Venlafaxine-associated nocturnal bruxism in a depressive patient successfully treated with buspirone

Bruxism, which is characterized by clenching and/or grinding of the dentition, is a common condition affecting approximately 8-21% of the population. It may be common during therapy with psychotropic medications, including antipsychotics and antidepressants. Bruxism associated with drugs can be destructive, resulting in severe consequences to health that include destruction of tooth structure, irreversible harm to the temporomandibular joint, severe myofascial pain, and muscle contraction headaches (Winocur, et al., 2003). Although selective serotonin reuptake inhibitor (SSRI)-associated bruxism has often been described in the literature (Gerber and Lynd, 1998; Winocur, et al., 2003), to our knowledge there are only two case reports describing venlafaxine-induced bruxism (Jaffee and Bostwick 2000; Brown and Hong, 1999). Here, we report a case of nocturnal bruxism likely induced by the antidepressant venlafaxine and successfully treated with buspirone. Mrs G was a 31-year-old separated woman with a primary school education admitted to our inpatient clinic. Upon examination, she was found to suffer from severe pervasive sadness, anhedonia, insomnia, moderate psychomotor retardation, feelings of worthlessness, distractibility, occasional passive suicidal ideation and decreased energy, concentration and self-esteem. She experienced these symptoms on most days and nearly every day during the month before admission. She stayed in bed most of the time, rarely took care of herself, and could not work at all. She had no personal history of substance abuse and no family history of mental illness. In addition, the patient started smoking cigarettes at an age of 25 and smoked 20 cigarettes per day. Also, she had not stopped smoking after being admitted into the hospital. She was diagnosed with major depressive disorder based on the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (Text Revision) (DSMIV-TR) (American Psychiatric Association, 2000). Initially, her 17-item Hamilton Depression Rating Scale (HAM-D) (Hamilton, 1960) total score was 27. Subsequently, extendedrelease (XR) venlafaxine was started at a dosage of 37.5 mg/day, which was titrated up to 150 mg/day. After a week of treatment with venlafaxine, she reported severe nocturnal bruxism. Her complaints included masseter tightness, headaches, tooth pain, and nocturnal tooth grinding. Her roommates reported loud nocturnal grinding noises. All the laboratory investigations were in the normal range and all the potential organic contributors to depression and to bruxism were excluded. In the past three years, she had two depressive episodes that required the use of antidepressant medications, including escitalopram (10 mg/day) and fluoxetine (20 mg/day). The patient and her family reported nocturnal bruxism symptoms associated with both of these medications. In addition, the patient indicated that her bruxism symptoms were similar to those she experienced with previous antidepressant medications, including escitalopram and fluoxetine. In an attempt to control the bruxism, clonazepam was initiated at a dose of 2 mg/day. At the end of the third week after hospitalization, there was no improvement in her bruxism, although her depressive symptoms partially remitted. Subsequently, clonezapam was gradually stopped, and buspirone was started at a dose of 10 mg/day, which was increased to 20 mg/day. She reported full resolution of headaches and bruxism within 10 days of the initiation of buspirone. At the fifth week after hospitalization, there was significant improvement of both depressive symptoms and bruxism symptoms. The patient’s total score on the HAM-D on the last week of admission was 5. Also, during the follow-up, there was no further appearance of nocturnal bruxism with venlafaxine and buspirone treatment. The neurochemical mechanisms underlying bruxism are little understood at present. Recent pharmacologic evidence suggests that the central dopaminergic system, especially within the mesocortical tract, may be involved in the pathophysiology Letter to the Editors