Use of buspirone in selective serotonin reuptake inhibitor-induced sleep bruxism

Abstract

Sleep bruxism is characterized by the involuntary clenching or grinding of the teeth during sleep and can cause severe health problems, including the destruction of tooth structure, temporo-mandibular joint dysfunction, myofascial pain, and severe sleep disturbances. Iatrogenic sleep bruxism may be common during treatment with psychotropic medications, such as anti-psychotics and antidepressants, especially selective serotonin reuptake inhibitors (SSRIs). Bruxism is a common movement disorder that affects 8–21% of the population. The majority of bruxism symptoms are mild or moderate, although rare but severe cases may lead to serious periodontal damage, temporo-mandibular dysfunction, sleep disturbances, jaw pain, and stiffness. As a result, such cases must be treated with medication. It has been hypothesized that the mechanism of SSRI-induced bruxism may involve excessive serotonergic action on the meso-cortical neurons arising from the ventral tegmental area. It has been argued that,the addition of buspirone, was necessitated by the high level of residual anxiety. As a result, these symptoms may have been prevented through the use of buspirone alone. Buspirone, is an agonist of the 5-HT1A receptor that increases dopaminergic neuron, firing in the ventral tegmental area and increases the synaptic release of dopamine in the prefrontal cortex. These effects ameliorate drug-induced bruxism. Buspirone can also ameliorate extrapyramidal side effects, such as akathisia and tardive dyskinesia, and this property may be an additional explanation for the bruxism-related effects of the drug. Furthermore, buspirone may be an effective treatment for the bruxism associated with the use of these medications.

Disclosure of interest

The authors have not supplied their declaration of competing interest.