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Sleep-related faciomandibular myoclonus: A sleep-related movement disorder different from bruxism
Abstract
We describe a 33-year-old man who presented with lip and tongue nibbling and bleeding during sleep. Videopolysomnography revealed myoclonic jerks involving the masticatory and facial muscles recurring mainly during NREM sleep. There was no tonic EMG masticatory activity typical of bruxism. EMG analysis demonstrated the recruitment of V- to VII innervated muscles and, in half of the episodes, also the sternocleidomastoideus. Our patient had sleep-related faciomandibular myoclonus (SFMM) with spontaneous jerks of oromasticatory and cervical muscles, occurring only during sleep. Tooth grinding, temporomandibular joint pain, abnormal tooth mobility, tooth wear, and other dental problems were clinically absent. We propose that, on the basis of the clinical and EMG features, SFMM may be considered a distinct disorder and different from sleep bruxism.
... A: orbicularis oculi; B: masseter; C: tibialis anterior. (Kato et al., 1999;Vetrugno et al., 2002;Loi et al., 2007;Wehrle et al., 2009;Dylgjeri et al., 2009), suggesting this condition is either rare or under-recognized. In a cohort of 41 patients with a clinical diagnosis of sleep bruxism (SB), four were found to have FMM rather than SB, based on sleep laboratory data (Kato et al., 1999). ...
... FMM is characterized by sudden forceful myoclonus of masticatory muscles causing vertical jaw movements occurring in isolation or clusters (Kato et al., 1999). Patients with FMM classically present with tongue biting during sleep (Vetrugno et al., 2002;Loi et al., 2007;Wehrle et al., 2009;Dylgjeri et al., 2009). This is seen most commonly in stage 1 and 2 sleep followed by rapid eye movement (REM) sleep and rarely in slow wave sleep (Kato et al., 1999). ...
... Sleep bruxism is characterized by rhythmic, involuntary contractions of masticatory muscles in sleep, most commonly in stage 1 and 2. It is clinically suspected by the presence of teeth grinding noises in sleep, abnormal tooth wear, morning stiffness or pain in jaw muscles and masseter muscle hypertrophy (Lavigne et al., 1996). In FMM, the myoclonic movement of the jaw produces a "tapping" or "clicking" sound of teeth as opposed to a "grinding" or "clenching" sound in SB (Vetrugno et al., 2002;Loi et al., 2007). In FMM, the EEG polygraphy demonstrates activation of masseter and temporalis muscles followed by orbicularis oris and oculi muscles 7-20 milliseconds later (Vetrugno et al., 2002;Loi et al., 2007). ...
Facio-mandibular myoclonus is a parasomnia characterized by forceful myoclonus of masticatory muscles in sleep. This condition typically presents with recurrent nocturnal tongue biting, which can be misdiagnosed for nocturnal seizures. The use of surface electromyographic channels over the facial muscles during video-EEG monitoring is helpful in confirming the diagnosis based on a typical burst pattern. This case report highlights difficulties in the diagnosis of facio-mandibular myoclonus and useful features which differentiate it from similar conditions.
... Two types of masticatory muscle activity have been documented during sleep: (1) rhythmic masticatory muscle activity (RMMA) [2], as seen in patients with sleep bruxism (SB); and (2) oromandibular myoclonus (OMM) or faciomandibular myoclonus (FMM). For purposes of our paper, the term OMM is used [13][14][15]. ...
... Tongue biting could be associated with epilepsy, but it is not involved in either RBD or idiopathic SB [2,13,26,27,31]. Other case reports present the counter-argument that sleep-related FMM may differ from SB [13,14,16,26]. It remains to be determined if OMM/FMM is a sign or risk factor associated with other neurologic conditions in a patient (e.g., epileptic manifestation) and by extrapolation if OMM/FMM is a risk factor for developing RBD with age. ...
We aimed to compare rhythmic masticatory muscle activity typical of sleep bruxism and oromandibular myoclonus (OMM) during rapid eye movement (REM) sleep in patients with idiopathic REM sleep behavior disorder (iRBD) and in Parkinson disease (PD) patients with RBD (PD-RBD).
Sleep polygraphic data were collected from 9 age-matched controls and 28 patients (mean±standard error of the mean, 66.0±1.7y) with a clinical and sleep laboratory diagnosis of RBD. Patients were divided into two groups: 13 patients with iRBD and 15 patients with PD-RBD. Rhythmic masticatory muscle activity, a marker of sleep bruxism, and OMM were scored blind to subject's diagnosis from jaw electromyographic recordings during sleep.
The rhythmic masticatory muscle activity index was significantly higher during REM sleep in iRBD subjects compared to controls (P<.01) and was significantly higher during non-REM (NREM) sleep in both subject groups compared to controls (P⩽.03). A positive sleep laboratory diagnosis of sleep bruxism was made in 25% of all patients. In iRBD, patients had more OMM during REM sleep than controls (2.4 times higher; P=.01).
In the presence of a high frequency of rhythmic masticatory muscle activity during REM sleep, RBD may be suspected and further neurologic assessment is recommended.
... Though the etiology of SRFMM remains poorly understood, it has been hypothesized that activation of V and VII cranial nerves may play a critical role. 11 SRFMM mostly manifests itself as an idiopathic myoclonus for the lack of definite neurologic deficits or EEG abnormalities. 8,12 However, in our work, there were one infant and three adults whose tongue biting was associated with acute brain trauma, drug therapy or brainstem ischemia, suggesting a symptomatic nature of SRFMM. ...
