The effects of electromyography-triggered neuromuscular electrical stimulation plus tilt sensor functional electrical stimulation training on gait performance in patients with subacute stroke: a randomized controlled pilot trial.

The effects of electromyography-triggered neuromuscular electrical stimulation and tilt sensor functional electrical stimulation on ankle dorsiflexion during walking are unclear. This study investigated whether combined electrical stimulation training affects gait performance in patients with stroke. Thirty-six patients were randomly assigned to a control (n = 13), electromyography-triggered neuromuscular electrical stimulation training (single electrical stimulation group, n = 12), or a combined electromyography-triggered neuromuscular electrical stimulation and tilt sensor functional electrical stimulation training (combined electrical stimulation group, n = 11) group. Both experimental groups undertook 60-minute interventions for two weeks. All patients' gait performances were evaluated according to walking speed and trunk acceleration during 10-meter walking tests undertaken pre-intervention and at two weeks post-intervention. A wireless triaxial accelerometer measured trunk acceleration, and the root mean square values of the vertical, mediolateral, and anterioposterior planes were calculated from randomly selected 10-step sequences. Compared with baseline, the 10-meter walking tests improved significantly after two weeks in the single and combined electrical stimulation groups. In the combined electrical stimulation group, the 10-meter walking tests scores and root mean square of the mediolateral plane improved significantly compared with those in the control group. Electromyography-triggered neuromuscular electrical stimulation and tilt sensor functional electrical stimulation training may improve body perturbation stability and walking quality.

Effects of neuromuscular electrical stimulation in patients with heart failure - review.

Research conducted in the last two decades suggests that neuromuscular electrical stimulation of the lower limb muscles (NMES) may be a "bridge" to conventional exercise or an alternative for patients with advanced chronic heart failure (CHF), non-compliant or non-responsive to physical training. Through stimulating the work of the skeletal muscles, NMES increases the functional capacity, muscle mass and endurance in patients with CHF. A beneficial effect of NMES on functional capacity, vascular endothelial function, quality of life and aerobic enzymes activity has been shown. A significant benefit of this novel therapy in heart failure is the fact that the procedure can be home-based, after prior guidance of the patient.

A role for nutritional intervention in addressing the aging neuromuscular junction.

The purpose of this review is to discuss the structural and physiological changes that underlie age-related neuromuscular dysfunction and to summarize current evidence on the potential role of nutritional interventions on neuromuscular dysfunction-associated pathways. Age-related neuromuscular deficits are known to coincide with distinct changes in the central and peripheral nervous system, in the neuromuscular system, and systemically. Although many features contribute to the age-related decline in neuromuscular function, a comprehensive understanding of their integration and temporal relationship is needed. Nonetheless, many nutrients and ingredients show promise in modulating neuromuscular output by counteracting the age-related changes that coincide with neuromuscular dysfunction. In particular, dietary supplements, such as vitamin D, omega-3 fatty acids, ß-hydroxy-ß-methylbutyrate, creatine, and dietary phospholipids, demonstrate potential in ameliorating age-related neuromuscular dysfunction. However, current evidence seldom directly assesses neuromuscular outcomes and is not always in the context of aging. Additional clinical research studies are needed to confirm the benefits of dietary supplements on neuromuscular function, as well as to define the appropriate population, dosage, and duration for intervention.

Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management.

Since the publication of the Duchenne muscular dystrophy (DMD) care considerations in 2010, multidisciplinary care of this severe, progressive neuromuscular disease has evolved. In conjunction with improved patient survival, a shift to more anticipatory diagnostic and therapeutic strategies has occurred, with a renewed focus on patient quality of life. In 2014, a steering committee of experts from a wide range of disciplines was established to update the 2010 DMD care considerations, with the goal of improving patient care. The new care considerations aim to address the needs of patients with prolonged survival, to provide guidance on advances in assessments and interventions, and to consider the implications of emerging genetic and molecular therapies for DMD. The committee identified 11 topics to be included in the update, eight of which were addressed in the original care considerations. The three new topics are primary care and emergency management, endocrine management, and transitions of care across the lifespan. In part 1 of this three-part update, we present care considerations for diagnosis of DMD and neuromuscular, rehabilitation, endocrine (growth, puberty, and adrenal insufficiency), and gastrointestinal (including nutrition and dysphagia) management.

