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Motor unit potential analysis of the palatal muscles in obstructive sleep apnea syndrome
Abstract
Objectives: Among different theories about pathogenesis of obstructive sleep apnea syndrome (OSAS), dysfunction of upper airway muscles still awaits to be delineated. The aim of this study is to examine differences in motor unit potential (MUP) parameters of upper airway muscles between OSAS patients and healthy controls. Methods: Ten male patients diagnosed as OSAS by whole-night polysomnography were analyzed for MUP parameters of genioglossus (GG) muscle, palatoglossus muscle (PG), palatopharyngeus muscle, and uvular (U) muscle. Eight healthy volunteer men matched by age were enrolled as a control group. Results: In PG muscle parameters, the mean MUP area was significantly smaller (P = 0.040) in OSAS patients than those in controls. On the other hand, U muscle parameters showed a significantly larger mean MUP area (P = 0.022) in OUAS patients compared to those in the control group. In OSAS patients, the percentages of polyphasic MUPs of GG and PG muscles were significantly high (P < 0.001 and P = 0.05, respectively). Body mass index was positively correlated with number of phases of GG muscle (rs = 0.63, P < 0.05) and duration of U muscle (rs = 0.71, P < 0.05) in OSAS patients. Other MUP parameters of palatal muscles were similar between the two groups. Conclusion: Our results showed that, although mild in severity, structural neurogenic and myogenic changes characterized as mild and nonuniform MUP changes may co-exist in OSAS patients. These changes in palatal muscles may be attributed to compensatory adaptation of muscle fibers to other precipitating factors in OSAS.
... The relative peak torque of the isokinetic concentric contraction of the right ankle flexor and extensor group, and the peak torque flexion-extension ratio display, the peak muscle moment of isokinetic concentric contraction of the right ankle plantar flexor group decreases with the increase of a given movement speed (60°/s-240°/s), the relative peak muscle torque of the right ankle plantar flexors decreased from 1.70N m/kg to 1.41N m/kg, and the peak muscle torque of the dorsiflexors decreased from 1.13 to 0.17N m/kg. 7,8 As shown in Table 2, the percentage decrease in the peak torque of isokinetic concentric contraction of the left and right knee flexor and extensor groups. 9 Figures 1 and 2 show the change curves of the average power and torque of the joint muscle group with the angular velocity. ...
Introduction
Taekwondo athletes' knee flexor and extensor muscle groups reveal the joint's biomechanical characteristics when tested and may suggest a direction for individual strength training in Tae Kwon Do athletes.
Objective
Evaluate the impact of muscle strengthening on joint strength in Tae Kwon Do athletes.
Methods
The study was conducted through a literature review, experimental test, and logical analysis.
Results
The strength of the flexion muscle group in Taekwondo athletes was significantly higher than that of extension. The flexion-extension ratio is high. This characteristic may be related to the athletes' habit of supporting body weight with the left leg and attacking with the right leg.
Conclusion
Strength training of the knee flexors is indicated for Tae Kwon Do athletes, balancing the muscular balance by raising the flexor fatigue index close to that of the extensors, improving the strength and endurance of the knee flexor muscles. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.
Keywords:
Physical Education and Training; Athletes; Muscle Strength
Background
Obstructive sleep apnea syndrome (OSAS) is a common disorder with significant morbidity and mortality. We aimed to evaluate the predictive accuracy of the Berlin questionnaire in patients with suspected OSAS undergoing PSG in the sleep laboratory setting against those going through the Embletta™ portable diagnostic system (Embletta PDS) at home.
Methods
Patients with suspected OSAS were recruited from respiratory clinics to complete Berlin questionnaire and Epworth Sleepiness Score (ESS). Patients were randomized to undergo either home-based sleep test (group A) or hospital-based polysomnography (PSG) (group B).
Results
Three hundreds and sixteen subjects with newly referred suspected OSAS were recruited and randomized into group A (n = 157) and group B (n = 159). The prevalence of moderate to severe OSAS defined as apnea-hypopnea index (AHI) ≥ 15/h was 54%. The Berlin questionnaire identified 69.7% (n = 99) of subjects as high risk in group A and 77.5% (n = 100) in group B. The sensitivity, specificity, negative predictive value (NPV), and positive predictive value (PPV) of the questionnaire to predict an AHI ≥ 15/h as diagnosed by PSG was 78, 23, 67 and 35%. When compared with Embletta PDS, the specificity and NPV increased to 48 and 63%. The area under the Receiver Operator Curve (ROC) based on PSG (AUC = 0.539, 95%CI 0.417, 0.661) and based on home Embletta (AUC = 0.712, 95%CI 0.617, 0.907).
Conclusions
The questionnaire was not reliable in predicting OSAS through PSG AHI whereas there was some predictive ability in discriminating patients with OSAS from normal subjects based on home Embletta sleep test.
Trial registration
The study was registered at ClinicalTrials.gov (Identifier: NCT01828216) on 10 April 2013.
The human soft palate plays an important role in respiration, swallowing, and speech. These motor activities depend on reflexes mediated by sensory nerve endings. To date, the details of human sensory innervation to the soft palate have not been demonstrated. In this study, eight adult human whole‐mount (soft palate‐tongue‐pharynx‐larynx‐upper esophagus) specimens were obtained from autopsy. Each specimen was bisected in the midline, forming two equal and symmetrical halves. Eight hemi‐specimens were processed with Sihler's stain, a whole‐mount nerve staining technique. The remaining eight hemi‐soft palates were used for immunohistochemical study. The soft palatal mucosa was dissected from the oral and nasal sides and prepared for neurofilament staining. Our results showed that the sensory nerve fibers formed a dense nerve plexus in the lamina propria of the soft palatal mucosa. There was a significant difference in the innervation density between both sides. Specifically, the oral side had higher density of sensory nerve fibers than the nasal side of the soft palate. The mean number and percent area of the sensory nerve fibers in the mucosa of the nasal side was 78% and 72% of those in the mucosa of the oral side, respectively (P < 0.0001). The data presented here could be helpful for further investigating the morphological and quantitative alterations in the sensory nerves in certain upper airway disorders involving the soft palate such as obstructive sleep apnea (OSA) and for designing effective therapeutic strategies to treat OSA. Anat Rec, 2018. © 2018 Wiley Periodicals, Inc.
