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Journal articles on the topic 'Chronic low-frequency stimulation'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Hu, P., K. M. Zhang, J. J. Feher, et al. "Salbutamol and chronic low-frequency stimulation of canine skeletal muscle." Journal of Physiology 496, no. 1 (1996): 221–27. http://dx.doi.org/10.1113/jphysiol.1996.sp021679.

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2

KRAUS, WILLIAM E., CAROL E. TORGAN, and DORIS A. TAYLOR. "Skeletal Muscle Adaptation to Chronic Low-Frequency Motor Nerve Stimulation." Exercise and Sport Sciences Reviews 22, no. 1 (1994): 313–60. http://dx.doi.org/10.1249/00003677-199401000-00014.

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3

Shenkman, Boris S., Ekaterina V. Lyubaeva, Daniil V. Popov, et al. "Chronic effects of low-frequency low-intensity electrical stimulation of stretched human muscle." Acta Astronautica 60, no. 4-7 (2007): 505–11. http://dx.doi.org/10.1016/j.actaastro.2006.09.014.

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4

Petrie, Michael, Manish Suneja, and Richard K. Shields. "Low-frequency stimulation regulates metabolic gene expression in paralyzed muscle." Journal of Applied Physiology 118, no. 6 (2015): 723–31. http://dx.doi.org/10.1152/japplphysiol.00628.2014.

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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.

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5

Barnard, E. A., P. J. Barnard, J. C. Jarvis, and J. Lai. "Low frequency chronic electrical stimulation of normal and dystrophic chicken muscle." Journal of Physiology 376, no. 1 (1986): 377–409. http://dx.doi.org/10.1113/jphysiol.1986.sp016159.

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6

Klug, G. A., M. Biedermann, M. E. Houston, D. Stuart, M. Mumby, and J. T. Stull. "Chronic low frequency stimulation reduces myosin phosphorylation in rabbit fast twitch muscle." Canadian Journal of Physiology and Pharmacology 70, no. 6 (1992): 859–65. http://dx.doi.org/10.1139/y92-115.

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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.

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7

Song, Jason J. "Present and Potential Use of Spinal Cord Stimulation to Control Chronic Pain." Pain Physician 3;17, no. 3;5 (2014): 234–46. http://dx.doi.org/10.36076/ppj.2014/17/234.

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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

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8

Bang, Y., H. Jeon, and I. Yoon. "0354 EFFECTIVENESS OF LOW-FREQUENCY ELECTRICAL STIMULATION ON PATIENTS WITH CHRONIC INSOMNIA." Sleep 40, suppl_1 (2017): A132. http://dx.doi.org/10.1093/sleepj/zsx050.353.

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9

Theriault, R., G. Theriault, and J. A. Simoneau. "Human skeletal muscle adaptation in response to chronic low-frequency electrical stimulation." Journal of Applied Physiology 77, no. 4 (1994): 1885–89. http://dx.doi.org/10.1152/jappl.1994.77.4.1885.

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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.

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10

Belasen, Abigail, Khizer Rizvi, Lucy E. Gee, et al. "Effect of low-frequency deep brain stimulation on sensory thresholds in Parkinson's disease." Journal of Neurosurgery 126, no. 2 (2017): 397–403. http://dx.doi.org/10.3171/2016.2.jns152231.

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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.

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11

Donoghue, Pamela, Philip Doran, Paul Dowling, and Kay Ohlendieck. "Differential expression of the fast skeletal muscle proteome following chronic low-frequency stimulation." Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics 1752, no. 2 (2005): 166–76. http://dx.doi.org/10.1016/j.bbapap.2005.08.005.

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12

Scott, O. M., G. Vrbova, S. A. Hyde, and V. Dubowitz. "Effects of chronic low frequency electrical stimulation on normal human tibialis anterior muscle." Journal of Neurology, Neurosurgery & Psychiatry 48, no. 8 (1985): 774–81. http://dx.doi.org/10.1136/jnnp.48.8.774.

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13

Pette, D., and S. Dusterhoft. "Altered gene expression in fast-twitch muscle induced by chronic low-frequency stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 3 (1992): R333—R338. http://dx.doi.org/10.1152/ajpregu.1992.262.3.r333.

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Increased neuromuscular activity via chronic low-frequency stimulation induces multiple fast-to-slow transitions in phenotypic properties that ultimately lead to fiber type conversions in the fast-twitch muscle of small mammals. Most of these alterations occur in an ordered sequence and result from the sequentially altered expression of myofibrillar and other protein isoforms. These changes relate to altered levels of specific mRNAs, followed by alterations in protein synthesis. As shown by the exchange of myosin heavy chain isoforms, protein degradation may be an additional control factor involved in the rearrangement of the myofibrillar apparatus. The degree of the various fast-to-slow transitions is species dependent and may be related to differences in thyroid hormone levels. It is suggested that the drastically and persistently depressed phosphorylation potential of the ATP system possibly serves to trigger the transformation process.