Neuromuscular Electrical Stimulation and Anabolic Signaling in Patients with Stroke.

INTRODUCTION: Stroke results in limited ability to produce voluntary muscle contraction and movement on one side of the body, leading to further muscle wasting and weakness. Neuromuscular electrical stimulation is often used to facilitate involuntary muscle contraction; however, the effect of neuromuscular electrical stimulation on muscle growth and strengthening processes in hemiparetic muscle is not clear. This study examined the skeletal muscle anabolic response of an acute bout of neuromuscular electrical stimulation in individuals with chronic stroke and healthy older adults. METHODS: Eleven individuals (59.8 ± 2.7 years old) were divided into a chronic stroke group (n = 5) and a healthy older adult control group (n = 6). Muscle biopsies were obtained before and after stimulation from the vastus lateralis of the hemiparetic leg for the stroke group and the right leg for the control group. The neuromuscular electrical stimulation protocol consisted of a 60-minute, intermittent stimulation train at 60 Hz. Phosphorylation of mammalian target of rapamycin and ribosomal protein S6 kinase beta-1 were analyzed by Western blot. FINDINGS: An acute bout of neuromuscular electrical stimulation increased phosphorylation of mammalian target of rapamycin (stroke: 56.0%; control: 51.4%; P = .002) and ribosomal protein S6 kinase beta-1 (stroke: 131.2%; control: 156.3%; P = .002) from resting levels to post-neuromuscular electrical stimulation treatment, respectively. Phosphorylated protein content was similar between stroke and control groups at both time points. CONCLUSION: Findings suggest that paretic muscles of patients with chronic stroke may maintain ability to stimulate protein synthesis machinery in response to neuromuscular electrical stimulation.

Vitamin D and/or calcium deficient diets may differentially affect muscle fiber neuromuscular junction innervation.

INTRODUCTION: There is evidence that supports a role for Vitamin D (Vit. D) in muscle. The exact mechanism by which Vit. D deficiency impairs muscle strength and function is not clear. METHODS: Three-week-old mice were fed diets with varied combinations of Vit. D and Ca2+ deficiency. Behavioral testing, genomic and protein analysis, and muscle histology were performed with a focus on neuromuscular junction (NMJ) -related genes. RESULTS: Vit. D and Ca2+ deficient mice performed more poorly on given behavioral tasks than animals with Vit. D deficiency alone. Genomic and protein analysis of the soleus and tibialis anterior muscles revealed changes in several Vit. D metabolic, NMJ-related, and protein chaperoning and refolding genes. CONCLUSIONS: These data suggest that detrimental effects of a Vit. D deficient or a Vit. D and Ca2+ deficient diet may be a result of differential alterations in the structure and function of the NMJ and a lack of a sustained stress response in muscles. Muscle Nerve 54: 1120-1132, 2016.

Modelling the response to low-frequency repetitive nerve stimulation of myasthenia gravis and Lambert-Eaton myasthenic syndrome.

Myasthenia gravis (MG) is an autoimmune postsynaptic disorder of neuromuscular transmission caused, in most patients, by antibodies against postsynaptic acetylcholine receptors. Lambert-Eaton myasthenic syndrome (LEMS) is a presynaptic autoimmune disease in which there is a reduction in Ca2+ entry with each impulse due to the action of antibodies against Ca2+ channels. These diseases have a distinct pattern of response to low-frequency repetitive nerve stimulation which allows its recognition in a particular subject. Nevertheless, the physiologic basis of this response is not entirely known. A model of the time-course of release probability of neuromuscular junctions that incorporates facilitation and a depression-recovery mechanism has been developed with the aim to investigate these response patterns. When the basal value of release probability was in the physiologic range, as in MG, release probability showed an increment after its initial decrease only if the recovery from depression was accelerated by presynaptic residual Ca2+. Otherwise, when the basal release probability was low, as in LEMS, a progressive reduction in the release probability without any late increase was only obtained if the efficacy of Facilitation and Ca2+-dependent recovery from depression were reduced.

