Letters to the Editor / Brain Stimulation 7 (2014) 486e497

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(INR), a calculation made to normalize prothrombin time and used as a standard for monitoring the effects of warfarin, was not immediately obtained by the patient, but 5 days later was 1.7 (goal of INR 2e3). With Ophthalmology, he reported sharp constant pain behind his left eye and feeling “waves moving” through his head and eyes during rTMS sessions. He denied any drainage, flashes, floaters, or trauma. His ophthalmologic history was notable for a previous left SCH 18 months prior, with no history of trauma at that time. His blood pressure was 143/92. Exam revealed a small SCH on the right inferior aspect of his left eye, but otherwise was normal. After his SCH resolved, rTMS was resumed. At that time, MADRS was 19, PCL-M was 68, and PHQ-9 was 19. Due to the SCH, rTMS protocol was switched to 1 Hz over 1 s for total of 1200 pulses delivered over 20 min at 110% of MT, with MT of 1.06 and coil angle of þ20. He experienced right eye pain radiating to his teeth and jaw. Coil angle was changed to 0 and MT decreased to 80% to help him better acclimate to rTMS. At the 6th session, MT was increased to 100% and he experienced left eye photophobia but no ocular hemorrhage. He reported noticeable improvements in his mood and anxiety level at session 10 and at the time of his last session 22, MADRS was 15 and at 3 week follow-up PCL-M decreased to 48 and PHQ-9 decreased to 11 with no evidence of any reoccurrence of SCH.

effect. Asking patients about ophthalmologic symptoms should be included as part of routine monitoring of rTMS side effects.

Discussion

http://dx.doi.org/10.1016/j.brs.2014.02.013

While rTMS in depression has been widely used, very few studies of rTMS in PTSD patients have been published so far. These studies have shown mixed results as to whether high frequency versus low frequency rTMS is effective for PTSD [1,2]. Electrophysiological studies suggest that low frequency rTMS (1 Hz) excites neurons within the stimulated field [3]. A meta-analysis of functional imaging studies in PTSD patients showed hypoactivation within the ventromedial prefrontal cortex (PFC) and hyperactivation of the amygdala [4]. This PTSD model would predict that high frequency rTMS to the PFC would be effective for PTSD, while low frequency ineffective. In our patient, low frequency rTMS was effective, which is consistent with a previous finding that showed increased activation of the PFC in PTSD [5]. Treatment with rTMS is generally safe and well tolerated with the most common side effects being headache and discomfort at the stimulation site [6] and the most serious but rare adverse effect being seizures [7]. These adverse effects have been positively correlated with both intensity and frequency of stimulation [7]. There has been one previous case report of posterior vitreous detachment and retinal tear after rTMS [8] but no other reports of ophthalmologic side effects. This is the first reported association of rTMS with SCH. Spontaneous, nontraumatic cases of SCH self-resolve over two to three weeks and require no treatment. The major risk factors are trauma and contact lens use in younger patients and hypertension and diabetes in older patients, though in the majority of cases the cause is unknown [9]. Patients receiving anticoagulation therapy are also at risk, but the prevalence of ocular hemorrhage in patients receiving warfarin is small [10]. Our patient was on warfarin though his INR was subtherapeutic at the time of the onset of the SCH. The patient also had the risk factor of hypertension, but his blood pressure was within range of his baseline readings. His risk for SCH likely increased due to receiving high frequency rTMS, as more side effects have been reported with high frequency stimulation. There was also no reoccurrence of SCH with low frequency rTMS. Although it cannot be determined that rTMS caused his SCH, the onset of the SCH after receiving rTMS makes this a possible side

Financial disclosures: The authors declare no financial interests or potential conflicts of interest. The views expressed herein are our own and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the U.S. Government. We are military service members. This work was prepared as part of our official duties. Title 17, USC, x 105 provides that ‘Copyright protection under this title is not available for any work of the United States Government.’ Title 17, USC, x 101 defines a U.S. Government work as a work prepared by a military service member or employee of the U.S. Government as part of that person’s official duties.

Bianca Cabrera Karris* Marc Capobianco Department of Mental Health, Naval Medical Center San Diego, 34800 Bob Wilson Drive, San Diego, CA 92134, USA author. Tel.: þ1 858 774 2002. E-mail addresses: [email protected], [email protected] (B.C. Karris)