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14

Kang, Lucia H. D., and Joseph F. Y. Hoh. "Chronic Low-Frequency Stimulation Transforms Cat Masticatory Muscle Fibers into Jaw-Slow Fibers." Journal of Histochemistry & Cytochemistry 59, no. 9 (2011): 849–63. http://dx.doi.org/10.1369/0022155411413817.

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15

Green, Howard J., and D. Pette. "Early metabolic adaptations of rabbit fast-twitch muscle to chronic low-frequency stimulation." European Journal of Applied Physiology 75, no. 5 (1997): 418–24. http://dx.doi.org/10.1007/s004210050182.

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16

Parreño, Matilde, Albert Pol, Joan Cadefau, et al. "Changes of skeletal muscle proteases activities during a chronic low-frequency stimulation period." Pfl�gers Archiv European Journal of Physiology 442, no. 5 (2001): 745–51. http://dx.doi.org/10.1007/s004240100595.

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17

J. Nuhr, M. "Beneficial effects of chronic low-frequency stimulation of thigh muscles in patients with advanced chronic heart failure." European Heart Journal 25, no. 2 (2004): 136–43. http://dx.doi.org/10.1016/j.ehj.2003.09.027.

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18

Deley, Gaëll, Gaëlle Kervio, Bénédicte Verges, et al. "Neuromuscular Adaptations to Low-Frequency Stimulation Training in a Patient with Chronic Heart Failure." American Journal of Physical Medicine & Rehabilitation 87, no. 6 (2008): 502–9. http://dx.doi.org/10.1097/phm.0b013e318174e29c.

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19

Rosenblatt, J. David, William M. Kuzon, Michael E. Houston, Nancy H. McKee, and Michael J. Plyley. "MYOSIN LIGHT CHAINS IN REGENERATING RAT SKELETAL MUSCLE FOLLOWING CHRONIC, LOW-FREQUENCY, ELECTRICAL STIMULATION." Quarterly Journal of Experimental Physiology 73, no. 4 (1988): 619–22. http://dx.doi.org/10.1113/expphysiol.1988.sp003181.

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20

Cassidy, Jessica M., Haitao Chu, David C. Anderson, et al. "A Comparison of Primed Low-frequency Repetitive Transcranial Magnetic Stimulation Treatments in Chronic Stroke." Brain Stimulation 8, no. 6 (2015): 1074–84. http://dx.doi.org/10.1016/j.brs.2015.06.007.

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21

Scott, O. M., S. A. Hyde, G. Vrbová, and V. Dubowitz. "Therapeutic possibilities of chronic low frequency electrical stimulation in children with Duchenne muscular dystrophy." Journal of the Neurological Sciences 95, no. 2 (1990): 171–82. http://dx.doi.org/10.1016/0022-510x(90)90240-n.

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22

Kleinjung, Tobias, Thomas Steffens, Philipp Sand, et al. "Which tinnitus patients benefit from transcranial magnetic stimulation?" Otolaryngology–Head and Neck Surgery 137, no. 4 (2007): 589–95. http://dx.doi.org/10.1016/j.otohns.2006.12.007.

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Objectives Chronic tinnitus is associated with hyperactivity of the central auditory system. Low-frequency repetitive transcra-nial magnetic stimulation (rTMS) of the temporal cortex has been proposed as a treatment for chronic tinnitus. This study determined the factors that predict a beneficial outcome with rTMS treatment. Study Design Forty-five patients with chronic tinnitus underwent 10 sessions of low-frequency rTMS to their left auditory cortex. The treatment outcome was assessed with a tinnitus questionnaire. Therapeutic success was related to the patients' clinical characteristics. Results A significant reduction in tinnitus complaints occurred after rTMS. In the questionnaire, 40% of the patients improved by five points or more. Treatment responders were characterized by shorter duration of tinnitus complaints and no hearing impairment. Conclusion Tinnitus-related neuroplastic changes might be less pronounced in patients with normal hearing and a short history of complaints. This could explain why those patients benefitted more from rTMS treatment.

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Jürgens, TP, V. Busch, O. Opatz, WJ Schulte-Mattler, and A. May. "Low-Frequency Short-Time Nociceptive Stimulation of the Greater Occipital Nerve does not Modulate the Trigeminal System." Cephalalgia 28, no. 8 (2008): 842–46. http://dx.doi.org/10.1111/j.1468-2982.2008.01612.x.

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Occipital stimulation in a small group of refractory chronic migraine and cluster headache patients has been suggested as a novel therapeutic approach with promising results. In an earlier study we have shown that a drug-induced block of the greater occipital nerve (GON) inhibits the nociceptive blink reflex (nBR). Now, we sought to examine the effects of low-frequency (3 Hz) short-time nociceptive stimulation of the GON on the trigeminal system. We recorded the nBR responses before and after stimulation in 34 healthy subjects. Selectivity of GON stimulation was confirmed by eliciting somatosensory evoked potentials of the GON upon stimulation. In contrast to an anaesthetic block of the occipital nerve, no significant changes of the R2-latencies and R2-response areas of the nBR can be elicited following GON stimulation. Various modes of electrical stimulation exist with differences in frequency, stimulus intensity, duration of stimulation and pulse width. One explanation for a missing modulatory effect in our study is the relatively short duration of the stimulation.

