Tonic EMG Activity Research Articles

Sleep related injury and its correlates in isolated rapid eye movement sleep behavior disorder

ObjectivesTo evaluate factors associated with sleep related injury (SRI) and persistent SRI (pSRI) in patients with isolated rapid eye movement sleep behavior disorder (iRBD). MethodsThis is a retrospective cohort study. A total of 388 patients with iRBD were involved for a comprehensive review of sleep related injuries. SRI is defined as a lifetime history of injurious behaviors to self and/or bed partner, and pSRI is considered if injurious symptoms continued to occur frequently (≥ 1/month). Correlations of SRI/pSRI with clinical, lifestyle and polysomnographic characteristics were analyzed. ResultsLifetime SRI was reported in 322 (83%) patients (66.3 ± 8.5 years old, male 77.0%), with 19.3% having severe injuries, including fractures (2.5%) and subdural hemorrhage (1.2%), while 7.5% required medical attendance. SRI was related to more severe depressive features (Padj = 0.017), current alcohol drinking (Padj = 0.014) and higher mentalis phasic and tonic EMG activity (Padj = 0.042 and 0.048). After a mean follow-up of 5.1 years, 18.2% of SRI patients (38/209) had pSRI despite intense treatment. Frequent nightmare at baseline (OR [95% CI] = 1.43 [1.01, 2.03]), restless leg syndrome (OR [95% CI] = 5.68 [1.42, 22.64]) and adult-onset sleepwalking (OR [95% CI] = 2.52 [1.10, 5.76]) were associated with an increased risk of pSRI. ConclusionsSRI is common in patients with iRBD and 18% had pSRI despite intensive treatment, emphasizing the importance of bedside safety. The identification of risk factors for SRI and pSRI underscores the need for systematic clinical screening and targeted interventions for at-risk patients.

Chemogenetic Activation of Hypoglossal Motoneurons in Neuromuscular Disease

The tongue is essential for breathing, swallowing, mastication, speech, coughing, and suckling. Many conditions and neuromuscular diseases are associated with lingual dysfunction, making it a priority to develop treatments which can improve tongue motor function. Our laboratory established that intralingual delivery of adeno‐associated virus serotype 9 (AAV9) encoding a particular gene can drive expression of that gene in hypoglossal motoneurons (XII MNs). This method can also drive expression of designer receptors exclusively activated by designer drugs (DREADDs) in XII MNs (Fleury‐Curado et al, 2021). Here we tested if intralingual delivery of AAV9‐hSyn‐hM3(Gq)‐mCherry could drive functional DREADD expression in XII MNs in a mouse model exhibiting tongue neuromuscular pathology. Specifically, we studied a mouse model of Pompe disease (Gaa‐/‐). The prevalence of Pompe disease is estimated to be 1 per 8,700 live births and is associated with macroglossia, dysphagia, dysarthria, sleep disordered breathing, and XII MN pathology. Intralingual injections of AAV9‐hSyn‐hM3(Gq)‐mCherry (2.4 x 1011 vg) or saline (sham) were administered to the base of tongue in anesthetized Pompe mice (AAV9‐DREADD n=11, saline n=4) or wild type (C57BL//6J mice (AAV9‐DREADD, n=5) at 4‐6 weeks of age. Lingual EMG activity was measured during spontaneous breathing under isoflurane anesthesia 12 weeks later. Tonic and phasic inspiratory EMG responses to intraperitoneal injection of saline (i.e., vehicle) or the DREADD ligand JHU37160‐dihydrochloride (J60) were assessed. Saline produced no significant changes in lingual EMG measures. All Pompe mice studied responded to J60 with an increase in tonic lingual EMG activity (time to response, TTR = 219±68 seconds; 1034±350% baseline at 30 min). Only 1 of 5 mice showed discernable increase in tonic EMG output after J60. The DREADD ligand produced an increase in phasic inspiratory bursting in all Pompe mice (TTR = 197±78 seconds; 506±248% baseline at 30 min). The increase in phasic bursting also occurred in all WT mice (TTR = 161±22 seconds; 512±151% baseline at 30 min). The DREADD ligand also caused a decrease in respiratory rate (bursts per minute) that was more pronounced in Pompe mice (79±5% baseline at 30 min post‐J60) compared to WT mice (91±12% baseline at 30 min post‐J60. Histological evaluation of the medulla confirmed expression of the mCherry fluorophore in XII MNs in all animals that received intralingual injection of AAV9‐hSyn‐hM3(Gq)‐mCherry. We conclude that intralingual delivery of an AAV9 vector encoding a DREADD can drive functional expression of DREADDs in XII MNs in a mouse model of Pompe disease that displays lingual myofiber atrophy and XII MN pathology. Thus, the ongoing neuromuscular pathology did not prevent the efficacy of chemogenetic tongue muscle activation. Indeed, the DREADD ligand caused a robust increase in both tonic and phasic lingual EMG activity in Pompe mice. The tonic EMG response appears to be more consistent in Pompe vs WT mice.

