Academic literature on the topic 'Chronic low-frequency stimulation'

The altered metabolic state after a spinal cord injury compromises systemic glucose regulation. Skeletal muscle atrophies and transforms into fast, glycolytic, and insulin-resistant tissue. Osteoporosis is common after spinal cord injury and limits the ability to exercise paralyzed muscle. We used a novel approach to study the acute effect of two frequencies of stimulation (20 and 5 Hz) on muscle fatigue and gene regulation in people with chronic paralysis. Twelve subjects with chronic (>1 yr) and motor complete spinal cord injury (ASIA A) participated in the study. We assessed the twitch force before and after a single session of electrical stimulation (5 or 20 Hz). We controlled the total number of pulses delivered for each protocol (10,000 pulses). Three hours after the completion of the electrical stimulation (5 or 20 Hz), we sampled the vastus lateralis muscle and examined genes involved with metabolic transcription, glycolysis, oxidative phosphorylation, and mitochondria remodeling. We discovered that the 5-Hz stimulation session induced a similar amount of fatigue and a five- to sixfold increase ( P < 0.05) in key metabolic transcription factors, including PGC-1α, NR4A3, and ABRA as the 20-Hz session. Neither session showed a robust regulation of genes for glycolysis, oxidative phosphorylation, or mitochondria remodeling. We conclude that a low-force and low-frequency stimulation session is effective at inducing fatigue and regulating key metabolic transcription factors in human paralyzed muscle. This strategy may be an acceptable intervention to improve systemic metabolism in people with chronic paralysis.

The effect of 1 – 12 days of electrical stimulation (10 Hz) on the ability to phosphorylate the P-light chain of myosin was studied in rabbit tibialis anterior muscle. Myosin phosphorylation was induced by exposure of the stimulated muscle and that of the contralateral leg to a single conditioning stimulus train (5 Hz) for 25 s via the motor nerve. Isometric tension was measured as were the myosin light chain composition and the activities of the enzymes responsible for phosphorylation and dephosphorylation. A computer simulation of the potential effect of a stimulation-induced disruption of Ca2+ metabolism on phosphorylation was also performed. Chronic stimulation for as little as 1 day eliminated light chain phosphorylation and reduced the myosin light chain kinase activity by approximately 36%. Conversely, phosphatase activity and light chain composition were unaffected. The model demonstrated that a slight depression in the magnitude of the Ca2+ transient could potentially attenuate phosphorylation. The data suggest that phosphorylation of myosin is extremely sensitive to prolonged muscle activity. Furthermore, it appears more likely that this sensitivity is related to regulation of intracellular free Ca2+ than to the other elements of the calmodulin-dependent system for myosin phosphorylation examined.Key words: myosin phosphorylation, muscle, contraction, stimulation.

Background: Spinal cord stimulation is an intervention that has become increasingly popular due to the growing body of literature showing its effectiveness in treating pain and the reversible nature of the treatment with implant removal. It is currently approved by the FDA for chronic pain of the trunk and limbs, intractable low back pain, leg pain, and pain from failed back surgery syndrome. In Europe, it has additional approval for refractory angina pectoris and peripheral limb ischemia. Objective: This narrative review presents the current evidence supporting the use of spinal cord stimulation for the approved indications and also discusses some emerging neuromodulation technologies that may potentially address pain conditions that traditional spinal cord stimulation has difficulty addressing. Study Design: Narrative review. Results: Spinal cord stimulation has been reported to be superior to conservative medical management and reoperation when dealing with pain from failed back surgery syndrome. It has also demonstrated clinical benefit in complex regional pain syndrome, critical limb ischemia, and refractory angina pectoris. Furthermore, several cost analysis studies have demonstrated that spinal cord stimulation is cost effective for these approved conditions. Despite the lack of a comprehensive mechanism, the technology and the complexity in which spinal cord stimulation is being utilized is growing. Newer devices are targeting axial low back pain and foot pain, areas that have been reported to be more difficult to treat with traditional spinal cord stimulation. Percutaneous hybrid paddle leads, peripheral nerve field stimulation, nerve root stimulation, dorsal root ganglion, and high frequency stimulation are actively being refined to address axial low back pain and foot pain. High frequency stimulation is unique in that it provides paresthesia free analgesia by stimulating beyond the physiologic frequency range. The preliminary results have been mixed and a large randomized control trial is underway to evaluate the future of this technology. Other emerging technologies, including dorsal root ganglion stimulation and hybrid leads, also show some promising preliminary results in non-randomized observational trials. Limitation: This review is a primer and not an exhaustive review for the current evidence supporting the use of spinal cord stimulation and precursory discussion of emerging neuromodulation technologies. This review does not address peripheral nerve stimulation and focuses mainly on spinal cord stimulation and touches on peripheral nerve field stimulation. Conclusions: Spinal cord stimulation has demonstrated clinical efficacy in randomized control trials for the approved indications. In addition, several open label observational studies on peripheral nerve field stimulation, hybrid leads, dorsal root ganglion stimulation, and high frequency stimulation show some promising results. However, large randomized control trials demonstrating clear clinical benefit are needed to gain evidence based support for their use. Key words: Spinal cord stimulation, chronic pain; low back pain, high frequency stimulation, peripheral nerve field stimulation, dorsal root ganglion stimulation, failed back surgery syndrome, complex regional pain syndrome, critical limb ischemia, refractory angina pectoris