Objective
A collapsible upper airway is a common cause of obstructive sleep apnea. The exact pathophysiology leading to a more collapsible airway is not well understood. A progressive neuropathy of the soft palate and pharyngeal dilators may be associated with the progression of snoring to OSA. The purpose of this study is to systematically review the international literature investigating the neurophysiologic changes in the soft palate and uvula that contribute to progression from snoring to OSA.
Methods
PubMed/MEDLINE and 4 other databases were systematically searched through July 4, 2017. Eligibility: (1) Patients: controls, snoring or OSA patients (2) Intervention: neuromuscular evaluation of the palate and/or uvula (3) Comparison: differences between controls, snoring and OSA patients (4) Outcomes: neuromuscular outcomes (5) Study design: Peer reviewed publications of any design.
Results
845 studies were screened, 76 were downloaded in full text form and thirty-one studies met criteria. Histological studies of the soft palate demonstrated diffuse inflammatory changes, muscular changes consistent with neuropathy, and neural aberrancies. Sensory testing studies provided heterogeneous outcomes though the majority favored neuronal dysfunction. Studies have consistently demonstrated that increasing severity of snoring and sleep apnea is associated with worsening sensory nerve function of the palate in association with atrophic histological changes to the nerves and muscle fibers of the soft palate and uvula.
Conclusions
Recent evidence highlighted in this systematic review implicates the role of neurogenic pathology underlying the loss of soft palate and/or uvular tone in the progression of snoring to sleep apnea.
Introduction:
Obstructi ve sleep apnoea is an increasingly prevalent clinical condition with significant impact on individuals and public health. Continuous positive airway pressure therapy is the standard treatment, but adherence is limited and alternative treatments are needed. In this context, non-invasive and invasive methods for the electrical stimulation of upper airway dilator muscles have been demonstrated to be effective in selected patients. Areas covered: This review will cover investigations on the clinical effects, safety, and tolerability of non-invasive and invasive electrical stimulation of the upper airway for the management of obstructive sleep apnoea. Following a search of the relevant literature published on PubMed this review is focused mainly on data obtained from randomized clinical trials and clinical studies. Expert commentary: The available evidence provides a rationale to consider upper airway electrical stimulation as treatment for selected patients with obstructive sleep apnoea, who have poor adherence or experience difficulties with continuous positive airway pressure therapy. Non-invasive stimulation using transcutaneous electrodes and implantable hypoglossal nerve stimulator technologies may provide an alternative to continuous positive airway pressure for the treatment of obstructive sleep apnoea via restoration of neuromuscular tone and improved upper airway patency.
Obstructive sleep apnea syndrome (OSAS) is characterized by hypotonia of lingual and suprahyoid muscles. Genioglossus muscle is responsible for protrusion and depression of the tongue. Its dysfunction results in occlusion of the upper airways and greater incidence of apnea-hypopnea events during sleep. The aim of this prospective study was to compare the effects of daytime transcutaneous electrical stimulation of the genioglossus muscle and standard continuous positive airway pressure (CPAP) therapy on the quality of sleep, in patients with OSAS. During a 4-week study period, 19 patients with OSAS were subjected to daytime transcutaneous electrical stimulation of the genioglossus muscle before sleep and another 19 subjects underwent standard CPAP therapy. Polysomnography (apnea-hypopnea index, AHI), Epworth Sleepiness Scale (ESS) and Pittsburgh Sleep Quality Index (PSQI) were used to diagnose OSAS and to verify the efficacy of both treatments. Electrical stimulation treatment was reflected by a decrease in PSQI (p = 0.012) but did not influence ESS and AHI values (p > 0.05). In turn, CPAP therapy resulted in a significant decrease in ESS and AHI values (p < 0.001) but exerted no effect on PSQI (p = 0.089). Despite improvement of sleep quality, electrical stimulation does not seem to reduce AHI values in patients with OSAS. Daytime electrical stimulation can be considered as an adjunct treatment in OSAS. Future prospective studies should center on the identification of patients with OSAS who may benefit most from transcutaneous electrical stimulation.
As the adipose tissue in epineurium is related to some extent to amount of body fat, it is possible that the amount of such fat may affect the nerve conduction. In this study, we have analyzed effect of Body Mass Index (BMI) on various parameters of nerve conduction study in one hundred seventy five healthy volunteers between ages of 18 and 66 years. BMI was determined and nerve conduction studies were performed prospectively in all the subjects using standardized techniques. Prolongation of distal motor latency (DML) was observed with increasing BMI except in motor Peroneal nerve. (In Median Nerve, P<005). F-Wave minimum latency was also found to be significantly prolonged in (P<0.05) in motor Tibial nerve. Higher BMI was found to be non-significantly associated with lower amplitude (both sensory and motor) except for peroneal nerve. Motor as well as sensory conduction velocity showed non-significant slowing along increasing BMI except sural and motor-sensory ulnar nerve in younger age group. This study demonstrated that various parameters of nerve conduction study can be affected by BMI. So, this biological factor has to be taken into consideration while interpreting nerve conduction studies.
Obese patients develop obstructive sleep apnea syndrome (OSAS), at least in part because of a narrowed upper airway. However, many obese adolescents do not develop OSAS, despite having a presumably narrower airway. The reasons for this phenomenon are unclear. The authors hypothesized that obese controls have a compensatory neuromuscular response to subatmospheric pressure loads during sleep, making them less likely to develop upper airway collapse.
Patients underwent pressure-flow measurements during sleep while wearing intraoral electrodes to measure genioglossal electromyography (EMGgg). Two techniques were applied to decrease nasal pressure (P(N)) to subatmospheric levels, resulting in an activated and relatively hypotonic upper airway.
