Buspirone as an antidote to SSRI-induced bruxism in 4 cases

One hypothesis to explain selective serotonin reuptake inhibitor (SSRI)-induced bruxism states that SSRIs increase extrapyramidal serotonin levels, thereby inhibiting dopaminergic pathways controlling movement. Previous reports have emphasized buspirone's postsynaptic dopaminergic effect as a partial antidote to the suppressed dopamine levels.

Four patients, recently started on treatment with the SSRI sertraline, presented with new-onset complaints attributable to SSRI-induced bruxism. All 4 responded to adjunctive buspirone, a serotonin-1A (5-HT1A) receptor agonist, with relief of bruxism and associated symptoms.

We expand the hypothesis put forth in previous reports by proposing that buspirone is not only acting postsynaptically in the extrapyramidal system, but also presynaptically on serotonergic neurons that influence masticatory modulation in the mesocortical tract. Our 4 cases support the concept of buspirone acting as a full agonist at the presynaptic 5-HT1A somatodendritic receptors located on the cell bodies of raphe serotonergic neurons that project to the ventral tegmental area (VTA) of the midbrain. These serotonergic neurons modulate the firing of the mesocortical tract, which itself projects from the VTA to the prefrontal cortex and acts on masticatory muscle activity through inhibiting spontaneous movements such as bruxism. While the literature is confusing and contradictory on definitions of bruxism and etiologies of incompletely understood movement disorders, we believe SSRI-induced bruxism is best conceptualized as a form of akathisia.