Journal of ECT • Volume 30, Number 4, December 2014

Kailash Sureshkumar, MD, DNB Srikala Bharath, DPM, MD, DCAP FRCPsych Kesavan Muralidharan, MD Preeti Sinha, MD Shilpa Veluthethodi Sivaraman, MBBS Department of Psychiatry NIMHANS Bangalore, India [email protected]

REFERENCES 1. Judd LL, Akiskal HS. Depressive episodes and symptoms dominate the longitudinal course of bipolar disorder. Curr Psychiatry Rep. 2003;5: 417–418 2. Slotema CW, Blom JD, Hoek HW, et al. Should we expand the toolbox of psychiatric treatment methods to include repetitive transcranial magnetic stimulation (rTMS)? A meta-analysis of the efficacy of rTMS in psychiatric disorders. J Clin Psychiatry. 2010;71: 873–884. 3. Ella R, Zwanzger P, Stampfer R, et al. Switch to mania after slow rTMS of the right prefrontal cortex. J Clin Psychiatry. 2002;63:249. 4. Cohen RB, Brunoni Adre R, Paulo S, et al. Clinical predictors associated with duration of repetitive transcranial magnetic stimulation treatment for remission in bipolar depression: a naturalistic study. J Nerv Ment Dis. 2010;198:679–681. 5. Dolberg OT, Dannon PN, Schreiber S, et al. Transcranial magnetic stimulation in patients with bipolar depression: a double blind, controlled study. Bipolar Disord. 2002:4(suppl 1):94–95.

Electroconvulsive Therapy for Frontotemporal Dementia With Comorbid Major Depressive Disorder To the Editor: he behavioral variant of frontotemporal dementia (FTD) may present with depression in addition to changes in behavior and personality. Selective serotonin reuptake inhibitors and trazodone may be useful in the treatment of depression in FTD.1 Less well researched is the use of electroconvulsive therapy (ECT) for severe or treatment-resistant cases. We describe ECT done for a patient with initial diagnoses of major depressive disorder with psychotic features and dementia not otherwise specified according


© 2014 Lippincott Williams & Wilkins

to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision diagnostic criteria.2 Later, his diagnosis was clarified to be the behavioral variant of FTD. A 70-year-old white man was brought to the emergency room by his ex-wife. His history was significant for a recent hospitalization on the neurology service at another hospital with confusion, having been found driving the wrong way on a 1-way street. His medical workup included computed tomography (CT) of the head, brain magnetic resonance imaging, brain singlephoton emission CT scan, electroencephalography, lumbar puncture, CT of the chest/abdomen/pelvis, ultrasound of the scrotum and thyroid, and extensive blood work to search for the etiology of his confusion, without significant results. Frontotemporal dementia had been considered at the time: he lacked empathy while interacting with his family after a prolonged absence; engaged in perseverative behavior, insisting on repetitively cleaning his room and belongings; and demonstrated deficits in executive function with relative sparing of his shortterm memory, thus fulfilling the criteria for possible behavioral variant of FTD.3 His Montreal Cognitive Assessment score was 25/30 and Frontal Assessment Battery score was 12/18, highlighting the preponderance of the executive functioning deficits rather than short-term memory loss in his presentation. He was prescribed citalopram and discharged. However, his depression worsened, and he started to demonstrate command auditory hallucinations to hang himself, excessive guilt, and shame. He falsely believed that he had a criminal record. He was admitted to the inpatient psychiatric ward at the Veterans Affairs Medical Center. Most of the patient’s history was obtained from his ex-wife. While family history was largely unknown, one of their 3 children was diagnosed with bipolar disorder. The patient had his own business as a physical therapist. He had not had close relationships with friends or family, and his marriage was strained for many years, culminating in a divorce. At the age of 64 years, he sold his business, and his family lost track of him for a few years. It turned out that in the interim he had moved to a small town, where he lived in a neat apartment devoid of personal effects. Because of the patient's severe depression, psychosis, and acute suicidal ideation, he was offered treatment with ECT. He expressed desire for improvement, was able to discuss the risks and benefits of the