Sleep laboratory.
There were 35 obese patients with OSAS, 28 obese controls, and 43 lean controls.
In the activated state, the two control groups had a flatter slope of the pressure-flow relationship and a more negative critical closing pressure (less collapsible) than the OSAS group. In the hypotonic state, the lean controls had a flatter slope of the pressure-flow relationship than the OSAS and obese control groups. In the activated state, the slope of EMGgg versus P(N) was greater in the obese control group than in the OSAS or lean control groups (P = 0.002 and P = 0.028, respectively); there were no differences in the hypotonic state.
Obese controls have vigorous upper airway neuromuscular responses during sleep. Upper airway reflexes normally decline during adolescent development. It is speculated that obese adolescents without OSAS maintain protective upper airway reflexes during adolescent development, whereas those who go on to develop OSAS do not. CITATION: Huang J; Pinto SJ; Yuan H; Katz ES; Karamessinis LR; Bradford RM; Gallagher PR; Hannigan JT; Nixon T; Ward MB; Lee YN; Marcus CL. Upper airway collapsibility and genioglossus activity in adolescents during sleep. SLEEP 2012;35(10):1345-1352.
Obstructive sleep apnea patients experience recurrent upper airway (UA) collapse due to decreases in the UA dilator muscle activity during sleep. In contrast, activation of UA dilators reduces pharyngeal critical pressure (Pcrit, an index of pharyngeal collapsibility), suggesting an inverse relationship between pharyngeal collapsibility and dilator activity. Since most UA muscles display phasic respiratory activity, we hypothesized that pharyngeal collapsibility is modulated by respiratory drive via neuromuscular mechanisms. Adult male Sprague-Dawley rats were anesthetized, vagotomized, and ventilated (normocapnia). In one group, integrated genioglossal activity, Pcrit, and maximal airflow (V(max)) were measured at three expiration and five inspiration time points within the breathing cycle. Pcrit was closely and inversely related to phasic genioglossal activity, with the value measured at peak inspiration being the lowest. In other groups, the variables were measured during expiration and peak inspiration, before and after each of five manipulations. Pcrit was 26% more negative (-15.0 ± 1.0 cmH(2)O, -18.9 ± 1.2 cmH(2)O; n = 23), V(max) was 7% larger (31.0 ± 1.0 ml/s, 33.2 ± 1.1 ml/s), nasal resistance was 12% bigger [0.49 ± 0.05 cmH(2)O/(ml/s), 0.59 ± 0.05 cmH(2)O/(ml/s)], and latency to induced UA closure was 14% longer (55 ± 4 ms, 63 ± 5 ms) during peak inspiration vs. expiration (all P < 0.005). The expiration-inspiration difference in Pcrit was abolished with neuromuscular blockade, hypocapnic apnea, or death but was not reduced by the superior laryngeal nerve transection or altered by tracheal displacement. Collectively, these results suggest that pharyngeal collapsibility is moment-by-moment modulated by respiratory drive and this phasic modulation requires neuromuscular mechanisms, but not the UA negative pressure reflex or tracheal displacement by phasic lung inflation.
Objective
The objective of this study was to verify a possible correlation between the etiology of uvulopalatal ptosis and decrease in palatopharyngeal muscle tone, due to a reduction of the number of nerve fibers in surgical specimens obtained from snoring patients.
Design/setting of the study
We have designed a comparative retrospective, case–control, double-blind, immunohistochemical and histomorphometric study of human uvula innervation in 51 apneic snoring patients who underwent uvulopalatopharyngoplasty (UPPP) and 47 normal subjects collected in a 5-year-long period in the Departments of Otolaryngology of Desio and Forlì Hospital, Italy.
Patients
Case study was chosen in patients who underwent UPPP, variably associated with other disobstructive surgical procedures for treatment of obstructive sleep apnea syndrome, classified according to current clinical, polysomnographic, endoscopic, and imaging criteria. Control subjects were recruited at the Institute of Legal Medicine, University of Milan, according to strong inclusion and exclusion criteria. The main outcome measure of the study was the number of nerve fibers in the patients' uvula evaluated histologically and repeated two times by two different people, in all the areas of the specimens. Finally, we correlated the area of the histological section with the number of fibers contained therein.
Results
The number of nerve fibers varied from a minimum of 58 to a maximum of 163 in normal subjects. In the snoring patient population, the number of nerve fibers varied from a minimum of 22 to a maximum of 126 (statistically significant difference, p < 0.0001). In conclusion, our results direct toward a clear neurogenetic predisposition to uvulopalatal ptosis, marked ab initio by a lower set of motor nerve fibers, which may be the initial stage of another subsequent morphological and functional abnormality.
In this study, we quantified the profiles of phasic activity in respiratory muscles (diaphragm, genioglossus and external intercostal) and non-respiratory muscles (neck and extensor digitorum) across REM sleep. We hypothesized that if there is a unique pontine structure that controls all REM sleep phasic events, the profiles of the phasic twitches of different muscle groups should be identical. Furthermore, we described how respiratory parameters (e.g., frequency, amplitude, and effort) vary across REM sleep to determine if phasic processes affect breathing.
Electrodes were implanted in Wistar rats to record brain activity and muscle activity of neck, extensor digitorum, diaphragm, external intercostal, and genioglossal muscles. Ten rats were studied to obtain 313 REM periods over 73 recording days. Data were analyzed offline and REM sleep activity profiles were built for each muscle. In 6 animals, respiratory frequency, effort, amplitude, and inspiratory peak were also analyzed during 192 REM sleep periods.
