Antidepressant-induced bruxism: need for buspirone?

Abstract

Bruxism is an involuntary grinding of the teeth which can occur during daytime or night. An estimated 85–90% of the population brux at some time during their lives, but it is clinically significant in only 5% of them. In such cases it can result in significant periodontal damage and can produce significant sleep disturbance in the bed partner of the person (Moore et al., 2000). Reports of SSRI-induced bruxism have appeared in the literature (Bostwick and Jaffee, 1999; Ellison and Stanziani, 1993; Wise, 2001). Recently venlafaxine has also been reported to cause bruxism (Jaffee and Bostwick, 2000; Pavlovic, 2004). It has been hypothesized that serotonergic drugs mediate excess-ive serotonergic action on mesocortical neurons arising from the ventral tegmental area leading to dopaminergic deficit which in turn causes akathisia-like movement of jaw muscles leading to bruxism (Bostwick and Jaffee, 1999). Buspirone a partial agonist at 5-HT1A receptors has been found to improve bruxism caused by SSRIs and venlafaxine (Bostwick and Jaffee, 1999; Jaffee and Bostwick, 2000; Pavlovic, 2004). It has been suggested that buspirone-mediated dopaminergic activity in the mesocortical pathway is responsible for an improvement in bruxism (Bostwick and Jaffee, 1999). However, drug-induced movement disorders do respond to reduction in doses of the drugs. It is noteworthy that in none of these reports any attempt to decrease the dose of the culprit antidepressant was made. We hereby report cases of bruxism induced by high dose of escitalopram (first report of escitalopram-induced bruxism) and venlafaxine, who were treated by dose adjustment. Subsequently we discuss the need for buspirone in such cases.