Functional and Morphological Correlates in the Drosophila LRRK2 loss-of-function Model of Parkinson's Disease: Drug Effects of Withania somnifera (Dunal) Administration.

The common fruit fly Drosophila melanogaster (Dm) is a simple animal species that contributed significantly to the development of neurobiology whose leucine-rich repeat kinase 2 mutants (LRRK2) loss-of-function in the WD40 domain represent a very interesting tool to look into physiopathology of Parkinson's disease (PD). Accordingly, LRRK2 Dm have also the potential to contribute to reveal innovative therapeutic approaches to its treatment. Withania somnifera Dunal, a plant that grows spontaneously also in Mediterranean regions, is known in folk medicine for its anti-inflammatory and protective properties against neurodegeneration. The aim of this study was to evaluate the neuroprotective effects of its standardized root methanolic extract (Wse) on the LRRK2 loss-of-function Dm model of PD. To this end mutant and wild type (WT) flies were administered Wse, through diet, at different concentrations as larvae and adults (L+/A+) or as adults (L-/A+) only. LRRK2 mutants have a significantly reduced lifespan and compromised motor function and mitochondrial morphology compared to WT flies 1% Wse-enriched diet, administered to Dm LRRK2 as L-/A+and improved a) locomotor activity b) muscle electrophysiological response to stimuli and also c) protected against mitochondria degeneration. In contrast, the administration of Wse to Dm LRRK2 as L+/A+, no matter at which concentration, worsened lifespan and determined the appearance of increased endosomal activity in the thoracic ganglia. These results, while confirming that the LRRK2 loss-of-function in the WD40 domain represents a valid model of PD, reveal that under appropriate concentrations Wse can be usefully employed to counteract some deficits associated with the disease. However, a careful assessment of the risks, likely related to the impaired endosomal activity, is required.

Activity-dependent degeneration of axotomized neuromuscular synapses in Wld S mice.

Activity and disuse of synapses are thought to influence progression of several neurodegenerative diseases in which synaptic degeneration is an early sign. Here we tested whether stimulation or disuse renders neuromuscular synapses more or less vulnerable to degeneration, using axotomy as a robust trigger. We took advantage of the slow synaptic degeneration phenotype of axotomized neuromuscular junctions in flexor digitorum brevis (FDB) and deep lumbrical (DL) muscles of Wallerian degeneration-Slow (Wld(S)) mutant mice. First, we maintained ex vivo FDB and DL nerve-muscle explants at 32°C for up to 48 h. About 90% of fibers from Wld(S) mice remained innervated, compared with about 36% in wild-type muscles at the 24-h checkpoint. Periodic high-frequency nerve stimulation (100 Hz: 1s/100s) reduced synaptic protection in Wld(S) preparations by about 50%. This effect was abolished in reduced Ca(2+) solutions. Next, we assayed FDB and DL innervation after 7 days of complete tetrodotoxin (TTX)-block of sciatic nerve conduction in vivo, followed by tibial nerve axotomy. Five days later, only about 9% of motor endplates remained innervated in the paralyzed muscles, compared with about 50% in 5 day-axotomized muscles from saline-control-treated Wld(S) mice with no conditioning nerve block. Finally, we gave mice access to running wheels for up to 4 weeks prior to axotomy. Surprisingly, exercising Wld(S) mice ad libitum for 4 weeks increased about twofold the amount of subsequent axotomy-induced synaptic degeneration. Together, the data suggest that vulnerability of mature neuromuscular synapses to axotomy, a potent neurodegenerative trigger, may be enhanced bimodally, either by disuse or by hyperactivity.

Neuromuscular Electrical Stimulation for Treatment-Refractory Chronic Dysphagia in Tube-Fed Patients: A Prospective Case Series.