Respiratory muscle phasic activity increased in the second part of the REM period. For example, genioglossal activity increased in the second part of the REM period by 63.8% compared to the average level during NREM sleep. This profile was consistent between animals and REM periods (η(2)=0.58). This increased activity seen in respiratory muscles appeared as irregular bursts and trains of activity that could affect rythmo-genesis. Indeed, the increased integrated activity seen in the second part of the REM period in the diaphragm was associated with an increase in the number (28.3%) and amplitude (30%) of breaths. Non-respiratory muscle phasic activity in REM sleep did not have a profile like the phasic activity of respiratory muscles. Time in REM sleep did not have an effect on nuchal activity (P=0.59).
We conclude that the concept of a common pontine center controlling all REM phasic events is not supported by our data. There is a drive in REM sleep that affects specifically respiratory muscles. The characteristic increase in respiratory frequency during REM sleep is induced by this drive.
Single motor unit recordings of the human genioglossus muscle reveal motor units with a variety of discharge patterns. Integrated multiunit electromyographic recordings of genioglossus have demonstrated an abrupt increase in the muscle's activity at arousal from sleep. The aim of the present study was to determine the effect of arousal from sleep on the activity of individual motor units as a function of their particular discharge pattern.
Genioglossus activity was measured using intramuscular fine-wire electrodes inserted via a percutaneous approach. Arousals from sleep were identified using the ASDA criterion and the genioglossus electromyogram recordings analyzed for single motor unit activity.
Sleep research laboratory.
Sleep and respiratory data were collected in 8 healthy subjects (6 men).
138 motor units were identified during prearousalarousal sleep: 25% inspiratory phasic, 33% inspiratory tonic, 4% expiratory phasic, 3% expiratory tonic, and 35% tonic. At arousal from sleep inspiratory phasic units significantly increased the proportion of a breath over which they were active, but did not appreciably increase their rate of firing. 80 new units were identified at arousals, 75% were inspiratory, many of which were active for only 1 or 2 breaths. 22% of units active before arousal, particularly expiratory and tonic units, stopped at the arousal.
Increased genioglossus muscle activity at arousal from sleep is primarily due to recruitment of inspiratory phasic motor units. Further, activity within the genioglossus motoneuron pool is reorganized at arousal as, in addition to recruitment, approximately 20% of units active before arousals stopped firing.
Patients with the sleep apnea/hypopnea syndrome (SAHS) often have more apneas supine that sitting. We have shown radiologically that although the retropalatal airway narrows on lying down, the retroglossal airway widens. We have thus investigated the effect of posture on genioglossal EMG activity in 10 normal subjects and 10 patients with SAHS (58 +/- 29 SD apneas + hypopneas/h) using peroral intramuscular EMG electrodes. Data were analyzed by three-way analysis of variance, with diagnosis, posture, and route as factors. Peak inspiratory and tonic expiratory genioglossal EMG were both than sitting, with no significant difference between normal subjects and SAHS higher (p < 0.001) supine patients, although there was a trend (p < 0.09) toward the supine posture having a greater effect on peak inspiratory EMG in the SAHS patients. There was no significant effect of breathing route on either peak inspiratory (p > 0.9) or tonic expiratory (p > 0.8) genioglossal EMG, but there were significant differences between the groups (p < 0.01), the SAHS patients having higher and the normal subjects lower EMG tone with nasal in comparison with oral breathing on both inspiration and expiration. This study therefore shows that both body posture and breathing route are important determinants of genioglossal EMG tone.
Introduction: Upper airway imaging can often identify the anatomical risk factors for sleep apnea and provide sufficient insight into the pathophysiology of obstructive sleep apnea (OSA). Materials and Methods: We conducted a case-control, observational study at a tertiary care hospital in North India. All cases and controls underwent lateral cephalometry and magnetic resonance imaging (MRI) for craniofacial and upper airway evaluation. Only the cases had polysomnography testing for confirmation of OSA and assessing the severity of disease. Results: Forty cases and an equal number of matched controls were recruited. On X-ray cephalometry, it was observed that the cases had a significantly larger hyoid mandibular distance and soft palate length; and shorter mandibular length. The MRI cephalometric variables were significantly different, the soft palate length, tongue length, and submental fat were longer while the retropalatal and retroglossal distance was shorter amongst the cases. A statistically significant positive correlation was found between the cephalometric parameters and the indices of severity of OSA. An increased hyoid mandibular distance and soft palate length, and a decrease in the lower anterior facial height were found to be predictive of severe OSA (Apnea-Hypopnea Index->30/h). An increased hyoid mandibular distance, soft palate length, and the tongue length and a reduced mandibular length were found to be predictive of need for continuous positive airway pressure (CPAP) pressures of ≥15 cm H 2 O. There were significant differences between the cephalometric parameters of the Indian OSA patients and patients from other ethnicities reported in the literature. Conclusions: OSA patients had a significantly smaller upper airway compared to age-, sex-, and body mass index-matched controls and cephalometric variables correlated with the indices of OSA severity. The cephalometric assessment was also predictive of severe OSA and the need for higher pressures of CPAP. This indicates the important role of upper airway anatomy in the pathogenesis of OSA.
Introduction
In addition to dyscoordination of upper airway dilator muscles activity, sleep may also alter the pattern of intra-muscular activation of single motor units (SMUs). Such changes should be identifiable by a state dependent change in EMG power spectrum, i.e., a shift in centroid frequency (ƒc) during sleep.
Methods
EMGs of the genioglossus and four other peri-pharyngeal muscles were recorded in OSA patients (n = 8), age-matched healthy subjects (n = 7), and 5 young healthy subjects, and ƒc was calculated for wakefulness and sleep periods.
Results
ƒc decreased with the onset of sleep and returned to baseline levels after arousal. ƒc of all muscles decreased similarly and significantly during sleep in the OSA and the age-matched healthy subjects, but not in the young subjects.
Conclusions
The pattern of decrease in ƒc is compatible with altered synchronization of SMUs during sleep. We speculate that these changes may contribute to the failure of dilator muscles to improve flow limitation during sleep in older subjects.