Letters to the Editor

proposed treatment, and was able to consent to it. The ECT treatment was applied 3 times a week with brief pulse constant current stimulation using a Thymatron System IV (Somatics, LLC, Lake Bluff, Ill). The initial stimulus setting of 35% of the maximal charge was implemented (100% for the Thymatron machine = 504 mC). Right unilateral electrode placement with ultrabrief pulse (0.3 millisecond) was used. Anesthesia was implemented with methohexital and succinylcholine, respective doses of which were 100 mg intravenously and 80 mg intravenously. An electroencephalogram was recorded during the treatment. Cardiac rhythm, blood, pressure, heart rate, and oxygenation were monitored before, during, and after the treatments. His seizures averaged 60 seconds in duration with high amplitude spike and wave activity and excellent postictal suppression. During the third treatment, his electrocardiogram (electrocardiogram) showed ST-segment depression. An exercise stress test was positive. Atenolol and aspirin were initiated per advice of cardiology. Three more ECT treatments were performed, with no further cardiovascular symptoms. His citalopram dose was increased to 20 mg daily, he participated in the ward milieu, and he received supportive psychotherapy from his treatment team. His depressive and psychotic symptoms resolved, with no worsening in cognition as demonstrated by the lack of change in his Montreal Cognitive Assessment score. After the index ECT course, the patient received several monthly maintenance treatments. The patient’s family was unable to meet his needs, and he transitioned to an assisted living facility, where his behavior worsened. He was hospitalized again, to manage his behavioral disturbance and find an alternative placement. He presented with apathy, poor judgment, and behavioral problems, which included getting into physical fights with other patients, having stubborn refusal to cooperate with staff requests, and pouring water on his roommates while they slept. A repeat single-photon emission CT scan showed mild decrease of tracer uptake in the bilateral mesial temporal lobes and bilateral orbitofrontal cortex with the right side of the brain affected to a greater degree than the left. This finding along with his clinical presentation led to the probable diagnosis of the behavioral variant of FTD according to the international consensus criteria.3 The patient’s progressive difficulty in making decisions regarding his medical care led us to terminate the maintenance ECT treatment. Fortunately, he was able to transition to a different assisted

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


Journal of ECT • Volume 30, Number 4, December 2014

Letters to the Editor

living facility that provided supportive care for his symptoms. In conclusion, patients with FTD may present with mood and psychotic symptoms severe enough to necessitate ECT. Existing literature on using ECT in FTD is limited but encouraging, with several case reports describing improvements in the patients’ behavior and mood during the treatment. A retrospective chart review of ECT in patients with dementia, including several patients with FTD, suggests that ECT is a safe and effective treatment for agitation and aggression, also demonstrating efficacy for mood symptoms.4 Our case adds to the growing body of evidence that ECT is effective in managing neuropsychiatric symptoms related to FTD, with low potential for cognitive adverse effects and should be considered when severe depression, suicidal ideation, psychosis, or treatment resistance are of concern. To minimize the potential for impaired cognition, we suggest unilateral mode of ECT delivery with ultrabrief pulse and closely monitoring the cognition and behavior during the course of treatment.

Anna Borisovskaya, MD Acting Associate Professor University of Washington Seattle, WA [email protected]

Jay Augsburger, MD Veterans Affairs Medical Center Seattle, WA

Marcella Pascualy, MD Associate Professor University of Washington Seattle, WA

The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Caselli RJ, Yaari R. Medical management of frontotemporal dementia. Am J Alzheimers Dis Other Demen. 2008;22:489–498. 2. American Psychiatric Association & American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR. Washington, DC: American Psychiatric Association; 2000. 3. Arvanitakis Z. Update on frontotemporal dementia. Neurologist. 2010;16:16–22. 4. Ujkaj M, Davidoff DA, Seiner SJ, et al. Safety and efficacy of electroconvulsive therapy for the treatment of agitation and aggression in patients with dementia. Am J Geriatr Psychiatry. 2012;20:61–72.