The purpose of the study was to verify the influence of several weeks of chronic low-frequency electrical stimulation (LFES) on the metabolic profile and functional capacity of human skeletal muscle. Knee extensor muscles (KEM) of eight subjects were electrically stimulated at 8 Hz for 8 h/day and 6 days/wk. Vastus lateralis muscle samples were taken before, after 4 wk, and after 8 wk of LFES, and activities of anaerobic (creatine kinase, phosphofructokinase, glyceraldehyde-3-phosphate dehydrogenase) and aerobic-oxidative (citrate synthase, 3-hydroxyacyl-CoA dehydrogenase, cytochrome-c oxidase) enzyme markers were determined. KEM dynamic performance was also assessed before, after 4 wk, and after 8 wk of LFES. Activity levels of anaerobic enzymes were not altered, whereas the activity levels of citrate synthase (29%),3-hydroxyacyl-CoA dehydrogenase (22%), and cytochrome-c oxidase (25%) were significantly increased after 4 wk of LFES but were not further increased after 4 additional wk of LFES. KEM performance was also improved (P < 0.05) but leveled off after 4 wk of LFES. Although significant changes were observed, the results of the present study suggest that the muscle characteristics investigated in the current study have a limited capacity of adaptation in response to this form of chronic LFES.

OBJECTIVE Chronic pain is a major distressing symptom of Parkinson's disease (PD) that is often undertreated. Subthalamic nucleus (STN) deep brain stimulation (DBS) delivers high-frequency stimulation (HFS) to patients with PD and has been effective in pain relief in a subset of these patients. However, up to 74% of patients develop new pain concerns while receiving STN DBS. Here the authors explore whether altering the frequency of STN DBS changes pain perception as measured through quantitative sensory testing (QST). METHODS Using QST, the authors measured thermal and mechanical detection and pain thresholds in 19 patients undergoing DBS via HFS, low-frequency stimulation (LFS), and off conditions in a randomized order. Testing was performed in the region of the body with the most pain and in the lower back in patients without chronic pain. RESULTS In the patients with chronic pain, LFS significantly reduced heat detection thresholds as compared with thresholds following HFS (p = 0.029) and in the off state (p = 0.010). Moreover, LFS resulted in increased detection thresholds for mechanical pressure (p = 0.020) and vibration (p = 0.040) compared with these thresholds following HFS. Neither LFS nor HFS led to changes in other mechanical thresholds. In patients without chronic pain, LFS significantly increased mechanical pain thresholds in response to the 40-g pinprick compared with thresholds following HFS (p = 0.032). CONCLUSIONS Recent literature has suggested that STN LFS can be useful in treating nonmotor symptoms of PD. Here the authors demonstrated that LFS modulates thermal and mechanical detection to a greater extent than HFS. Low-frequency stimulation is an innovative means of modulating chronic pain in PD patients receiving STN DBS. The authors suggest that STN LFS may be a future option to consider when treating Parkinson's patients in whom pain remains the predominant complaint.

Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive technique used to modulate cortical excitability of excitatory and inhibitory neural networks, the effects of which often outlast initial application. Although rTMS is used both clinically and experimentally, the potential deleterious consequences, especially when delivered chronically, remain unclear and its safety is still largely unknown. Our current study evaluates the effects of prolonged chronic low-frequency rTMS on the immunoreactivity of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (Iba1) for the assessment of glial activation in a feline model of rTMS facilitated visuospatial neglect recovery. Conscious subjects were treated daily with 1 Hz rTMS (60% machine output) for 20' over the course of 14 weeks. In comparison with control animals receiving sham treatment, quantitative analysis of protein concentrations by optical density revealed no significant alterations in localized GFAP levels following chronic 1Hz rTMS. Iba1 visualization was unattained resulting presumably from inadequacies with species cross-reactivity of primary antibodies. Visual assessment of morphology showed no alterations typically associated with histopathology or indications of glial proliferation. These results suggest that extensive low-frequency rTMS does not induce reactive gliosis or gross histopathology, affording continued evidence for the safety of rTMS.

Skeletal muscle is a heterogeneous, multinucleated, post-mitotic tissue that contains many functionally diverse fibre types that are capable of adjusting their phenotypic properties in response to altered contractile demands. This plasticity, or adaptability of skeletal muscle is largely dictated by variations in motoneuron firing patterns. For example, in response to increased tonic firing of slow motoneurons, which occurs during bouts of endurance training or chronic low-frequency stimulation (CLFS), skeletal muscle adapts by transforming from a faster to a slower phenotypic profile. CLFS is an animal model of endurance training that induces fast-to-slow fibre type transformations in the absence of fibre injury in the rat. The underlying signaling mechanisms regulating this fast-to-slow fibre type transformation, however, remain to be fully elucidated. It has been suggested that myogenic stem cells, termed satellite cells, may regulate and/or facilitate this transformational process. Therefore, the signaling mechanisms involved in CLFS-induced satellite cell activation as well as the role satellite cells may play in CLFS-induced skeletal muscle adaptation were investigated in rat. A pharmacological inhibitor of nitric oxide (NO) synthase, Nω-nitro-L-arginine methyl ester, was used to investigate CLFS-induced satellite cell activation in the absence of endogenous NO production. Results suggest that NO is required for early CLFS-induced satellite cell activation, but a yet-to-be defined pathway exists that is able to fully compensate in the absence of prolonged NO production. A novel method of satellite cell ablation (i.e. weekly focal γ-irradiation application) was used to investigate CLFS-induced skeletal muscle adaptation in the absence of a viable satellite cell population. Myosin heavy chain (MHC), an important structural and regulatory protein component of the contractile apparatus, was used as a cellular marker of the adaptive response to CLFS. Findings suggest that satellite cell activity may be required for early fast-to-slow MHC-based transformations to occur at the protein level without delay in the fast fibre population, and may also play an obligatory role in the final transformation from fast type IIA to slow type I fibres. Interestingly, additional results show that NO appears to be a key mediator of MHC isoform gene expression during CLFS-induced fast-to-slow fibre type transformations.