2006
DOI: 10.1093/sleep/29.3.307
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The Effect of 2 Sympatholytic Medications—Propranolol and Clonidine—On Sleep Bruxism: Experimental Randomized Controlled Studies

Abstract: Although propranolol did not affect sleep bruxism, clonidine decreased sympathetic tone in the minute preceding the onset of sleep bruxism, thus reducing sleep bruxism by preventing the sequence of autonomic to motor activation of sleep bruxism. This further supports the role of sympathetic activity in the pathophysiology of sleep bruxism. Because morning hypotension was seen in 19% of patients, further dose-dependant research is required to assess the safety of clonidine for the management of sleep bruxism.

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Cited by 98 publications
(96 citation statements)
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“…Although the hypothesis has been formulated that GABA may play a role in SB, any relationship seems to be merely indirect, since GABA is implicated in almost all the neuronal systems that control wakefulness, sleep and motor activity. Its best-known pharmacological analogues, diazepam and clonazepam, produce a reduction of SB, but they also have severe, undesirable collateral effects, such as sleepiness, dizziness and risk of addiction (15). According to the concepts explained above, SB may be divided into primary or idiopathic SB, that is present without any apparent cause, and secondary SB, due to traumatic injuries, diseases or sometimes pharmacological treatments for other diseases, such as Parkinson's disease (iatrogenic bruxism).…”
Section: Etiopathogenesismentioning
confidence: 99%
“…Although the hypothesis has been formulated that GABA may play a role in SB, any relationship seems to be merely indirect, since GABA is implicated in almost all the neuronal systems that control wakefulness, sleep and motor activity. Its best-known pharmacological analogues, diazepam and clonazepam, produce a reduction of SB, but they also have severe, undesirable collateral effects, such as sleepiness, dizziness and risk of addiction (15). According to the concepts explained above, SB may be divided into primary or idiopathic SB, that is present without any apparent cause, and secondary SB, due to traumatic injuries, diseases or sometimes pharmacological treatments for other diseases, such as Parkinson's disease (iatrogenic bruxism).…”
Section: Etiopathogenesismentioning
confidence: 99%
“…8,21 Regarding to the pharmacological treatments, clonidine has a major role, but is associated with secondary adverse effects, demonstrating the necessity for further controlled RCTs with longer follow-up time to verify its real efficacy and safety. 6 Thus, clonazepam becomes a safer alternative and with satisfactory results in the short term. 7,18 It is important to mention here that the clonazepam, like other benzodiazepine drugs, may exacerbate OSAS.…”
Section: Discussionmentioning
confidence: 99%
“…Another drug that also shows good results in the control and management of SB is L-dopa. 11 In relation to amitriptyline, there is no scientific evidence to justify its use in patients with SB, 13,17 same fact occurs with propranolol, 6 tryptophan 3 and bromocriptine. 10 Target of many current studies in the Orofacial Pain investigations, due to its analgesic and antinociceptive properties, botulinum toxin has yet no RCTs analyzing its role in the treatment of SB.…”
Section: Discussionmentioning
confidence: 99%
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“…Bruksizm etiyolojisine ilikin propanolol ve klonidin ile ilgili çalımalar da mevcuttur. Propanolol, non selektif beta bloker, bruksizmde ve buna bağlı ritmik çiğneme kas aktivitesinde anlamlı bir azalmaya sebep olmazken, klonidin, alfa agonist, santral sinir sistemini aktive ederek bruksizmde anlamlı bir oranda azalma sağlar 67,68 .…”
Section: Etiyolojiunclassified