The Experts below are selected from a list of 318 Experts worldwide ranked by ideXlab platform
Kevin L. Kilgore - One of the best experts on this subject based on the ideXlab platform.
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counted cycles method to measure the block inception time of kilohertz frequency mammalian Motor Nerve block
Journal of Neuroscience Methods, 2020Co-Authors: Niloy Bhadra, M R Gerges, Douglas Michael Ackermann, Kevin L. Kilgore, Emily FoldesAbstract:Abstract Background Kilohertz frequency alternating currents (KHFAC) produce rapid Nerve conduction block of mammalian peripheral Nerves and have potential clinical applications in reducing Nerve hyperactivity. However, there are no experimental measurements of the block inception time (BIT) for the complete block of mammalian Motor axons, i.e. the time from the start of delivery of the KHFAC to the axons reaching a fully blocked state. New method A “counted cycles” method (CCM) was designed to exploit characteristics of the onset response, which is typical of KHFAC block, to measure the BIT with a millisecond time resolution. Randomized and repeated experiments were conducted in an in-vivo rodent model, using trains of KHFAC over a range of complete cycle counts at three frequencies (10, 20, and 40 kHz). Results Complete Motor Nerve conduction block was obtained in the rat sciatic Nerve (N = 4) with an average BIT range of 5 ms–10 ms. The fastest BIT measured was 2.5 ms–5 ms. There was no statistical difference between the block inception times for the three frequencies tested. Comparison with existing methods There are no comparable methods to measure the KHFAC BIT. Conclusion The KHFAC BIT is faster than previously estimated. KHFAC Motor Nerve block is established in milliseconds. These results may assist in the design of methods to eliminate the onset response produced by KHFAC Nerve block.
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high frequency electrical conduction block of mammalian peripheral Motor Nerve
Muscle & Nerve, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:A quick-acting, quick-reversing method for blocking action potentials in peripheral Nerves could be used in the treatment of muscle spasticity and pain. A high-frequency alternating-current (HFAC) sinusoidal waveform is one possible means for providing this type of block. HFAC was used to block peripheral Motor Nerve activity in an in vivo mammalian model. Frequencies from 10 to 30 kHZ at amplitudes of between 2 and 10 V were investigated. A complete and reversible Motor block was obtained at all frequencies. The block threshold amplitudes showed a linear relationship with frequency, the lowest threshold being at 10 kHZ. HFAC block has three phases: an onset response; a period of asynchronous firing; and a steady state of complete or partial block. The onset response and the asynchronous firing can be minimized by using an optimal frequency–amplitude combination. In general, the onset response was lowest for the combination of 30 kHZ and 10 V. Muscle Nerve, 2005
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block of mammalian Motor Nerve conduction using high frequency alternating current
International IEEE EMBS Conference on Neural Engineering, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:High frequency alternating current waveforms have been shown to produce a rapidly reversible Nerve block in animal models. Acute in-vivo experiments were carried out in a rat model. A blocking electrode was placed on the sciatic Nerve and Motor Nerve block quantified by measuring force output of the gastrocnemius muscle. Sinusoidal waveforms in the range of 10 kHz to 30 kHz were tested. The results indicate that a 100% Nerve block of Motor activity can be accomplished at all the frequencies tested. The block is complete and quickly reversible. Block thresholds (peak to peak voltage of the waveform) were measured and showed a linear relationship to frequency. Block was obtained with the lowest voltage at 10 KHz. It was also demonstrated that the block is not produced indirectly through fatigue. This type of Nerve block may have multiple applications in the treatment of spasticity and pain
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High-frequency electrical conduction block of mammalian peripheral Motor Nerve
Muscle and Nerve, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:A quick-acting, quick-reversing method for blocking action potentials in peripheral Nerves could be used in the treatment of muscle spasticity and pain. A high-frequency alternating-current (HFAC) sinusoidal waveform is one possible means for providing this type of block. HFAC was used to block peripheral Motor Nerve activity in an in vivo mammalian model. Frequencies from 10 to 30 kHZ at amplitudes of between 2 and 10 V were investigated. A complete and reversible Motor block was obtained at all frequencies. The block threshold amplitudes showed a linear relationship with frequency, the lowest threshold being at 10 kHZ. HFAC block has three phases: an onset response; a period of asynchronous firing; and a steady state of complete or partial block. The onset response and the asynchronous firing can be minimized by using an optimal frequency-amplitude combination. In general, the onset response was lowest for the combination of 30 kHZ and 10 V.