OBJECTIVE: The aim of this study was to evaluate the role of neuromuscular electrical stimulation (NMES) in tube-fed patients with severe and chronic dysphagia refractory to traditional swallowing therapy (TT). PATIENTS AND METHODS: A total of 11 consecutive dysphagic patients with tube-dependent nutrition and who had not responded to 6 months of TT were enrolled. Each patient received NMES for 30 min and TT for 30 min, twice a day, 5 days per week for 4 weeks. In order to evaluate the swallowing impairment, each patient underwent a fiberoptic endoscopic examination of swallowing immediately before the beginning of the treatment, after 2 weeks and after 4 weeks. RESULTS: All enrolled patients managed to complete the swallowing treatment protocol for at least 2 weeks. After the 4-week treatment, 6 of 11 enrolled patients passed to a total oral diet with single or multiple consistencies despite specific food limitations or special preparation or compensation. Five patients, all affected by the most severe form of dysphagia, maintained tube-dependent nutrition. CONCLUSION: NMES as adjunctive treatment to TT may offer a new possibility for the management of tube-fed patients who are refractory to TT.

Técnica neuromuscular de la vaina rectal abdominal / No disponible

La Técnica Neuromuscular (TNM) permite simultanear exploración, diagnóstico y tratamiento, y tiene como objetivo normalizar el tejido muscular y conjuntivo. La técnica permite localizar las induraciones y/o dificultades del deslizamiento dentro de tejido conjuntivo, que se interpretan como una disminución de las propiedades viscoelásticas de dicho tejido, lo que limita la doble función de filtro iónico y difusión de nutrientes. Consta de una serie de trazos realizados con el pulgar, de forma lenta, que permiten centrar la atención tanto en la sensación palpatoria como en la respuesta del paciente. La técnica abdominal básica trata las zonas abdominales y consta de varias partes. Debe prestarse especial atención a la línea alba y la vaina rectal abdominal, por su gran variedad de factores funcionales y estructurales, y su repercusión tanto a nivel local como sobre la salud en su conjunto (AU)

No disponible

Neuromuscular electrical stimulation as a method to maximize the beneficial effects of muscle stem cells transplanted into dystrophic skeletal muscle.

Cellular therapy is a potential approach to improve the regenerative capacity of damaged or diseased skeletal muscle. However, its clinical use has often been limited by impaired donor cell survival, proliferation and differentiation following transplantation. Additionally, functional improvements after transplantation are all-too-often negligible. Because the host microenvironment plays an important role in the fate of transplanted cells, methods to modulate the microenvironment and guide donor cell behavior are warranted. The purpose of this study was to investigate whether the use of neuromuscular electrical stimulation (NMES) for 1 or 4 weeks following muscle-derived stem cell (MDSC) transplantation into dystrophic skeletal muscle can modulate the fate of donor cells and enhance their contribution to muscle regeneration and functional improvements. Animals submitted to 4 weeks of NMES after transplantation demonstrated a 2-fold increase in the number of dystrophin+ myofibers as compared to control transplanted muscles. These findings were concomitant with an increased vascularity in the MDSC+NMES group when compared to non-stimulated counterparts. Additionally, animals subjected to NMES (with or without MDSC transplantation) presented an increased maximal specific tetanic force when compared to controls. Although cell transplantation and/or the use of NMES resulted in no changes in fatigue resistance, the combination of both MDSC transplantation and NMES resulted in a faster recovery from fatigue, when compared to non-injected and non-stimulated counterparts. We conclude that NMES is a viable method to improve MDSC engraftment, enhance dystrophic muscle strength, and, in combination with MDSC transplantation, improve recovery from fatigue. These findings suggest that NMES may be a clinically-relevant adjunct approach for cell transplantation into skeletal muscle.

C-terminal Agrin Fragment as a potential marker for sarcopenia caused by degeneration of the neuromuscular junction.