Upper airway patency to airflow and the occurrence of obstructive sleep apnea involve a complex interplay between pharyngeal anatomy and synergic co‐activation of peri‐pharyngeal muscles. In previous studies we observed large differences in the response to sleep‐associated flow limitation between the genioglossus and other (non‐GG) peri‐pharyngeal muscles. We hypothesized that similar differences are present also during wakefulness. In the present study we compared the response to inspiratory loading of the genioglossus electromyogram and four other peri‐pharyngeal muscles. Studies were performed in eight obstructive sleep apnea patients, seven age‐matched healthy subjects and five additional younger subjects. Electromyogram activity was evaluated over a range of negative oesophageal pressures and expressed as % of maximal electromyograms. In healthy subjects, the slope response to inspiratory loading (electromyogram/pressures) was similar for the genioglossus and non‐GG muscles studied. However, the electromyogram responses were significantly higher in the young subjects compared with older subjects. In contrast, in the obstructive sleep apnea patients, the electromyogram/pressure response of the non‐GG muscles was similar to that of the age‐matched healthy subjects, whereas the slope response of the genioglossus electromyogram was significantly higher than non‐GG muscles. We conclude that both age and the presence of obstructive sleep apnea affect the response of peri‐pharyngeal muscles to inspiratory loading. In patients with obstructive sleep apnea the genioglossus seems to compensate for mechanical disadvantages, but non‐GG muscles apparently are not included in this neuromuscular compensatory mechanism. Our current and previous findings suggest that attempts to improve obstructive sleep apnea with myofunctional therapy should put added emphasis on the training of non‐GG muscles.
Objective:
Both myopathic and neuropathic tongue protruder muscle changes have been demonstrated to occur in obstructive sleep apnea (OSA) patients using different methods. We tried to elucidate this dilemma using quantitative electromyographic (EMG) methods.
Methods:
In a group of consecutive patients with suspected OSA a full overnight polysomnography (PSG) and quantitative needle EMG of the tongue protruder, biceps brachii and vastus lateralis muscles were performed. EMG findings were compared to control subjects.
Results:
Of 23 patients, 8 were classified as simple snorers and the remaining 15 as OSA patients by PSG. Motor unit potential (MUP) parameters obtained in tongue protruder muscles, but not biceps brachii or vastus lateralis muscles, were significantly larger in patients compared to controls. However, no correlation was found between tongue protruder muscle MUP parameters and patient characteristics.
Discussion:
Our study confirmed previous findings of neuropathic changes in the tongue protruder muscles of OSA patients, and extended these to simple snorers. Changes were limited to the upper airway muscle, and could not been explained by the severity or duration of the sleep breathing disorder. The possible role of denervation injury caused by the upper airway vibrations should be tested in the future by appropriately designed studies.
Upper airway patency closely contact with neuromuscular airway regulation during respiratory, especially the activity of the pharyngeal dilators. The genioglossus is the largest pharyngeal dilators with its contraction playing the most important role in keeping the pharyngeal airway open. In healthy individuals, genioglossus activation shows a negative correlation with pharyngeal collapsibility and upper airway resistance. Negative pressure during inspiration can stimulate airway mechanoreceptors to produce a muscle reflex activity. However, in obstructive sleep apnea (OSA) patients, the muscles cannot always compensate for the increased mechanical load, resulting in frequent obstructive breathing events. A number of studies have shown that the collapsibility of upper airway during sleep in OSA patients is closely related to the activity of genioglossus electromyography(GGEMG). The present article describes the current understanding regarding the characters of GGEMG during sleep in healthy adults, as well as the pathophysiology of GGEMG in OSA patients.
In patients with OSA, substantial increases in genioglossus (GG) activity during hypopneas/apneas usually fail to restore normal airflow. We have previously suggested that sleep-induced alteration in tongue muscle coordination may explain this finding, as retractor muscles co-activation was reduced during sleep, as compared to wakefulness. The present study was undertaken to evaluate if these alterations in dilator muscle activation during sleep play a role in the pathogenesis of OSA, and whether co-activation of additional peri-pharyngeal muscles (non-GG muscles: styloglossus, geniohyoid, sternohyoid and sterno-cleido-mastoid) is also impaired during sleep. We compared GG and non-GG muscles EMG activity in 8 OSA patients and 12 healthy subjects during wakefulness, while breathing through inspiratory resistors, to the activity observed during sleep, towards the end of flow limitation, before arousal, at equivalent esophageal pressures. During wakefulness, resistive breathing triggered increases in both GG and non-GG muscles activity. During sleep, flow limitation was associated with increases in GG EMG that reached, on the average, more than two-fold the level observed while awake. In contrast, EMGs of the non-GG muscles, recorded simultaneously, reached on the average only about 2/3 the wakefulness level. We conclude that during sleep GG activity may increase to levels that exceed substantially those sufficient to prevent pharyngeal collapse during wakefulness, whereas other peri-pharyngeal muscles do not co-activate during sleep in both OSA and healthy subjects. We speculate that upper airway muscle dyssynchrony during sleep may explain why GG EMG activation fails to alleviate flow limitation and stabilize airway patency during sleep.
Upper airway muscle motoneurons, as assessed at the level of the motor unit, have a range of different discharge patterns, varying as to whether their activity is modulated in phase with the respiratory cycle, are predominantly inspiratory or expiratory, or are phasic as opposed to tonic. Two fundamental questions raised by this observation are: how are synaptic inputs from premotor neurons distributed over motoneurons to achieve these different discharge patterns; and how do different discharge patterns contribute to muscle function? We and others have studied the behavior of genioglossus (GG) and tensor palatini (TP) single motor units at transitions from wakefulness to sleep (sleep onset), from sleep to wakefulness (arousal from sleep), and during hypercapnia. Results indicate that decreases or increases in GG and TP muscle activity occur as a consequence of derecruitment or recruitment, respectively, of phasic and tonic inspiratory-modulated motoneurons, with only minor changes in rate coding. Further, sleep-wake state and chemical inputs to this "inspiratory system" appear to be mediated through the respiratory pattern generator. In contrast, phasic and tonic expiratory units and units with a purely tonic pattern, the "tonic system," are largely unaffected by sleep-wake state, and are only weakly influenced by chemical stimuli and the respiratory cycle. We speculate that the "inspiratory system" produces gross changes in upper airway muscle activity in response to changes in respiratory drive, while the "tonic system" fine tunes airway configuration with activity in this system being determined by local mechanical conditions.