Background
Sleep-related facial mandibular myoclonus (SRFMM) remains rare in clinical practice. The aim of this study was to provide a comprehensive understanding of the electroclinical manner, therapeutic regimen, and prognosis of SRFMM.
Methods
Twenty-three patients who were diagnosed with SRFMM by clinical manifestation, video-electroencephalography (EEG) and electromyography over bilateral masseter and temporalis muscles were enrolled. Clinical and electrophysiological evaluation as well as follow-up information were recorded and analyzed.
Results
The cohort involved 4 infants and 19 adults with a mean onset age of 43.5 years for SRFMM, among whom 19 were male. Twenty-one patients complained of tongue injuries and disturbed night-time sleep. SRFMM in 4 patients were ascribed to oral aripiprazole, brainstem ischemia and brain trauma. In 62 SRFMM episodes, 93.5% occurred in NREM sleep and 6.5% in REM sleep, and all events were associated with EEG arousals. In 13 patients with or without clonazepam, the motor events gradually disappeared, and the rest turned to be sporadic.
Conclusion
SRFMM is a characteristic parasomnia manifested by tongue biting and accompanying facial mandibular myoclonus, leading to disrupted sleep. Besides adults, infants can also experience SRFMM with spontaneous remission. Most patients respond well to clonazepam, eventually with favorable prognosis.
... However, hypnic jerks in general are common and do not routinely cause such reliable tongue injury. The consistency with which patients bite their tongues during sleep suggests that the biting may be due to sleep-related faciomandibular myoclonus, a type of focal hypnic jerk that has since been described and is known to cause similar injury, and typically is responsive to treatment with clonazepam [21]. Worthy of note, patient three also is noted to regularly bite and lacerate his tongue when he sneezes. ...
Background:
Geniospasm is a rare genetic disorder characterized by paroxysmal rhythmic or irregular movements of the chin and lower lip due to repetitive contractions of the mentalis muscle. Pathophysiology is poorly understood, and optimal treatment has not been established.
Methods:
Geniospasm was characterized in a series of patients after evaluation in our clinics, and a comprehensive review of all cases in the medical literature was performed.
Results:
We evaluated four patients (1 female) in four families with geniospasm, aged 4 months to 9 years. Bothersome symptoms were present in one patient, who was treated with regular injections of onabotulinumtoxinA, with complete resolution of symptoms and no adverse effects. 9 patients in the literature have had similar outcomes.
Conclusions:
Limited data exist with regard to the effective treatment of geniospasm. Several treatments have been used historically, with variable outcomes. Our results, together with those of prior reported cases, demonstrate benefit of the use of botulinum toxin injections for management of this condition.
... Patients with oromandibular myoclonus may complain of nocturnal tongue biting and insomnia. OMM is a different entity from SB, although approximately 10% of SB patients exhibit OMM [121,122]. OMM can be found in patients with RBD and epilepsy. In patients with sleep-related epilepsy, nocturnal seizures are associated with a variety of movements in the limbs (e.g., bicycling legs) and the mouth (e.g., chewing automatism). ...
... 84 Familial patterns can be traced for OMM. 208 Approximately 10% of SB patients can exhibit OMM, although OMM is a different entity from SB. 84,209 Patients with oromandibular myoclonus may complain of nocturnal tongue biting. ...
Sleep bruxism (SB) is a sleep-related movement disorder characterized by rhythmic jaw muscle contractions with tooth-grinding sounds. SB may cause tooth wear, jaw muscle pain and discomfort, dental restoration failure, and temporal headache. A diagnosis of SB is confirmed using polysomnography and audio-video recordings. Although the causes of SB remain to be determined, the pathophysiology may be related to sleep homeostasis, neurochemicals, psychological factors, heritability, and the maintenance of oropharyngeal functions such as breathing and oral mucosa lubrication. The current trend in SB management is oriented toward the protection of orodental structures and the reduction of several risks rather than a cure. Behavioral, dental, and pharmacologic management is proposed because evidence-based data and safety assessments are missing.
... Patients with oromandibular myoclonus may complain of nocturnal tongue biting and insomnia. OMM is a different entity from SB, although approximately 10% of SB patients exhibit OMM [121,122]. OMM can be found in patients with RBD and epilepsy. In patients with sleep-related epilepsy, nocturnal seizures are associated with a variety of movements in the limbs (e.g., bicycling legs) and the mouth (e.g., chewing automatism). ...
Occlusal overload during sleep is a significant clinical issue that has negative impacts on the maintenance of teeth and the longevity of dental prostheses. Sleep is usually viewed as an 'out-of-functional' mode for masticatory muscles. However, orodental structures and prostheses are not free from occlusal loads during sleep since masticatory muscles can be activated at a low level within normal sleep continuity. Thus, an increase in masticatory muscle contractions, by whatever the cause, can be associated with a risk of increased occlusal loads during sleep. Among such conditions, sleep bruxism (SB) is a type of sleep-related movement disorders with potential load challenge to the tooth and orofacial structures. Patients with SB usually report frequent tooth grinding noises during sleep and there is a consecutive increase in number and strength of rhythmic masticatory muscle activity (RMMA). Other types of masticatory muscle contractions can be non-specifically activated during sleep, such as brief contractions with tooth tapping, sleep talking, non-rhythmic contractions related to non-specific body movements, etc.; these occur more frequently in sleep disorders. Studies have shown that clinical signs and symptoms of SB can be found in patients with sleep disorders. In addition, sleep becomes compromised with aging process, and a prevalence of most sleep disorders is high in the elderly populations, in which prosthodontic rehabilitations are more required. Therefore, the recognition and understanding of the role of sleep disorders can provide a comprehensive vision for prosthodontic rehabilitations when prosthodontists manage complex orodental cases needing interdisciplinary collaborations between dentistry and sleep medicine.
