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A case of venlafaxine-induced bruxism alleviated by duloxetine substitution
Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (2011) 307
Contents lists available at ScienceDirect
Progress in Neuro-Psychopharmacology & Biological Psychiatry j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p n p
Letter to the Editor (Case report) A case of venlafaxine-induced bruxism alleviated by duloxetine substitution Sir: Bruxism, characterized by clenching and/or grinding of dentition, is a common condition affecting 8–21% of the population (Attansio, 1997). Selective serotonin reuptake inhibitors (SSRIs) have been the most commonly reported antidepressant agents to cause bruxism and distress patients' lives (Winocur et al., 2003). The serotonin–norepinephrine reuptake inhibitor (SNRI) venlafaxine, but not duloxetine, has also been reported to be associated with bruxism in sporadic cases (Alonso-Navarro et al., 2009; Jaffee and Bostwick, 2000; Brown and Hong, 1999; Kuloglu et al., 2010). To our knowledge, there has been no report on relieving bruxism symptoms with an SNRI substitution. Mrs. A, 72-year-old married woman without any previous personal or familial history of movement disorders, was diagnosed with major depressive disorder 2.5 years ago. She had a full remission from depression under venlafaxine 75 mg/day for 2 years. Six months ago, she had a relapse of depression with severe anxiety, low mood, easily tearing, negative thinking, nihilistic delusions, and suicidal ideation for 2 weeks and then received a titrated dose of venlafaxine to 150 mg/day. She had a partial remission but developed bruxism with clenching and grinding the teeth and worsened anxiety. Blood count, biochemistry, and thyroid functions were normal, and brain CT showed only age-related brain atrophy. SNRI-induced bruxism was suspected and venlafaxine 150 mg/day was shifted to duloxetine 30 mg/day to prevent a relapse of depression. Her bruxism improved gradually and disappeared 3 weeks later after switching to duloxetine. She had remained free from depressive symptoms and bruxism in the following 6 months. The mechanism for SNRI-induced bruxism may be due to disrupted serotonergic modulation of dopaminergic neurons in the mesocortical tract, which plays a role of controlling muscular or motor activity (Kishi, 2007). Our patient developed typical bruxism 3 weeks after treatment of venlafaxine 150 mg/day, while bruxism gradually disappeared within 3 weeks after a substitution with duloxetine. Although the improvement of bruxism with duloxetine substitution could not rule out the possibility of spontaneous amelioration over time after discontinuing venlafaxine, the observed benefit of duloxetine in this case might still be associated with a relatively lower affinity for serotonin reuptake in duloxetine as compared to venlafaxine (Montgomery, 2010). However, the controlled trials of duloxetine in patients with iatrogenic and idiopathic bruxism are needed to substantiate this anecdotal observation. References Alonso-Navarro H, Prietu MM, Ruiz-Ezquerro JJ, Jimenez-Jimenez FJ. Bruxism possibly induced by venlafaxine. Clin Neuropharmacol 2009;32:111–2. Attansio R. An overview of bruxism and its management. Dent Clin North Am 1997;41: 229–41.
0278-5846/$ – see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.pnpbp.2010.11.025
Brown ES, Hong SC. Antidepressant-induced bruxism successfully treated with gabapentin. J Am Dent Assoc 1999;130:1467–9. Jaffee MS, Bostwick JM. Buspirone as an antidote to venlafaxine-induced bruxism. Psychosomatics 2000;41:535–6. Kishi Y. Paroxetine-induced bruxism effectively treated with tandospirone. J Neuropsychiatry Clin Neurosci 2007;19:90–1. Kuloglu M, Ekinci O, Caykoylu A. Venlafaxine-associated nocturnal bruxism in a depressive patient successfully treated with buspirone. J Psychopharmacol 2010;24:627–8. Montgomery SA. Tolerability of serotonin norepinephrine reuptake inhibitor antidepressants. CNS Spectr 2010;2008:27–33. Winocur E, Gavish A, Voikovitch M, Emodi-Perlman A, Eli I. Drugs and bruxism: a critical review. J Orofac Pain 2003;17:99-111.
Jane Pei-Chen Chang Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan Graduate Institute of Clinical Medical Science College of Medicine, China Medical University & Hospital, Taichung, Taiwan Chia-Cheng Wu Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan China Medical University Beigang Hospital, China Medical University & Hospital, Taichung, Taiwan Kuan-Pin Su Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan Graduate Institute of Clinical Medical Science College of Medicine, China Medical University & Hospital, Taichung, Taiwan Corresponding author. Department of Psychiatry, China Medical University Hospital, No.2 Yuh-Der Road, Taichung 404, Taiwan. Tel.: +886 4 22052121x1074. E-mail address: [email protected].