The prevalence of obstructive sleep apnoea (OSA) increases with age, yet the risk factors for OSA in older people remain poorly understood. This study aimed to define the age-related changes in upper airway morphology in carefully matched groups of healthy older (>60 years, n = 11) and younger (<40 years, n = 14) males, using direct (magnetic resonance imaging (MRI)) and indirect (acoustic reflection) imaging. The median (interquartile range) combined retropalatal and retroglossal pharyngeal length was greater in older than in younger males (older 8.8 (7.8-9.0) cm, younger 7.8 (7.0-8.3) cm; p = 0.03), as was the soft palate cross-sectional area (older 43.1 (36.0-48.8) cm(2), younger 35.3 (30.5-40.5) cm(2); p = 0.03), parapharyngeal fat pad diameter (older 1.7 (1.4-2.2) cm, younger 1.2 (1.0-1.8) cm; p = 0.03) and cross-sectional area of the fat pads (older 13.8 (9.1-17.1) cm(2); younger 7.4 (5.9-13.0) cm(2); p = 0.02) as measured by MRI. Using acoustic reflection, pharyngeal calibre (older 4.8 (3.8-6.6) cm(2), younger 3.4 (2.8-4.6) cm(2); p = 0.03), pharyngeal volume (older 35.1 (30.9-55.4) cm(3), younger 27.2 (22.7-44.2) cm(3); p = 0.04) and glottis area (older 2.7 (2.1-3.9) cm(2), younger 1.3 (1.1-1.9) cm(2); p = 0.003) were also larger in older participants compared with younger participants. There was no difference in craniofacial measures between groups, including volumetric data and hyoid bone position. The larger pharyngeal calibre observed in older males may be compensating for an age-related enlargement in pharyngeal soft tissue that predisposes to OSA.
Obstructive Sleep Apnea (OSA) is a common sleep disorder characterized by repetitive collapse of the upper airway (UA). One treatment option is a mandibular advancement splint (MAS) which protrudes the lower jaw, stabilizing the airway. However not all patients respond to MAS therapy and individual effects are not well understood. Simulations of airway behavior may represent a non-invasive means to understand OSA and individual treatment responses. Our aims were (1) to analyze UA occlusion and flow dynamics in OSA using the fluid structure interaction (FSI) method, and (2) to observe changes with MAS. Magnetic resonance imaging (MRI) scans were obtained at baseline and with MAS in a known treatment responder. Computational models of the patients' UA geometry were reconstructed for both conditions. The FSI model demonstrated full collapse of the UA (maximum 5.83mm) pre-treatment (without MAS). The UA collapse was located at the oropharynx with low oropharyngeal pressure (-51.18Pa to -39.08Pa) induced by velopharyngeal jet flow (maximum 10.0m/s). By comparison, simulation results from the UA with MAS, showed smaller deformation (maximum 2.03mm), matching the known clinical response. Our FSI modeling method was validated by physical experiment on a 1:1 flexible UA model fabricated using 3D steriolithography. This is the first study of airflow dynamics in a deformable UA structure and inspiratory flow. These results expand on previous UA models using computational fluid dynamics (CFD), and lay a platform for application of computational models to study biomechanical properties of the UA in the pathogenesis and treatment of OSA.
The upper airway is a complex, multifunctional, dynamic neuromechanical system. Its patency during breathing requires moment-to-moment coordination of neural and mechanical behavior and varies with posture. Failure to continuously recruit and coordinate dilator muscles to counterbalance the forces that act to close the airway results in hypopneas or apneas. Repeated failures lead to obstructive sleep apnea (OSA). Obesity and anatomical variations such as retrognathia increase the likelihood of upper airway collapse by altering the passive mechanical behavior of the upper airway. This behavior depends on the mechanical properties of each upper airway tissue in isolation, their geometrical arrangements, and their physiological interactions. Recent measurements of respiratory-related deformation of the airway wall have shown that there are different patterns of airway soft tissue movement during the respiratory cycle. In OSA patients airway dilation appears less coordinated compared to healthy subjects (matched for body mass index). Intrinsic mechanical properties of airway tissues are altered in OSA patients, but the factors underlying these changes have yet to be elucidated. How neural drive to the airway dilators relates to the biomechanical behavior of the upper airway (movement and stiffness) is still poorly understood. Recent studies have highlighted that the biomechanical behavior of the upper airway cannot be simply predicted from electromyographic activity (EMG) of its muscles.
Dysphagia (impaired swallowing) is common in patients with Parkinson disease (PD) and is related to aspiration pneumonia, the primary cause of death in PD. Therapies that ameliorate the limb motor symptoms of PD are ineffective for dysphagia. This suggests that the pathophysiology of PD dysphagia may differ from that affecting limb muscles, but little is known about potential neuromuscular abnormalities in the swallowing muscles in PD. This study examined the fiber histochemistry of pharyngeal constrictor and cricopharyngeal sphincter muscles in postmortem specimens from 8 subjects with PD and 4 age-matched control subjects. Pharyngeal muscles in subjects with PD exhibited many atrophic fibers, fiber type grouping, and fast-to-slow myosin heavy chain transformation. These alterations indicate that the pharyngeal muscles experienced neural degeneration and regeneration over the course of PD. Notably, subjects with PD with dysphagia had a higher percentage of atrophic myofibers versus with those without dysphagia and controls. The fast-to-slow fiber-type transition is consistent with abnormalities in swallowing, slow movement of food, and increased tone in the cricopharyngeal sphincter in subjects with PD. The alterations in the pharyngeal muscles may play a pathogenic role in the development of dysphagia in subjects with PD.
