic syndrome (International Statistical Classification of Diseases, 10th Revision; World Health Organization, 1992) and nicotine dependence. The manic episode responded to a combination of olanzapine plus lithium and valproate. The patient had a breakthrough depressive episode, which was characterized by pervasive low mood, lack of interest, low energy, decreased sleep, and poor social interaction with significant sociooccupational dysfunction. The depression did not improve much despite adequate treatment trials with fluoxetine and agomelatine, while the patient was being compliant on lithium and valproate. At admission, the patient scored 24 on the 21-item Hamilton Depression Rating Scale, 22 on the Beck Depression Inventory, and 4 on the Clinical Global Impression scale, indicating that
A
he was moderately ill. Initially, lithium, valproate, and agomelatine were augmented with cognitive behavior therapy and day structuring to which the patient failed to respond. After discussing with the patient about the merits and demerits of ECT and rTMS, the patient preferred rTMS in view of its benign adverse effect profile as a further augmentation strategy to the aforementioned treatment. He was prescribed rTMS after obtaining written informed consent and ruling out contraindications to rTMS. The patient received 10 sessions (5 sessions per week 2 weeks) of highfrequency rTMS to the left dorsolateral prefrontal cortex4 5.5 cm anterior to the motor cortical area corresponding to the right thumb at 100% resting-motor threshold. Ten trains were administered in each session at 15-Hz frequency for 10 seconds, with an intertrain interval of 60 seconds, for a total of 1500 pulses per session. The patient received a total of 15,000 pulses over 2 weeks. Although a few studies4 suggest that the efficacy of rTMS is better if given for more than 2 weeks, we could not extend treatment with rTMS as the patient had requested for discharge because of compelling personal reasons. After 2 weeks of rTMS, the patient reported a subjective improvement in mood from 4 to 8 on a scale of zero to 10, with zero being severely depressed mood and 10 being normal mood. There was an improvement in the 21-item Hamilton Depression Rating Scale scores from 24 to 14 and the Beck Depression Inventory scores from 22 to 12, which was approximately 40% to 45% improvement in the scores of both scales. Clinically, his mood, sleep, social interaction, and involvement in ward activities improved. The Clinical Global Impression scale—Severity of Illness score improved from 4 to 2 (borderline, mentally ill). The patient reported headache on a few occasions after rTMS, which subsided spontaneously. This improvement was maintained for the next 4 days after which the patient was discharged. Our report suggests that high-frequency rTMS to the left dorsolateral prefrontal cortex is efficacious as an augmentation treatment for BD. This is in line with some of the published literature, including a randomized controlled trial of high-frequency rTMS for BD5 and a retrospective naturalistic study, where 56 patients with BD remitted with highfrequency rTMS.4 Furthermore, apart from headache, our patient did not experience any of the other reported adverse effects of rTMS. However, rTMS for BD needs to be explored further in well-designed trials before it can be routinely recommended in clinical practice. © 2014 Lippincott Williams & Wilkins
Copyright © 2014 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