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Bergeron, David, Sami Obaid, Marie-Pierre Fournier-Gosselin, Alain Bouthillier, and Dang Khoa Nguyen. "Deep Brain Stimulation of the Posterior Insula in Chronic Pain: A Theoretical Framework." Brain Sciences 11, no. 5 (2021): 639. http://dx.doi.org/10.3390/brainsci11050639.

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Introduction: To date, clinical trials of deep brain stimulation (DBS) for refractory chronic pain have yielded unsatisfying results. Recent evidence suggests that the posterior insula may represent a promising DBS target for this indication. Methods: We present a narrative review highlighting the theoretical basis of posterior insula DBS in patients with chronic pain. Results: Neuroanatomical studies identified the posterior insula as an important cortical relay center for pain and interoception. Intracranial neuronal recordings showed that the earliest response to painful laser stimulation occurs in the posterior insula. The posterior insula is one of the only regions in the brain whose low-frequency electrical stimulation can elicit painful sensations. Most chronic pain syndromes, such as fibromyalgia, had abnormal functional connectivity of the posterior insula on functional imaging. Finally, preliminary results indicated that high-frequency electrical stimulation of the posterior insula can acutely increase pain thresholds. Conclusion: In light of the converging evidence from neuroanatomical, brain lesion, neuroimaging, and intracranial recording and stimulation as well as non-invasive stimulation studies, it appears that the insula is a critical hub for central integration and processing of painful stimuli, whose high-frequency electrical stimulation has the potential to relieve patients from the sensory and affective burden of chronic pain.

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Carroll, Stefanie, Pierluigi Nicotera, and Dirk Pette. "Calcium transients in single fibers of low-frequency stimulated fast-twitch muscle of rat." American Journal of Physiology-Cell Physiology 277, no. 6 (1999): C1122—C1129. http://dx.doi.org/10.1152/ajpcell.1999.277.6.c1122.

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Ca2+transients were investigated in single fibers isolated from rat extensor digitorum longus muscles exposed to chronic low-frequency stimulation for different time periods up to 10 days. Approximately 2.5-fold increases in resting Ca2+ concentration ([Ca2+]) were observed 2 h after stimulation onset and persisted throughout the stimulation period. The elevated [Ca2+] levels were in the range characteristic of slow-twitch fibers from soleus muscle. In addition, we noticed a transitory elevation of the integral [Ca2+] per pulse with a maximum (∼5-fold) after 1 day. Steep decreases in rate constant of [Ca2+] decay could be explained by an immediate impairment of Ca2+ uptake and, with longer stimulation periods, by an additional loss of cytosolic Ca2+ binding capacity resulting from a decay in parvalbumin content. A partial recovery of the rate constant of [Ca2+] decay in 10-day stimulated muscle could be explained by an increasing mitochondrial contribution to Ca2+ sequestration.

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Kaye, Alan D. "High Frequency Spinal Cord Stimulation for Complex Regional Pain Syndrome: A Case Report." January 2018 1, no. 21;1 (2017): E177—E182. http://dx.doi.org/10.36076/ppj.2017.1.e177.

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Complex regional pain syndrome (CRPS) is a chronic, debilitating, neuropathic pain condition which is often misdiagnosed, difficult to manage, and lacks proven methods for remission. Most available methods provide some relief to a small percentage of patients. Recent FDA approval and superiority of the Nevro Senza 10-kHz high frequency (HF10) spinal cord stimulation (SCS) therapy over traditional low-frequency spinal cord stimulation for treatment of chronic back and leg pain may provide a new interventional therapeutic option for patients suffering from CRPS. We provide a case report of a 53-year-old Caucasian woman who suffered with CRPS in the right knee and thigh for over 7 years. Implantation of the HF10 device provided over 75% relief of pain, erythema, heat, swelling, and tissue necrosis to the entire region within 1 month of treatment. Because the HP10 therapy provides pain relief without paresthesia typical of traditional low-frequency, this system may provide relief for patients suffering from chronic pain. Key words: Complex regional pain syndrome, spinal cord stimulation, Nevro Senza HF10, erythema, knee, thigh

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27

Lindelof, Kim, Kerstin Jung, Jens Ellrich, Rigmor Jensen, and Lars Bendtsen. "Low-frequency electrical stimulation induces long-term depression in patients with chronic tension-type headache." Cephalalgia 30, no. 7 (2010): 860–67. http://dx.doi.org/10.1177/0333102409354783.