* Corresponding

Received 31 January 2014 Available online 24 March 2014 References [1] Cohen H, Kaplan Z, Kotler M, Kouperman I, Moisa R, Grisaru N. Repetitive transcranial magnetic stimulation of the right dorsolateral prefrontal cortex in posttraumatic stress disorder: a double-blind, placebo-controlled study. Am J Psychiatry 2004;161(3):515e24. [2] Nam D, Pae C, Chae J. Low-frequency, repetitive transcranial magnetic stimulation for the treatment of patients with posttraumatic stress disorder: a double-blind, sham-controlled study. Clin Psychopharmacol Neurosci 2013;11(2):96e102. [3] Speer AM, Kimbrell TA, Wassermann EM, et al. Opposite effects of high and low frequency rTMS on regional brain activity in depressed patients. Biol Psychiatry 2000;48(12):1133e41. [4] Etkin A, Wager TD. Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. Am J Psychiatry 2007;164:1476e88. [5] Zubieta JK, Chinitz JA, Lombardi U, Fig LM, Cameron OG, Liberzon I. Medial frontal cortex involvement in PTSD symptoms: a SPECT study. J Psychiatr Res 1999;33(3):259e64. [6] George MS, Lisanby SH, Avery D, et al. Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: a sham-controlled randomized trial. Arch Gen Psychiatry 2010;67(5):507e16. [7] Rossi S, Hallett M, Rossini P, Pascual-Leone A, The Safety of TMS Consensus Group. Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research. Clin Neurophysiol 2009;120(12):2008e39. [8] Kung S, Ahuja Y, Iezzi R, Sampson SM. Posterior vitreous detachment and retinal tear after repetitive transcranial magnetic stimulation. Brain Stimul 2011;4(4):218e21. [9] Tarlan B, Kiratli H. Subconjunctival hemorrhage: risk factors and potential indicators. Clin Ophthalmol 2013;7:1163e70. [10] Superstein R, Gomolin JE, Hammouda W, Rosenberg A, Overbury O, Arsenault C. Prevalence of ocular hemorrhage in patients receiving warfarin therapy. Can J Ophthalmol 2000;35(7):385e9.

rTMS for Treatment of Depression in a Patient With Cerebral Amyloid Angiopathy: A Case Report on Safety and Efficacy Dear Editor, We report on the safety and efficacy of low frequency repetitive transcranial magnetic stimulation (rTMS) on a patient presenting

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Letters to the Editor / Brain Stimulation 7 (2014) 486e497

Figure 1. The left-hand image (A) shows a susceptibility weighted MRI sequence revealing numerous micro hemorrhages in the patient. The right-hand image (B) shows PiB-PET imaging, showing high levels of cortical uptake indicating amyloid deposition.

with a long history of medication-resistant depression and known co-morbid cerebral amyloid angiopathy (CAA). rTMS is effective in treating medication-resistant depression and its use is quickly growing [1]. Its broader use, however, raises concerns about the safety of TMS particularly in patient populations where there may either be a higher risk for side-effects or a lower likelihood of showing a positive response to treatment. There are currently two forms of rTMS with substantial evidence for efficacy in the treatment of depression, high-frequency rTMS (5e20 Hz) to the left dorsolateral prefrontal cortex (DLPFC) and low-frequency rTMS (1 Hz) to the right DLPFC [2]. While lowfrequency rTMS to right DLPFC has not been tested in large multicenter trials, a meta-analysis of smaller trials lends evidence for its efficacy [3]. To date, there have been no seizures reported from low frequency right DLPFC protocols and 1 Hz rTMS is being used as a treatment for epilepsy [4]. CAA is a neurovascular disease characterized by b-amyloid fibrils deposited in the walls of cerebral blood vessels [5]. These deposits weaken the vessel walls and predispose patients to complications such as intracerebral hemorrhage, microbleeds, and cognitive impairment. CAA microbleeds are believed to occur in greater than 30% of adults over the age of 70, and are potentially even more prevalent given the amount of asymptomatic individuals with microbleeds [6]. Currently, there is no evidence reported in the literature regarding the safety of brain stimulation techniques such as rTMS in patients with CAA. Given the seizure risk of rTMS and the treatment’s unknown effects on weakened cerebrovasculature, it is unclear whether patients with CAA who could benefit from rTMS treatment should be subjected to an induction and maintenance course of stimulation.

Patient presentation This 73 year-old male retired physician, who is married without children, has a long history of chronic medicationresistant depression dating back to adolescence. He had a strong maternal family history of depression. Around age 50 he was initiated on therapy with paroxetine, which was discontinued a

couple of months later due to side effects. Over the course of the next few years he attempted trials of medications from several classes of anti-depressant medications including bupropion, venlafaxine, St. John’s Wart, nefazodone, remeron, risperidone, and mirtazapine. Venlafaxine was the only agent to show minor improvement in mood, but was ultimately discontinued due to intolerable side effects. The rest were either not beneficial, not tolerable, or both. In the late 1990s the patient was hospitalized and received over twenty sessions of electroconvulsive therapy. These also had no positive effect on his depression and caused severe memory loss, including some degree of retrograde amnesia that did not fully resolve. Since then he has continued to try various combinations of anti-depressant medications with little to no success. The patient recently experienced episodes of acute vertigo for which he received an MRI to investigate. The MRI unexpectedly showed approximately 40 microbleeds (Fig. 1A), leading to a diagnosis of probable CAA [7]. No parenchymal hemorrhages have occurred and he has been followed with serial imaging for a number of years. During his course, he participated in a CAA research study that included amyloid imaging with Pittsburgh Compound B (PiB). This study (obtained as described with the patient’s informed consent) demonstrated increased cortical PiB retention (Fig. 1B) in a pattern consistent with CAA [8].

