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Letters to the Editor / Brain Stimulation 8 (2015) 838e849

potentiation/depression effects in brain slice preparations compared to constant frequency stimulation [6]. It is additionally possible that, similarly to other forms of noninvasive brain stimulation techniques delivered at intensities below those needed for synaptic activation, like transcranial alternating current stimulation, ScTBS might induce subthreshold changes in the membrane potentials of affected neurons, thus altering their firing rate [7]. Further studies are needed to fully understand the clinical utility of invasive chronic ScTBS in ET patients. Supplementary video related to this article can be found at http://dx.doi.org/10.1016/j.brs.2015.05.003. Conflict of interest: None. Authors contributions: Marina Picillo organized and executed the study and drafted the manuscript. Elena Moro, Mark Edwards, Vincenzo Di Lazzaro, Andres M. Lozano revised the manuscript for intellectual content. Alfonso Fasano conceived and designed the study and drafted and revised the manuscript for intellectual content. Study funding: No targeted funding reported. Full financial disclosures: MP received salary from the University of Salerno, Italy and research grants from the Division of Neurology e University of Toronto and the Michael J. Fox Foundation. EM has received honoraria from Medtronicfor consulting service and lecturing. ME receives funding from NIHR, Parkinson’s UK and the Medical Research Council. VDL received personal fees from Medtronic during the conduct of the Crystal study. AML received speaker and/or consulting honoraria fromBoston Scientific, Medtronic, St. Jude, Schering, Elekta, InSightec; he is the co-founder ofFunctional Neuromodulation Ltd and deputy editor of Brain Stimulation Journal. AF received speaker and/or consulting honoraria from Abbvie, Boston Scientific, Chiesi pharmaceuticals, Medtronic, TEVA Canada, UCB pharma and research grants from NeurecaOnlus, AFaR, the Division of Neurology e University of Toronto and the Michael J. Fox Foundation. He is in the editorial board of BioMed Research International, Case Reports in Neurological Medicine and Plos One.

Marina Picillo Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson’s Disease Toronto Western Hospital, Toronto, ON, Canada Division of Neurology, University of Toronto, Toronto, ON, Canada Centre for Neurodegenerative Diseases (CEMAND) Department of Medicine and Surgery, University of Salerno Salerno, Italy Elena Moro Service de Neurologie, CHU Grenoble, Joseph Fourier University INSERM U836, Grenoble, France Mark Edwards UCL Institute of Neurology, Queen Square, London, UK Vincenzo Di Lazzaro Institute of Neurology, Campus Bio Medico University, Rome, Italy Andres M. Lozano Division of Neurosurgery Toronto Western Hospital e UHN University of Toronto, Toronto, ON, Canada Alfonso Fasano* Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson’s Disease, Toronto Western Hospital, Toronto, ON, Canada Division of Neurology, University of Toronto, Toronto, ON, Canada * Corresponding author. Division of Neurology, University of Toronto, Movement Disorders Centre, Toronto Western Hospital , 399 Bathurst St, 7 Mc412,

Toronto, ON, Canada M5T 2S8. Tel.: þ1 416 603 5800x5961; fax: þ1 416 603 5004. E-mail address: [email protected] (A. Fasano) Received 2 May 2015 Available online 10 June 2015 http://dx.doi.org/10.1016/j.brs.2015.05.003

References [1] Huang YZ, Edwards MJ, Rounis E, Bhatia KP, Rothwell JC. Theta burst stimulation of the human motor cortex. Neuron 2005;45:201e6. [2] Halliday DM, Conway BA, Farmer SF, Shahani U, Russell AJ, Rosenberg JR. Coherence between low-frequency activation of the motor cortex and tremor in patients with essential tremor. Lancet 2000;355:1149e53. [3] Chuang WL, Huang YZ, Lu CS, Chen RS. Reduced cortical plasticity and GABAergic modulation in essential tremor. Mov Disord 2014;29:501e7. [4] Hellriegel H, Schulz EM, Siebner HR, Deuschl G, Raethjen JH. Continuous thetaburst stimulation of the primary motor cortex in essential tremor. Clin Neurophysiol 2012;123:1010e5. [5] Moro E, Schwalb JM, Piboolnurak P, et al. Unilateral subdural motor cortex stimulation improves essential tremor but not Parkinson’s disease. Brain 2011;134: 2096e105. [6] Larson J, Wong D, Lynch G. Patterned stimulation at the theta frequency is optimal for the induction of hippocampal long-term potentiation. Brain Res 1986;368(2):347e50. [7] Brittain J-S, Probert-Smith P, Aziz TZ, Brown P. Tremor suppression by rhythmic transcranial current stimulation. Curr Biol 2013;23(5):436e40. [8] Haubenberger D, Kalowitz D, Nahab FB, Toro C, Ippolito D, Luckenbaugh DA, et al. Validation of digital spiral analysis as outcome parameter for clinical trials in essential tremor. Mov Disord 2011;26(11):2073e80.

