Fluoxetine-Induced Sleep Bruxism Rapidly Treated With Once-Nightly Dosing of Buspirone in a 6-Year-Old Girl.

Fluoxetine is a selective serotonin reuptake inhibitor that is commonly used in children and adolescents. Several reports exist regarding the relationship of fluoxetine use and sleep bruxism. We report the case of a 6-year-old girl who was successfully treated with once-nightly dosing of buspirone for fluoxetine-induced sleep bruxism, which was confirmed with clear on-off-on treatment sequence.

Association between psychotropic medications and presence of sleep bruxism: A systematic review.

The purpose of this study was to systematically review the literature for studies that investigated the association between use of psychotropic medications and presence of sleep bruxism (SB). Observational studies were selected in a two-phase process. Searches were performed on six electronic databases, and a grey literature search was conducted on three databases. SB diagnosis was based on questionnaires or clinical examinations; no polysomnography examinations were performed. Risk of bias was assessed using the Joanna Briggs Institute Critical Appraisal Checklist for Analytical Cross-Sectional Studies. Overall quality of evidence was evaluated according to the Grading of Recommendations Assessment, Development and Evaluation criteria. Five analytical cross-sectional studies were included, evaluating antidepressants, anticonvulsants and psychostimulants. One study was judged as low risk of bias, three as moderate risk and one high risk. Antidepressants were evaluated in adult populations only; duloxetine (Odds Ratio [OR] = 2.16; 95% Confidence Interval [95% CI] = 1.12-4.17), paroxetine (OR = 3.63; 95% CI = 2.15-6.13) and venlafaxine (OR = 2.28; 95% CI = 1.34-3.86) were positively associated with SB risk. No increased odds of SB were observed considering use of citalopram, escitalopram, fluoxetine, mirtazapine and sertraline. With regard to anticonvulsants, only barbiturates were associated with SB in children (OR = 14.70; 95% CI = 1.85-116.90), while no increased odds were observed for benzodiazepine, carbamazepine and valproate. The only psychostimulant evaluated was methylphenidate, and an association with SB was observed in adolescents (OR = 1.67; 95% CI = 1.03-2.68). Findings from this SR suggested that medications such as duloxetine, paroxetine, venlafaxine, barbiturates and methylphenidate might be associated with SB; however, overall quality of evidence was considered very low, and therefore, caution is recommended.

BiteStrip analysis of the effect of fluoxetine and paroxetine on sleep bruxism.

OBJECTIVE: The relationship between sleep bruxism (SB) and selective serotonin reuptake inhibitors (SSRIs) is still under debate because of the lack of well-designed objective studies. The current study investigates possible effects of SSRIs, fluoxetine, and paroxetine on SB in patients with anxiety and depression. MATERIALS AND METHODS: Thirty users of SSRIs for treatment of depression or anxiety were enrolled in the study. After clinical and anamnestic examination, 15 fluoxetine and 15 paroxetine users were included. For an objective evaluation of SB, a single-use disposable home screening device, BiteStrip, was used prior to the first SSRI intake and was repeated on the 7th and 15th days. Patients' self-reported data also were obtained for assessment of patient awareness. RESULTS: BiteStrip scores were significantly higher on the 7th and 15th days than the first measurement (p<0.01). There was an increase in 26 (86.6%) patients' bruxism scores on the 7th day. There was also an increase in 27 (90%) patients' bruxism scores on the 15th day. But according to patients' self-reports, only 6 patients had an awareness that bruxism symptoms were initiated or exacerbated 15days after starting fluoxetine or paroxetine. CONCLUSION: Fluoxetine and paroxetine, SSRIs used for the treatment of anxiety and depression, may initiate or aggravate SB. Clinicians should consider that SSRIs may be the cause of SB when SSRI users are referred to dental clinics for SB symptoms. As there is a shortage of researches on this subject, further studies are necessary to confirm the existence of SSRI-induced SB.

Association between sleep bruxism and alcohol, caffeine, tobacco, and drug abuse: A systematic review.