Histopathological alterations and a reduced number of capillaries have been observed in the palate muscles of snorers with obstructive sleep apnea syndrome (OSAS). These changes may create a substrate for decreased microcirculation, impaired aerobic metabolism and muscle dysfunction and contribute to upper airway obstruction during sleep.
The aim was to analyze mitochondria distribution and oxidative enzyme activity in relation to capillary supply in the palate muscles of patients with a history of long-term snoring and OSAS.
Palatopharyngeus (PP) and uvula (UV) muscle samples were obtained from 8 patients undergoing uvulopalatopharyngoplasty due to habitual snoring and OSAS. The muscles were analyzed with enzyme- and immunohistochemistry and morphometry.
Abnormalities in the internal organization of mitochondria and oxidative activity were observed in 39 ± 15% of the fibers in the PP and 4 ± 3% in the UV, but not in control samples. The majority of these fibers had a lobulated contour and trabecular internal organization of mitochondria. The number of capillaries around abnormal fibers (PP 0.9 ± 0.3, UV 0.4 ± 0.1) was lower than in fibers of a normal appearance in both patients (PP 1.4 ± 0.6, UV 1.2 ± 0.3) and references (PP 2.7 ± 0.7, UV 1.9 ± 0.9) (p < 0.05).
Abnormal mitochondrial distribution, a low capillary supply and signs of impaired oxidative activity suggest that muscle dysfunction of the palate muscles in long-term snorers may contribute to the upper airway obstruction during sleep. The cause of these abnormalities remains unclear, but local muscle and nerve trauma due to vibration and stretch is a possible etiology.
This study aims to use clinical scales in a standardized fashion in evaluating the frequency of a high and narrow hard palate and/or small and retroplaced mandible in children with polysomnographically demonstrated sleep-disordered breathing (SDB).
This is a retrospective review of clinical and polysomnographic data from children (2-17 years old) with SDB. Exclusion criteria were obesity, presence of a syndromic disorder, and incomplete chart information. Data on demographics, reason for referral, sleep history, Mallampati scale, size of the tonsils (Friedman scale), bite occlusion (dental positioning), and correlating clinical presentation and comparative physical exam of nasomaxillary and mandibular features (using subjective grading scales) were collected, as were results of pre- and post- treatment polysomnography.
Data from 400 children were analyzed. With increasing age, fewer referrals were made for abnormal breathing during sleep and more were made for daytime impairment and generally poor sleep. There were 290 children (72.6%) who had tonsils graded 3+ or 4+, but 373 (93.3%) had craniofacial features considered to be risk factors for SDB, including small mandible and/or high and narrow hard palate associated with a narrow nasomaxillary complex. Mean pretreatment apnea-hypopnea index (AHI) was 14.6 ± 17.1 and AHI was similar in the three age groups. Initial treatment was adenotonsillectomy. Follow-up was obtained in 378 subjects, and 167 cases demonstrated residual AHI. Incomplete response to adenotonsillectomy was seen more often in children with Mallampati scale scores of 3 and 4.
Non-obese children with SDB had different initial clinical complaints based on age. Independently of age, facial anatomic structures limiting nasal breathing and those considered to be risk factors for SDB were commonly seen in the total group. Clinical assessment of craniofacial features considered as risk factors for SDB and more particularly a Mallampati scale score of 3 or 4 can be useful in identifying children who may be more at risk for limited response to adenotonsillectomy, suggesting a subsequent need for post-surgery polysomnography.
Chronic stimulation of the hypoglossus nerve may provide a new treatment modality for obstructive sleep apnoea (OSA). In previous studies we observed large differences in response to stimulation of the genioglossus (GG). We hypothesised that both individual patient characteristics and the area of the GG stimulated are responsible for these differences. In the present study, we compared the response to GG electrical stimulation at the anterior area (GGa-ES), which activates the whole GG and the posterior area (GGp-ES), which activates preferentially the longitudinal fibres. Studies were performed in 14 propofol-sedated OSA patients. The parameters evaluated included cephalometry, pressure-flow relationship and pharyngeal shape and compliance assessed by pharyngoscopy. Compared with GGa-ES, GGp-ES resulted in significantly larger decreases in the critical value of end-expiratory pressure (P(crit)) (from 3.8 ± 2.2 to 2.9 ± 3.3 and -2.0 ± 3.9 cmH(2)O, respectively (p<0.001)). Both tongue size and velopharyngeal shape (anteroposterior to lateral ratio) correlated significantly with the decrease in P(crit) during GGp-ES (R = 0.53 and -0.66, respectively; p<0.05). In the patients with the larger tongue size (n = 7), the decrease in P(crit) reached 8.0 ± 2.2 cmH(2)O during GGp-ES. We conclude that directing stimulation to longitudinal fibres of the GG improves the flow-mechanical effect. In addition, patients with large tongues and narrow pharynx tend to respond better to GGp-ES.
Pulmonary aspiration is the consequence of abnormal entry of fluid, particulate material, or endogenous secretions into the airway. The two main types of aspiration scenarios include anterograde aspiration, which occurs during swallowing, and retrograde aspiration, which can occur during gastroesophageal reflux (GER) events. The important structures that protect against aspiration include the aerodigestive apparatus: pharynx, upper esophageal sphincter, esophageal body, glottis and vocal cords, and airway. In this article we review the neuroanatomy, physiology, and pathophysiology pertinent to glottic reflexes and airway aspiration across the age spectrum from neonates to adults. We also discuss recent advances in our understanding of glottal reflexes and the relationship of these reflexes to developmental anatomy and physiology, the pathophysiology of aspiration, and aerodigestive interactions.