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Repetitive low-frequency electrical stimulation (LFS) induces pain inhibition in healthy volunteers and in animals, but it is unknown whether it has an analgesic effect in patients with headache. The aim of this study was to investigate if LFS could induce prolonged pain inhibition, called long-term depression (LTD), in patients with chronic tension-type headache (CTTH). Twenty CTTH patients and 20 healthy volunteers were exposed to 20 min LFS (1 Hz) to the forehead. LTD was measured as a decrease in pain response to electrical stimulation in a 1-h post-LFS period following LFS. The LFS induced a significant and stable inhibition of pain (LTD) both in patients with CTTH (post-LFS average decrease in pain rating: 19.6 ± 3.9%, all P < 0.005, Holm–Sidak) and in healthy controls (30.1 ± 5.0%, all P < 0.001, Holm–Sidak). During the LFS period, the pain ratings decreased consistently in both groups. In conclusion, a significant and stable pain inhibition (LTD) can be induced in CTTH patients by LFS.

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Munson, John B., Robert C. Foehring, Lorne M. Mendell, and Tessa Gordon. "Fast-to-Slow Conversion Following Chronic Low-Frequency Activation of Medial Gastrocnemius Muscle in Cats. II. Motoneuron Properties." Journal of Neurophysiology 77, no. 5 (1997): 2605–15. http://dx.doi.org/10.1152/jn.1997.77.5.2605.

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Munson, John B., Robert C. Foehring, Lorne M. Mendell, and Tessa Gordon. Fast-to-slow conversion following chronic low-frequency activation of medial gastrocnemius muscle in cats. II. Motoneuron properties. J. Neurophysiol. 77: 2605–2615, 1997. Chronic stimulation (for 2–3 mo) of the medial gastrocnemius (MG) muscle nerve by indwelling electrodes renders the normally heterogeneous MG muscle mechanically and histochemically slow (type SO). We tested the hypothesis that motoneurons of MG muscle thus made type SO by chronic stimulation would also convert to slow phenotype. Properties of all single muscle units became homogeneously type SO (slowly contracting, nonfatiguing, nonsagging contraction during tetanic activation). Motoneuron electrical properties were also modified in the direction of type S, fatigue-resistant motor units. Two separate populations were identified (on the basis of afterhyperpolarization, rheobase, and input resistance) that likely correspond to motoneurons that had been fast (type F) or type S before stimulation. Type F motoneurons, although modified by chronic stimulation, were not converted to the type S phenotype, despite apparent complete conversion of their muscle units to the slow oxidative type (type SO). Muscle units of the former type F motor units were faster and/or more powerful than those of the former type S motor units, indicating some intrinsic regulation of motor unit properties. Experiments in which chronic stimulation was applied to the MG nerve cross-regenerated into skin yielded changes in motoneuron properties similar to those above, suggesting that muscle was not essential for the effects observed. Modulation of group Ia excitatory postsynaptic potential (EPSP) amplitude during high-frequency trains, which in normal MG motoneurons can be either positive or negative, was negative in 48 of 49 chronically stimulated motoneurons. Negative modulation is characteristic of EPSPs in motoneurons of most fatigue-resistant motor units. The general hypothesis of a periphery-to-motoneuron retrograde mechanism was supported, although the degree of control exerted by the periphery may vary: natural type SO muscle appears especially competent to modify motoneuron properties. We speculate that activity-dependent regulation of the neurotrophin-(NT) 4/5 in muscle plays an important role in controlling muscle and motoneuron properties.

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Fujii, Hiromitsu, Sohei Tokunaka, and Sunao Yachiku. "EFFECTS OF CHRONIC LOW-FREQUENCY ELECTRICAL STIMULATION ON THE EXTERNAL URETHRAL SPHINCTER OF MALE RABBITS." Japanese Journal of Urology 86, no. 7 (1995): 1240–48. http://dx.doi.org/10.5980/jpnjurol1989.86.1240.

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30

Garcia, René, Guillaume Spennato, Linda Nilsson-Todd, Jean-Luc Moreau, and Olivier Deschaux. "Hippocampal low-frequency stimulation and chronic mild stress similarly disrupt fear extinction memory in rats." Neurobiology of Learning and Memory 89, no. 4 (2008): 560–66. http://dx.doi.org/10.1016/j.nlm.2007.10.005.

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Prats, C. "Glycogen depletion and resynthesis during 14 days of chronic low-frequency stimulation of rabbit muscle." Biochimica et Biophysica Acta (BBA) - General Subjects 1573, no. 1 (2002): 68–74. http://dx.doi.org/10.1016/s0304-4165(02)00332-x.

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高, 伟. "Randomized Controlled Trials on Treatment of Chronic Headache by Low Frequency Transcutaneous Eletrical Nerve Stimulation." International Journal of Psychiatry and Neurology 08, no. 02 (2019): 19–23. http://dx.doi.org/10.12677/ijpn.2019.82004.