BACKGROUND: The aim of this systematic review was to answer the focused question, "In adults, is there any association between sleep bruxism (SB) and alcohol, caffeine, tobacco, or drug abuse?" TYPES OF STUDIES REVIEWED: This systematic review included studies in which the investigators assessed SB diagnosis by using questionnaires, clinical assessment, or polysomnography and evaluated its association with alcohol, caffeine, tobacco, or drug abuse. The authors graded SB as possible, probable, or definitive. The authors developed specific search strategies for Latin American and Caribbean Health Sciences Literature, PsycINFO, PubMed, ScienceDirect, and Web of Science. The authors searched the gray literature by using Google Scholar and ProQuest. The authors evaluated the methodological quality of the included studies by using the Meta-Analysis of Statistics Assessment and Review Instrument. RESULTS: From among 818 studies, the authors selected 7 for inclusion in which samples ranged from 51 through 10,229 participants. SB was associated highly with alcohol and tobacco use. In 1 study, the investigators noted a positive and weak association for heavy coffee drinkers. The odds for SB seem to increase almost 2 times for those who drank alcohol, almost 1.5 times for those who drank more than 8 cups of coffee per day, and more than 2 times for those who were current smokers. The abuse of methylenedioxymethamphetamine associated with SB remained without sufficient evidence. CONCLUSIONS AND PRACTICAL IMPLICATIONS: On the basis of limited evidence, SB was associated positively with alcohol, caffeine, and tobacco. The association between the studied drugs could not be discredited; however, there is still a need for stronger evidence based on studies with greater methodological rigor.

Antidepressant-Induced Sleep Bruxism: Prevalence, Incidence, and Related Factors.

OBJECTIVE: The relationship between sleep bruxism and antidepressant drugs in patients remains unclear. In this study, we aimed to investigate the incidence rate of antidepressant-related bruxism and to examine whether antidepressant use is associated with this adverse effect in the patients. METHODS: The study sample was gathered from 2 hospitals. A total of 807 patients who met the inclusion criteria were included in the study. The sample was divided into 2 groups: the antidepressant group (n = 506) and the control group (n = 301). Sleep bruxism was established with reports from the study participants on the basis of the International Classification of Sleep Disorders: Diagnosis and Coding Manual Second Edition. RESULTS: The prevalence of bruxism was significantly higher in the antidepressant group (24.3%) than in the control group (15.3%). The incidence of antidepressant-induced bruxism was 14.0%. The antidepressants most associated with bruxism were paroxetine, venlafaxine, and duloxetine. The patients experiencing antidepressant-induced bruxism had higher age compared with those who did not experience this adverse effect. CONCLUSIONS: The results of the present study suggest that bruxism is frequently observed in women taking antidepressants and that it seems to be associated with antidepressant use at least in some patients.

Duloxetine-induced Sleep Bruxism in Fibromyalgia Successfully Treated With Amitriptyline.

A 44-year-old woman, who was suffering from widespread musculoskeletal pain, fatigue, and sleep disorder, was diagnosed as fibromyalgia. There was no apparent organic disease. Duloxetine therapy was introduced with a dose of 60 mg/day at bedtime. A few days later her husband noted severe teeth clenching and associated loud grinding noises during sleep. Then, duloxetine dosage was reduced to 30 mg/day. The bruxism continued with this dosage, thus the therapy was discontinued. The bruxism resolved after cessation. Three weeks later, duloxetine therapy was restarted at the dosage of 60 mg/day. On the third day of the therapy, bruxism started again and amitriptyline therapy at the dosage of 10 mg/day was added to duloxetine therapy. The dosage of amitriptyline was incrementally adjusted to 25 mg/ day. On the fourth day of the combined therapy, bruxism symptoms improved. Two months later, the bruxism symptoms were resolved and the complaints for fibromyalgia were under control. Although bruxism has been reported due to venlafaxine use, there is only one duloxetine-induced bruxism case in the literature which was treated with buspirone. However, we report duloxetine-induced bruxism treated successfully with amitriptyline in a patient with fibromyalgia. Tricyclic antidepressants have a suppression effect on the REM phase of the sleep cycle; this may help to cease the bruxism symptoms appearing in that phase of the sleep cycle. This is the first reported case of fibromyalgia with duloxetine-induced sleep bruxism successfully treated with amitriptyline.