Acute and Reproducible Mood Improvement Due to Nucleus Accumbens Deep Brain Stimulation Dear Editors, Deep brain stimulation (DBS) has demonstrated an antidepressant efficacy in patients suffering from treatment-refractory major depressive disorder (MDD), through modulation of brain regions belonging to cortico-subcortical networks involved in mood control [1e5]. However, many aspects of this approach are still under investigation, including the DBS short-term effects and optimal stimulation programming. Here we report very acute, quantified and reproducible mood changes induced by NAcc-DBS in a refractory MDD patient. Mrs M., aged 41, nurse, had been suffering from MDD since 1997. The current MDD episode began in 2003 and was worsening over time, becoming severe and resistant to a combination of psychotherapy, pharmacotherapy and electroconvulsive therapy. She received several antidepressant medications, at recommended doses and durations, with SSRIs, SNRIs, tricyclic agents and MAOI, with no significant efficacy. Augmentation strategies with mood stabilizers and antipsychotic agents were also used without significant clinical improvement. The current MDD episode, lasting for 8 years, was considered as highly treatment-refractory. In 2011, she participated in a DBS trial [6] comparing the efficacy of stimulation of the NAcc and caudate nucleus. At inclusion, the Hamilton Depression Rating Score (HDRS-17) was 24. Bilateral DBS electrodes were implanted stereotactically, allowing to stimulate either the NAcc or the caudate nucleus, depending on the

Letters to the Editor / Brain Stimulation 8 (2015) 838e849

selected contacts. During the trial, chronic stimulation of the NAcc (4 months) or the caudate (4 months), using predefined stimulation parameters (4 V, 130 Hz, 90 ms), did not result in any significant mood change (HDRS-17 respectively 25 and 26). After the end of the study (June 2012, M10), the stimulation voltage was increased to 5 V on the most distal contact of each electrode, located in the NAcc. Within a few hours, these new settings led to a dramatic improvement of the patient’s mood, reaching criteria for clinical remission (HDRS-17 ¼ 3), and remaining stable for 11 months. In May 2013 (M21), she displayed an acute depressive relapse (HDRS-17 ¼ 33), concomitant with the stimulation discontinuation due to battery depletion. After battery replacement, the slow increase of the stimulation amplitude, up to 6 V, and the use of additional contacts (0-1-Cþ) resulted in only mild mood improvement (HRDS-17 ¼ 24). Due to this poor outcome, the patient claimed that the stimulation be switched off (M30). Within the few hours following the stimulation stop, she experienced a rapid mood worsening, confirmed by psychometric assessment (HDRS-17 ¼ 36). Consequently, the stimulation was switched on again, from 0 to 6 V directly, according to the last settings. Within 1 h, she experienced radical changes, with dramatic mood improvement, alleviation of moral pain, disappearance of psychomotor retardation, reappearance of long-lost desires and wishes of social contacts. This acute remission state (HDRS-17 ¼ 3) was maintained for one month, until a new relapse occurred very suddenly (in a few hours delay), once again concomitant with stimulation disruption due to rapid battery depletion. Therefore, a rechargeable device was implanted. The day after the surgery, without stimulation, the psychiatric examination pointed out a frank depressive symptomatology (HDRS-17 ¼ 27). Once again, switching on the stimulator resulted in a very fast mood improvement, the HDRS-17 score improved from 27 to 2 within 2 h. Six months later, this clinical remission was sustained. This case describes acute and reproducible improvements of mood, related to the DBS of the NAcc in a severe and treatmentrefractory MDD patient. Similar acute or very rapid mood changes have been previously described in MDD patients treated by DBS of other targets, including the ventral striatum [4], the subcallosal cingulate gyrus [2] and the medial forebrain bundle [5]. This suggests that such an acute effect is not specific to the NAcc-DBS, but can be induced by the stimulation of several structures belonging to mood control networks. In our case, the amplitude and dynamics of the mood changes were systematically quantified by HDRS-17 assessment. These acute mood changes, observed after DBS initiation and discontinuation, contrast with the usual slow mood improvement observed in MDD patients responding to antidepressant medication, and the delayed mood worsening observed after medication disruption. This suggests that DBS and pharmacological treatments may have different mechanisms of action on mood regulation networks. As the patient was not blind to the stimulation parameters adjustments, a placebo effect cannot be excluded. However this is very unlikely, considering several arguments. No change was observed after the first stimulator replacement and gradual increase of the stimulation amplitude. The depression recurrences occurred twice after stimulation discontinuation due to battery depletion, unknown by the patient. Last, severe and treatment resistant MDD patients are usually less prone to placebo effect [7]. One can hypothesize that NAcceDBS-induced acute mood changes might have been related to hypomania, as already observed after DBS of the sub-thalamic nucleus in Parkinson’s disease patients [8] and in obsessive compulsive disorder patients treated by NAcc-DBS [9]. However clinical assessment of our patient did not reveal hypomanic symptoms. Interestingly, acute mood improvements were only observed when stimulation amplitude was abruptly set to 6 V, whereas

