• Journal of Dental Rehabilitation and Applied Science
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• v.28 no.1
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• pp.87-101
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• 2012

Bruxism is extensively defined as a diurnal or nocturnal parafunctional habit of tooth clenching or grinding. The etiology of bruxism may be categorized as central factors or peripheral factors and according to previous research results, central factors are assumed to be the main cause. Bruxism may cause tooth attrition, cervical abfraction, masseter hypertrophy, masseter or temporalis muscle pain, temporomandibular joint arthralgia, trismus, tooth or restoration fracture, pulpitis, trauma from occlusion and clenching in particularly may cause linea alba, buccal mucosa or tongue ridging. An oral appliance, electromyogram or polysomnogram is used as a tool for diagnosis and the American Sleep Disorders Association has proposed a clinical criteria. However the exact etiology of bruxism is yet controversial and the selection of treatment should be done with caution. When the rate of bruxism is moderate or greater and is accompanied with clinical symptoms and signs, treatment such as control of dangerous factors, use of an oral appliance, botulinum toxin injection, pharmacologic therapy and biofeedback therapy may be considered. So far, oral appliance treatment is known to be the most rational choice for bruxism treatment. For patients in need of esthetic correction of hypertrophic masseters, as well as bruxism treatment, botulinum toxin injection may be a choice.

• Sleep Medicine and Psychophysiology
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• v.4 no.2
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• pp.164-171
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• 1997

Introduction : Periodic limb movement disorder (PLMD) is shown to common in patients with OSA and may become evident or worsened when treated with nasal continuous positive airway pressure (CPAP). Whether this is due to im proved sleep continuity. adverse nocturnal body positioning, uncovered by CPAP, or due to the CPAP stimulus is still debat-ed. We hypothesized that the increase in PLM activity following CPAP is associated with more supine-sleeping tendencies when being treated with CPAP. In the present work, we compared differences in the PLMD index (PLMI) and sleeping position of patients with sleep disordered breathing before and after CPAP treatment. Method : We studied 16 patients (mean age 46 yr, 9M, 7F) with OSA (11 patients) or UARS (5 patients) who either had PLMD on initial polysomnogram (baseline PSG) or on nasal CPAP trial (CPAP PSG). All periodic leg movements were scored on anterior tibialis EMG during sleep according to standard criteria (net duration; 0.5-5.0 seconds, intervals; 4-90 seconds. 4 consecutive movements). Paired t-tests compared PLMD index (PLMI), PLMD-related arousal index (PLMD-ArI), respiratory disturbance index (RDI), and supine sleeping position spent with baseline PSG and CPAP PSG. Results : Ten patients (63%) on baseline PSG and fifteen patients (94%) on CPAP PSG had documented PLMD ($PLMI{\ge}5$) respectively with significant increase on CPAP PSG(p<0.05). Ten patients showed the emergence (6/10 patients) or substantial worsening (4/10 patients) of PLMD during CPAP trial. Mean CPAP pressure was $7.6{\pm}1.8\;cmH_2O$. PLMI tended to increase from baseline PSG to CPAP PSG, and significantly increase when excluding 2 outlier (baseline PSG, $19.0{\pm}25.8/hr$ vs CPAP PSG, $29.9{\pm}12.5/hr$, p<0.1). PLMD-ArI showed no significant change, but a significant decrease was detected when excluding 2 outlier (p<0.1). There was no significant sleeping positional difference (supine vs non-supine) on baseline PSG, but significantly more supine position (supine vs non-supine, p<0.05) on CPAP PSG. There was no significant difference in PLMI during supine-sleeping and nonsupine-sleeping position on both of baseline PSG and CPAP PSG. There was also no significant difference in PLMI during supine-sleeping position between baseline PSG and CPAP PSG. With nasal CPAP, there was a highly significant reduction in the RDI (baseline PSG, $14.1{\pm}21.3/hr$ vs CPAP PSG, $2.7{\pm}3.9/hr$, p<0.05). Conclusion : This preliminary data confirms previous findings that CPAP is a very effective treatment for OSA, and that PLMD is developed or worsened with treatment by CPAP. This data also indicates that supine-sleeping position is more common when being treated with CPAP. However, there was no clear evidence that supine position is the causal factor of increased PLMD with CPAP. It is, however, suggested that the relative movement limitation induced by CPAP treatment could be a contributory factor of PLMD.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.590-596
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• 2001

The hallmarks of sleep apnea syndrome include daytime hypersomnolence, snoring, obesity, disturbed nocturnal sleep, and apneic episodes. Thyroid deficiency states are now a well recognized cause of sleep apnea. Central, obstructive, and mixed patterns of sleep apnea may be observed in hypothyroidism. A-33-yr-old man was admitted complaining of daytime hypersomnolence, snoring, sleep apnea and obesity. A polysomnogram showed obstructive pattern of sleep apnea syndrome. Physical examination and hormonal study revealed a narrowing of the upper airway and primary hypothyroidism. Dilated cardiomyopathy was diagnosed by echocardiogram. The poctients was treated for obstructive sleep apnea syndrome with nasal continuous positive airway pressure(CPAP) for 2 months and the underlying hypothyroidism with thyroid hormone therapy. This successfully controlled the snoring, sleep apnea, and other apnea-related symptoms. Here, we describe our experience of nasal CP AP and thyroid hormone therapy in a patient with primary hypothyroidism associated with obstructive sleep apnea syndrome and dilated cardiomyopathy with review of the relevant literature.

• Sleep Medicine and Psychophysiology
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• v.9 no.1
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• pp.48-55
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• 2002

Objective: Stress is known to be a common cause of short-term insomnia and insomniacs often complain that stress induces sleep problems. However, previous studies on the correlation between stress and sleep do not show consistent results. We aimed to investigate the effects of minor stressful events on sleep among college students. Method: Physically and mentally healthy college student volunteers filled out a self-assessment questionnaire to evaluate their stress and sleep. To find out the status of average stress and sleep, the volunteers filled out K-DSI and daily sleep assessments on three consecutive days. In addition, we surveyed the amount of caffeine beverage intake and assessed the degree of depression and anxiety. Results: The total number of students participating in this study was 202, 101 men and 101 women. Minor stress turned out to significantly affect non-restorative sleep and secondary symptoms of insomnia (awakening difficulty, displeasure, feeling of dissatisfaction with sleep, physical uneasiness or pain at awakening, daytime sleepiness, depressive moods, tiredness and concentration difficulty). However, global PSQI score, self-reported sleeping hours, sleep latency, awakening frequency, frequency and duration of napping, were not explained by stress scores. Conclusion: In this study, minor stresses seemed to affect sleep, especially secondary symptoms caused by non-restorative sleep. We can thus infer that minor stresses impair the restorative effects of sleep by inducing arousal, and the direct relationship the two can be confirmed by polysomnogram.