Targeted Retrograde Chemogenetic Approach to Treat Sleep Apnea

IntroductionObstructive Sleep Apnea (OSA) is a prevalent condition and a major cause of morbidity and mortality. The tongue and specifically genioglossus (GG) muscle have been implicated in the pathogenesis of upper airway (UA) obstruction during sleep. Nasal positive airway pressure can treat OSA but poor adherence severely limits its effectiveness. There is an urgent need for pharmacotherapy that reverses neuromuscular defects in upper airway function. We have previously shown that diet induced obese C57BL/6J (DIO) mice have OSA, similar to humans. We have also recently demonstrated that Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) deployed by intracerebral injection can be expressed in hypoglossal motor neurons and that activation of these DREADDs by specific ligand increased GG activity and improved pharyngeal patency. The goal of our novel approach is to avoid intracranial injection and improve specificity of DREADD delivery to hypoglossal motor neurons innervating genioglossus muscle. We hypothesize that tongue injecting retrograde adeno‐associated virus type 9 (AAV9) carrying excitatory DREADDs will (1) deploy DREADDs in hypoglossal motor neurons; (2) improve UA patency and (3) and treat sleep apnea in DIO mice.MethodsDREADDs (AAV9‐hSyn‐hM3(Gq)‐mCherry n=10) or Control AAV9‐hSyn‐GFP (n=5) were delivered bilaterally by tongue injection in DIO mice. Six weeks after gene delivery, mice were injected with specific ligand (J60) and saline intraperitoneally (IP) one week apart in a random order: we performed GG electromyography (EMGGG), UA dynamic MRI, positron emission tomography (PET) scan and sleep studies.ResultsDREADDs or control virus were expressed in the tongue and hypoglossal nucleus in all mice. In DREADD‐transfected mice, administration of J60 resulted in (1) 7.05 fold increase in EMGGG activity (p<0.001); (2) pharyngeal dilation at the rim of the soft palate (0.46 ±0.03mm2 to 1.16±0.05mm2, p<0.05) by MRI; (3) increased tongue metabolic activity (2.21± 0.28 to 4.14 ± 0.31 g/ml, p<0.001) by PET scan; (4) increased minute ventilation (22.53 ± 10.39 to 60.18 ± 33.28 mL/min) and maximal inspiratory flow (1.58 ± 0.58 to 4.11 ± 1.98 mL/sec) during sleep, treating sleep apnea. No changes were seen following j60 injection in mice injected with control virus or saline injection.ConclusionTongue injection of retrograde AAV9 carrying DREADDs successfully deployed DREADDs in hypoglossal motor neurons. Activation of these DREADDs by specific ligand (J60) treated OSA.Support or Funding InformationRO1HL138932, AHA 19CDA34660245, ATS Foundation Unrestricted Grant(A) Whole body PET scan in mouse treated with retrograde excitatory DREADD after Saline (left) or J60 (right). Note the increase in tongue metabolic activity marked by the intense uptake after J60 (right). (B) Plotted Standardized Uptake Values (SUVs) in these animals. *, p < 0.001.Figure 1(A) Representative genioglossal electromyography (EMGGG), recorded at baseline (left) and after J60 administration (right). Note the increase in both phasic and tonic EMG activity. (B) Plotted EMG responses to J60 or saline in the same DREADD treated animals. *, p < 0.001.Figure 2

