Buspirone in the Treatment of Fluoxetine-Induced Sleep Bruxism

Introduction

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) commonly used in psychiatric disorders such as major depressive disorder, anxiety disorders, and obsessive-compulsive disorder in children and adolescents (Brambilla et al. 2005). It is a highly tolerable drug with low anticholinergic side effects (Wernicke 1985). Common side effects of fluoxetine are tremor, anxiety, sleep problems, and gastrointestinal symptoms, including nausea, diarrhea, weight loss, vomiting, and anorexia (Brambilla et al. 2005). Sleep bruxism is characterized as dysfunctional joint movements, such as clenching and gritting of the teeth during sleep, which lead to problems such as headache, temporomandibulary articular dysfunction, hypertrophy of the masseter muscle, periodontal diseases, and weakening of the teeth (Clark and Ram 2007). Despite the fact that there have been no controlled studies on the relationship between fluoxetine and sleep bruxism, several researchers have reported that fluoxetine can induce sleep bruxism (Ellison and Stanziani 1993; Fitzgerald and Healy 1995). In this study, we present a 7-year-old child with separation anxiety disorder (SAD) who displayed sleep bruxism with fluoxetine treatment that disappeared with buspirone treatment.

Case Report

A 7-year-old boy was referred to our outpatient clinic by his school due to problems adapting to primary school. He described his fear that something would happen to his mother that would prevent her from returning to pick him up. He also complained of headaches and stomachaches in mornings before going to school everyday. His mother had remained at the school all day for 2 months since the term began because her son could not stay at school alone. He had been placed back in kindergarten because of these problems in separating from his mother. However, because he could not comply with the kindergarten for the same problems, he was taken out of the school by his family 2 weeks after admission.

He was diagnosed with SAD based on both his clinical evaluation and the information received from his teachers and family; fluoxetine 15 mg/day was started. At the fourth week of medical treatment, the patient's complaints had improved dramatically, and he was able to attend school alone with only minor anxiety symptoms. However, his mother reported that he had started to grind his teeth for 1–2 hours every night. No nocturnal abnormal movements or daytime dyskinesia involving any other part of the body was noted by his mother. Because his SAD symptoms had improved, the fluoxetine treatment was continued, and buspirone 5 mg three times per day was added based on previous reports of its effectiveness in sleep bruxism (Sabuncuoglu et al. 2009; Yüce et al. 2013). After 5 days of buspirone treatment, a significant reduction in the sleep bruxism was observed, and the family did not note any adverse reactions. By the end of the first month of buspirone treatment, his family reported no bruxism symptoms for the past 3 weeks.

Discussion

Sleep bruxism is a jaw muscle activity that occurs during sleep and is characterized by repeated clenching or grinding of the teeth, which may result in damage to the temporomandibular joint and teeth and also produce headache and facial pain (Lobbezoo et al. 2013). The cause of sleep bruxism is not exactly known and is assumed to have a multifactorial etiology (Shetty et al. 2010). Several cases of drug-induced bruxism have been reported in patients taking antidepressants, sedatives, anxiolytics, and dopamine-related agents (Winocur et al. 2003). Likewise, fluoxetine-induced sleep bruxism has been noted in a number of case reports (Ellison and Stanziani 1993; Sabuncuoglu et al. 2009) in addition to cases associated with other SSRIs (Lobbezoo et al. 2001; Wise 2001; Uca et al. 2015). However, the reports concerning the relationship between fluoxetine and sleep bruxism have only included adult or adolescent cases. In this study, we established the relationship between fluoxetine and sleep bruxism in a child.

Methylphenidate and atomoxetine are commonly used drugs for attention-deficit hyperactivity disorder (ADHD) in childhood and have been reported to cause sleep bruxism in children (Gara and Robert 2000; Mendhekar and Andrea 2008; Mendhekar and Lohıa 2009; Yüce et al. 2013; Sivri and Bilgiç 2015). As in the present case, the addition of buspirone has been found to improve sleep bruxism related to atomoxetine use in a boy with ADHD (Yüce et al. 2013). In addition, adult and adolescent cases have illustrated that buspirone can be effective in the treatment of fluoxetine-induced sleep bruxism as in our case (Ellison and Stanziani 1993; Sabuncuoglu et al. 2009), in contrast to unresponsive cases. (Fitzgerald and Healy 1995). To the best of our knowledge, this is the first report of fluoxetine-related bruxism treated with buspirone in children.

Two opposite hypotheses have been suggested as the neurobiological explanation for bruxism. According to the hypothesis related to dopamine excess, hyperdopaminergic (or hypocholinergic) situations may cause bruxism because of exaggeration of the normal functioning of the jaw muscle (Bostwick and Jaffee 1999). This assumption is based on previous reports that dopaminergic agents (i.e., methylphenidate, l-Dopa) may cause bruxism (Kenneth and Magee 1970; Mendhekar and Andrea 2008). However, other reports indicate that hypodopaminergic medications also cause bruxism, which is in contrast to the hypothesis related to dopamine excess. This assumption suggests that bruxism instead occurs as a result of dopamine depletion when hypodopaminergic agents (i.e., antipsychotics) are administered (Mendhekar and Andrade 2009; Caykoylu et al. 2011). According to this hypothesis, bruxism is a movement disorder—like akathisia—related to a paucity of dopamine in the extrapyramidal system (Bostwick and Jaffee 1999). Previous reports suggest that SSRI-induced bruxism is associated with the dopamine decrease that occurs as a result of increased serotonin levels in the mesocortical track (Falisi et al. 2014), supporting the hypothesis related to dopamine paucity. Buspirone, a 5-HT1A receptor partial agonist in the presynaptic and postsynaptic areas, has been observed to improve both idiopathic and drug-induced bruxism (Ellison and Stanziani 1993; Sabuncuoglu et al. 2009; Orsagh-Yentis et al. 2011; Yüce et al. 2013). It is suggested that because of its partial agonistic activity on the postsynaptic 5-HT1A receptors, competition is created between buspirone and serotonin to bind with the 5-HT1A receptors and results in reduced serotonergic activity, which leads to increased dopaminergic activity (Orsagh-Yentis et al. 2011). This pathway might be responsible for buspirone's effectiveness in SSRI-induced bruxism.

In conclusion, this report suggests that clinicians should be aware of the possibility of fluoxetine-induced bruxism in childhood just as in adulthood. Further systematic studies will be required to establish the relationship between fluoxetine and bruxism and also to clarify the effectiveness of buspirone.