SIR: Several case reports have shown that selective serotonin reuptake inhibitors (SSRIs) induced bruxism.1 This letter reports a patient with paroxetine-induced bruxism who was effectively treated with tandospirone, a partial agonist of the 5-hydoxytryptamine (5-HT)1A receptor. Tandospirone is less potent at dopamine D2 receptor than buspirone.2
"Mr. Y," an 81-year-old depressed Japanese man, received a 4-month trial of sulpiride, a common antidepressant medication used in primary care clinics in Japan. Since his depressive symptoms did not improve, he was referred to the psychiatry clinic. At that time, he experienced all nine criteria for major depressive disorder outlined in DSM-IV.3 He agreed to a trial which replaced sulpiride with paroxetine.
A regimen of paroxetine was started with a bedtime dose of 10mg. After 7 days at this dosage with no reported adverse effects, the dosage was increased to 20mg/day. At the 14-day follow-up, depressive symptoms remained, although his mood had improved. The dosage was again increased to 30mg/day. At the 21-day follow-up, his depressive symptoms were under better control. He was very pleased with this treatment. However, he complained of "night-and-day jaw clenching" and "sore jaws and teeth." His wife also witnessed his symptoms. Within a week of adding tandospirone, 10mg p.o. t.i.d., to the regimen, he reported that his jaws no longer clenched and that sore jaws and teeth improved.
This case report shows that the patient developed bruxism after starting on a regimen of paroxetine. It has been postulated that disturbances in the central dopaminergic system, especially within the mesocortical tract, are linked to bruxism.4 SSRI-induced bruxism is considered to be a consequence of serotonergically mediated inhibition of the dopaminergic system. In addition, in this case, elderly age and prior neuroleptic exposure (sulpiride: D2 and D3 antagonist) before starting paroxetine predisposed him to develop bruxism.
It has been reported that buspirone, a partial agonist of the 5-HT1A receptor, ameliorates SSRI-induced bruxism.1,4 This case suggests that tandospirone also improves paroxetine-induced bruxism. Several mechanisms can be considered in explaining why 5-HT1A agonists relieve SSRI-induced bruxism. It has been shown that systematic administration of 5-HT1A receptor agonists increases dopamine release in the prefrontal cortex.5 This effect is considered a major factor in ameliorating bruxism.
The precise mechanism of how 5-HT1A receptors regulate dopamine release is not known; however, several mechanisms have been postulated. Presynaptically, agonist activation of the somatodendritic 5-HT1A autoreceptors in the raphe, which reduces 5-HT cell firing, synthesis, and release of 5-HT, is considered to increase dopaminergic neuron firing in the ventral tegmental area and synaptic release of dopamine in the prefrontal cortex.4 Postsynaptic effects are also suggested since 5-HT1A receptors are localized on nonserotonergic neurons in various brain regions, including the prefrontal cortex. It has been shown that dopamine release is modulated by postsynaptic 5-HT1A receptors in the prefrontal cortex.6
This case adds to the literature by suggesting that SSRI-induced bruxism can be treated with tandospirone, a 5-HT1A receptor agonist.