Cases reported "Sleep Bruxism"

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1/9. Idiopathic myoclonus in the oromandibular region during sleep: a possible source of confusion in sleep bruxism diagnosis.

    As part of a larger study, polysomnographic and audiovisual data were recorded over 2 nights in 41 subjects with a clinical diagnosis of sleep bruxism (SB). Electromyographic (EMG) events related to SB were scored according to standard criteria (Lavigne et al. J Dent Res 1996;75:546-552). Post hoc analysis revealed that rapid shock-like contractions with the characteristics of myoclonus in the jaw muscles were observed in four subjects. EMG bursts characterized as myoclonus were significantly shorter in duration than bursts classified as SB. None of the subjects had any history of myoclonus while awake. Myoclonic episodes were more frequent in sleep stages 1 and 2 than in REM. Half of the episodes contained one or two contractions whereas the other half had three or more repetitive contractions. SB and myoclonus coexisted in one subject. To rule out sleep epilepsy, full electroencephalogram montage was done in three subjects and no epileptic spikes were noted. Our results suggest that approximately 10% of subjects clinically diagnosed as SB could present oromandibular myoclonus during sleep. ( info)

2/9. A vibratory stimulation-based inhibition system for nocturnal bruxism: a clinical report.

    For the single subject tested to date, the bruxism-contingent vibratory-feedback system for occlusal appliances effectively inhibited bruxism without inducing substantial sleep disturbance. Whether the reduction in bruxism would continue if the device no longer provided feedback and whether the force levels applied are optimal to induce suppression remain to be determined. ( info)

3/9. Polysomnographic assessment of spells in sleep: nocturnal seizures versus parasomnias.

    A dilemma can arise when attempting to distinguish a nocturnal seizure from a parasomnia because both phenomena can be characterized by a general increase in motor and autonomic activity with a transient reduction in the level of consciousness. An additional problem is that an accurate clinical diagnosis generally relies heavily on a detailed history. As sleep related disorders occur at a time when the patient is not fully cognizant, polysomnographic analysis can on occasion supplement for the intrinsic paucity of detailed history. Simultaneously, correlating the clinical and polysomnographic analysis immediately prior to, during, and following an event of interest, can be helpful in differentiating nocturnal seizures from parasomnias. ( info)

4/9. Familial nocturnal facio-mandibular myoclonus mimicking sleep bruxism.

    A mother and son presented with a multi-decade history of nocturnal tongue biting and bleeding. In both patients, video polysomnographic recordings documented bursts of electromyographic activity originating in the masseter and spreading to orbicularis oris and oculi muscles, present only during sleep. Faciomandibular myoclonic activity during sleep mimics sleep bruxism and may be familial. ( info)

5/9. Use of the Calmset 3 biofeedback/relaxation system in the assessment and treatment of chronic nocturnal bruxism.

    Biofeedback and nocturnal alarms using electromyographic (EMG) activity of the masseter muscles have often been used to treat nocturnal bruxism. However, although use of EMG activated nocturnal alarms has been successful, the clinical utility of the devices reported in the literature to date is questionable. For instance, many of the devices are cumbersome and specifically designed and constructed by the investigators. Hence, the purpose of the present investigation was to test the clinical utility of the Calmset (Thought technology Limited, Montreal, canada), a commercially available, user-friendly, compact, and portable EMG biofeedback instrument that may be used as an EMG activated nocturnal alarm. To meet this objective, the Calmset was used both to facilitate assessment and to treat an individual with chronic nocturnal bruxism. The results indicated that the patient exhibited fewer bruxing episodes following treatment and that treatment gains were maintained 6 months following termination of treatment. Advantages and disadvantages of using the Calmset are discussed. ( info)

6/9. A proposed mechanism for diurnal/nocturnal bruxism: hypersensitivity of presynaptic dopamine receptors in the frontal lobe.

    There are many reports in the literature concerning nocturnal bruxism, however, diurnal (non-sleep)/nocturnal bruxism is rarely mentioned. We report three patients with diurnal/nocturnal bruxism. They differed from the usual features of nocturnal bruxism in hypoperfusion of the left frontal lobe, a poor response to l-dopa or bromocriptine therapy and a favourable response to metoclopramide. Hypersensitive presynaptic dopamine receptors may be the underlying pathology responsible for this type of bruxism. Regional differences in dopamine receptor pharmacology may explain the perplexing relationship of bruxism to both hyper- and hypo-dopaminergic states. ( info)

7/9. Tiagabine may reduce bruxism and associated temporomandibular joint pain.

    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. ( info)

8/9. Bruxism in children: a warning sign for psychological problems.

    Bruxism is nonfunctional clenching or grinding of the teeth. It is a destructive habit that may result in tooth wear. Although research on bruxism is extensive, its etiology remains debatable. The literature suggests that bruxism is correlated with both experienced and anticipated life stress. The purpose of this report is to describe 2 cases of severe bruxism in children of similar age with different life histories and to discuss the factors that could have triggered this parafunctional condition. ( info)

9/9. Bilateral temporalis muscle hypertrophy: a case report.

    Although masseteric hypertrophy is common and can be accompanied by temporalis hypertrophy, temporalis hypertrophy by itself is an exceptional finding. A patient, a chronic bruxer who was receiving psychiatric care and psychotherapeutic medications, complained of moderate discomfort and swelling in both temporal areas. It is believed that the patient's long-term stress-related sleeping problem was causing her bruxism. Of great interest was the fact that chronic bruxing had resulted in the rare occurrence of temporalis muscle hypertrophy without a coexisting masseteric hypertrophy. ( info)


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