Denervation of oropharyngeal muscles in obstructive sleep apnea (OSA) has been suggested by needle electromyography (EMG) and muscle biopsy, but little is known about oropharyngeal nerve conduction abnormalities in OSA. We sought to compare hypoglossal nerve conduction studies in patients with and without OSA. Unilateral hypoglossal nerve conduction studies were performed on 20 subjects with OSA and 20 age-matched controls using standard techniques. Median age was 48 years in OSA subjects and 47 years in controls. Hypoglossal compound muscle action potential (CMAP) amplitudes were significantly reduced (P = 0.01, Wilcoxon signed-rank test), but prolongation of latencies in OSA subjects did not reach significance in comparison to those of controls. Among a subgroup of subjects without polyneuropathy (15 pairs), reduced amplitudes in OSA subjects retained borderline significance (P = 0.05). Hypoglossal nerve conduction abnormalities may distinguish patients with OSA from controls. These abnormalities could potentially contribute to, or arise from, OSA.
To establish the inter-rater reliability of decomposition-based quantitative electromyography (DQEMG) derived motor unit number estimates (MUNEs) and quantitative motor unit (MU) analysis.
Using DQEMG, two examiners independently obtained a sample of needle and surface-detected motor unit potentials (MUPs) from the tibialis anterior muscle from 10 subjects. Coupled with a maximal M wave, surface-detected MUPs were used to derive a MUNE for each subject and each examiner. Additionally, size-related parameters of the individual MUs were obtained following quantitative MUP analysis.
Test-retest MUNE values were similar with high reliability observed between examiners (ICC=0.87). Additionally, MUNE variability from test-retest as quantified by a 95% confidence interval was relatively low (+/-28 MUs). Lastly, quantitative data pertaining to MU size, complexity and firing rate were similar between examiners.
MUNEs and quantitative MU data can be obtained with high reliability by two independent examiners using DQEMG.
Establishing the inter-rater reliability of MUNEs and quantitative MU analysis using DQEMG is central to the clinical applicability of the technique. In addition to assessing response to treatments over time, multiple clinicians may be involved in the longitudinal assessment of the MU pool of individuals with disorders of the central or peripheral nervous system.
In interpretation of diagnostic findings the probability that an abnormal test accurately indicates pathology (i.e., the positive predictive value), and a normal test accurately excludes pathology (i.e., the negative predictive value) is the most important. For motor unit potential (MUP) analysis no such data has been published; hence this was the aim of this study.
In 31 patients with facioscapulohumeral muscular dystrophy (FSHD) and 34 controls the biceps brachii and vastus lateralis muscles were examined by concentric needle electromyography (EMG), using template operated MUP analysis. These results were compared to non-parametric reference data obtained in another group of 34 (biceps brachii) and 46 (vastus lateralis) control subjects.
For the biceps brachii muscles sensitivity was 59%, specificity 91%, the positive predictive value 85%, and negative predictive value 72% with at least two criteria (mean values or outliers for MUP thickness, amplitude and duration) below the reference intervals. In addition, all subjects with three abnormal EMG criteria were FSHD patients, and 90% of subjects with normal EMG were controls.
Template operated MUP analysis demonstrated reasonable predictive value for diagnosis and exclusion of myopathy.
Quantitative MUP analysis seems to be useful for the preliminary diagnosis of FSHD in patients with appropriate clinical picture.
Sleep apnea is worse in the supine posture and is associated with retropalatal airway narrowing or occlusion. We have, therefore, examined the effects of posture, negative pressure, and route of respiration on palatal muscle activity in 13 nonsnoring awake male subjects by using electromyography. Electromyographic activity of the levator palatini and palatoglossus was expressed as a percentage of maximum activity. Both the levator palatini (P = 0.002) and palatoglossus (P = 0.002) exhibited phasic inspiratory activity. Overall, posture did not affect the levator palatini (F = 1.58; P = 0.23) or palatoglossus (F = 0.98; P = 0.34) activity, but analysis by route of respiration showed the palatoglossus to be more active when the subjects were nose breathing supine (F = 6.64; P = 0.02). Levator palatini activity was lower when nose breathing was compared with mouth breathing in both the erect and supine postures (F = 6.67; P < 0.02). Nose breathing with the mouth held open caused an increase in palatoglossal activity (P = 0.04). Negative-pressure application (0 to -12.5 cmH2O) caused significant increases in levator palatini (P < 0.001) and palatoglossus (P < 0.001) activity, 100 ms after pressure stimulus, irrespective of route. However, the palatoglossus required significantly greater negative pressures to cause activation when applied via the nose compared with the mouth (P < 0.05). These observations indicate that the levator palatini and palatglossus have respiratory activity and are reflexly activated by negative pressure.
This article reviews studies of upper airway muscles in humans, with emphasis on muscle fiber structural and electrophysiological changes observed in patients with obstructive sleep apnea syndrome (OSAS). The concept of OSAS as a progressive disease is discussed and also possible causes. These include local nervous lesions in the upper airway, both motor and sensory. Previous muscle biopsy studies have given evidence for motor neuron lesions such as, e.g., the phenomenon of type grouping in histological sections. New data obtained with concentric needle EMG recordings from the palatopharyngeus muscles are also presented. In 10/12 OSAS patients there were typical findings indicating motor neuropathy (reduced EMG activity at maximal voluntary effort, long and polyphasic motor-unit potentials and, in two cases, spontaneous denervation activity), whereas such findings were only present in 3/15 patients with habitual snoring. This supports the hypothesis that progression from habitual snoring to the clinical disease of OSAS could be attributed to peripheral neurogenic lesions.
Multi-MUP analysis of palatal muscles in healthy men
- F K Savrun
- B Benbir
- R Inan
- A Kaytaz
- H Kaynak
Savrun FK, Benbir B, Inan R, Kaytaz A, Kaynak H. Multi-MUP
analysis of palatal muscles in healthy men. J Turk Sleep Med
JTSM 2014;1:43-5.
Clinical Neurophysiology of Disorders of Muscle and Neuromuscular Junction, Including Fatigue
- E Stalberg
- J R Daube
Stalberg E, Daube JR. Electromyographic methods. In:
Stålberg E, editor. Clinical Neurophysiology of Disorders
of Muscle and Neuromuscular Junction, Including Fatigue.
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