INTRODUCTION: Sarcopenia is considered to be an enormous burden for both the individuals affected and for society at large. A multifactorial aetiology of this geriatric syndrome has been discussed. Amongst other pathomechanisms, the degeneration of the neuromuscular junction (NMJ) may be of major relevance. The intact balance between the pro-synaptic agent agrin and the anti-synaptic agent neurotrypsin ensures a structurally and functionally intact NMJ. Excessive cleavage of the native motoneuron-derived agrin by neurotrypsin into a C-terminal Agrin Fragment (CAF) leads to functional disintegration at the NMJ and may consecutively cause sarcopenia. The present study evaluates the hypothesis that CAF serum concentration is a potential marker for the loss of appendicular lean mass in older adults. It also explores how CAF concentration is influenced by vitamin D supplementation and physical exercise. METHOD: Serum was taken from 69 (47 female) prefrail community-dwelling older adults participating in a training intervention study to measure the CAF concentration using the Western blot technique. All participants were supplemented orally with vitamin D3 before the training intervention period commenced. Appendicular lean mass (aLM) was evaluated by dual energy X-ray absorptiometry. Multiple linear regression models were used to identify factors significantly associated with CAF concentration. RESULTS: Appendicular lean mass, age and sex were identified as significant explanatory factors for CAF concentration. Gait speed and hand grip strength were not associated with CAF concentration. Male participants showed a strong correlation (r=-0.524) between CAF serum concentration and aLM, whereas this was not the case (r=-0.219) in females. Vitamin D supplementation and physical exercise were significantly associated with a reduction in CAF concentration, especially in participants with initially high CAF concentrations. CONCLUSIONS: C-terminal Agrin Fragment could be a potential marker for identifying sarcopenia in a subgroup of affected individuals in the future. The decline of muscle mass seems to be a CAF-associated process in males, whereas the situation in females may be more complex and multifactorial. CAF concentration is reduced by vitamin D supplementation and physical exercise and therefore suggests a potentially positive effect on NMJs. Further prospective studies of sarcopenic patients in addition to muscle biopsy and electromyographical investigations are planned to verify the external validity of the CAF concept.

Effects of home-based resistance training and neuromuscular electrical stimulation in knee osteoarthritis: a randomized controlled trial.

BACKGROUND: Quadriceps femoris muscle (QFM) weakness is a feature of knee osteoarthritis (OA) and exercise programs that strengthen this muscle group can improve function, disability and pain. Traditional supervised resistance exercise is however resource intensive and dependent on good adherence which can be challenging to achieve in patients with significant knee OA. Because of the limitations of traditional exercise programs, interest has been shown in the use of neuromuscular electrical stimulation (NMES) to strengthen the QFM. We conducted a single-blind, prospective randomized controlled study to compare the effects of home-based resistance training (RT) and NMES on patients with moderate to severe knee OA. METHODS: 41 patients aged 55 to 75 years were randomised to 6 week programs of RT, NMES or a control group receiving standard care. The primary outcome was functional capacity measured using a walk test, stair climb test and chair rise test. Additional outcomes were self-reported disability, quadriceps strength and cross-sectional area. Outcomes were assessed pre- and post-intervention and at 6 weeks post-intervention (weeks 1, 8 and 14 respectively). RESULTS: There were similar, significant improvements in functional capacity for the RT and NMES groups at week 8 compared to week 1 (p ≤ 0.001) and compared to the control group (p < 0.005), and the improvements were maintained at week 14 (p ≤ 0.001). Cross sectional area of the QFM increased in both training groups (NMES: +5.4%; RT: +4.3%; p = 0.404). Adherence was 91% and 83% in the NMES and RT groups respectively (p = 0.324). CONCLUSIONS: Home-based NMES is an acceptable alternative to exercise therapy in the management of knee OA, producing similar improvements in functional capacity. TRIAL REGISTRATION: Current Controlled Trials ISRCTN85231954.

Neuromuscular electrical stimulation increases muscle protein synthesis in elderly type 2 diabetic men.

Physical activity is required to attenuate the loss of skeletal muscle mass with aging. Short periods of muscle disuse, due to sickness or hospitalization, reduce muscle protein synthesis rates, resulting in rapid muscle loss. The present study investigates the capacity of neuromuscular electrical stimulation (NMES) to increase in vivo skeletal muscle protein synthesis rates in older type 2 diabetes patients. Six elderly type 2 diabetic men (70 ± 2 yr) were subjected to 60 min of one-legged NMES. Continuous infusions with L-[ring-¹³C6]phenylalanine were applied, with blood and muscle samples being collected regularly to assess muscle protein synthesis rates in both the stimulated (STIM) and nonstimulated control (CON) leg during 4 h of recovery after NMES. Furthermore, mRNA expression of key genes implicated in the regulation of muscle mass were measured over time in the STIM and CON leg. Muscle protein synthesis rates were greater in the STIM compared with the CON leg during recovery from NMES (0.057 ± 0.008 vs. 0.045 ± 0.008%/h, respectively, P < 0.01). Skeletal muscle myostatin mRNA expression in the STIM leg tended to increase immediately following NMES compared with the CON leg (1.63- vs. 1.00-fold, respectively, P = 0.07) but strongly declined after 2 and 4 h of recovery in the STIM leg only. In conclusion, this is the first study to show that NMES directly stimulates skeletal muscle protein synthesis rates in vivo in humans. NMES likely represents an effective interventional strategy to attenuate muscle loss in elderly individuals during bed rest and/or in other disuse states.

