Tonic EMG Activity Research Articles

M-H-074 TONIC AND PHASIC MUSCLE ACTIVITY IN REM SLEEP BEHAVIOR DISORDER

Introduction and Objectives: REM sleep behavior disorder (RBD) is characterized by the loss of the normal REM sleep skeletal muscle atonia, resulting in complex motor behaviors associated with dream mentation. The polysomnographical hallmarks of RBD include tonic/phasic loss of the muscle atonia of REM sleep (REM sleep without atonia; RWA). However, scoring RWA is not well established. We will describe our methods of scoring RWA and will discuss some unsolved issues of RWA scoring. Materials and Methods: The diagnosis of RBD was made based on the International Classification of Sleep Disorders 2nd criteria. The subjects were 20 consecutive patients (19 male and 1 female, mean age: 67.9±7.8 years) who underwent full PSG. In our RWA scoring based on “The AASM Manual for Scoring 2007”, increased EMG activity was counted separately according to the EMG activity patterns; tonic EMG, phasic pattern, and combined EMG activities. If chin EMG activity was present for more than 50% of each 30-second epoch, that epoch was scored as tonic. Phasic EMG density was scored from the chin EMG and represented the percentage of 3 second mini-epochs containing EMG activity lasting 0.1 to 5 seconds. We calculated the percentage of RWA, tonic REM, phasic and REM density. Results: The mean values of the proportions of REM and RWA as a percentage of total sleep time were 19.7±6.3% and 7.2±4.6%. The mean values of tonic REM percentage and phasic EMG activity during REM sleep were 26.0±19.8% and 18.7±7.9%. Conclusion: Some groups have reported cut off or mean values of RWA to diagnose RBD or to identify a predictor for the development of neurodegenerative diseases. Compared to this data, our tonic REM percentage and phasic activity was low. The causes of differences were unclear. Further investigation including a large scale study population will be necessary to clarify the adequate values.

GABAergic control of micturition within the periaqueductal grey matter of the male rat.

In urethane-anaesthetised rats continuous infusion of saline into the bladder (6 ml h⁻¹) evoked periodic sharp rises in intravesicular pressure accompanied by rhythmic bursting of external urethral sphincter (EUS) EMG and expulsion of urine from the urethral meatus. Microinjection of the GABA agonist muscimol (250 pmol) into the caudal ventrolateral periaqueductal grey (PAG), but not at other sites in the PAG, either depressed reflex voiding frequency (-60%, n = 7) and tonic EUS EMG activity (-38%, n = 6) or completely inhibited voiding (four sites). Microinjection of the GABA antagonist bicuculline (BIC; 1 nmol) into the same region, to reduce ongoing GABA tone, increased reflex voiding frequency (+467%, n = 16) and tonic activity in the EUS (+56%, n = 7) whilst bursting activity in the EUS became desynchronised. Although muscimol failed to change reflex micturition when microinjected into the dorsal caudal PAG, microinjection of BIC at these sites evoked pronounced autonomic arousal and increased reflex voiding frequency (+237%, n = 34). The results demonstrate that the functional integrity of synapses in the caudal ventrolateral PAG is essential to permit micturition. Transmission through the region is normally regulated by a tonic GABAergic inhibitory influence. In contrast, the functional integrity of the dorsal caudal PAG is not essential for reflex micturition. However, micturition may be initiated from this region via projections to the caudal ventrolateral PAG, as part of the behavioural response to psychological threat or other stressful stimuli.

BPCO, sindrome delle apnee ostruttive del sonno e disturbi del sonno

To 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).In 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.Sixty-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).Clinical 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.