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Billet, B., K. Hanssens, O. De Coster, et al. "Wireless high-frequency dorsal root ganglion stimulation for chronic low back pain: A pilot study." Acta Anaesthesiologica Scandinavica 62, no. 8 (2018): 1133–38. http://dx.doi.org/10.1111/aas.13138.

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Putman, Charles T., Walter T. Dixon, Jean A. Pearcey, et al. "Chronic low-frequency stimulation upregulates uncoupling protein-3 in transforming rat fast-twitch skeletal muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 6 (2004): R1419—R1426. http://dx.doi.org/10.1152/ajpregu.00421.2004.

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The purpose of this investigation was to examine the temporal changes in uncoupling protein (UCP)-3 expression, as well as related adaptive changes in mitochondrial density and fast-to-slow fiber type transitions during chronically enhanced contractile activity. We examined the effects of 1–42 days of chronic low-frequency electrical stimulation (CLFS), applied to rat tibialis anterior (TA) for 10 h/day, on the expression of UCP-3 and concomitant changes in myosin heavy chain (MHC) protein expression and increases in oxidative capacity. UCP-3 protein content increased from 1 to 12 days, reaching 1.5-fold over control ( P < 0.0005); it remained elevated for up to 42 days. In contrast, UCP-3 mRNA decreased in response to CLFS, reaching a level that was threefold lower than control ( P < 0.0007). The activities of the mitochondrial reference enzymes citrate synthase (EC 4.1.3.7) and 3-hydroxyacyl-CoA-dehydrogenase (EC 1.1.1.35), which are known to increase in proportion to mitochondrial density, progressively increased up to an average of 2.3-fold ( P < 0.00001). These changes were accompanied by fast-to-slow fiber type transitions, characterized by a shift in the pattern of MHC expression ( P <0.0002): MHCI and MHCIIa expression increased by 1.7- and 4-fold, whereas MHCIIb displayed a 2.4-fold reduction. We conclude that absolute increases in UCP-3 protein content in the early adaptive phase were associated with the genesis of mitochondria containing a normal complement of UCP-3. However, during exposure to long-term CLFS, mitochondria were generated with a lower complement of UCP-3 and coincided with the emergence of a growing population of oxidative type IIA fibers.

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Slmoneau, J. A., Y. G??llnas, A. Lachance, R. Th??rlault, and G. Th??riault. "438 CHANGES IN HUMAN SKELETAL MUSCLE ENERGY METABOLISM INDUCED BY CHRONIC LOW-FREQUENCY ELECTRICAL STIMULATION." Medicine & Science in Sports & Exercise 22, no. 2 (1990): S73. http://dx.doi.org/10.1249/00005768-199004000-00438.

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Krentz, Joel R., Maria Gallo, Karen J. B. Martins, et al. "The Effects of Creatine and Chronic Low Frequency Stimulation on Muscle Fiber Cross-Sectional Area." Medicine & Science in Sports & Exercise 42 (May 2010): 373. http://dx.doi.org/10.1249/01.mss.0000384669.12706.ed.

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Ohlendieck, K., G. R. Frömming, B. E. Murray, et al. "Effects of chronic low-frequency stimulation on Ca2+-regulatory membrane proteins in rabbit fast muscle." Pflügers Archiv - European Journal of Physiology 438, no. 5 (1999): 700–708. http://dx.doi.org/10.1007/s004249900115.

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Koranda, Jessica L., Jackson J. Cone, Daniel S. McGehee, Mitchell F. Roitman, Jeff A. Beeler, and Xiaoxi Zhuang. "Nicotinic receptors regulate the dynamic range of dopamine release in vivo." Journal of Neurophysiology 111, no. 1 (2014): 103–11. http://dx.doi.org/10.1152/jn.00269.2013.

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Nicotinic acetylcholine receptors (nAChRs) are expressed presynaptically on dopamine axon terminals, and their activation by endogenous acetylcholine from striatal cholinergic interneurons enhances dopamine release both independently of and in concert with dopamine neuron activity. Acute nAChR inactivation is believed to enhance the contrast between low- and high-frequency dopamine cell activity. Although these studies reveal a key role for acute activation and inactivation of nAChRs in striatal microcircuitry, it remains unknown if chronic inactivation/desensitization of nAChRs can alter dopamine release dynamics. Using in vivo cyclic voltammetry in anaesthetized mice, we examined whether chronic inactivation of nAChRs modulates dopamine release across a parametric range of stimulation, varying both frequency and pulse number. Deletion of β2*nAChRs and chronic nicotine exposure greatly diminished dopamine release across the entire range of stimulation parameters. In addition, we observed a facilitation of dopamine release at low frequency and pulse number in wild-type mice that is absent in the β2* knockout and chronic nicotine mice. These data suggest that deletion or chronic desensitization of nAChRs reduces the dynamic range of dopamine release in response to dopamine cell activity, decreasing rather than increasing contrast between high and low dopamine activity.