Responses to anterior and posterior perturbations in Parkinson’s disease with early postural instability: role of axial and limb rigidity

We studied 12 patients with Parkinson's disease (PD): 6 with postural instability (Hoehn and Yahr Stage 3) and 6 without (Stage 2 or 2.5), using a quantitative test based on the clinical pull test. Their findings were compared with those for 12 healthy controls. The patients on their usual medications were pulled either forwards or backwards at the level of the shoulders and asked not to take a step in a series of five trials. Acceleration was monitored for the upper trunk, sacrum, and both tibias. EMG was measured in soleus and tibialis anterior (TA) muscles in all and for thigh and truncal muscles in a subgroup. A target of 0.2g trunk acceleration was used, but smaller perturbations were used in very unstable patients. All the Stage 3 patients lost balance in at least one trial for the posterior perturbations but none for the anterior ones. None of the Stage 2 patients lost balance. There was increased tonic EMG and agonist activity but no difference in EMG onset or initial force production compared to healthy controls. For posterior perturbations, there were two related disorders that separated the PD patients from controls. There was a significantly higher ratio of sacral-to-applied acceleration and both PD groups showed reduced knee acceleration and shortened latency, more so for the Stage 3 group. The increased sacral-to-C7 acceleration ratio was correlated with the tonic level of activation of the hamstrings (HS), quadriceps, and lumbar paraspinal muscles (PS), while the tibial acceleration latency was also correlated with the level of tonic PS activation. We also found that the size of balance responses, 0-200ms post-perturbation, correlated significantly with the level of tonic activation in nearly all the muscles studied. We confirmed that PD patients show greater instability posteriorly than anteriorly to applied perturbations. Our findings support increasing axial and limb rigidity as the cause of the impaired pull test rather than postural bradykinesia and suggest that tonic truncal and thigh muscle activation may be an important underlying cause.

Anticipatory Inhibition of EMG Activity of the Human M. Soleus at Voluntary Contraction of Its Antagonists

Quantitative changes in background tonic EMG activity of m. soleus within a premotor period of voluntary contraction of its antagonists were examined in healthy humans. The above activity was recorded in the lying position at voluntary moderate tonic tension of this muscle and in the upright position, where the body was supported by both legs. The effect of voluntary flexion of the ipsilateral ankle joint (a simple motor reaction to a light signal) was examined. It was found that the intensity of soleus EMG in both tested positions, began to decrease 30–60 msec before the appearance of EMG activity recorded from the ankle flexor m. tibialis anterior, and such inhibition reached the maximum at the end of the premotor period. The observed dynamics of tonic EMG in the m. soleus show that an anticipatory drop in the activity of soleus motoneurons develops before the beginning of voluntary movements. Possible physiological mechanisms underlying this phenomenon are discussed. We believe that, within the premotor period, impulsation coming via mostly the corticospinal tract to soleus motoneurons decreases due to the action of central motor commands, and this leads to lowering of tonic tension of this muscle.