Polysomnographic diagnosis of idiopathic REM sleep behavior disorder

The presence of either excessive tonic chin EMG activity during REM sleep, or excessive phasic submental or limb EMG twitching is required to diagnose REM sleep behavior disorder (RBD). The aim was to identify cut-off values and to assess the sensitivity and specificity of these values taken separately or combined to diagnose idiopathic RBD patients. Eighty patients presenting with a clinical diagnosis of idiopathic RBD and 80 age- and gender-matched normal controls were studied in the sleep laboratory. Receiver operating characteristic curves were drawn to find optimal cut-off values for three REM sleep EMG parameters. Tonic and phasic EMG activity were measured in the chin, but not in the limbs. Videos were examined during the recording but were not systematically reviewed by the authors. Total correct classification of 81.9% was found for tonic chin EMG density ≥30%; 83.8% for phasic chin EMG density ≥15% and 75.6% for ≥24 leg movements per hour of REM sleep. Five patients did not fulfill any of these three polysomnographic (PSG) criteria. Conversely, one subject of the control group met the PSG criteria for RBD. This study estimates the diagnostic value of a visual scoring method for the diagnosis of idiopathic RBD and establishes cut-off values to be used in clinical and research set-ups. For the five RBD patients who did not show chin EMG abnormalities, it cannot be excluded that they had increased phasic EMG activity in the upper limbs and presented visible motor activity.

Airway Dilator Muscle Activity and Lung Volume During Stable Breathing in Obstructive Sleep Apnea

Many patients with obstructive sleep apnea (OSA) have spontaneous periods of stable flow limited breathing during sleep without respiratory events or arousals. In addition, OSA is often more severe during REM than NREM and more severe during stage 2 than slow wave sleep (SWS). The physiological mechanisms for these observations are unknown. Thus we aimed to determine whether the activity of two upper airway dilator muscles (genioglossus and tensor palatini) or end-expiratory lung volume (EELV) differ between (1) spontaneously occurring stable and cyclical breathing and (2) different sleep stages in OSA. Physiologic observation. Sleep physiology laboratory. 15 OSA patients with documented periods of spontaneous stable breathing. Subjects were instrumented with intramuscular electrodes for genioglossus and tensor palatini electromyograms (EMG(GG) and EMG(TP)), chest and abdominal magnetometers (EELV measurement), an epiglottic pressure catheter (respiratory effort), and a mask and pneumotachograph (airflow/ventilation). Patients slept supine overnight without CPAP. Peak and Tonic EMG(GG) were significantly lower during cyclical (85.4 +/- 2.7 and 94.6 +/- 4.7 % total activity) than stable breathing (109.4 +/- 0.4 and 103 +/- 0.8% total activity, respectively). During respiratory events in REM, tonic EMG(GG) activity was lower than during respiratory events in stage 2 (71.9 +/- 5.1 and 119.6 +/- 5.6% total activity). EMG(GG) did not differ between stable stage 2 and stable SWS (98.9 +/- 3.2 versus 109.7 +/- 4.4% total activity), nor did EMG(TP) or EELV differ in any breathing condition/sleep stage. Increased genioglossus muscle tone is associated with spontaneous periods of stable flow limited breathing in the OSA subjects studied. Reductions in genioglossus activity during REM may explain the higher severity of OSA in that stage. Increased lung volume and tensor palatini activity do not appear to be major mechanisms enabling spontaneous stable flow limited breathing periods.

Diagnosis of REM Sleep Behavior Disorder by Video-Polysomnographic Study: Is One Night Enough?

Clinical features of RBD were typically episodic with limited data on the night-to-night reliability of the diagnostic video-PSGs. We aimed to assess on whether a single night study was adequate. Retrospective review. Sleep laboratory. 55 RBD patients with at least 2 consecutive video-PSGs. N/A. We analyzed 2 consecutive video-PSGs using REM-related EMG activity (REMREEA), REM sleep without atonia (RSWA), and video analysis of motor events. A weak first night effect with increased REM sleep latency, increased stage 1 sleep, and increased arousal index were found. No differences were found in phasic and tonic EMG activity scores between night 1 and night 2. The presence of OSAS, use of CPAP, and clonazepam treatment did not affect the night-to-night variability and diagnostic accuracy. The kappas were 0.64, 0.51, and 0.31 between night 1 and night 2 for 10% REMREEA, RSWA, and video analysis respectively. Over 80% of patients could be diagnosed by various criteria in the first night, but the diagnostic ability could be enhanced to nearly 95% when combining PSG with video analysis. While both of the EMG criteria as well as the combination criteria had good reliability, video-analysis had poorer night-to-night reliability. A single night of video-PSG was adequate in the diagnosis of RBD in most clinical patients and the combination of PSG and video analysis could enhance the detection rate further. Our findings have important resource implications.