... 20 SB usually follows an arousal, and sometimes concludes with a swallow, and can occur in any stage of sleep but most often nonrapid eye movement (NREM) stage 1 or NREM stage 2. SB is probably an extreme audible expression of another brainstem masticatory CPG, rhythmic masticatory muscle activity. 21 Sleep-related faciomandibular myoclonus (FM) is another primary sleep-related movement disorder that at first glance resembles SB but is characterized on polysomnography by spontaneous myoclonic jerks of the facial, masticatory, and sometimes sternocleidomastoid muscles during NREM sleep without the tonic electromyographic masticatory activity typical of SB. 22 Sleep-related FM can cause repetitive tongue biting and bleeding, and has been mistaken for sleep-related epilepsy. 23 Biting often accompanying aggression has rarely been observed to occur during epileptic seizures. ...
Central pattern generators (CPGs) are genetically determined neural circuits that produce self-sustained patterns of behavior that subserve innate motor activities essential for survival. In higher primates, CPGs are largely under neocortical control. Certain motor manifestations observed in parasomnias and epileptic seizures share similar semiological features resembling motor behaviors, which can be the expression of the same CPG. Epilepsy and sleep can lead to a temporary loss of control of neocortex on lower neural structures. We suggest that this transitory neocortical dysfunction facilitates the emergence of stereotyped inborn motor patterns that depend on the activation of the same CPGs.
... The observations of several studies suggest that EMG phenotypes of motor activity may differ between the sleep states (4,28). In general, craniofacial muscles may show a mixture of tonic and phasic activities during NREM sleep, while during REM sleep, phasic muscle bursts occur repetitively in craniofacial muscles in mice, rats, guinea pigs, and human infants (1,4,12,(25)(26)(27)40). Excessive transient motor activities in the craniofacial muscles or jaw movements often occur with characteristic or stereotypic patterns predominantly in favorable sleep state(s) in patients with sleep bruxism (19,35), oromandibular myoclonus (29,39,58), sleep apnea syndrome (55), parasomnias (56), and REM sleep behavior disorders (13). A variety of intrinsic motor patterns during sleep represents the nature of transient excitatory inputs to craniofacial muscles under the distinct inhibitory processes during sleep states, and modifications of intrinsic motor patterns may give pathological implications for understanding sleep-related motor activity and clinical manifestation such as muscle pain and fatigue (24,34). ...
Sleep-related movement disorders are characterized by the specific phenotypes of muscle activities and movements during sleep. However, the state-specific characteristics of muscle bursts and movement during sleep are poorly understood. In this study, jaw-closing and -opening muscle electromyographic (EMG) activities and jaw movements were quantified to characterize phenotypes of motor patterns during sleep in freely-moving and head-restrained guinea pigs. During non-REM (NREM) sleep, both muscles were irregularly activated in terms of duration, activity and intervals. During REM sleep, clusters of phasic bursts occurred in the two muscles. Compared to NREM sleep, burst duration, activity and intervals were less variable during REM sleep for both muscles than during NREM sleep. Although burst activity was lower during the two sleep states than during mastication, burst duration and intervals during REM sleep were distributed within a similar range to those during mastication. A trigger-averaged analysis of muscle bursts revealed that the temporal association between the bursts of the jaw-closing and -opening muscles during REM sleep was analogous to the temporal association during natural chewing. The burst characteristics of the two muscles reflected irregular patterns of jaw movements during NREM sleep and repetitive alternating bilateral movements during REM sleep. The distinct patterns of jaw muscle bursts and movements reflect state-specific regulations of the jaw motor system during sleep states. Phasic activations in the antagonistic jaw muscles during REM sleep are regulated, at least in part, by the neural networks involving masticatory pattern generation, demonstrating that waking jaw motor patterns are replayed during sleep periods.
... Oromandibular myoclonus (OMM) has been reported in subjects with or without SB (Kato et al., 1999;Loi et al., 2007). It is characterized by shock-like jaw movements with sudden, short-duration muscle bursts. ...
The masseter muscle is involved in the complex and coordinated oromotor behaviors such as mastication during wakefulness. The masseter electromyographic (EMG) activity decreases but does not disappear completely during sleep: the EMG activity is generally of low level and inhomogeneous for the duration, amplitude and intervals. The decreased excitability of the masseter motoneurons can be determined by neural substrates for NREM and REM sleep. The masseter EMG activity is increased in association with the level of arousal fluctuations within either sleep state. In addition, there are some motor events such as REM twitches, swallowing and rhythmic masticatory muscle activity (RMMA), whose generation might involve the additional activation of specific neural circuits. Sleep bruxism (SB) is characterized by exaggerated occurrence of RMMA. In SB, the rhythmic activation of the masseter muscle can reflect the rhythmic motor inputs to motoneurons through, at least in part, common neural circuits for generating masticatory rhythm under the facilitatory influences of transient arousals. However, it remains elusive as to which neural circuits determine the genesis of sleep bruxism. Based on the available knowledge on the masseter EMG activity during sleep, this review presents that the variety of the masseter EMG phenotypes during sleep can result from the combinations of the quantitative, spatial and temporal neural factors eventually sending net facilitatory inputs to trigeminal motoneurons under sleep regulatory systems.