0727 TONIC AND PHASIC CHIN EMG DENSITY IN IDIOPATHIC REM SLEEP BEHAVIOR DISORDER

In 2010, our group published a scoring method for REM sleep phasic and tonic EMG activity in REM sleep behavior disorder (RBD). Cut-off values were reported in a large population of RBD and healthy subjects, but this method was based on 20 sec epochs which limits it current used as a diagnostic tool. The aims of the present study were to confirm results of the previous study in a different RBD cohort using 30 sec epochs, to assess the sensitivity and specificity of cut-off values for tonic and phasic values to diagnose RBD (taken separately or combined), to correlate tonic and phasic values with clinical markers of neurodegeneration, and to look at changes of REM sleep EMG abnormalities over times. Fifty-nine patients with a clinical diagnosis of idiopathic RBD and 50 age- and gender-matched healthy subjects were studied in our sleep laboratory. Tonic and phasic EMG activity were recorded and scored according to our method described previously using 30 sec epochs. Receiver operating curves were drawn to find optimal cut-off values for REM sleep EMG parameters. Clinical markers of neurodegeneration were also studied and a subgroup of patients was recorded again after 12 months. Total correct classification of 89% was found for tonic or phasic chin EMG density ≥15%. This correct classification score increased to 97% when both criteria were applied. A significant positive correlation (r=0.321) was found between tonic EMG and UPDRSIII. Recordings performed after 12 months showed a significant increase of 20% of tonic EMG density. This study confirms the value of a scoring method based on chin EMG and establishes cut-off values to be used for the diagnosis of RBD. Results further document the status of tonic and not phasic REM density as a marker of ongoing neurodegeneration and disease progression. Canadian Institutes of Health Research (CIHR) and by the W Garfield Weston Foundation.

Postural responses in the upper limbs evoked by axial impulses: a role for reticulospinal projections.

We studied the short-latency (SL) postural effects of axial impulses in 11 subjects (22±2years old). Recordings were made bilaterally from soleus and tibialis anterior (TA) muscles. We confirmed that with leaning anteriorly and posteriorly, reflex EMG increases occurred in both muscle groups at short latency following brief perturbations applied over C7 or the sternum (soleus mean latencies 57.5 and 66.4ms; TA mean 51.7 and 55.4ms, respectively). While the size of the SL reflexes was affected by the direction of lean when standing we found that light touch did not affect the amplitudes or latencies significantly. We investigated the presence of SL responses in the upper limb muscle triceps brachii during an isometric contraction and when the arm muscles had a direct role in supporting approximately 40% of the body weight. Similar levels of tonic EMG activity occurred in triceps in both conditions but significantly larger SL reflexes occurred when used posturally compared to the isometric contraction (23.0 vs 3.3%) while the reverse occurred for SL responses in soleus and TA, which were significantly attenuated. The responses were present with the head in the neutral position but with head rotation were larger contralateral to the direction of rotation. Calculations based upon the relative latencies suggest that the pathway responsible is not the corticospinal tract. We conclude that axially evoked SL postural reflexes are unaffected by light tactile input but are present in upper limb muscles when used for postural support. We propose that the pathway mediating these responses is the reticulospinal tract.

Dynamics of the H Reflex and Tonic Activity in the Human m.Soleus at a Voluntary Movement of the Upper Limb

In tests on healthy volunteers, we examined the effects of voluntary flexion of the elbow joint on the magnitude of the H reflex recorded from the ipsilateral m. soleus and on tonic EMG activity of this muscle. The H reflex was subjected to two-phase modulation; a period of facilitation lasting up to 300 msec was replaced by subsequent long-lasting inhibition. Tonic EMG-activity of the m. soleus induced by moderate voluntary contraction of its antagonist did not undergo significant changes under these conditions. As is supposed, changes in the intensity of background presynaptic inhibition exerted on afferents of the H reflex arc are the reason for the observed shifts in the magnitude of this reflex.

Beware: Recruitment of Muscle Activity by the EEG-Neurofeedback Trainings of High Frequencies.

EEG-neurofeedback (NFB) became a very popular method aimed at improving cognitive and behavioral performance. However, the EMG frequency spectrum overlies the higher EEG oscillations and the NFB trainings focusing on these frequencies is hindered by the problem of EMG load in the information fed back to the subjects. In such a complex signal, it is highly probable that the most controllable component will form the basis for operant conditioning. This might cause different effects in the case of various training protocols and therefore needs to be carefully assessed before designing training protocols and algorithms. In the current experiment a group of healthy adults (n = 14) was trained by professional trainers to up-regulate their beta1 (15–22 Hz) band for eight sessions. The control group (n = 18) underwent the same training regime but without rewards for increasing beta. In half of the participants trained to up-regulate beta1 band (n = 7) a systematic increase in tonic EMG activity was identified offline, implying that muscle activity became a foundation for reinforcement in the trainings. The remaining participants did not present any specific increase of the trained beta1 band amplitude. The training was perceived effective by both trainers and the trainees in all groups. These results indicate the necessity of proper control of muscle activity as a requirement for the genuine EEG-NFB training, especially in protocols that do not aim at the participants’ relaxation. The specificity of the information fed back to the participants should be of highest interest to all therapists and researchers, as it might irreversibly alter the results of the training.