Niloy Bhadra - One of the best experts on this subject based on the ideXlab platform.
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counted cycles method to measure the block inception time of kilohertz frequency mammalian Motor Nerve block
Journal of Neuroscience Methods, 2020Co-Authors: Niloy Bhadra, M R Gerges, Douglas Michael Ackermann, Kevin L. Kilgore, Emily FoldesAbstract:Abstract Background Kilohertz frequency alternating currents (KHFAC) produce rapid Nerve conduction block of mammalian peripheral Nerves and have potential clinical applications in reducing Nerve hyperactivity. However, there are no experimental measurements of the block inception time (BIT) for the complete block of mammalian Motor axons, i.e. the time from the start of delivery of the KHFAC to the axons reaching a fully blocked state. New method A “counted cycles” method (CCM) was designed to exploit characteristics of the onset response, which is typical of KHFAC block, to measure the BIT with a millisecond time resolution. Randomized and repeated experiments were conducted in an in-vivo rodent model, using trains of KHFAC over a range of complete cycle counts at three frequencies (10, 20, and 40 kHz). Results Complete Motor Nerve conduction block was obtained in the rat sciatic Nerve (N = 4) with an average BIT range of 5 ms–10 ms. The fastest BIT measured was 2.5 ms–5 ms. There was no statistical difference between the block inception times for the three frequencies tested. Comparison with existing methods There are no comparable methods to measure the KHFAC BIT. Conclusion The KHFAC BIT is faster than previously estimated. KHFAC Motor Nerve block is established in milliseconds. These results may assist in the design of methods to eliminate the onset response produced by KHFAC Nerve block.
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high frequency electrical conduction block of mammalian peripheral Motor Nerve
Muscle & Nerve, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:A quick-acting, quick-reversing method for blocking action potentials in peripheral Nerves could be used in the treatment of muscle spasticity and pain. A high-frequency alternating-current (HFAC) sinusoidal waveform is one possible means for providing this type of block. HFAC was used to block peripheral Motor Nerve activity in an in vivo mammalian model. Frequencies from 10 to 30 kHZ at amplitudes of between 2 and 10 V were investigated. A complete and reversible Motor block was obtained at all frequencies. The block threshold amplitudes showed a linear relationship with frequency, the lowest threshold being at 10 kHZ. HFAC block has three phases: an onset response; a period of asynchronous firing; and a steady state of complete or partial block. The onset response and the asynchronous firing can be minimized by using an optimal frequency–amplitude combination. In general, the onset response was lowest for the combination of 30 kHZ and 10 V. Muscle Nerve, 2005
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block of mammalian Motor Nerve conduction using high frequency alternating current
International IEEE EMBS Conference on Neural Engineering, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:High frequency alternating current waveforms have been shown to produce a rapidly reversible Nerve block in animal models. Acute in-vivo experiments were carried out in a rat model. A blocking electrode was placed on the sciatic Nerve and Motor Nerve block quantified by measuring force output of the gastrocnemius muscle. Sinusoidal waveforms in the range of 10 kHz to 30 kHz were tested. The results indicate that a 100% Nerve block of Motor activity can be accomplished at all the frequencies tested. The block is complete and quickly reversible. Block thresholds (peak to peak voltage of the waveform) were measured and showed a linear relationship to frequency. Block was obtained with the lowest voltage at 10 KHz. It was also demonstrated that the block is not produced indirectly through fatigue. This type of Nerve block may have multiple applications in the treatment of spasticity and pain
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High-frequency electrical conduction block of mammalian peripheral Motor Nerve
Muscle and Nerve, 2005Co-Authors: Niloy Bhadra, Kevin L. KilgoreAbstract:A quick-acting, quick-reversing method for blocking action potentials in peripheral Nerves could be used in the treatment of muscle spasticity and pain. A high-frequency alternating-current (HFAC) sinusoidal waveform is one possible means for providing this type of block. HFAC was used to block peripheral Motor Nerve activity in an in vivo mammalian model. Frequencies from 10 to 30 kHZ at amplitudes of between 2 and 10 V were investigated. A complete and reversible Motor block was obtained at all frequencies. The block threshold amplitudes showed a linear relationship with frequency, the lowest threshold being at 10 kHZ. HFAC block has three phases: an onset response; a period of asynchronous firing; and a steady state of complete or partial block. The onset response and the asynchronous firing can be minimized by using an optimal frequency-amplitude combination. In general, the onset response was lowest for the combination of 30 kHZ and 10 V.