... ) Sleep-related faciomandibular myoclonus Spontaneous myoclonic jerks of the facial, masticatory, and sometimes sternocleidomastoid muscles during NREM sleep without the tonic EMG masticatory activity typical of sleep bruxism (Loi et al., 2007) Spontaneous myoclonic jerks in facial, masseter, and neck muscles during NREM sleep Sleep-related release of brainstem central pattern generators May cause tongue-biting; Sometimes mistaken for sleep-related epilepsy (Dylgjeri et al., 2009) Excessive fragmentary myoclonus Small muscle twitches about the mouth, fingers, or toes or small muscle twitches that resemble muscle fasciculations because they cause no movement across a joint space (Broughton et al., 1985) ...
Sleep specialists are frequently referred adults with epilepsy to evaluate their sleep/wake complaints, sometimes to determine whether their paroxysmal nocturnal behaviors are epileptic or not. Many patients with epilepsy have at least one parasomnia (some more than one), and the sleep specialists are often asked to differentiate and treat these. Sleep specialists review which primary sleep disorders are more common in adults with epilepsy and how to evaluate and best treat these. The authors summarize (1) how to evaluate and differentiate parasomnias using video-polysomnography; (2) the value of sleep deprivation and loud auditory stimuli to increase the likelihood of provoking a non-rapid eye movement arousal parasomnia with a single night of video-polysomnography; and (3) how to score excessive muscle activity during rapid eye movement sleep to confirm a diagnosis of rapid eye movement sleep behavior disorder. The clinical semiology and video-polysomnography features of simple and complex sleep-related movement disorders and parasomnias are reviewed.
Bleeding tongue biting episodes during sleep are a rare and alarming situation that can negatively impact the child's and parents' sleep, affecting their quality of life. Although highly suspicious of epilepsy, a differential diagnosis should be made with sleep-related movement disorders such as bruxism, hypnic myoclonus, facio-mandibular myoclonus, and geniospasm when this hypothesis is excluded. The clinical history, electroencephalogram, and video-polysomnography are essential for diagnostic assessment. Treatment with clonazepam can be necessary in the presence of frequent tongue biting, causing severe injuries and sleep disturbance. This study reports the challenging case of managing and diagnosing a 2-year-old boy with recurrent tongue biting during sleep since he was 12 months old, causing bleeding lacerations, frequent awakenings, and significant sleep impairment with daytime consequences for him and his family.
Sleep is universally encountered, and complaints about its disruption are common. Included in this list are a variety of movement abnormalities that occur in association with sleep. Often misdiagnosed, many of these problems are disruptive and affect the quality of life. This chapter reviews the sleep–wake cycle and divides sleep-related movement disorders into three major categories: I. Involuntary movements that occur around the time of sleep (myoclonus, those associated with dyssomnias, parasomnias, and other); II. Hyperkinetic movement disorders that are present during the daytime and persist during sleep; III. Seizures during and around the time of sleep. This chapter emphasizes the first category describing salient clinical features, and pathophysiology, diagnosis, and treatment are emphasized.
Sleep-related movement disorders are characterized by simple, stereotyped, movements which perturb sleep. The diagnosis of a sleep-related movement disorder requires the subjective complaint of nocturnal sleep disturbance or diurnal sleepiness or fatigue. This category includes restless leg syndrome, periodic limb movement disorder (PLMD), sleep-related leg cramps, sleep-related bruxism, sleep-related rhythmic movement disorder, benign sleep myoclonus of infancy, propriospinal myoclonus at sleep onset and sleep-related movement disorder either unspecified, due to drug or substance intake, or a medical condition. Other motor entities producing no known clinical consequences are included in the “isolated symptoms and normal variants” category.
Purpose
Sleep-related facio-mandibular myoclonus(SRFMM) is a rare and under-recognized stereotyped parasomnia. SRFMM can present with isolated tongue biting, which can be misdiagnosed as epilepsy and sleep bruxism. We aimed to investigate the clinical characteristics and demographics of patients with SRFMM.
Methods
We reported a case of SRFMM and presented a literature review on SRFMM. We searched the Medline, Pubmed, and Web of Science database using the following search algorithm: "facio-mandibular myoclonus" or "masticatory myoclonus" or "tongue biting" limited to publications in English.
Results
In total, nine studies were included. In addition to our case, a total of 17 patients were analyzed. SRFMM was found to be more prevalent in males, with a mean age of 48.2 years old. Most of the patients experienced tongue biting during non-rapid eye movement sleep. A majority of the patients were misdiagnosed with epilepsy or sleep bruxism. The simultaneous video EEG and surface EMG was beneficial in confirming the diagnosis of SRFMM. In some patients, clonazepam was reported to ameliorate the tongue biting event.
Conclusion
This study represents a comprehensive summary of SRFMM, which has unique clinical features. Extra-caution may be needed in these cases as it may puzzle neurologists in terms of management.