Effects of neuromuscular electrical stimulation, laser therapy and LED therapy on the masticatory system and the impact on sleep variables in cerebral palsy patients: a randomized, five arms clinical trial.

BACKGROUND: Few studies demonstrate effectiveness of therapies for oral rehabilitation of patients with cerebral palsy (CP), given the difficulties in chewing, swallowing and speech, besides the intellectual, sensory and social limitations. Due to upper airway obstruction, they are also vulnerable to sleep disorders. This study aims to assess the sleep variables, through polysomnography, and masticatory dynamics, using electromiography, before and after neuromuscular electrical stimulation, associated or not with low power laser (Gallium Arsenide- Aluminun, =780 nm) and LED (= 660 nm) irradiation in CP patients. METHODS/DESIGN: 50 patients with CP, both gender, aged between 19 and 60 years will be enrolled in this study. The inclusion criteria are: voluntary participation, patient with hemiparesis, quadriparesis or diparetic CP, with ability to understand and respond to verbal commands. The exclusion criteria are: patients undergoing/underwent orthodontic, functional maxillary orthopedic or botulinum toxin treatment. Polysomnographic and surface electromyographic exams on masseter, temporalis and suprahyoid will be carry out in all sample. Questionnaire assessing oral characteristics will be applied. The sample will be divided into 5 treatment groups: Group 1: neuromuscular electrical stimulation; Group 2: laser therapy; Group 3: LED therapy; Group 4: neuromuscular electrical stimulation and laser therapy and Group 5: neuromuscular electrical stimulation and LED therapy. All patients will be treated during 8 consecutive weeks. After treatment, polysomnographic and electromiographic exams will be collected again. DISCUSSION: This paper describes a five arm clinical trial assessing the examination of sleep quality and masticatory function in patients with CP under non-invasive therapies. TRIAL REGISTRATION: The protocol for this study is registered with the Brazilian Registry of Clinical Trials - ReBEC RBR-994XFS.

Neuromuscular electrical stimulation training results in enhanced activation of spinal stabilizing muscles during spinal loading and improvements in pain ratings.

Low back pain is associated with dysfunction in recruitment of muscles in the lumbopelvic region. Effective rehabilitation requires preferential activation of deep stabilizing muscle groups yet training these muscles poses challenges in a clinical setting. This study was carried out in order to quantify the response of deep stabilizing muscles (transverses abdominis and deep fibres of multifidus) to a period of training using a novel neuromuscular electrical stimulation (NMES) application in a group of patients with chronic low back pain. Analysis of results revealed clinically and statistically significant improvements in indicators of both muscle groups' performance, as evidenced by ultrasound evaluation of activation during voluntary activity. These improvements were associated with significant improvements in self reported pain levels, suggesting that NMES has an important role to play in CLBP rehabilitation.

The influence of orthopaedic implants on patient tolerance of neuromuscular electrical stimulation (NMES).