Task‐related changes in propriospinal excitation from hand muscles to human flexor carpi radialis motoneurones

This study addresses whether there is excitation from human hand muscles to flexor carpi radialis (FCR) motoneurones mediated through propriospinal circuits and, if so, whether it is used in specific motor tasks. Electrical stimuli to the ulnar nerve at wrist level produced an excitation in FCR motoneurones with characteristics typical of a propriospinally mediated effect: low threshold (0.6 x motor threshold (MT)), a group I effect that was not reproduced by purely cutaneous stimuli, long central delay (4.1 +/- 0.4 ms in single units), suppression when the stimulus intensity was increased, and facilitation of the corticospinal excitation at the premotoneuronal level. Ulnar-induced propriospinally mediated excitation was compared during selective voluntary contractions of the FCR and, at equivalent level of FCR EMG, during tasks in which the FCR was activated automatically in postural contractions rather than voluntarily (grip, pinching and pointing). The excitation was significantly greater during grip (and pinching) than during voluntary FCR contractions and pointing, whether measured in single motor units or tonic EMG activity, or whether the response to motor cortex stimulation was assessed as the compound motor-evoked potential or the corticospinal peak in single units. The discrepancy between the tasks appeared with ulnar intensities above 0.8 x MT and was then present across a wide range of stimulus intensities. This suggests a reduction in the corticospinal control of 'feedback inhibitory interneurones' mediating peripheral inhibition to propriospinal neurones during grip and pinching. The resulting more effective background excitation of propriospinal neurones by the peripheral input from hand muscles could contribute to stabilizing the wrist during grip.

Negative myoclonus. An overview of its clinical features, pathophysiological mechanisms, and management

Negative myoclonus (NM) is an unspecific motor disorder that can characterize a variety of neurological conditions. From the clinical point of view, NM appears as a shock-like involuntary jerky movement caused by a sudden, brief interruption of muscle activity. Asterixis is a type of NM that occurs typically in toxic-metabolic encephalopathies. NM of epileptic nature, or epileptic negative myoclonus (ENM), is defined as an interruption of tonic muscle activity, which is time-locked to an epileptic EEG abnormality, without evidence of an antecedent positive myoclonia in the agonist–antagonist muscles. ENM can be observed in idiopathic, cryptogenic, and symptomatic epileptic disorders. Pathophysiological hypotheses on the origin of NM involve subcortical as well as cortical mechanisms. Recent neuroimaging and neurophysiologic investigations, including intracerebral recordings and electrical stimulation procedures in epileptic patients, suggest the participation of premotor, primary motor, primary sensory, and supplementary motor areas in the genesis of NM. Polygraphic monitoring is essential for the diagnosis of NM, allowing the demonstration of brief interruptions of a tonic EMG activity, not preceded by a positive myoclonus in the agonist and antagonist muscles of the affected limb. Simultaneous EEG-EMG monitoring demonstrating the association of NM with an epileptic potential is consistent with the diagnosis of ENM. Evolution and prognosis of NM is mainly related to aetiology. In childhood idiopathic partial epilepsy, ENM can respond to some drugs (in particular, ethosuximide), whereas other medications (such as carbamazepine or phenytoin) have been reported to induce or worsen it.