Specific patterns of laryngeal electromyography during wakefulness are associated to sleep disordered breathing and nocturnal stridor in multiple system atrophy

BackgroundNocturnal stridor and respiratory abnormalities are important features of multiple system atrophy (MSA) with relevance to patient survival, and they are detected and evaluated mainly through video-polysomnography (video-PSG). Diurnal laryngoscopy seems to yield abnormal findings only in the presence of significant vocal cord (VC) dysfunction. AimTo assess whether specific electrophysiological patterns of diurnal EMG of VC muscles may indicate nocturnal stridor or respiratory dysfunctions in MSA patients. Materials and methodsSeventeen patients with probable MSA were examined. A full-night video-PSG to collect standard breathing parameters (apnea/hypopnea index, mean HbSAO2, oxygen desaturation index, total sleep time with HbSaO2 below 90%) was performed in all the patients. Laryngoscopy and EMG investigation of adductor (thyroarytenoid-TA) and abductor (posterior cricoarytenoid-PCA) muscles of the VCs were also performed. ResultsBoth the laryngeal EMG abnormalities (based on MUAP analysis and kinesiologic EMG investigation of VC muscles) and the laryngoscopic alterations correlated with video-PSG respiratory abnormalities. Specific patterns of EMG findings were consistently found in MSA subjects with nocturnal stridor detected at PSG. In particular, the following EMG findings were related to the severity of breathing abnormalities and the presence of stridor on video-PSG: neurogenic pattern on MUAP analysis of the PCA, paradoxical activation of the TA during inspiration and tonic EMG activity of the TA during quiet breathing. ConclusionsElectromyographic/kinesiologic investigation of VC muscles during wakefulness provides additional information on the pathophysiology of the respiratory abnormalities in MSA patients that could be useful for guiding the choice of the best appropriate treatment and care.

The role of the supporting lower limb function in the premotor changes in the H-reflex of m. soleus

In studies on healthy humans we examined changes in the H reflex amplitude and the intensity of background EMG of the soleus muscle within the premotor period of voluntary extension of the contralateral ankle joint. The tested persons were in the lying prone position with relaxed legs, or in the standing position with support on both feet or only on one foot with additional hand support. The soleus H reflex was induced using the standard technique by transcutaneous stimulation (1 ms long current pulses) of the tibial nerve afferents in the region of the popliteal dimple. Using superficial electrodes, we recorded the integral EMG reflex discharge from the m. soleus, amplified, and visualized it using a two-channel digital oscillograph, Handiscope HS3 (TiePieEngeneering, Netherlands). In other tests, we also recorded tonic background EMG activity from the soleus muscle. After fullwave rectification and low-frequency filtration we estimated the area under the integral curve enveloping oscillations of the above mentioned EMG. In the lying position the extension of contralateral ankle joint evoked anticipatory facilitation of the testing soleus H-reflex. It manifested in 90–60 ms and reached the maximum 30 ms before the conditioning movement. Considerable changes of the soleus background EMG-activity did not occur during the premotor period. Consequently, it is supposed that the mechanism leading to the H-reflex facilitation is the decrease of presynaptic inhibition at 1a. In the standing position with support on both feet contralateral ankle joint extension caused anticipatory inhibition of the soleus H-reflex and simultaneous suppression of background EMG 90–60 ms before the conditioning movement. These results indicate the anticipatory changes of muscle tone and suggest participation of postsynaptic mechanism in the inhibition of the testing H-reflex. When the moving contralateral extremity had no support, the contralateral ancle joint extension did not cause anticipatory inhibition but facilitation of the soleus H-reflex. Its time course was similar to that observed in the lying position. The considerable changes of the soleus background EMG-activity did not arise. The results of the experiments indicate that the nature of premotor changes in the spinal neuron circuits, associated with the lower limb muscles, depends not only on the type of upcoming voluntary movement. Being caused by the contralateral limb movements, they depend greatly on the fulfillment or nonfulfillment of the support function by the lower limbs.

