Romanelli F, Adler D A, Bungay K M
University of Kentucky Medical Center, Lexington 40536, USA.
Ann Pharmacother. 1996 Nov;30(11):1246-8. doi: 10.1177/106002809603001107.
To report the case of a patient with possible paroxetine-induced bruxism that was effectively treated with buspirone.
A 20-year-old woman with no active medical conditions besides acne and no history of dental problems was seen in an outpatient psychiatry clinic for the evaluation of ongoing depression. The patient was prescribed paroxetine 10 mg every morning. After 5 days of therapy the patient reported no adverse effects, and the paroxetine dosage was increased to 20 mg every morning. Due to increased somnolence, the dosing schedule was subsequently changed to 20 mg hs. Two months later during a dental visit for a tooth extraction, the dentist noted that the patient's teeth appeared damaged in what he believed to be a pattern consistent with the grinding and clenching of teeth. Prior to this time, dental examinations had not revealed any tooth damage. The patient was thought to have paroxetine-induced bruxism and, based on earlier case reports, was treated with buspirone 5 mg hs. On day 4 of buspirone therapy the patient reported a significant reduction in the extent of gritting, tooth pain, and jaw tenderness.
The selective serotonin reuptake inhibitors (SSRIs) fluoxetine and sertraline have been associated with bruxism in previous reports. This case suggests paroxetine-induced bruxism. The exact mechanism of SSRI-induced bruxism remains unclear. Many theories have been proposed, including sleep disturbance, serotonergic-mediated inhibition of dopamine manifesting as akathisia, and SSRI-induced anxiety. According to published reports, SSRI-induced bruxism may respond to therapy with buspirone. Consistent with these reports, this patient responded favorably to buspirone therapy.
Clinicians should be aware that the potential for paroxetine-induced bruxism exists and that buspirone may be an appropriate therapeutic intervention.
报告一例可能由帕罗西汀引起磨牙症的患者，该患者使用丁螺环酮治疗有效。
一名20岁女性，除痤疮外无其他活动性疾病，无牙科问题病史，因持续性抑郁在门诊精神科就诊。患者每天早晨服用10毫克帕罗西汀。治疗5天后，患者报告无不良反应，随后帕罗西汀剂量增至每天早晨20毫克。由于嗜睡加重，给药方案随后改为每晚20毫克。两个月后，患者因拔牙就诊牙科时，牙医注意到患者的牙齿出现了他认为与磨牙和紧咬牙一致的损伤模式。在此之前，牙科检查未发现任何牙齿损伤。该患者被认为患有帕罗西汀引起的磨牙症，根据早期病例报告，给予每晚5毫克丁螺环酮治疗。在丁螺环酮治疗的第4天，患者报告磨牙程度、牙痛和颌部压痛明显减轻。
选择性5-羟色胺再摄取抑制剂（SSRI）氟西汀和舍曲林在先前的报告中与磨牙症有关。该病例提示为帕罗西汀引起的磨牙症。SSRI引起磨牙症的确切机制尚不清楚。已提出许多理论，包括睡眠障碍、5-羟色胺介导的多巴胺抑制表现为静坐不能，以及SSRI引起的焦虑。根据已发表的报告，SSRI引起的磨牙症可能对丁螺环酮治疗有反应。与这些报告一致，该患者对丁螺环酮治疗反应良好。
临床医生应意识到存在帕罗西汀引起磨牙症的可能性，丁螺环酮可能是一种合适的治疗干预措施。