Physiologically adaptive changes of the L5 afferent neurogram and of the rat soleus EMG activity during 14 days of hindlimb unloading and recovery

The hindlimb unloading rat model (HU, Morey's model) is usually used to mimic and study neuromuscular changes that develop during spaceflights. This Earth-based model of microgravity induces a muscular atrophy of the slow postural muscle of hindlimbs, such as the soleus, a loss of strength, modifications of contraction kinetics, changes in histochemical and electrophoretical profiles and modifications of the tonic EMG activity. It has been suggested in the literature that some of these neuromuscular effects were due to a reduction of afferent feedback during HU. However, no direct data have confirmed this hypothesis. The aim of this study was to clearly establish if changes of the L5 afferent neurogram are closely related to the soleus EMG activity during and after 14 days of HU. Immediately after HU, the EMG activity of the soleus muscle disappeared and was associated with a decrease in the afferent neurogram. The soleus electromyographic and afferent activities remained lower than the pre-suspension levels until the sixth day of HU and were recovered between the sixth and the ninth day. On the twelfth and fourteenth days, they were increased beyond the pre-suspension levels. During the first recovery day, these activities were significantly higher than those on the fourteenth HU day and returned to the pre-suspension levels between the third and sixth recovery days. To conclude, our study directly demonstrates that the HU conditions cannot be considered as a functional deafferentation, as suggested in the literature, but only as a reduction of afferent information at the beginning of the HU period.

Timing of cortical excitability changes during the reaction time of movements superimposed on tonic motor activity

Seated subjects were instructed to react to an auditory cue by simultaneously contracting the tibialis anterior (TA) muscle of each ankle isometrically. Focal transcranial magnetic stimulation of the leg area of the motor cortex (MCx) was used to determine the time course of changes in motor-evoked potential amplitude (MEP) during the reaction time (RT). In one condition the voluntary contraction was superimposed on tonic EMG activity maintained at 10% of maximal voluntary contraction. In the other condition the voluntary contraction was made starting from rest. MEPs in the TA contralateral to the stimulation coil were evoked at various times during the RT in each condition. These were compared to the control MEPs evoked during tonic voluntary activity or with the subject at rest. The RT was measured trial by trial from the EMG activity of the TA ipsilateral to the magnetic stimulus, taking into account the nearly constant time difference between the two sides. The MEPs became far greater than control MEPs during the RT (mean = 332%, SD = 44 %, of control MEPs, P < 0.001) without any measurable change in the background level of EMG activity. The onset of this facilitation occurred on average 12.80 ms (SD = 7.55 ms) before the RT. There was no difference in the onset of facilitation between the two conditions. Because MEPs were facilitated without a change in the background EMG activity, it is concluded that this facilitation is specifically due to an increase of MCx excitability just before voluntary muscle activation. This conclusion is further reinforced by the observation that MEPs evoked by near-threshold anodal stimuli to the MCx were not facilitated during the RT, in contrast to those evoked by near-threshold transcranial magnetic stimulation. However, several observations in the present and previous studies indicate that MEP amplitude may be more sensitive to alpha-motoneuron activity than to motor cortical neuron activity, an idea that has important methodological implications.

Dysfunction of transcallosally mediated motor inhibition and callosal morphology in patients with schizophrenia.

In order to assess the functional integrity of motor pathways through the corpus callosum (CC) in patients with schizophrenia transcallosally mediated inhibition (TI) of voluntary tonic EMG activity of first dorsal interosseus muscle following ipsilateral focal transcranial magnetic stimulation (fTMS) was investigated. In addition thickness and length of CC were calculated. Twelve patients suffering from schizophrenia and 12 healthy controls were investigated. CC morphology was measured in mid-sagittal MRI-slices. Latency and duration of TI were calculated. In schizophrenics the duration of TI was significantly prolonged, whereas latencies were not. In addition, a lack of TI was found unilaterally in three patients. Measurements of CC revealed a significantly reduction of the length and thickness in the anterior part of CC in patients. These findings indicate that measurement of TI could be used to detect clinical silent affection of transcallosal motor pathways in schizophrenics. The effect of neuroleptic drugs has to be explored.

SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats.

The aim of the present study was to find out whether blockade of adenosine A(2A) receptors by a selective antagonist, SCH 58261, influenced parkinsonian-like muscle rigidity. Muscle tone was examined using a combined mechano- and electromyographic method which simultaneously measured muscle resistance (MMG) of a rat hindfoot to passive extension and flexion in the ankle joint and electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity produced by reserpine (5 mg/kg + alpha-methyl-p-tyrosine, 250 mg/kg) was antagonized by SCH 58261 (0.1-5 mg/kg). SCH 58261 (5 mg/kg) also reduced reserpine-enhanced tonic and reflex EMG activities in both the gastrocnemius and the tibialis muscles. Moreover, SCH 58261 in doses of 1 and 5 mg/kg abolished muscle resistance induced by haloperidol (0.5 mg/kg). However, only the highest dose of SCH 58261 (5 mg/kg) decreased tonic EMG activity enhanced by haloperidol. Administration of L-DOPA (75 and 100 mg/kg) dose-dependently decreased the muscle resistance as well as tonic EMG activity evoked by haloperidol. Combined administration of SCH 58261 (0.1 mg/kg) and L-DOPA (50 mg/kg) in doses which did not affect the haloperidol-induced muscle rigidity produced a pronounced synergistic effect. The ability of SCH 58261 to diminish the parkinsonian-like muscle rigidity and to potentiate the effect of L-DOPA in this model seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.

Quantitative measures of spasticity in post-stroke patients

Objective: Quantitative evaluation of muscle tone in post-stroke patients; correlation of biomechanical indices with conventional clinical scales and neurophysiological measures; characterization of passive and neural components of muscle tone.Methods: Mechanical stretches of the wrist flexor muscles of 53 post-stroke patients were imposed by means of a torque motor at constant speed. Patients were clinically studied using the Ashworth scale for spasticity and the Medical Research Council score for residual muscle strength. The neurophysiological measures were Hoffmann reflex latency, Hmax/Mmax ratio, stretch reflex threshold speed (SRTS), stretch reflex (SR) latency and area, passive (ISI) and total (TSI) stiffness indices.Results: Hmax/Mmax ratio, SR area, ISI and TSI values were significantly higher in patients, while SRTS was significantly lower. TSI, SRTS and SR area were highly correlated to the Ashworth score.Conclusions: This EMG-biomechanical technique allows an objective evaluation of changes in muscle tone in post-stroke patients, providing easily measurable, quantitative indices of muscle stiffness. The linear distribution of these measures is particularly indicated for monitoring changes induced by treatment. The apparatus seems suitable to characterize neural stiffness, while difficulties were found in isolating the passive components, because of the occurrence of tonic EMG activity in most spastic patients.

Effects of eye rotation on the sound-evoked post-auricular muscle response (PAMR)

One objective electrophysiological test for deafness involves presenting a brief acoustic stimulus to a subject and measuring the electrical activity evoked in the muscle located just behind the ear (the post-auricular muscle or PAM). We describe a method for enhancing this post-auricular muscle response (PAMR) using lateral eye movement, which increases both the tonic EMG activity in the PAM and the magnitude of the PAMR, and decreases response latency. EMG activity in most subjects tested (more than 30) increased almost instantly on rotation of the eyes, and thereafter grew more slowly with maintained lateral gaze, with the largest increase occurring with eye rotation towards rather than away from the measurement electrodes over the PAM. The EMG activity returned rapidly to near pre-rotation levels when the eyes were returned to the forwards position, with full recovery taking some minutes. While there was a similar increase and return of the PAMR amplitude with eye rotation, the time-course of these changes was somewhat different, largely because the EMG activity and the PAMR amplitude were not proportional. Rather the PAMR amplitude was a saturating function of EMG level, so that the PAMR response did not fall as markedly as the EMG when the eyes were returned to a forwards gaze, and the recovery of the PAMR amplitude to pre-rotation levels appeared to take longer. We discuss the neural mechanisms that may be responsible for this PAMR potentiation with eye movement and discuss its probable role in increasing variability in early studies which did not control for eye movement. We also discuss the utility of eye rotation in potentiating and stabilising the PAMR to allow its use in screening for deafness.