Neuromuscular electrical stimulation (NMES) is a potential deep vein thrombosis (DVT) preventative measure that is often over-looked. NMES could be used postoperatively in conjunction with pharmacological prophylaxis to further reduce the incidence rate of DVT following orthopaedic surgery. However, the use of NMES in the recovery period following orthopaedic surgery on patients with metallic hip/knee implants has not been tested to date. The presence of a metallic implant may interfere with the NMES generated electric field causing hypersensitivity at the implant site. This may essentially limit the use of NMES postoperatively. Consequently, patient tolerance of NMES must be assessed before any treatment can be administered. Five hip replacement patients and 5 knee replacement patients participated in this study that were at least 3 weeks post-op. NMES was applied to the calf muscles of each patient using skin surface electrodes and the stimulation intensity was slowly increased. Comfort was assessed by asking the patient to indicate the stimulation intensity corresponding to 4 thresholds: when they first felt the stimulus sensation (sensory threshold), when a muscle contraction was observed (motor threshold), when stimulation became uncomfortable (pain threshold) and when the stimulation became unbearable (pain tolerance). Patients also indicated their overall comfort level on a visual analogue scale and completed a short verbal interview detailing their experience of the NMES treatment. Results indicated that the presence of a metallic implant did not give rise to hypersensitivity to NMES. Patients found the application of calf muscle NMES comfortable and acceptable as a treatment. We conclude that use of NMES on postoperative orthopaedic patients can be safely considered as a DVT prevention method.

Low-intensity electrical stimulation ameliorates disruption of transverse tubules and neuromuscular junctional architecture in denervated rat skeletal muscle fibers.

We determine the effects of direct electrical stimulation (ES) on the histological profiles in atrophied skeletal muscle fibers after denervation caused by nerve freezing. Direct ES was performed on the tibialis anterior (TA) muscle after denervation in 7-week-old rats divided into groups as follows: control (CON), denervation (DN), or denervation with direct ES (subdivided into a 4 mA (ES4), an 8 mA (ES8), or a 16 mA stimulus (ES16). The stimulation frequency was set at 10 Hz, and the voltage was set at 40 V (30 min/day, 6 days/week, for 3 weeks). Ultrastructural profiles of the membrane systems involved in excitation-contraction coupling, and four kinds of mRNA expression profiles were evaluated. Morphological disruptions occurred in transverse (t)-tubule networks following denervation: an apparent disruption of the transverse networks, and an increase in the longitudinal t-tubules spanning the gap between the two transverse networks, with the appearance of pentads and heptads. These membrane disruptions seemed to be ameliorated by relatively low intensity ES (4 mA and 8 mA), and the area of longitudinally oriented t-tubules and the number of pentads and heptads decreased significantly (P < 0.01) in ES4 and ES8 compared to the DN. The highest intensity (16 mA) did not improve the disruption of membrane systems. There were no significant differences in the (alpha1s)DHPR and RyR1 mRNA expression among CON, DN, and all ES groups. After 3 weeks of denervation all nerve terminals had disappeared from the neuromuscular junctions (NMJs) in the CON and ES16 groups. However, in the ES4 and ES8 groups, modified nerve terminals were seen in the NMJs. The relatively low-intensity ES ameliorates disruption of membrane system architecture in denervated skeletal muscle fibers, but that it is necessary to select the optimal stimulus intensities to preserve the structural integrity of denervated muscle fibers.

Electrical stimulation promotes motor nerve regeneration selectivity regardless of end-organ connection.

Previous studies have demonstrated that end-organ deprivation after peripheral nerve injury results in targeting of regenerating nerve fibers into inappropriate pathways, which leads to poor functional recovery. Here we studied the effect of electrical stimulation on the regeneration selectivity of motor nerves after peripheral nerve injury and end-organ deprivation. We found that end-organ deprivation reduced regenerating selectivity of motor nerves, total number of regenerating motoneurons, and level of neural trophic factors in the regenerating pathways after nerve injury (p < 0.05). Electrical stimulation successfully promoted motor nerve regeneration selectivity regardless of end-organ connections (p < 0.05). This increased selectivity was accompanied by an increase in the protein level of neural trophic factors in the distal nerve stumps by 3 weeks after nerve injury (p < 0.05). There was a similar increase in the protein level of these neural trophic factors in denervated muscle. However, the RNA level of these factors decreased both in the distal nerves and in the muscle. Despite the promising effect of promoting motor nerve regeneration selectivity, electrical stimulation did not prevent motoneuron loss caused by end-organ deprivation. The present study suggests that end organs contribute to the development of selective motor nerve regeneration by increasing the neurotrophic factors in the regeneration pathways. Electrical stimulation is an efficient strategy to ameliorate the deteriorated regeneration microenvironment caused by end-organ deprivation and to promote motor nerve regeneration selectivity when end-organ connections are deprived.