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Abd-Elsayed, Alaa. "Comparison of Spinal Cord Stimulation Waveforms for Treating Chronic Low Back Pain: Systematic Review and Meta-Analysis." Pain Physician 5;23, no. 9;5 (2020): 451–60. http://dx.doi.org/10.36076/ppj.2020/23/451.

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Background: The treatment of chronic refractory low back pain (LBP) is challenging. Conservative and pharmacologic options have demonstrated limited efficacy. Spinal cord stimulation (SCS) has been shown to be effective in reducing chronic LBP in various contexts. With emerging SCS technologies, the collective evidence of novel waveforms relative to traditional tonic stimulation for treating chronic LBP has yet to be clearly characterized. Objectives: To provide evidence for various SCS waveforms—tonic, burst, and high frequency (HF)—relative to each other for treating chronic LBP. Study Design: Systematic review and meta-analysis. Methods: PubMed, Medline, Cochrane Library, prior systematic reviews, and reference lists were screened by 2 separate authors for all randomized trials and prospective cohort studies comparing different SCS waveforms for treatment of chronic LBP. Results: We identified 11 studies that included waveform comparisons for treating chronic LBP. Of these, 6 studies compared burst versus tonic, 2 studies compared burst versus HF, and 3 studies compared tonic versus HF. A meta-analysis of 5 studies comparing burst versus tonic was conducted and revealed pooled superiority of burst over tonic in pain reduction. One study comparing burst versus tonic was excluded given technical challenges in data extraction. Limitations: Both randomized controlled trials and prospective cohort studies were included for meta-analysis. Several studies included a high risk of bias in at least one domain. Conclusions: Burst stimulation is superior to tonic stimulation for treating chronic LBP. However, superiority among other waveforms has yet to be clearly established given some heterogeneity and limitations in evidence. Given the relative novelty of burst and HF SCS waveforms, evidence of longitudinal efficacy is needed. Key words: Chronic low back pain, spinal cord stimulation, tonic, burst, high frequency

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Hicks, A., K. Ohlendieck, S. O. Gopel, and D. Pette. "Early functional and biochemical adaptations to low-frequency stimulation of rabbit fast-twitch muscle." American Journal of Physiology-Cell Physiology 273, no. 1 (1997): C297—C305. http://dx.doi.org/10.1152/ajpcell.1997.273.1.c297.

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To examine mechanisms underlying force reduction after the onset of chronic low-frequency (10 Hz) stimulation (CLFS), we exposed rabbit tibialis anterior muscles to various durations of CLFS. To follow changes in isometric contractile properties and electromyographic (EMG) activity, we studied stimulated and contralateral muscles during a terminal test at 10 Hz for 10 min. In addition, activities and protein amounts of the sarcoplasmic reticulum Ca(2+)-ATPase, content of Na(+)-K(+)-ATPase, and expression patterns of triad junction components were examined. Force output and EMG amplitude declined abruptly soon after the onset of stimulation, suggesting refractoriness of a large fiber population. Although twitch force and to a lesser extent EMG activity gradually recovered after stimulation for 6 days and longer, the muscles exhibited profoundly altered properties, i.e., enhanced fatigue resistance, absence of twitch potentiation, and prolonged contraction and relaxation times. These changes were associated with significant increases in Na(+)-K(+)-ATPase concentration and significant decreases in Ca(2+)-ATPase, ryanodine receptor, dihydropyridine receptor, and triadin concentrations over the course of the 20 days of stimulation. Alterations in excitability, Ca2+ handling, and excitation-contraction coupling prior to changes in myofibrillar protein isoforms may thus be responsible for early functional alterations.

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Green, Alexander L., Shouyan Wang, Sarah L. F. Owen, David J. Paterson, John F. Stein, and Tipu Z. Aziz. "Controlling the Heart Via the Brain: A Potential New Therapy for Orthostatic Hypotension." Neurosurgery 58, no. 6 (2006): 1176–83. http://dx.doi.org/10.1227/01.neu.0000215943.78685.01.

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Abstract OBJECTIVE: Electrical stimulation of the midbrain is known to influence blood pressure in animals. In humans, it is used for the treatment of chronic neuropathic pain. Our aim was to assess whether orthostatic hypotension can be successfully treated with deep brain stimulation of the periventricular/periaqueductal gray areas in humans. METHODS: We recruited 11 patients who had chronic neuropathic pain and who had undergone implantation of a deep brain stimulator in the periventricular/periaqueductal gray areas. Patients were divided into three groups depending on whether they had orthostatic hypotension (one patient), mild orthostatic intolerance (five patients), or no orthostatic intolerance (five patients). Postoperatively, we continuously recorded blood pressure and heart rate with stimulation off and on and in both sitting and standing positions. From these values, we derived the blood pressure changing rate. Using autoregressive modeling techniques, we calculated changes in low- and high-frequency power spectra of heart rate and baroreflex sensitivity. RESULTS: Electrical stimulation reduced the decrease in systolic blood pressure on standing from 28.2 to 11.1% in one patient with orthostatic hypotension (P &lt; 0.001). In the mild orthostatic intolerance group, an initial drop in systolic blood pressure of 15.4% was completely reversed (P &lt; 0.001). There were no side effects in the remaining group. These changes were accompanied by increases in the blood pressure changing rate, the baroreflex sensitivity, and the baseline (sitting) low-frequency power of the RR interval, but not the high-frequency power. CONCLUSION: Electrical stimulation of the human periventricular/periaqueductal gray areas can reverse orthostatic hypotension. The cause seems to be an increase in sympathetic outflow and in baroreflex sensitivity. This has important implications for future therapies.