Effect of Two Antidepressant Drugs on REM Sleep and EMG Activity during Sleep

In a placebo-controlled study, the effects on sleep of single and repeated doses of imipramine and dexnafenodone, an antidepressant drug under development, were investigated in young, healthy volunteers. In contrast to placebo, both drugs suppressed REM sleep substantially after acute and repeated administration. As a consequence, REM sleep latencies increased under active treatment to mean values which were about two to four times larger than baseline values. Since the active inhibition of the muscle tone is a distinct feature of REM sleep, we studied the influence of the two antidepressant drugs on this variable. By means of computerised EMG analysis, tonic and transient EMG activity were computed for total recording time and for the different sleep stages. While tonic EMG activity during sleep was increased with both drugs, transient EMG events remained unaffected. Computerised analysis of the microstructure of sleep is an effective tool for studying the effect of antidepressant drugs on sleep.

Callosal and corticospinal tract function in patients with hydrocephalus: a morphometric and transcranial magnetic stimulation study.

In 15 patients with symptomatic hydrocephalus, pressure-induced morphological changes of the brain and the function of callosal and corticospinal fibres were studied. Morphometry of the corpus callosum (CC) was performed on midsagittal MR images. Focal transcranial magnetic stimulation of the motor cortex was used to assess simultaneously excitatory motor responses in contralateral hand muscle (corticospinally mediated effect) and inhibition of tonic EMG activity in ipsilateral hand muscles (transcallosal inhibition (TI) of the contralateral motor cortex). Before a shunt operation, the midsagittal area of the CC was reduced by 34% on average. The height and, to a lesser degree the length, of the CC were increased before the shunt operation. Thresholds and central motor latencies of corticospinally mediated responses were normal, response amplitudes were smaller than in normal subjects. Motor thresholds increased from 38, SD 5 to 52, SD 8% (P < 0.01) within 7 days after ventricular drainage, reflecting the increase in the distance between stimulation coil and brain. The threshold increase paralleled a restoration of normal anatomical conditions within 7 days after shunt operation and the improvement of motor symptoms and might be a predictor of successful decompression. Transcallosal inhibition could be elicited in all patients. The measurements of TI lay within the normal range except the duration, which was prolonged in 73% of 15 patients before shunt operation as a probable indicator of an increased dispersion of callosal conduction. The normalization of the area and shape of the CC after shunt operation and the normal corticospinal and callosal conduction times exclude degeneration, demyelination or functional block of a large proportion of callosal or corticospinal tract fibres or a substantial loss of nerve cells in motor cortex.

Control of upright standing posture during low-frequency linear oscillation

We examined the effects of anteroposterior movement of a sled on human upright standing. Each of six healthy men stood on the platform of a sled in the dark. The sinusoidal acceleration was provided, from 0.02 to 0.04 G, followed by 0.06 and 0.08 G, at a stroke length from 6 to 10 m and then to 14 m. Low acceleration (0.02 and 0.04 G) induced body sway, pivoting on the ankle joint. High acceleration (0.06 and 0.08 G) increased body sway, but the head-neck joint remained locked upright. The electromyographic recordings of the lower leg muscles revealed continuous tonic EMG activities of the gastrocnemius and tibialis anterior muscles at acceleration of 0.02 and 0.04 G, while reciprocal activation was observed at 0.06 and 0.08 G. During head movement, the neck muscles were slightly activated tonically at acceleration of 0.02 and 0.04 G, but they were markedly and tonically activated at 0.06 and 0.08 G. We speculate that the sled oscillation caused body sway in proportion to the acceleration, with the ankle joint playing a principal role. Analysis of neck movement also revealed that the head was held in a fixed upright position, indicating that the vestibulocollic reflex might tonically activate the neck muscles.