Neurophysiological assessment of REM sleep behaviour disorder

REM sleep behaviour disorder (RBD) is characterized by violent dream-enacting behaviours associated with nightmares and increased EMG activity during REM sleep. RBD may be secondary to neurological diseases, particularly Parkinson’s disease, dementia with Lewy bodies, or multiple system atrophy. The majority of patients with idiopathic RBD will develop one of these synucleinopathies, indicating that this parasomnia represents in most instances the prodromal state of a neurodegenerative disease. RBD is also a treatable condition associated with injury potential. Thus, a correct diagnosis of RBD has relevant prognostic and treatment implications. Video-polysomnography (video-PSG) is mandatory for a definite RBD diagnosis. Video-polysomnography will rule out other conditions that can mimic RBD, such as obstructive sleep apnoea or periodic limb movement disorder. Video-polysomnography is also essential to record REM sleep-related behaviours or demonstrate REM sleep without atonia (RWA). RWA is defined as either excessive tonic or phasic EMG activity during REM sleep. However, excessive EMG activity is usually based on the scorer’s subjective impression and objective quantification is not routinely performed. Several manual and computer-assisted scoring methods of EMG activity in the chin and limb muscles have been developed, and recently quantitative EMG cut-off values for RBD diagnosis have been proposed.

Relation between postural sway magnitude and metabolic energy cost during upright standing on a compliant surface

Postural control performance is often described in terms of postural sway magnitude, assuming that lower sway magnitude reflects better performance. However, people do not typically minimize sway magnitude when performing a postural control task. Possibly, other criteria are satisfied when people select the amount of sway they do. Minimal metabolic cost has been suggested as such a criterion. The aim of this study was to experimentally test the relation between sway magnitude and metabolic cost to establish whether metabolic cost could be a potential optimization criterion in postural control. Nineteen healthy subjects engaged in two experiments in which different magnitudes of sway were evoked during upright standing on a foam surface while metabolic energy expenditure, center of pressure (CoP) excursion, and muscle activation were recorded. In one experiment, sway was manipulated by visual feedback of CoP excursion. The other experiment involved verbal instructions of standing still, natural or relaxed. In both experiments, metabolic cost changed with sway magnitude in an asymmetric parabolic fashion, with a minimum around self-selected sway magnitudes and a larger increase at small compared with large sway magnitudes. This metabolic response was paralleled by a change in tonic and phasic EMG activity in the major leg muscles. It is concluded that these results are in line with the notion that metabolic cost can be an optimization criterion used to set postural control and as such could account for the magnitude of naturally occurring postural sway in healthy individuals, although the pathway remains to be elucidated.

Validation of an integrated software for the detection of rapid eye movement sleep behavior disorder.

Rapid eye movement sleep without atonia (RWA) is the polysomnographic hallmark of REM sleep behavior disorder (RBD). To partially overcome the disadvantages of manual RWA scoring, which is time consuming but essential for the accurate diagnosis of RBD, we aimed to validate software specifically developed and integrated with polysomnography for RWA detection against the gold standard of manual RWA quantification. Academic referral center sleep laboratory. Polysomnographic recordings of 20 patients with RBD and 60 healthy volunteers were analyzed. N/A. Motor activity during REM sleep was quantified manually and computer assisted (with and without artifact detection) according to Sleep Innsbruck Barcelona (SINBAR) criteria for the mentalis ("any," phasic, tonic electromyographic [EMG] activity) and the flexor digitorum superficialis (FDS) muscle (phasic EMG activity). Computer-derived indices (with and without artifact correction) for "any," phasic, tonic mentalis EMG activity, phasic FDS EMG activity, and the SINBAR index ("any" mentalis + phasic FDS) correlated well with the manually derived indices (all Spearman rhos 0.66-0.98). In contrast with computerized scoring alone, computerized scoring plus manual artifact correction (median duration 5.4 min) led to a significant reduction of false positives for "any" mentalis (40%), phasic mentalis (40.6%), and the SINBAR index (41.2%). Quantification of tonic mentalis and phasic FDS EMG activity was not influenced by artifact correction. The computer algorithm used here appears to be a promising tool for REM sleep behavior disorder detection in both research and clinical routine. A short check for plausibility of automatic detection should be a basic prerequisite for this and all other available computer algorithms.

