Bruxism Secondary to Chronic Antidopaminergic Drug Exposure

Micheli, Federico; Pardal, Manuel Fernández; Gatto, M. Lo; Asconapé, Jorge J.; Giannaula, Rolando; Parera, Ignacio Casas

doi:10.1097/00002826-199308000-00003

Cited by 70 publications

(35 citation statements)

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“…Interestingly, in SB patients with no medical or psychological disorder or using medication, a controlled study with L-dopa showed a modest (Ϸ 30%) but significant reduction in SB-related motor activity (Lobbezoo et al, 1997a). The specificity of DA in the genesis of SB remains equivocal, because an increase in tooth-grinding was reported in schizophrenic patients treated with a DA antagonist (e.g., haloperidol) (Micheli et al, 1993), and a recent controlled study with a modest DA agonist (e.g., bromocriptine) did not reveal any effect in SB patients (Lavigne et al, 2001d).…”

Section: Sb and Neurochemical Influencesmentioning

confidence: 99%

Neurobiological Mechanisms Involved in Sleep Bruxism

Lavigne

Kato

Kolta

et al. 2003

Critical Reviews in Oral Biology & Medicine

443

290

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Sleep bruxism (SB) is reported by 8% of the adult population and is mainly associated with rhythmic masticatory muscle activity (RMMA) characterized by repetitive jaw muscle contractions (3 bursts or more at a frequency of 1 Hz). The consequences of SB may include tooth destruction, jaw pain, headaches, or the limitation of mandibular movement, as well as tooth-grinding sounds that disrupt the sleep of bed partners. SB is probably an extreme manifestation of a masticatory muscle activity occurring during the sleep of most normal subjects, since RMMA is observed in 60% of normal sleepers in the absence of grinding sounds. The pathophysiology of SB is becoming clearer, and there is an abundance of evidence outlining the neurophysiology and neurochemistry of rhythmic jaw movements (RJM) in relation to chewing, swallowing, and breathing. The sleep literature provides much evidence describing the mechanisms involved in the reduction of muscle tone, from sleep onset to the atonia that characterizes rapid eye movement (REM) sleep. Several brainstem structures (e.g., reticular pontis oralis, pontis caudalis, parvocellularis) and neurochemicals (e.g., serotonin, dopamine, gamma aminobutyric acid [GABA], noradrenaline) are involved in both the genesis of RJM and the modulation of muscle tone during sleep. It remains unknown why a high percentage of normal subjects present RMMA during sleep and why this activity is three times more frequent and higher in amplitude in SB patients. It is also unclear why RMMA during sleep is characterized by co-activation of both jaw-opening and jawclosing muscles instead of the alternating jaw-opening and jaw-closing muscle activity pattern typical of chewing. The final section of this review proposes that RMMA during sleep has a role in lubricating the upper alimentary tract and increasing airway patency. The review concludes with an outline of questions for future research.

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Section: Sb and Neurochemical Influencesmentioning

confidence: 99%

Neurobiological Mechanisms Involved in Sleep Bruxism

Lavigne

Kato

Kolta

et al. 2003

Critical Reviews in Oral Biology & Medicine

443

290

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“…Bruxism on the other hand has been consistently implicated in tooth wear etiology (28,(35)(36)(37). Bruxism is defined as the oral activity characterized by grinding or clenching of teeth without the presence of food (38). The symptoms that confirm the presence of this disease are: grinding noise, pain in jaw muscles, pain in the temporomandibular joint (TMJ), headaches and neck pain.…”

Section: Introductionmentioning

confidence: 99%

Tooth wear among patients suffering from mental disorders

Piccoli¹

2014

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“…It has been reported that benzodiazepines, b-blockers, anticholinergic agents, botulinum toxin, and buspirone can be beneficial in bruxism treatment (Micheli et al 1993;Bader and Lavigne 2000;Winocur et al 2003;Clark and Ram 2007). There is no reliable information on the time range of the onset of medication-induced bruxism.…”

Section: Discussionmentioning

confidence: 99%

“…Substances related to dopaminergic, serotonergic, and adrenergic systems can increase or suppress bruxism activity (Ellison and Stanziani 1993;Micheli et al 1993;Winocur et al 2003). It is thought that atomoxetine's mechanism of action, which improves ADHD symptoms and sustains this effect, functions via very specific inhibition of presynaptic norepinephrine reuptake (Garnock-Jones and Keating 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Bruxism can occur in association with anxiety, benzodiazepines, use of alcohol, or selective serotonin reuptake inhibitors (SSRIs). It is thought that dopamine agonist medications can cause bruxism or worsen preexisting symptoms (Ellison and Stanziani 1993;Micheli et al 1993;Bader and Lavigne 2000;Wise 2001;Winocur et al 2003;Clark and Ram 2007). Bruxism can cause serious damage to tooth enamel, and temporomandibulary articular pain in severe cases (Bader and Lavigne 2000;Clark and Ram 2007).…”

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confidence: 99%

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