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Thomas, Christine K., Lisa Griffin, Sharlene Godfrey, Edith Ribot-Ciscar, and Jane E. Butler. "Fatigue of Paralyzed and Control Thenar Muscles Induced by Variable or Constant Frequency Stimulation." Journal of Neurophysiology 89, no. 4 (2003): 2055–64. http://dx.doi.org/10.1152/jn.01002.2002.

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Muscles paralyzed by chronic (>1 yr) spinal cord injury fatigue readily. Our aim was to evaluate whether the fatigability of paralyzed thenar muscles ( n = 10) could be reduced by the repeated delivery of variable versus constant frequency pulse trains. Fatigue was induced in four ways. Intermittent supramaximal median nerve stimulation (300-ms-duration trains) was delivered at 1) constant high frequency (13 pulses at 40 Hz each second for 2 min); 2) variable high frequency (each second for 2 min). The first two intervals of each variable frequency train were 5 and 20 ms. The remaining pulses were evenly distributed in time across 275 ms. The number of pulses varied for each subject such that the force time integral in the unfatigued state matched that evoked by a constant 40-Hz train; 3) constant low frequency (7 pulses at 20 Hz each second for 4 min); and 4) variable low frequency (each second for 4 min). The pulse pattern was the same as that for variable high frequency except that the force-time integral was matched to that produced by the constant low-frequency stimulation. These same experiments were performed on the thenar muscles of five able-bodied control subjects. The variable high-frequency trains used to fatigue paralyzed and control muscles had an average (± SE) of 12 ± 2 and 10 ± 1 pulses, respectively. Variable low-frequency trains had 7 ± 1 and 6 ± 1 pulses, respectively. Significant mean force declines of comparable magnitude (to 20–25% initial fatigue force or to 13–21% initial 50 Hz force) were seen in paralyzed muscles with all four stimulation protocols. The force reductions in paralyzed muscles were always accompanied by significant increases in half-relaxation time and decreases in force-time integral, irrespective of the stimulation protocol. Significant force decreases also occurred in control muscles during each fatigue test. Again, these force declines were similar whether constant or variable pulse patterns were used at high or low frequencies (to 40–60% initial fatigue force or to 29–36% initial 50 Hz force). The force reductions in control muscles were significantly less than those seen in paralyzed muscles, except when constant high-frequency stimulation was used. The variations in stimulation frequency, pulse pattern, and pulse number used in this study therefore had little influence on thenar muscle fatigue in control subjects or in spinal cord–injured subjects with chronic paralysis.

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Bolash, Robert, Michael Creamer, Richard Rauck, et al. "Wireless High-Frequency Spinal Cord Stimulation (10 kHz) Compared with Multiwaveform Low-Frequency Spinal Cord Stimulation in the Management of Chronic Pain in Failed Back Surgery Syndrome Subjects: Preliminary Results of a Multicenter, Prospective Randomized Controlled Study." Pain Medicine 20, no. 10 (2019): 1971–79. http://dx.doi.org/10.1093/pm/pnz019.

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Abstract Background This study aimed to evaluate the wireless Freedom Spinal Cord Stimulator (WSCS) System for the treatment of chronic back and/or leg pain associated with failed back surgery syndrome (FBSS) refractory to standard medical treatment utilizing 10-kHz stimulation (high-frequency [HF]) in comparison with 10–1,500-Hz stimulation (low-frequency [LF]) waveforms. Methods Ninety-nine subjects were randomized in a 1:1 ratio to receive either HF or LF stimulation waveforms utilizing the same Freedom WSCS System. All subjects were implanted with two 8-electrode arrays in the exact same anatomical positions within the dorsal epidural spinal column, with the top electrode positioned at the T8 and T9 vertebrae levels, respectively, and the wireless receiver placed under the skin in a subcutaneous pocket. Results Seventy-two (HF: N = 38; LF: N = 34) subjects had completed the six-month follow-up after an initial 30-day trial period at the time of this report. For both the HF and LF arms, mean visual analog scale (VAS) scores for back and leg pain decreased significantly: 77% and 76%, respectively, for the HF arm and 64% and 64%, respectively, for the LF arm. In addition, most subjects experienced significant improvements in VAS, Oswestry Disability Index, European Quality of Life 5 Dimension questionnaire, Patient Global Impression of Change, and sleep duration. Conclusions These preliminary results demonstrate that WSCS devices can reduce FBSS chronic pain substantially with both LF and HF stimulation waveforms over a seven-month period (30-day trial period and six-month post-trial evaluation).