Effect of natural trunk inclination on variability in soleus inhibition and tibialis anterior activation during gait initiation in young adults

BackgroundAnticipatory postural adjustments (APAs) of gait initiation (GI) permit first step execution. APAs are characterized by a structured pattern of soleus (SOL) inhibition followed by tibialis anterior (TA) activation. This pattern shows variability among young adults where SOL is not always inhibited before TA activation. Initial posture preceding GI could explain a part of this variability. The aim of the study was to investigate the effect of natural trunk inclination on APAs during GI. MethodsTwo groups of twelve subjects divided by natural trunk inclination angle performed five gait initiation trials. A regression model was computed to predict SOL inhibition and TA activation. ResultsBackward leaners showed less SOL inhibition in stance leg (25.8% of trials) compared to forward leaners (55.6% of trials). Regression model revealed that high tonic EMG activity in SOL in the stance leg is the variable that best explains SOL inhibition variation within trials but not TA activation. ConclusionSlight variations in APAs are due to natural trunk inclination but more contribution in APAs is due to initial posture, future step speed and initial tonic soleus activity. Absence of SOL inhibition could be in part explained by natural trunk inclination, where the backward inclination leads to lower tonic SOL activity in quiet standing. These effects could be due to inherent and functional variability, which depend on postural variation, muscular coordination and limb roles.

Neurophysiological Markers of Stress within a Recovery Period after Acute Complications of Cardiovascular Diseases

In the course of rehabilitation in a sanatorium, we provided polygraphic examination of a group of 14 men who endured myocardial infarction or stroke one to three months ago. Fourteen men of a comparable age (55 years, on average), healthy from the aspect of diseases of the cardiovascular system, served as the control group. Examination was performed using a flexible data acquisition and feedback platform «Nexus-10 Mark II» (the Netherlands) allowing us to simultaneously record ECG, EMG, EEG, respiratory movements, pulse blood filling, skin temperature, electrodermal resistance, and a few other indices. It was found that patients suffering from complications of pathologies of the cardiovascular system were characterized by a significant increase in the electrodermal conductivity, clearly expressed tachypnea, and some trends toward tachycardia and decrease in the skin temperature. According to indices of the heart rate variability (HRV), the mean value of the Bayevskii stress index in patients was about three times higher than the analogous value in the control group, while the total power of the HRV spectrum was dramatically lower. The amplitude of tonic EMG activity recorded from mm. trapezii in the resting state considerably exceeded the respective value in control subjects. The amplitude of 8-13 Hz EEG oscillations in the Cz lead in patients was somewhat lower than in the control group, and increase in this index in the test with closing of the eyes in these subjects was manifested much slightly than in the control. Parallel recording of physiological (first of all, neurophysiological) indices allows researchers to effectively identify objective markers of the stress state developed after complications of diseases of the cardiovascular system; the respective data can be used in the curative procedures with the control of functions of the organism using a feedback technology by the parameters of activity of the functional systems (biofeedback control).

Clinical manifestations of Parkinson disease and the onset of rapid eye movement sleep behavior disorder