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This chapter deals with motor functions and dysfunctions in sleep. A variety of motor disorders may appear during sleep interfering with sleep. After a brief summary of motor control in wakefulness the chapter addresses how this control changes during different stages of sleep and how its dyscontrol may arise and affect an individual. We classify motor disorders in sleep into two broad categories: Diurnal movement disorders persisting in sleep and those occurring exclusively in sleep. Following a brief description of these entities we conclude the chapter by addressing approach to these motor disorders in sleep and outlining principles of treatment.
Insomnia is the most common sleep complaint. Insomnia is not a disease but a symptom arising from multiple environmental, medical, and mental disorders. Insomnia can be transient, of short term, or chronic in its presentation. Degenerative and vascular diseases involving the central nervous system (CNS) may impair sleep either as a result of the brain lesion or because of illness-related personal discomfort.
Chronic insomnia can be caused by neurological conditions characterized by movement disorders starting or persisting during sleep that hinder sleep onset and/or sleep continuity.
Three specific neurological conditions, fatal familial insomnia, a human prion disease; Morvan syndrome, an autoimmune limbic encephalopathy; and Delirium tremens, the well-known alcohol or benzodiazepine withdrawal syndrome, share a common clinical phenotype characterized by an inability to sleep associated with motor and autonomic activation. Agrypnia excitata (AE) is the term, which aptly defines this generalized over-activation syndrome, whose pathogenetic mechanism consists in an intralimbic disconnection releasing the hypothalamus and brainstem reticular formation from corticolimbic control.
Sleep is universally encountered and complaints about its disruption are common. Included in this list are a variety of movement abnormalities that occur in association with sleep. Often misdiagnosed, many of these problems are disruptive and affect the quality of life. This chapter reviews the sleep–wake cycle and divides sleep-related movement disorders into three major categories: I. Involuntary movements that occur around the time of sleep (myoclonus, those associated with dyssomnias, parasomnias, and other); II. Hyperkinetic movement disorders that are present during the daytime and persist during sleep; III. Seizures during and around the time of sleep. This chapter emphasizes the first category describing salient clinical features, pathophysiology, diagnosis, and treatment are emphasized.
This chapter discusses the case of a 60-year-old man who was referred with a history of repeated episodes of tongue biting during sleep and finding it difficult to fall asleep because of racing thoughts and anxiety over whether he would be able to sleep on a given night. It presents the clinical history, examination, follow-up, treatment, diagnosis, and the results of the procedures performed on the patient. The case emphasizes the need to check patients' sleep-related spells by means of video-polysomnography (PSG) and detailed neurophysiological studies for a complete characterization with the aim of avoiding delays before establishing the correct diagnosis and promptly instituting the appropriate treatment. The PSG recording of the patient revealed that he suffered from nocturnal myoclonic jerks. Sleep-induced faciomandibular myoclonus in the patient recurred mainly during NREM sleep and seemed to have a subcortical origin.
This chapter focuses on motor functions and dysfunctions of sleep. Motor disturbances associated with sleep can be loosely sorted into two categories. In the first category, there are motor disturbances—diurnal movement disorders—present during the daytime that may have an impact on sleep, either directly through their motor effects or indirectly through a variety of other mechanisms. These are the typical movement disorders that are seen by a movement disorder specialist. In the second category, there are motor disturbances that are predominantly associated with sleep. They may be motor activity similar to what is normally found during waking hours that intrudes upon sleep or abnormal motor activity that does not occur during the wake state but is aroused by sleep. These are generally classified as sleep disorders and primarily are treated by a sleep disorder specialist. These two main categories are by no means completely unique, and it is not unusual for a patient with a disorder in one category to be seen by a specialist in the other category.
Background:
To investigate the association between each clinical diagnosis criterion for sleep bruxism (SB) and the frequency of jaw motor events during sleep.
Methods:
Video-polysomnography was performed on 17 healthy adult subjects (mean age, 26.7 ± 2.8 years), with at least one of the following clinical signs and symptoms of SB: (1) a report of frequent tooth grinding, (2) tooth attrition with dentine exposure through at least three occlusal surfaces, (3) morning masticatory muscle symptoms, and (4) masseter muscle hypertrophy. Episodes of rhythmic masticatory muscle activity (RMMA) and isolated tonic activity were scored visually. These variables were compared with regards to the presence or absence of each clinical sign and symptom.
Results:
In 17 subjects, 4.0 ± 2.5/h (0.1-10.2) RMMA and 1.0 ± 0.8/h (0-2.4) isolated tonic episodes were observed (total episodes: 5.0 ± 2.4/h (1.2-11.6)). Subjects with self-reported grinding sounds (n=7) exhibited significantly higher numbers of RMMA episodes (5.7 ± 2.3/h) than those without (n=10; 2.8 ± 1.8/h) (p=0.011). Similarly, subjects with tooth attrition (n=6) showed significantly higher number of RMMA episodes (5.6 ± 3.1/h) than those without (n=11; 3.2 ± 1.6/h) (p=0.049). The occurrence of RMMA did not differ between the presence and absence of morning masticatory muscle symptoms or muscle hypertrophy.
Conclusions:
Clinical signs and symptoms frequently used for diagnosing SB can represent different clinical and physiological aspects of jaw motor activity during sleep.