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Bang, Young Rong, Hong Jun Jeon, and In-Young Yoon. "Modest Effects of Low-frequency Electrical Stimulation on Patients with Chronic Insomnia in an Open Trial." Sleep Medicine Research 10, no. 1 (2019): 17–24. http://dx.doi.org/10.17241/smr.2019.00346.

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Deley, G., B. Verges, G. Kervio, B. Grassi, and J. M. Casillas. "Comparison of low-frequency electrical stimulation and conventional exercise training in patients with chronic heart failure." European Journal of Cardiovascular Prevention & Rehabilitation 12, no. 3 (2005): 291. http://dx.doi.org/10.1097/00149831-200506000-00049.

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Doucet, Barbara M., and Lisa Griffin. "High-Versus Low-Frequency Stimulation Effects on Fine Motor Control in Chronic Hemiplegia: A Pilot Study." Topics in Stroke Rehabilitation 20, no. 4 (2013): 299–307. http://dx.doi.org/10.1310/tsr2004-299.

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Barwood, Caroline H. S., Bruce E. Murdoch, Brooke-Mai Whelan, et al. "Modulation of N400 in chronic non-fluent aphasia using low frequency Repetitive Transcranial Magnetic Stimulation (rTMS)." Brain and Language 116, no. 3 (2011): 125–35. http://dx.doi.org/10.1016/j.bandl.2010.07.004.

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48

Ohlendieck, K., G. R. Frömming, B. E. Murray, et al. "Effects of chronic low-frequency stimulation on Ca 2+ -regulatory membrane proteins in rabbit fast muscle." Pfl�gers Archiv European Journal of Physiology 438, no. 5 (1999): 700–708. http://dx.doi.org/10.1007/s004240051096.

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49

Li, Wei, Yuye Yang, Qing Ye, Bo Yang, and Zhengrong Wang. "Effect of chronic and acute low-frequency repetitive transcranial magnetic stimulation on spatial memory in rats." Brain Research Bulletin 71, no. 5 (2007): 493–500. http://dx.doi.org/10.1016/j.brainresbull.2006.11.002.

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Puppa, Melissa J., E. Angela Murphy, Raja Fayad, Gregory A. Hand, and James A. Carson. "Cachectic skeletal muscle response to a novel bout of low-frequency stimulation." Journal of Applied Physiology 116, no. 8 (2014): 1078–87. http://dx.doi.org/10.1152/japplphysiol.01270.2013.

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While exercise benefits have been well documented in patients with chronic diseases, the mechanistic understanding of cachectic muscle's response to contraction is essentially unknown. We previously demonstrated that treadmill exercise training attenuates the initiation of cancer cachexia and the development of metabolic syndrome symptoms (Puppa MJ, White JP, Velazquez KT, Baltgalvis KA, Sato S, Baynes JW, Carson JA. J Cachexia Sarcopenia Muscle 3: 117–137, 2012). However, cachectic muscle's metabolic signaling response to a novel, acute bout of low-frequency contraction has not been determined. The purpose of this study was to determine whether severe cancer cachexia disrupts the acute contraction-induced response to low-frequency muscle contraction [low-frequency stimulation (LoFS)]. Metabolic gene expression and signaling was examined 3 h after a novel 30-min bout of contraction (10 Hz) in cachectic ApcMin/+(Min) and C57BL/6 (BL-6) mice. Pyrrolidine dithiocarbamate, a STAT/NF-κB inhibitor and free radical scavenger, was administered systemically to a subset of mice to determine whether this altered the muscle contraction response. Although glucose transporter-4 mRNA was decreased by cachexia, LoFS increased muscle glucose transporter-4 mRNA in both BL-6 and Min mice. LoFS also induced muscle peroxisome proliferator-activated receptor-γ and peroxisome proliferator-activated receptor-α coactivator-1 mRNA. However, in Min mice, LoFS was not able to induce muscle proliferator-activated receptor-α coactivator-1 targets nuclear respiratory factor-1 and mitochondrial transcription factor A mRNA. LoFS induced phosphorylated-S6 in BL-6 mice, but this induction was blocked by cachexia. Administration of pyrrolidine dithiocarbamate for 24 h rescued LoFS-induced phosphorylated-S6 in cachectic muscle. LoFS increased muscle phosphorylated-AMP-activated protein kinase and p38 in BL-6 and Min mice. These data demonstrate that cachexia alters the muscle metabolic response to acute LoFS, and combination therapies in concert with muscle contraction may be beneficial for improving muscle mass and function during cachexia.

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