Transcranial Magnetic Stimulation in a 15-Year-Old Patient With Autism and Comorbid Depression To the Editor: epression is a common co-occurring disorder in patients with autism, with prevalence rates from 1.5% to 10% for major depressive episodes.1 Transcranial magnetic stimulation (TMS) is a noninvasive neuromodulation technique that uses pulsating magnetic fields to depolarize cortical neurons. High frequency (≥5 Hz) TMS can induce excitatory responses and low frequency (≤1 Hz) induces inhibitory responses.2 Transcranial magnetic stimulation has been proposed as an antidepressant treatment in adolescents3 and in patients with autism to improve executive functioning.4 We present the case of an adolescent with autistic disorder and comorbid depression treated with TMS to illustrate this potential application. The patient's parents (guardians) provided permission for the treatment and for the use of protected health information. This is a 15-year-old adolescent boy with an autistic disorder diagnosis according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. He was diagnosed at the age of 5 years using the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule, in addition to expert clinical diagnosis. He lives with his parents and his fraternal twin, who was also diagnosed with an autistic disorder. He attends ninth grade in high school with paraprofessional assistance in the classroom. He has a family history of autistic disorder and depression in second-degree relatives. His autistic symptoms include limitations in social interactions, difficulties in coping with change, stereotypic movements and behaviors, as well as limited and stereotypical language use. He has a history of depression since early childhood, with depressive episodes that last several days, characterized by lack of motivation, decreased participation in activities, isolation, and crying spells. In addition, he exhibited irritability and longstanding extreme sensitivity to negative emotion expressed by his twin brother. He was prescribed 6/25 mg of olanzapine/ fluoxetine, 4 mg of guanfacine, and 0.5 mg of clonazepam 3 times daily. Previous psychotropic treatment has been ineffective or induced adverse effects. These included sertraline, paroxetine, risperidone, and aripiprazole. On the initial evaluation, his parents reported that his mood was down, with decreased motivation, variable energy level,


increased appetite, psychomotor slowing, irritability, tearfulness, and increased stereotypical phrase repetition. On the initiation of TMS, clonazepam was titrated down to avoid effects on motor threshold. To treat depressive symptoms, we chose low-frequency TMS over the right dorsolateral prefrontal cortex (DLPFC). The treatments were administered using a Magpro R30 stimulator (Tonica Electronik A/S, Farum, Denmark) using a cool-B65 figure 8 coil. The resting motor threshold (RMT) determined by the visualization of movement method was 89%.2 The DLPFC was localized 6 cm anterior in a parasagittal line to the RMT location. The TMS was delivered daily at 90% of the RMT, using 1 Hz, 10 seconds on, and 10 to 30 seconds off. The treatment was started at 150 pulses per session (PPS) and increased to 300 PPS by the second week. A total of 10 sessions of TMS over the right DLPFC were administered with improvement in the mood symptoms. Subsequently, we applied low-frequency TMS over the left DLPFC in an attempt to improve the core symptoms of autism, modeling previous studies to improve executive functioning in autism.4 The left RMT was 80%, and the left DLPFC was identified as 6 cm anterior in a parasagittal line to the RMT location. Stimulation was delivered at 90% of RMT, using 1 Hz, 10 seconds on, and 10 to 15 seconds off. The number of pulses per session was increased from 300 PPS to 600 PPS by the fourth week. On completion of 20 sessions, TMS was tapered in 6 sessions for 3 weeks. Stimulation was well tolerated, and adverse effects included mild headaches, jaw twitch during the stimulation, and transient dizziness immediately after the treatments. Improvement in both mood and some autism core features were reported by his parents and his educational team. His mood was described as “perkier”: he seemed more active and his energy improved. He seemed to be able to cope with daily stresses better and no longer had episodes of tearfulness. Improvements in communication and social interactions were noted. He made better eye contact, greeted people more consistently, and was more verbal. In addition, he seemed to be more supportive of the emotions of his parents and his twin brother. The academic tutor noticed that he focused better during school-related tasks. On mental status examination by his psychiatrist (author J.N.C.) after the completion of TMS treatment, the patient seemed more animated and spontaneously communicative than on any prior visit during the course of his treatment. In this case, we used slow TMS over the right DLPFC to treat depression because © 2014 Lippincott Williams & Wilkins

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

Electroconvulsive therapy for frontotemporal dementia with comorbid major depressive disorder.

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