ObjectiveTo identify whether the presence and/or timing of rapid eye movement (REM) sleep behavior disorder (RBD) onset were associated with differences in clinical features and sleep parameters of Parkinson disease (PD). MethodsIn all, 112 PD patients were enrolled and all underwent extensive clinical evaluations and video-polysomnography (PSG). Clinical features and PSG parameters were compared in PD patients with (PD+RBD) or without (PD−RBD) RBD, RBD preceding (RBD>PD), or not (PD⩾RBD) PD onset. ResultsSixty-three of the 112 PD patients were affected by RBD. Adjusted for age, gender, education, body mass index (BMI), levodopa equivalent daily dose (LED) and PD duration, PD+RBD patients had higher Hoehn & Yahr stage, higher scores for UPDRS parts I, II and III, more dyskinesia, higher ratio of axial/limb manifestations, and more hallucinations. Their cognitive and quality-of-life status was significantly lower (all P<0.05). For PSG, PD+RBD patients exhibited higher percentages of phasic and tonic EMG activities, lower apnea hypopnea (AHI) and oxygen desaturation index (ODI), and less time in arterial oxygen saturation (SaO2) <90% during REM sleep (all P<0.05). PD⩾RBD (n=22) patients did not significantly differ from RBD>PD (n=41) patients in clinical manifestations, whereas the PD⩾RBD subgroup had significantly higher UPDRS part I score, lower PDQ score and lower AHI during REM than the PD−RBD group (all P<0.05), but not RBD>PD subgroup. Correlation analysis showed that worse cognition was associated with shorter interval of RBD preceding PD onset (r=0.297, P=0.018), but not RBD duration (P=0.202). ConclusionsClinical manifestations of PD may vary depending on the presence and timing of RBD onset. These findings are compatible with the hypothesis that RBD may be a marker of complex subtypes of PD.

Loss of Rapid Eye Movement Sleep Atonia in Patients with REM Sleep Behavioral Disorder, Narcolepsy, and Isolated Loss of REM Atonia

To compare the amounts of REM sleep without atonia (RSWA) between patients with REM sleep behavior disorder (RBD), "isolated loss of REM atonia," narcolepsy, and control subjects and determine if there were threshold values for the amount of RSWA that differentiate each group from controls. Retrospective analyses of polysomnography (PSG) records were used employing strict quantitative criteria for the measurement of phasic and tonic EMG activity during REM sleep. The PSG recordings of 47 individuals were analyzed (RBD 16, isolated loss of REM atonia 11, narcolepsy 10, control 10). Patients with the diagnosis of isolated loss of REM atonia had significantly lower levels of EMG activity during REM sleep than those with RBD but higher than control subjects. RSWA was higher in narcolepsy than in loss of REM atonia but lower than for RBD patients. Receiver operating characteristic (ROC) curves provided threshold values with high specificity and sensitivity in all patient groups with a cutoff value ≥ 1.22% (100% correctly classified) for phasic and ≥ 3.17% for tonic (92% correctly classified) EMG activity in RBD. Quantification of REM sleep EMG activity can successfully differentiate RBD and isolated loss of REM atonia patients from controls. The consistently increased amount of RSWA in patients with narcolepsy indicates that this can be an additional marker for a diagnosis of narcolepsy. Longitudinal studies of patients with isolated loss of REM atonia are needed to evaluate if these patients are at risk of developing RBD or neurodegenerative disorders.

Does Controlling for the Magnitude of Tonic EMG Activity Decrease the Variability in the cVEMP Measures?

Does Controlling for the Magnitude of Tonic EMG Activity Decrease the Variability in the cVEMP Measures?

種々の疾患にともなう首下がり症候群の病態生理学的分析―表面筋電図所見と理学療法の効果から―

Dropped head syndrome is seen in various diseases. We investigated its pathophysiological mechanisms with physical and radiological examination, surface EMG and responses to physiotherapy. Subjects had dropped head as a complaint, but their primary diagnoses were various. We investigated 16 cases: 5 cases of Parkinson disease, 5 cases of multiple system atrophy predominant parkinsonism, 3 cases of cervical spondylosis and 3 cases with other diagnoses. We found that patients had common findings such as bulging of cervical muscles, and tonic EMG activities mainly in the extensors in the sitting and standing position, but in the flexors of the neck only in the supine position. Of the 16 cases, 14 were treated with physiotherapy to improve the alignment of the pelvis and whole vertebral column; 6 of the 14 cases (63%) showed remarkable improvement. We conclude that the primary reason of dropped head syndrome is unknown in Parkinson disease and cervical spondylosis, but also that many of the patients have secondary changes in alignment of the skeletomuscular system which could be treated with physiotherapy.