Insomnia is the most common sleep complaint. Insomnia is not a disease but a symptom arising from multiple environmental, medical, and mental disorders. Insomnia can be transient, short-term, or chronic in its presentation. Degenerative and vascular diseases involving the central nervous system (CNS) may impair sleep either as a result of the brain lesion or because of illness-related personal discomfort.
Chronic insomnia can be caused by neurological conditions characterized by movement disorders starting or persisting during sleep that hinder sleep onset and/or sleep continuity.
Three specific neurological conditions, Fatal familial insomnia, a human prion disease, Morvan’s chorea, an autoimmune limbic encephalopathy, and Delirium tremens, the well-known alcohol or benzodiazepine withdrawal syndrome, share a common clinical phenotype characterized by an inability to sleep associated with motor and autonomic activation. Agrypnia excitata (AE) is the term which aptly defines this generalized overactivation syndrome, whose pathogenetic mechanism consists in an intralimbic disconnection releasing the hypothalamus and brainstem reticular formation from corticolimbic control.
Pregnancy is a time of extensive physiologic, physical, and hormonal changes. These changes can significantly disrupt a woman’s
sleep and can result in symptoms of daytime sleepiness and fatigue. Understanding how sleep is altered during pregnancy and
recognizing sleep disorders that commonly develop during pregnancy may enable healthcare professionals to identify and treat
sleep problems. Sleep is vital to the health and well-being of pregnant women. By counseling women on strategies to optimize
sleep, healthcare professionals may improve the quality of nighttime sleep and reduce daytime sleepiness and fatigue.
KeywordsEstrogen-Progesterone-Pregnancy-Insomnia-Sleep-disordered breathing-Restless legs syndrome
Sleep complaints are common among older adults. About 20% of older adults who responded to the 2003 National Sleep Foundation
poll admitted taking a sleep pill prescribed by a doctor or use over-the-counter sleep pills or drink alcohol, wine, or beer
to promote sleep with 15% admitting using these aids every or almost every night. Overall, those who report a good health
have a better quality of sleep than those who estimate having a fair or poor health. Sleep patterns are affected by age-related
changes in circadian rhythms, medications, pain and medical conditions, neurodegenerative diseases, excessive daytime sleep,
and specific sleep pathologies. Inadequate quality and quantity of sleep impact daytime alertness, physical, mood, and cognitive
function. Neuropsychiatric disorders (e.g., depression and dementia), digestive system diseases (e.g., esophageal reflux),
pain, heart disease, and chronic pulmonary problems increase risk of insomnia. Insomnia itself may increase risk of chronic
disease.
KeywordsElderly-Insomnia-Depression-Dementia-Pain-Medications-Neurodegenerative conditions-Daytime alertness
Patients with sleep-disordered breathing, particularly obstructive sleep apnea, may present with insomnia-predominant symptoms
rather than classic sleep apnea symptoms. As polysomnography is not typically performed in the evaluation of insomnia, it
is the challenge of the clinician to obtain a thorough history to determine if there are other signs or symptoms that may
lead one to consider the diagnosis of sleep-disordered breathing in this group of patients. Treatment of concurrent sleep-disordered
breathing and insomnia may also pose a challenge, as both disorders may need to be addressed for successful resolution of
symptoms.
KeywordsInsomnia-Obstructive sleep apnea-Sleep-related breathing disorders
Virtually any medical condition can cause sleep disruption. The incidence of insomnia increases with age as medical problems
increasingly occur, and patients with chronic insomnia are more likely to develop adverse health outcomes due to medical disease.
There are multiple ways in which insomnia may be caused or aggravated by medical illness or bodily injury. Unpleasant stimuli
can directly impede initiation of sleep, or they may cause frequent arousals or awakenings. Changes in basic systemic physiology
(such as disorders of ventilation) may produce similar disruption in sleep continuity. There may be humoral changes that have
direct neurochemical or neurophysiological effects, augmenting vigilance and lowering the threshold to arousal from sleep.
The effects of acute and subacute sleep disruption can lead to chronic psychophysiological insomnia by creating the anticipation
of disturbed sleep and by altering circadian entrainment, further accentuating the disruptive effects of the underlying medical
condition. Difficulties with insomnia may persist long after the causative medical condition has been effectively managed.
KeywordsEczema-End-stage renal disease-Gastroesophageal reflux disease-Congestive heart failure-Asthma-Allergies-Hyperthyroidism-Arthritis
Because our circadian rhythms have a strong influence on sleepiness/alertness, inappropriate timing of these rhythms with
respect to the attempted sleep period can produce insomnia. Relatively delayed circadian rhythms have been associated with
sleep-onset insomnia and advanced or early timed rhythms have been associated with early morning awakening insomnia. Therefore,
management of these insomnias need to include treatments, such as bright light and melatonin, that will retime the circadian
rhythms to be more in synchrony with the timing of sleep.
KeywordsCircadian rhythms, Delayed sleep phase-Advanced sleep phase-Insomnia-Bright-light therapy-Melatonin
Several movement disorders may occur during nocturnal rest disrupting sleep. A part of these complaints is characterized by relatively simple, non-purposeful and usually stereotyped movements. The last version of the International Classification of Sleep Disorders includes these clinical conditions (i.e. restless legs syndrome, periodic limb movement disorder, sleep-related leg cramps, sleep-related bruxism and sleep-related rhythmic movement disorder) under the category entitled sleep-related movement disorders. Moreover, apparently physiological movements (e.g. alternating leg muscle activation and excessive hypnic fragmentary myoclonus) can show a high frequency and severity impairing sleep quality. Clinical and, in specific cases, neurophysiological assessments are required to detect the presence of nocturnal movement complaints. Patients reporting poor sleep due to these abnormal movements should undergo non-pharmacological or pharmacological treatments.