Treatment plan The patient was referred to our clinic by his psychiatrist for possible treatment with TMS given the refractory nature of his symptoms. There were no focal findings on his neurological exam and no signs of any cognitive symptoms. One concern that arose in the evaluation was whether the combination of rTMS and CAA might increase the risk of a seizure. After explaining the potential risks of the treatment and with his consent, therapy was started with 1hz to the right DLPFC as defined by 5.5 cm anterior to motor threshold site. Motor threshold was defined as the intensity over the motor hotspot at which 50% of pulses produced a discernable visual motor response in the patients’ hand. Stimulation intensity was set to 110% of the resting motor threshold,

Letters to the Editor / Brain Stimulation 7 (2014) 486e497

Zachary A. Gray Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, Boston, MA, USA

and rTMS was applied at 1 Hz for 1600 pulses per day for 3 weeks. A Magstim Super Rapid2 repetitive stimulator (Magstim Company Ltd., Whitland, Carmarthenshire, UK) was used to conduct all rTMS sessions.

Steven M. Greenberg Department of Neurology, Stroke Research Centre, Massachusetts General Hospital, Boston, MA, USA

Patient response The patient tolerated the treatments well and showed an excellent response with a decrease in his Beck Depression Inventory II (BDI-II) from a baseline of 21 to 1 at the end of the initial course. His Hamilton Rating Scale for Depression (HAM-D) dropped from a 10 at initial evaluation to a 1 at the end of his induction course. His observed affect (assessed by clinicians involved in his treatment) was reported to be noticeably improved e he was said to be more engaged and alert, and was able to both enjoy and deliver humor. There was no exacerbation of microbleeds due to CAA on visual inspection of a follow-up MRI.

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Daniel Z. Press, TMS Program Clinical Director* Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, Boston, MA, USA * Corresponding

author. Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, 330 Brookline Ave., KS-158, Boston, MA 02215, USA. E-mail address: [email protected] Received 20 February 2014 Available online 24 March 2014

http://dx.doi.org/10.1016/j.brs.2014.02.013

Discussion The patient’s treatment was completed successfully and without complication. He received a total of 15 daily sessions over three weeks, during which he entered full remission. Since completion of induction, this patient has continued maintenance sessions of rTMS due to episodic and mild recurrence of decreased mood. He continues to show a good response. Low frequency rTMS was performed without complications in a patient with CAA and medication-resistant depression. Whether risks could emerge with additional patients and whether high frequency left DLPFC treatments can be performed safely remains unanswered. At least initially, low frequency right DLPFC treatment should incur a lower risk of complications, particularly seizures, in patients with CAA and for whom rTMS is medically indicated. DP is the clinical director for the TMS Program at Beth Israel Deaconess Medical Center. The PiB Scan was covered by NIH Grant R01 AG26484 on which SG is the PI.

References [1] George MS, Taylor JJ, Short EB. The expanding evidence base for rTMS treatment of depression. Curr Opin Psychiatry 2013;26:13e8. [2] Fregni F, Pascual-Leone A. Transcranial magnetic stimulation for the treatment of depression in neurologic disorders. Curr Psychiatry Rep 2005;7:381e90. [3] Berlim MT, Van den Eynde F, Jeff Daskalakis Z. Clinically meaningful efficacy and acceptability of low-frequency repetitive transcranial magnetic stimulation (rTMS) for treating primary major depression: a meta-analysis of randomized, double-blind and sham-controlled trials. Neuropsychopharmacology 2013;38: 543e51. [4] Rossi S, Hallett M, Rossini PM, Pascual-Leone A. Safety, ethical considerations, and application guidelines for the use of transcranial magnetic stimulation in clinical practice and research. Clin Neurophysiol 2009;120:2008e39. [5] Biffi A, Greenberg SM. Cerebral amyloid angiopathy: a systematic review. J Clin Neurol 2011;7:1e9. [6] Viswanathan A, Greenberg SM. Cerebral amyloid angiopathy in the elderly. Ann Neurol 2011;70:871e80. [7] Knudsen KA, Rosand J, Karluk D, Greenberg SM. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston Criteria. Neurology 2001;56:537e9. [8] Johnson KA, Gregas M, Becker JA, et al. Imaging of amyloid burden and distribution in cerebral amyloid angiopathy. Ann Neurol 2007;62:229e34.

rTMS for treatment of depression in a patient with cerebral amyloid angiopathy: a case report on safety and efficacy.

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