Susan E Mackinnon - One of the best experts on this subject based on the ideXlab platform.
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supercharge end to side anterior interosseous to ulnar Motor Nerve transfer restores intrinsic function in cubital tunnel syndrome
Plastic and Reconstructive Surgery, 2020Co-Authors: Jana Dengler, Andrew Yee, Lorna C. Kahn, Utku Can Dolen, Jennifer Megan M Patterson, Kristen M Davidge, Susan E MackinnonAbstract:Background The supercharge end-to-side anterior interosseous Nerve-to-ulnar Motor Nerve transfer offers a viable option to enhance recovery of intrinsic function following ulnar Nerve injury. However, in the setting of chronic ulnar Nerve compression where the timing of onset of axonal loss is unclear, there is a deficit in the literature on outcomes after supercharge end-to-side anterior interosseous Nerve-to-ulnar Motor Nerve transfer. Methods A retrospective study of patients who underwent supercharge end-to-side anterior interosseous Nerve-to-ulnar Motor Nerve transfer for severe cubital tunnel syndrome over a 5-year period was performed. The primary outcomes were improvement in first dorsal interosseous Medical Research Council grade at final follow-up and time to reinnervation. Change in key pinch strength; grip strength; and Disabilities of the Arm, Shoulder and Hand questionnaire scores were also evaluated using paired t tests and Wilcoxon signed rank tests. Results Forty-two patients with severe cubital tunnel syndrome were included in this study. Other than age, there were no significant clinical or diagnostic variables that were predictive of failure. There was no threshold of compound muscle action potential amplitude below which supercharge end-to-side anterior interosseous Nerve-to-ulnar Motor Nerve transfer was unsuccessful. Conclusions This study provides the first cohort of outcomes following supercharge end-to-side anterior interosseous Nerve-to-ulnar Motor Nerve transfer in chronic ulnar compression neuropathy alone and underscores the importance of appropriate patient selection. Prospective cohort studies and randomized controlled trials with standardized outcome measures are required. Clinical question/level of evidence Therapeutic, IV.
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refining indications for the supercharge end to side anterior interosseous to ulnar Motor Nerve transfer in cubital tunnel syndrome
Plastic and Reconstructive Surgery, 2020Co-Authors: Hollie A Power, Amy M Moore, Lorna C. Kahn, Megan M Patterson, Susan E MackinnonAbstract:: The supercharge end-to-side anterior interosseous to ulnar Motor Nerve transfer has gained popularity over the past decade as a method of augmenting intrinsic muscle reinnervation in patients with acute neurotmetic ulnar Nerve injuries. Controversy remains regarding its efficacy and appropriate clinical indications in cubital tunnel syndrome, where the timing of onset of axonal loss is less clear. The authors present guidelines for patient selection, surgical technique, and postoperative rehabilitation based on their clinical experience with the technique in this patient population. CLINICAL QUESTION/LEVEL OF EVIDENCE:: Therapeutic, V.
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the supercharge end to side anterior interosseous to ulnar Motor Nerve transfer for restoring intrinsic function clinical experience
Plastic and Reconstructive Surgery, 2015Co-Authors: Kristen M Davidge, Amy M Moore, Susan E MackinnonAbstract:Background:The authors reviewed their initial clinical experience with the supercharge end-to-side anterior interosseous–to–ulnar Motor Nerve transfer and refined their indications for this technique.Methods:A retrospective cohort study was performed of all patients undergoing the supercharge end-to
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Two-level Motor Nerve transfer for the treatment of long thoracic Nerve palsy.
Journal of neurosurgery, 2011Co-Authors: Wilson Z. Ray, Mitchell A. Pet, Michael C. Nicoson, Andrew Yee, Lorna C. Kahn, Susan E MackinnonAbstract:The authors report a case of long thoracic Nerve (LTN) palsy treated with two-level Motor Nerve transfers of a pectoral fascicle of the middle trunk, and a branch of the thoracodorsal Nerve. This procedure resulted in near-total improvement of the winged scapula deformity, and a return of excellent shoulder function. A detailed account of the postoperative physical therapy regimen is included, as this critical component of the favorable result cannot be overlooked. This case establishes the two-level Motor Nerve transfer as a new option for treating LTN palsy, and demonstrates that Nerve transfers should be considered in the therapeutic algorithm of an idiopathic mononeuritis.