Several issues remain to be clarified in the future research and management of SB. It is important to differentiate SB from other normal sleep orofacial activities and concomitant sleep disorders. Other orofacial activities may obscure the diagnosis of SB and may give an ambiguous clinical picture when evaluating treatment efficacy. Laboratory recordings provide a more specific diagnosis. Most of the clinical signs (e.g., tooth wear, masseter hypertrophy) are not exclusive to SB but could be concomitant with other habits or activities during wakefulness. No pathologic features in the central nervous system, such as a dysfunction of the dopaminergic system, have been observed in SB patients. Recent neurophysiologic studies have suggested that SB is a powerful microarousal event associated with central and autonomic nervous system activity during sleep. The additive contribution of psychosocial stress cannot be overlooked.
There have been no recent major breakthroughs in SB management. Cognitive and behavioral managements, which include stress management, lifestyle changes, or improved coping mechanisms, may be beneficial. Oral splint appliances are useful to protect teeth from damage. A few medications (e.g., benzodiazepines, muscle relaxants) may be helpful for a short-term period, particularly when there is secondary pain, but controlled studies are needed to assess their efficacy, safety, and patient acceptance and tolerance.
Patients with multiple sclerosis (MS) report sleep disturbances more frequently than the general population. Besides specific sleep disturbances, many other conditions could impair nocturnal rest in this population. In addition, information regarding the role of disrupted sleep on quality of life (QoL) in MS patients is lacking. This study was performed to bridge this gap.
A total of 120 patients with MS were enrolled into the study. Demographic, socioeconomic and clinical characteristics (clinical course and duration of MS, EDSS score, therapeutic information, presence of pain, presence of sexual and/or bladder dysfunction, localization of demyelinating plaques, and presence of anxiety and depression) were collected. The Pittsburgh Sleep Quality Index (PSQI), the Charlson Comorbidity Index (CCI) and the Italian version of the 36-item Short Form (SF-36) were used to assess quality of sleep, comorbidity and QoL, respectively.
Nearly half (47.5%) of MS patients were classified as "poor sleepers," having significantly higher EDSS (3.1+/-1.4 vs. 2.3+/-1.4, p=0.009) and CCI scores (0.19+/-0.4 vs. 0.03+/-0.2, p=0.009) than "good sleepers." In addition, pain due to MS was more common among "poor sleepers" (33.3% vs. 17.7%, p=0.05). Scores for each domain of the SF-36, and the mental component summary (MCS) and physical component summary (PCS) scores were significantly lower in poor sleepers than in good sleepers (p<0.001 for each score). Of the different variables associated with MCS, the only independent predictors of mental status were: presence of sexual and/or bladder dysfunction and global PSQI score. The independent predictors for physical status (PCS) were age, EDSS score and global PSQI score.
Poor sleep is common in patients with MS, representing an independent predictor of QoL. Patients with MS who are poor sleepers should receive immediate assessment and treatment, bearing in mind that, in addition to specific sleep disturbances, other clinical conditions (both related and unrelated to MS) can disrupt nocturnal sleep.
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.
A patient with post-hypoxic myoclonus, sensitive to therapy with 5-hydroxytryptophan and clonazepam, was subjected to detailed electrophysiological investigation. Brief generalised jerks followed the critical stimulus of muscle stretch. The electroencephalogram showed generalised spikes that were associated with, but not time locked to, the myoclonus. The cranial nerve nuclei were activated upward. Analysis of the findings suggests that the mechanism of the myoclonus is hyperactivity of a reflex mediated in the reticular formation of the medulla oblongata.
Tonic and rhythmic activity of the masticatory muscles accompanied by a loud and grating or clicking sound characterizes bruxism, a well-recognized parasomnia. We describe a 63-year-old man who complained of insomnia due to repeated tongue nibbling during sleep. Nocturnal polysomnographic recordings showed brief (50-100-ms) myoclonic jerks of myloioideus and masseter muscles occurring during phase 1 of sleep and leading to troublesome tongue nibbling with arousal of the patient. Hypnograms showed reduction of phase 2 and absent phases 3-4 and REM. Different pharmacological treatments including clomipramine, benzodiazepines, and carbamazepine were ineffective. A purposive interdental plate was placed to prevent jaw closings during sleep: masticatory myoclonus still persisted, but it did not provoke arousals; insomnia disappeared and night hypnograms improved.
The current study explores the proposition that a treating clinician's etiologic model influences patients' reports of tooth grinding, the validity of, and subsequent research findings relying on these measures. The investigation compares self-reports of tooth grinding and related clinical variables for 151 cases of temporomandibular pain and dysfunction syndrome (TMPDS) treated by a clinician who does not explicitly support the grinding theory of the etiology of TMPDS, and 139 healthy controls. Cases were no more likely than well controls to report ever-grinding, but were actually significantly less likely than well controls to report current grinding. They were also significantly more likely to report that a dentist had told them they ground. Findings suggest that studies using self-report, clinician-report of tooth grinding (or both) are methodologically inadequate for addressing the relationship between tooth grinding and TMPDS.
