Duloxetine-Induced Subcortical Growth in a Patient With Major Depressive Disorder and Panic Disorder

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Back to table of contents Previous article Next article LettersFull AccessDuloxetine-Induced Subcortical Growth in a Patient With Major Depressive Disorder and Panic DisorderChien-Han Lai, M.D., M.Sc.Chien-Han LaiSearch for more papers by this author, M.D., M.Sc.Published Online:1 Apr 2011AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Duloxetine's role in human subcortical structures is still unclear. Here, we presented a case of major depressive disorder (MDD) with panic disorder (PD) responding to duloxetine treatment. the patient's putamen and brainstem volume increased after 6 weeks of therapy.Case ReportsMr. H is a 38-year-old male patient with a single MDD-with-PD episode for 1 year (Hamilton Rating Scale for Depression [Ham-D]): 43; Panic Disorder Severity Scale [PDSS]: 27). He received the following antidepressant therapy: fluoxetine, venlafaxine, escitalopram, and mirtazapine each for 3–4 months without much improvement (Ham-D lowest score: 35; PDSS lowest score: 23). Because of nonresponse to previous antidepressants, he started to receive duloxetine 30 mg initially with abrupt switching from mirtazapine 60 mg/day (Ham-D: 41; PDSS: 25), and was titrated to 60 mg within 2 weeks without any significant side effects except mild nausea and sedation. After 6 weeks of therapy, his MDD and PD symptoms improved (Ham-D: 20; PDSS: 11). Structural brain MRI scans were obtained with a 3T GE version scanner. Scans with three-dimensional fast spoiled gradient-echo recovery (3D-FSPGR) T1W1 (TR=11.2 msec, TE=5.2 msec, matrix=256 x 256, field of view=260 mm, number of excitation=1, slice thickness=1 mm, 180 slices; no gap) were performed at first visit and 6th-week visit. Structural MRI was processed with FMRIB's Integrated Registration and Segmentation Tool function (FIRST Version 1.2) of FSL (FMRIB Software Library; Version 4.1.1; Oxford, England) to perform subcortical brain segmentation using a shape and appearance model. The volume changes are listed as follows (Table 1).TABLE 1. Subcortical Volume Increase After 6 Weeks of Antidepressant TherapyTABLE 1. Subcortical Volume Increase After 6 Weeks of Antidepressant TherapyEnlarge tableDiscussionSheline has proposed a theory of a limbic-cortical-striatal-pallidal-thalamic circuit (including putamen) in MDD pathogenesis. MDD patients seemed to “over-recruit” a memory system sensitive to negative stimuli, which also includes caudate-putamen areas. They had increased linear-increase activities of putamen with other limbic structures to sad faces.1 PD patients had reduced putamen activation while performing a nondominant hand-motor task, and putamen dysfunction might play a role in PD.2 A comprehensive meta-analysis showed moderate putamen volume reduction in MDD patients.3 Yoo et al.4 reported that PD patients had gray-matter volume decrease, and the reduction severity might be correlated with PD symptom severity. Duloxetine might improve the symptoms of MDD and PD through the growth effects in the putamen. Gorman et al.5 proposed a neuroanatomical “fear network” with projections to the brainstem in PD. This system provides an explanation of conditioned fear response.5 Serotonin transporter binding abnormalities in the brainstem were also observed in MDD patients. This patient's brainstem regeneration after duloxetine treatment might be related to serotonin-reuptake inhibition and serotonin level elevation at the brainstem. From the above findings, a possible role serotonin and norepinephrine reuptake-inhibition could explain “subcortical growth” with duloxetine in this patient with MDD and PD.Dept. of Psychiatry Buddhist Tzu-Chi General Hospital Taipei Branch Taipei, TaiwanInstitute of Brain Science National Yang Ming University Taipei City, TaiwanI thank Dr. Yuan-Yu Hsu (Department of Medical Imaging, Buddhist Tzu-Chi General Hospital Taipei Branch) for MRI acquisition help and technique assistance.1. Surguladze S , Brammer MJ , Keedwell P , et al.: A differential pattern of neural response toward sad versus happy facial expressions in major depressive disorder. Biol Psychiatry 2005; 57:201–209Crossref, Medline, Google Scholar2. Marchand WR , Lee JN , Healy L , et al.: An fMRI motor activation paradigm demonstrates abnormalities of putamen activation in females with panic disorder. J Affect Disord 2009; 116:121–125Crossref, Medline, Google Scholar3. Koolschijn PC , van Haren NE , Lensvelt-Mulders GJ , et al.: Brain volume abnormalities in major depressive disorder: a meta-analysis of magnetic resonance imaging studies. Hum Brain Mapp 2009; 30:3719–3735Crossref, Medline, Google Scholar4. Yoo HK , Kim MJ , Kim SJ , et al.: Putaminal gray matter volume decrease in panic disorder: an optimized voxel-based morphometry study. Eur J Neurosci 2005; 22:2089–2094Crossref, Medline, Google Scholar5. Gorman JM , Kent JM , Sullivan GM , et al.: Neuroanatomical hypothesis of panic disorder, revised. Am J Psychiatry 2000; 157:493–505Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByNone Volume 23Issue 2 Spring 2011Pages E42-E43 Metrics I thank Dr. Yuan-Yu Hsu (Department of Medical Imaging, Buddhist Tzu-Chi General Hospital Taipei Branch) for MRI acquisition help and technique assistance.PDF download History Published online 1 April 2011 Published in print 1 April 2011