Hugh J Willison - One of the best experts on this subject based on the ideXlab platform.
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the pre synaptic Motor Nerve terminal as a site for antibody mediated neurotoxicity in autoimmune neuropathies and synaptopathies
Journal of Anatomy, 2014Co-Authors: Simon N Fewou, Jaap J Plomp, Hugh J WillisonAbstract:The pre-synaptic Motor Nerve terminal is a highly complex and dynamic compartment within the lower Motor neuron responsible for converting electrical signals into secreted chemicals. This self-renewing process of synaptic transmission is accomplished by the calcium-triggered fusion of neurotransmitter-containing vesicles with the plasma membrane and the subsequent retrieval and recycling of vesicle components. Besides this conventional physiological role, the highly active process of vesicle fusion and re-uptake into endosomal sorting pathways acts as a conduit for entry of a range of substances into the intracellular compartment of the Motor Nerve terminal. Whilst this entry portal sub-serves many vital physiological processes, such as those mediated by neurotrophin trafficking, there is also the potential for substantial pathological consequences resulting from uptake of noxious agents, including autoantibodies, viruses and toxins. These may act locally to induce disease within the Nerve terminal, or traffic beyond to the Motor neuron cell body and central nervous system to exert their pathological effects. This review focuses on the recent evidence that the ganglioside-rich pre-synaptic membrane acts as a binding site for potentially neurotoxic serum autoantibodies that are present in human autoimmune Motor neuropathies. Autoantibodies that bind surface antigens induce membrane lytic effects, whereas their uptake attenuates local injury and transfers any potential pathological consequences to the intracellular compartment. Herein the thesis is explored that a balance exists between local injury at the exofacial leaflet of the pre-synaptic membrane and antibody uptake, which dictates the overall level and site of Motor Nerve injury in this group of disorders.
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the role of complement and complement regulators in mediating Motor Nerve terminal injury in murine models of guillain barre syndrome
Journal of Neuroimmunology, 2008Co-Authors: Hugh J Willison, Susan K Halstead, Erin Beveridge, Femke M P Zitman, Kay N Greenshields, Paul B Morgan, Jaap J PlompAbstract:Recent research into the Guillain-Barre syndromes (GBS) has focused on anti-ganglioside antibodies that correlate with specific clinical phenotypes. Our increasing understanding of the role of antibodies in mediating GBS has naturally focused our attention on complement involvement in the pathological procession. We have studied the axonal and glial components of the murine Motor Nerve terminal as a model site of antibody and complement mediated injury. Such studies are providing us with clear information on the molecular components underlying our clinicopathological model for GBS and have lead us to the testing of emerging complement therapeutics that are potentially suitable for human use.
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Anti-ganglioside antibodies and the presynaptic Motor Nerve terminal.
Annals of the New York Academy of Sciences, 2008Co-Authors: Hugh J Willison, Jaap J PlompAbstract:The Guillain Barre syndromes (GBS) are the world's leading cause of acute autoimmune neuromuscular paralysis. Understanding the pathophysiological events of GBS, and improving immunotherapies are fundamental to improving the clinical outcome. Recent research into GBS and the Miller Fisher syndrome (MFS) variant has focused on the forms mediated by anti-ganglioside antibodies in which correlations have been established between anti-ganglioside antibodies and specific clinical phenotypes, notably between anti-GM1/GD1a antibodies and the acute Motor axonal variant and anti-GQ1b/GT1a antibodies and MFS. Anti-ganglioside antibodies can arise through molecular mimicry with GBS-associated Campylobacter jejuni oligosaccharides. Our work has focused on axonal and glial components of the Motor Nerve terminal as a model site of injury, and through combined active and passive immunization paradigms in glycosyltransferase knockout mice we have developed murine neuropathy phenotypes mediated by anti-ganglioside antibodies. Several determinants influence disease expression including the level of immunological tolerance to microbial glycans that mimic self gangliosides, the degree of complement activation, and the ganglioside density in target tissue. Such studies provide us with clear information on an antibody-mediated pathogenesis model for GBS and should lead to rational therapeutic testing of agents that are potentially suitable for use in man.