FFT analysis of EEG during stage 2-to-REM transitions in narcoleptic patients and normal sleepers

The EEG in REM sleep is markedly different from the EEG in non-REM sleep; however, very little research has been conducted analyzing the transition from NREM to REM sleep. The purpose of this study was to describe the changes in EEG power spectra that coincide with significant physiological events throughout the transition from stage 2 to REM sleep. Furthermore, a comparison of the stage 2 to REM transition between narcoleptic patients and normal sleepers was conducted. Five female and five male patients diagnosed with narcolepsy-cataplexy and 10 normal sleepers matched for age and gender participated. Analyses were based on the consecutive appearance of 3 common physiological indicators of REM sleep: First, a decrease in tonic submental EMG activity; second, the appearance of saw tooth waves; and third, the appearance of rapid eye movements. Systematic changes in EEG power density were evident for delta, theta, alpha and sigma frequencies, across the stage 2-REM transition. These changes appeared to be relatively continuous throughout this transition rather than changing dramatically following the onset of any one of the 3 primary physiological indicators of REM sleep. Furthermore, the transition from stage 2 to stage REM appeared to be similar for narcoleptic patients and normal sleepers.

Breathing when chest wall muscle are tonically contracted for isometric, non-respiratory tasks.

We have previously shown that regional chest wall impedance increases when the chest wall muscles are tonically contracted to perform isometric, non-respiratory tasks. To test how this affects breathing, we measured respiratory frequency, tidal volume, end-tidal PCO2, electromyographic activity (EMG) at four points on the chest wall surface, and regional displacements across six planes of the chest wall during maintenance of three different postures that necessitated strong tonic respiratory muscle contraction. These postures included a static push-up, a bilateral leg-lift and a partial sit-up. The subjects (n = 8) were able to maintain the postures for 1.5-2.5 min, and strong tonic EMG activity was observed in each posture at all points measured. The rate and depth of breathing and pattern of regional chest wall displacements were variable within the group of subjects and among the three postures. However, minute ventilation increased and end-tidal PCO2 decreased in each subject during each posture (P < 0.05). In six of the eight subjects, transdiaphragmatic pressure (Pdi) was measured during 1 min of the same exercises. The ratio of the breathing fluctuation in Pdi to tidal volume was at least twice as high compared with rest, except for two subjects during the leg-lifts. We conclude that strong tonic contraction of the chest wall muscles impedes, but does not limit, breathing, and that there is no single breathing strategy used during such conditions.

Antiparkinsonian effect of flupirtine in monoamine-depleted rats.

Excitatory amino acid receptor antagonists lead to marked suppression of parkinsonian-like symptoms in rodent and primate models of Parkinson's disease and are able to potentiate the ability of L-DOPA to reverse akinesia and ameliorate muscular rigidity displayed in these animal models. Flupirtine, which is clinically used as a non-opioid analgesic agent, has some N-methyl-D-aspartate (NMDA) antagonistic properties in several in vivo and in vitro experiments. We now report that in monoamine depleted rats (pretreated with reserpine, 5 mg/kg, and alpha-methyl-para-tyrosine, 250 mg/ kg i.p.) flupirtine dose-dependently (1-20 mg/kg i.p.) suppressed rigidity, measured as tonic EMG activity in the gastrocnemius muscle, but had no effect on akinesia, measured as locomotor activity. In addition, it potentiated the antiparkinsonian effect of L-DOPA on akinesia and rigidity in this rodent model of Parkinson's disease. These effects of flupirtine are of particular clinical relevance, since flupirtine is devoid of the typical side effects of NMDA-receptor antagonists.