Although bruxism has been regarded as having a possibly important role in the aetiology of craniomandibular disorders, the activity of masticatory muscles relative to mandibular position during sleep grinding as recorded by electromyography (EMG) has not yet been clarified. Surface EMGs of the bilateral superficial masseter muscles were recorded simultaneously with mandibular position during sleep from 12 volunteers for three consecutive nights. The incidence of two mandibular positions were recorded with magnetic sensors for both left- and right-sided mandibular grinding. One of the mandibular positions was the canine edge-to-edge position, and the other was the midpoint between the intercuspal position and the canine edge-to-edge position. The mode of the working/ balancing activity ratio ranged from 1/10 to 2/10, showing the marked predominance of balancing side masseter muscle activity during sleep grinding. During sleep grinding, EMG bursts of masseter muscle were observed mainly with mediotrusive mandibular movement from the canine edge-to-edge position. From the results of the present study, it is suggested that muscular dynamics during sleep are unique compared to that during voluntary clenching, and exert a greater mechanical load to the balancing side temporomandibular joint.
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.
The aim of this study was to clarify the relationship between the mandibular position with tooth contacts and jaw-closing muscle activity during sleep using electromyography and newly devised equipment for detecting tooth contacts and also to confirm the validity of this system. Five males volunteered for this study and three of them reported their bruxing during sleep. Occurrences of tooth contacts at eccentric mandibular positions in addition to the intercuspal position during sleep were detected using micro photo sensors and sensor targets prepared for the individuals. Electromyographic activities (EMG) from right and left masseter and anterior temporal muscles were also recorded. Results of the polygraphic recordings demonstrated that the mandibular positions during bruxism could be distinguished clearly whether it's in the right or left position, or has no lateral deviation, and further, that bruxing events could be categorized based on mandibular position pattern. The relationship between the mandibular position and muscle activity could be evaluated using this system. The study suggested the validity of the system for measuring nocturnal bruxing events.
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.
Sleep bruxism (SB) is a stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep. The majority of the population will at some time during their lifetime grind or clench their teeth. It becomes a pathological condition when the subject presents severe tooth damage or complains of non-restorative sleep. The prevalence of SB is difficult to estimate, since quite often the subjects are unaware of having the disorder. There is no gender difference. SB is more frequent in the younger generation, with a decline over age. The symptom recognized in children can persist in adulthood. The aetio-pathophysiology is still unclear. SB has been associated with tooth interference, psychosocial and environmental factors, brain transmitters and basal ganglia dysfunction. Attempts have been made to specify the personality traits of bruxers, reported to be greater anxiety or vulnerability to stress; however, this is still controversial. SB subjects were observed to present vigilance-sleepiness and somatic problems. However, they are generally good sleepers. Some authors reported SB during all sleep stages, others observed the majority of bruxe episodes during light sleep and REM and often associated with arousal transients. No abnormalities of the autonomic nervous system could be shown in awake SB subjects. While some studies have shown an association between SB and PLM or breathing disorders, others did not confirm this. There is no specific treatment for SB: each subject has to be individually evaluated and treated. Three management alternatives are used: dental, pharmacological and psychobehavioural.
One of the most significant characteristics of the temporomandibular joint (TMJ) is that it is in fact composed of two joints. Several finite element simulations of the TMJ have been developed but none of them analysed the different responses of its two sides during nonsymmetrical movement. In this paper, a lateral excursion of the mandible was introduced and the biomechanical behaviour of both sides was studied. A three-dimensional finite element model of the joint comprising the bone components, both articular discs, and the temporomandibular ligaments was used. A fibre-reinforced porohyperelastic model was introduced to simulate the behaviour of the articular discs, taking into account the orientation of the fibres in each zone of these cartilage components. The mandible movement during its lateral excursion was introduced as the loading condition in the analysis. As a consequence of the movement asymmetry, the discs were subjected to different load distributions. It was observed that the maximal shear stresses were located in the lateral zone of both discs and that the lateral attachment of the ipsilateral condyle-disc complex suffered a large distortion, due to the compression of this disc against the inferior surface of the temporal bone. These results may be related with possible consequences of a common disorder called bruxism. Although it would be necessary to perform an exhaustive analysis of this disorder, including the contact forces between the teeth during grinding, it could be suggested that a continuous lateral movement of the jaw may lead to perforations of both discs in their lateral part and may damage the lateral attachments of the disc to the condyle.
Monitoring and staging human sleep Principles and practice of sleep medicine
- Carskadon Ma M Kryger
- Roth T Dement
Carskadon MA, Rechthschaffen A. Monitoring and staging human sleep. In: Kryger M, Roth T, Dement WC, editors. Principles and practice of sleep medicine, 4th ed. Philadelphia: W.B. Saunders Company; 2005. p 1359-1377.
Sleep bruxism Principles and practice of sleep med-icine
- Lavigne Gj
- C Manzini
- Kato
Lavigne GJ, Manzini C, Kato T. Sleep bruxism. In: Kryger M, Roth T, Dement W, editors. Principles and practice of sleep med-icine, 4th ed. Philadelphia: W.B. Saunders Company; 2005. p 946-959.
Sleep bruxism: an overview of an oromandibular sleep movement disorder
- Bader