Psychotropic drugs and bruxism.

INTRODUCTION: Sleep and awake bruxism is defined as 'a parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth'. Some evidence suggests that bruxism may be caused by, or associated with, alterations in the CNS neurotransmission. Several classes of psychotropic drugs interfering with CNS activity may potentially contribute to bruxism. Thus, the purpose of this study was to examine relevant peer-reviewed papers to identify and describe the various classes of psychotropic substances that may cause, exacerbate or reduce bruxism as the result of their pharmacological action in CNS neurons. AREAS COVERED: A literature search from 1980 to the present was performed using PubMed database. The term 'bruxism' was used in association with 'psychotropic', 'dopamine (DA)', 'serotonin', 'histamine', 'antipsychotics', 'antidepressants', 'antihistaminergics' and 'stimulants'. EXPERT OPINION: Studies on the effects of DA agonists (Levo-DOPA, psychostimulants) and antagonists (antipsychotics) identified a central role of DA in the pathogenesis of pharmacologically induced bruxism. Important information from studies on drugs acting on serotonin neurotransmission (antidepressants) was recognized. Other mechanisms involving different neurotransmitters are emerging. This is the case of antihistaminergic drugs which may induce bruxism as a consequence of their disinhibitory effect on the serotonergic system.

Ketotifen-induced nocturnal bruxism.

UNLABELLED: Nocturnal bruxism is a common oromandibular movement disorder highly prevalent in children, but its pathophysiological mechanism has not been fully explained. Iatrogenic sleep bruxism has been described following treatment with several psychotropic medications. However, no case of antihistamine-induced bruxism has been reported to date. Herein, we describe a 4-year-old child who experienced nocturnal bruxism during treatment for bronchospasm and rhinitis with the antihistamine ketotifen. Drug rechallenge was also performed. CONCLUSION: The present case adds useful information to our knowledge of bruxism. Complex and poorly understood interactions between multiple central nervous system neurotransmitters, such as histamine, serotonin, and dopamine, are involved.

Legal psychoactive substances as risk factors for sleep-related bruxism: a nationwide Finnish Twin Cohort study.

AIMS: Different psychoactive factors including alcohol, coffee and tobacco, are considered as risk factors for bruxism. Often, heavy drinking and generous intake of coffee are correlated with smoking. Interactions between these agents may confound studies. The aim was to investigate the possible independent effects of drinking alcohol and coffee consumption on the occurrence of bruxism. METHODS: Data derived from the Finnish Twin Cohort study consisting of 12,502 twin individuals (45.6% men, 54.4% women, mean age 44 years) born during the 1930-1957. The twins responded to a questionnaire sent in 1990 (response rate of 77%) consisting of 103 multiple-choice questions, seven dealing with tobacco use, four on alcohol use, one about coffee consumption and two with bruxism. RESULTS: Increasing alcohol intake raised the risk for weekly bruxism even when adjusted for smoking status [heavy drinking odds ratio (OR) 1.9; 95% CI 1.23-2.84, binge drinking OR 1.6; 95% CI 1.28-2.12, and passing-out due to excessive alcohol intoxication at least twice within the previous year OR 1.5; 95% CI 1.09-2.18]. The situation was similar to that for coffee consumption of more than eight cups per day (OR 1.4; 95% CI 1.01-1.98). Interaction analyses for 'smoking with risk factors' revealed no statistically significant interactions. Current smoking was an independent risk factor for bruxism in all models (OR 2.3-2.7). CONCLUSION: Given the observed associations between alcohol drinking, binge drinking, passing-out due to excessive alcohol intake and coffee consumption, the results support our hypothesis of an independent association of both alcohol use, and coffee consumption with bruxism.