Tiagabine May Reduce Bruxism and Associated Temporomandibular Joint Pain
Abstract
Tiagabine is an anticonvulsant gamma-aminobutyric acid reuptake inhibitor commonly used as an add-on treatment of refractory partial seizures in persons over 12 years old. Four of the 5 cases reported here indicate that tiagabine might also be remarkably effective in suppressing nocturnal bruxism, trismus, and consequent morning pain in the teeth, masticatory musculature, jaw, and temporomandibular joint areas. Tiagabine has a benign adverse-effect profile, is easily tolerated, and retains effectiveness over time. Bed partners of these patients report that grinding noises have stopped; therefore, the tiagabine effect is probably not simply antinociceptive. The doses used to suppress nocturnal bruxism at bedtime (4–8 mg) are lower than those used to treat seizures.
Bruxism is the jaw clenching or grinding of teeth that usually occurs during sleep.1–5 It is synonymous with trismus when referring to tonic jaw clenching, and considerable jaw pain and tooth ischemic pain in particular can be generated by this form. Lifetime occurrence of at least some orofacial pain from a night of bruxing or daytime episodes of clenching or grinding, particularly at a time of unusual stress, approaches 100%. Point prevalence is estimated at 5–10% of the adult population,5,6 and a minority of these individuals develop consequent temporomandibular joint (TMJ) or orofacial pain syndromes, excessive tooth wear, or tooth fracture.7,8
Rhythmic nocturnal masticatory muscle activity in bursts of 3–5 at 1 Hz, with occlusal force generated between 3 and 80 N (N ≈ 100 g), is commonly seen. The relationship between the rhythmic and the tonic forms of bruxism is unclear, but both forms cause pain.2 Sleep bruxism is thought to occur during microarousals or arousal transients.1,6,9 Pain, TMJ structural damage, tooth damage, and nonrestorative sleep are serious consequences of bruxism for some patients and are poorly controlled by current treatments. Better bruxism treatments are needed.
Not only is bruxism more commonly a problem in individuals with depression and anxiety disorders, but also the medicines used to treat anxiety and depression can themselves often create a new iatrogenic or worsen a preexisting bruxism even when they successfully treat the target psychiatric problem.10 Bruxism is more common in cerebral palsy, Down syndrome, autism, and other developmentally delayed or intellectually impaired populations. For unknown reasons, bruxism is a common mammalian response to stress; for example, rats also experience sleep bruxism during periods of stress.11
Ascription of bruxism to malocclusion and other peripheral afferent stimuli is now considered to be incorrect. Current data indicate that central primary efferents are the common and prominent drivers of bruxism.1,3,5,7,12–14 For example, heart rate increases are seen just before initiation of jaw musculature contractions of a bruxism bout, and cortical electroencephalogram activity increases 4 seconds before bruxism onset.2 The finding of reduced slow-wave sleep (stage III–VI) in bruxism13 and its occurrence during microarousals from sleep may be relevant to tiagabine's salutary effects, as discussed below.1,5,9