29 September 2010
Contents lists available at ScienceDirect
Progress in Neuro-Psychopharmacology & Biological Psychiatry j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p n p
Letter to the Editor (Case report) A case of venlafaxine-induced bruxism alleviated by duloxetine substitution Sir: Bruxism, characterized by clenching and/or grinding of dentition, is a common condition affecting 8–21% of the population (Attansio, 1997). Selective serotonin reuptake inhibitors (SSRIs) have been the most commonly reported antidepressant agents to cause bruxism and distress patients' lives (Winocur et al., 2003). The serotonin–norepinephrine reuptake inhibitor (SNRI) venlafaxine, but not duloxetine, has also been reported to be associated with bruxism in sporadic cases (Alonso-Navarro et al., 2009; Jaffee and Bostwick, 2000; Brown and Hong, 1999; Kuloglu et al., 2010). To our knowledge, there has been no report on relieving bruxism symptoms with an SNRI substitution. Mrs. A, 72-year-old married woman without any previous personal or familial history of movement disorders, was diagnosed with major depressive disorder 2.5 years ago. She had a full remission from depression under venlafaxine 75 mg/day for 2 years. Six months ago, she had a relapse of depression with severe anxiety, low mood, easily tearing, negative thinking, nihilistic delusions, and suicidal ideation for 2 weeks and then received a titrated dose of venlafaxine to 150 mg/day. She had a partial remission but developed bruxism with clenching and grinding the teeth and worsened anxiety. Blood count, biochemistry, and thyroid functions were normal, and brain CT showed only age-related brain atrophy. SNRI-induced bruxism was suspected and venlafaxine 150 mg/day was shifted to duloxetine 30 mg/day to prevent a relapse of depression. Her bruxism improved gradually and disappeared 3 weeks later after switching to duloxetine. She had remained free from depressive symptoms and bruxism in the following 6 months. The mechanism for SNRI-induced bruxism may be due to disrupted serotonergic modulation of dopaminergic neurons in the mesocortical tract, which plays a role of controlling muscular or motor activity (Kishi, 2007). Our patient developed typical bruxism 3 weeks after treatment of venlafaxine 150 mg/day, while bruxism gradually disappeared within 3 weeks after a substitution with duloxetine. Although the improvement of bruxism with duloxetine substitution could not rule out the possibility of spontaneous amelioration over time after discontinuing venlafaxine, the observed benefit of duloxetine in this case might still be associated with a relatively lower affinity for serotonin reuptake in duloxetine as compared to venlafaxine (Montgomery, 2010). However, the controlled trials of duloxetine in patients with iatrogenic and idiopathic bruxism are needed to substantiate this anecdotal observation. References Alonso-Navarro H, Prietu MM, Ruiz-Ezquerro JJ, Jimenez-Jimenez FJ. Bruxism possibly induced by venlafaxine. Clin Neuropharmacol 2009;32:111–2. Attansio R. An overview of bruxism and its management. Dent Clin North Am 1997;41: 229–41.
0278-5846/$ – see front matter © 2010 Elsevier Inc. All rights reserved. doi:10.1016/j.pnpbp.2010.11.025
Brown ES, Hong SC. Antidepressant-induced bruxism successfully treated with gabapentin. J Am Dent Assoc 1999;130:1467–9. Jaffee MS, Bostwick JM. Buspirone as an antidote to venlafaxine-induced bruxism. Psychosomatics 2000;41:535–6. Kishi Y. Paroxetine-induced bruxism effectively treated with tandospirone. J Neuropsychiatry Clin Neurosci 2007;19:90–1. Kuloglu M, Ekinci O, Caykoylu A. Venlafaxine-associated nocturnal bruxism in a depressive patient successfully treated with buspirone. J Psychopharmacol 2010;24:627–8. Montgomery SA. Tolerability of serotonin norepinephrine reuptake inhibitor antidepressants. CNS Spectr 2010;2008:27–33. Winocur E, Gavish A, Voikovitch M, Emodi-Perlman A, Eli I. Drugs and bruxism: a critical review. J Orofac Pain 2003;17:99-111.
Jane Pei-Chen Chang Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan Graduate Institute of Clinical Medical Science College of Medicine, China Medical University & Hospital, Taichung, Taiwan Chia-Cheng Wu Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan China Medical University Beigang Hospital, China Medical University & Hospital, Taichung, Taiwan Kuan-Pin Su Department of Psychiatry, China Medical University & Hospital, Taichung, Taiwan Graduate Institute of Clinical Medical Science College of Medicine, China Medical University & Hospital, Taichung, Taiwan Corresponding author. Department of Psychiatry, China Medical University Hospital, No.2 Yuh-Der Road, Taichung 404, Taiwan. Tel.: +886 4 22052121x1074. E-mail address: [email protected].
29 September 2010