Jaap J Plomp - One of the best experts on this subject based on the ideXlab platform.
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the pre synaptic Motor Nerve terminal as a site for antibody mediated neurotoxicity in autoimmune neuropathies and synaptopathies
Journal of Anatomy, 2014Co-Authors: Simon N Fewou, Jaap J Plomp, Hugh J WillisonAbstract:The pre-synaptic Motor Nerve terminal is a highly complex and dynamic compartment within the lower Motor neuron responsible for converting electrical signals into secreted chemicals. This self-renewing process of synaptic transmission is accomplished by the calcium-triggered fusion of neurotransmitter-containing vesicles with the plasma membrane and the subsequent retrieval and recycling of vesicle components. Besides this conventional physiological role, the highly active process of vesicle fusion and re-uptake into endosomal sorting pathways acts as a conduit for entry of a range of substances into the intracellular compartment of the Motor Nerve terminal. Whilst this entry portal sub-serves many vital physiological processes, such as those mediated by neurotrophin trafficking, there is also the potential for substantial pathological consequences resulting from uptake of noxious agents, including autoantibodies, viruses and toxins. These may act locally to induce disease within the Nerve terminal, or traffic beyond to the Motor neuron cell body and central nervous system to exert their pathological effects. This review focuses on the recent evidence that the ganglioside-rich pre-synaptic membrane acts as a binding site for potentially neurotoxic serum autoantibodies that are present in human autoimmune Motor neuropathies. Autoantibodies that bind surface antigens induce membrane lytic effects, whereas their uptake attenuates local injury and transfers any potential pathological consequences to the intracellular compartment. Herein the thesis is explored that a balance exists between local injury at the exofacial leaflet of the pre-synaptic membrane and antibody uptake, which dictates the overall level and site of Motor Nerve injury in this group of disorders.
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the role of complement and complement regulators in mediating Motor Nerve terminal injury in murine models of guillain barre syndrome
Journal of Neuroimmunology, 2008Co-Authors: Hugh J Willison, Susan K Halstead, Erin Beveridge, Femke M P Zitman, Kay N Greenshields, Paul B Morgan, Jaap J PlompAbstract:Recent research into the Guillain-Barre syndromes (GBS) has focused on anti-ganglioside antibodies that correlate with specific clinical phenotypes. Our increasing understanding of the role of antibodies in mediating GBS has naturally focused our attention on complement involvement in the pathological procession. We have studied the axonal and glial components of the murine Motor Nerve terminal as a model site of antibody and complement mediated injury. Such studies are providing us with clear information on the molecular components underlying our clinicopathological model for GBS and have lead us to the testing of emerging complement therapeutics that are potentially suitable for human use.
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Anti-ganglioside antibodies and the presynaptic Motor Nerve terminal.
Annals of the New York Academy of Sciences, 2008Co-Authors: Hugh J Willison, Jaap J PlompAbstract:The Guillain Barre syndromes (GBS) are the world's leading cause of acute autoimmune neuromuscular paralysis. Understanding the pathophysiological events of GBS, and improving immunotherapies are fundamental to improving the clinical outcome. Recent research into GBS and the Miller Fisher syndrome (MFS) variant has focused on the forms mediated by anti-ganglioside antibodies in which correlations have been established between anti-ganglioside antibodies and specific clinical phenotypes, notably between anti-GM1/GD1a antibodies and the acute Motor axonal variant and anti-GQ1b/GT1a antibodies and MFS. Anti-ganglioside antibodies can arise through molecular mimicry with GBS-associated Campylobacter jejuni oligosaccharides. Our work has focused on axonal and glial components of the Motor Nerve terminal as a model site of injury, and through combined active and passive immunization paradigms in glycosyltransferase knockout mice we have developed murine neuropathy phenotypes mediated by anti-ganglioside antibodies. Several determinants influence disease expression including the level of immunological tolerance to microbial glycans that mimic self gangliosides, the degree of complement activation, and the ganglioside density in target tissue. Such studies provide us with clear information on an antibody-mediated pathogenesis model for GBS and should lead to rational therapeutic testing of agents that are potentially suitable for use in man.