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gradual increase of the stimulation amplitude (using the same stimulation contacts and frequency) did not result in similar clinical improvement. This might suggest that the DBS-related modulation of the neural networks involved in mood control needs to reach rapidly a “threshold” to be efficient, in order to overcome neural processes related with the chronic depressive state. This point has to be considered when programming the stimulation parameters in patients experiencing depression relapse despite continuous stimulation, or after stimulator replacement.

Bruno Giordana Michel Benoit Nelly Darmon Department of Psychiatry, Hopital Pasteur CHU de Nice, 06000 Nice, France Jerome Yelnik CRICM UPMC/INSERM UMR S 975, CNRS UMR 7225 La Salpêtrière Hospital, Paris, France Bruno Millet Service de Psychiatrie adulte, Batiment La Force Hopital Pitié Salpêtrière, 75013 Paris, France Denys Fontaine* Department of Neurosurgery, Hopital Pasteur CHU de Nice, 06000 Nice, France IGCN-EA 7282 (Image-Guided Clinical Neuroscience and Connectomics), UMR 6284 ISIT, UdA Clermont-Ferrand, France * Corresponding

author. Service de Neurochirurgie, Hospital Pasteur, 30 Avenue de la voie romaine, 06000 Nice, France. Tel.: þ33 492038450; fax: þ33 492038528. E-mail address: [email protected] (D. Fontaine) Received 2 April 2015 Available online 10 June 2015

http://dx.doi.org/10.1016/j.brs.2015.05.004

References [1] Lozano A, Mayberg H, Giacobbe P, Hamani C, Craddock R, Kennedy S. Subcallosal cingulate gyrus deep brain stimulation for treatment-resistant depression. Biol Psychiatry 2008;64:461e7. [2] Mayberg H, Lozano A, Voon V, et al. Deep brain stimulation for treatmentresistant depression. Neuron 2005;45:651e60. [3] Malone D, Dougherty D, Rezai A, et al. Deep brain stimulation of the ventral capsule/ventral striatum for treatment-resistant depression. Biol Psychiatry 2009;65:267e75. [4] Schlaepfer T, Cohen M, Frick C, et al. Deep brain stimulation to reward circuitry alleviates anhedonia in refractory major depression. Neuropsychopharmacology 2008;33:368e77. [5] Schlaepfer T, Bewernick B, Kayser S, Madler B, Coenen V. Rapid effects of deep brain stimulation for treatment-resistant major depression. Biol Psychiatry 2013;73:1204e12. [6] Millet B, Jaafari N, Polosan M, et al. Limbic versus cognitive target for deep brain stimulation in treatment-resistant depression: accumbens more promising than caudate. Eur Neuropsychopharmacol 2014;24:1229e39. [7] Schatzberg A, Kraemer H. Use of placebo control groups in evaluating efficacy of treatment of unipolar major depression. Biol Psychiatry 2000;47:736e44. [8] Mallet L, Schupbach M, N’Diaye K, et al. Stimulation of subterritories of the subthalamic nucleus reveals its role in the integration of the emotional and motor aspects of behavior. Proc Natl Acad Sci U S A 2007;104:10661e6. [9] Denys D, Mantione M, Figee M, et al. Deep brain stimulation of the nucleus acccumbens for treatment refractory obsessive compulsive disorder. Arch Gen Psychiatry 2010;67:1061e8.

Acute and Reproducible Mood Improvement Due to Nucleus Accumbens Deep Brain Stimulation.

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