WorldCat Linked Data Explorer

Turtle N-Triple JSON-LD RDF/XML HTML Contact Us Home

http://worldcat.org/entity/work/id/1348551029

Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies

This book covers the computer simulation of demyelinating neuropathies and neuronopathies and compares models with clinical findings. Through the approximation of nerve excitation and conduction, the authors show how the versatile structure of nerve fibers relates to different modes of focal prospects, inward and outward currents, conduction velocity, and errant transmission. They also explain how mathematical models elucidate emerging fine distinctions between hereditary and acquired neuronal diseases, including Charcot-Marie-Tooth, chronic inflammatory demyelinating polyneuropathy, Guillain-

Open All Close All

type

about

http://schema.org/about

contributor

creator

description

http://schema.org/description

  • "This book covers the computer simulation of demyelinating neuropathies and neuronopathies and compares models with clinical findings. Through the approximation of nerve excitation and conduction, the authors show how the versatile structure of nerve fibers relates to different modes of focal prospects, inward and outward currents, conduction velocity, and errant transmission. They also explain how mathematical models elucidate emerging fine distinctions between hereditary and acquired neuronal diseases, including Charcot-Marie-Tooth, chronic inflammatory demyelinating polyneuropathy, Guillain-"@en
  • ""Preface Preface v vi Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies (PISD) are specifi c indicators for CIDP and its subtypes; (3) the severe focal demyelinations, each of them internodal and paranodal, paranodalinternodal (IFD and PFD, PIFD), are specifi c indicators for acquired demyelinating neuropathies such as GBS and MMN; (4) the simulated progressively greater degrees of axonal dysfunctions termed ALS1, ALS2 and ALS3 are specifi c indicators for the motor neuron disease ALS Type1, Tape2 and Type3; and (5) the obtained excitability properties in the simulated demyelinating neuropathies are quite different from those in the simulated ALS subtypes, because of the different fi bre electrogenesis. The results show that the abnormalities in the axonal excitability properties in the ALS1 subtype are near normal. The results also show that in the simulated hereditary, chronic and acquired demyelinating neuropathies, the slowing of action potential propagation, based on the myelin sheath dysfunctions, is larger than this, based on the progressively increased uniform axonal dysfunctions in the simulated ALS2 and ALS3 subtypes. Conversely, the abnormalities in the accommodative and adaptive processes are larger in the ALS2 and ALS3 subtypes than in the demyelinating neuropathies. The increased axonal superexcitability in the ALS2 and ALS3 subtypes leads to repetitive discharges (action potential generation) in the nodal and internodal axolemma beneath the myelin sheath along the fi bre length in response to the applied long-duration subthreshold polarizing current stimuli (accommodative processes) and to the applied long-duration suprathreshold depolarizing current stimuli (adaptive processes)"--"@en
  • ""Preface Preface v vi Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies (PISD) are specifi c indicators for CIDP and its subtypes; (3) the severe focal demyelinations, each of them internodal and paranodal, paranodalinternodal (IFD and PFD, PIFD), are specifi c indicators for acquired demyelinating neuropathies such as GBS and MMN; (4) the simulated progressively greater degrees of axonal dysfunctions termed ALS1, ALS2 and ALS3 are specifi c indicators for the motor neuron disease ALS Type1, Tape2 and Type3; and (5) the obtained excitability properties in the simulated demyelinating neuropathies are quite different from those in the simulated ALS subtypes, because of the different fi bre electrogenesis. The results show that the abnormalities in the axonal excitability properties in the ALS1 subtype are near normal. The results also show that in the simulated hereditary, chronic and acquired demyelinating neuropathies, the slowing of action potential propagation, based on the myelin sheath dysfunctions, is larger than this, based on the progressively increased uniform axonal dysfunctions in the simulated ALS2 and ALS3 subtypes. Conversely, the abnormalities in the accommodative and adaptive processes are larger in the ALS2 and ALS3 subtypes than in the demyelinating neuropathies. The increased axonal superexcitability in the ALS2 and ALS3 subtypes leads to repetitive discharges (action potential generation) in the nodal and internodal axolemma beneath the myelin sheath along the fi bre length in response to the applied long-duration subthreshold polarizing current stimuli (accommodative processes) and to the applied long-duration suprathreshold depolarizing current stimuli (adaptive processes)"--"
  • ""Preface Preface v vi Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies (PISD) are specifi c indicators for CIDP and its subtypes; (3) the severe focal demyelinations, each of them internodal and paranodal, paranodalinternodal (IFD and PFD, PIFD), are specifi c indicators for acquired demyelinating neuropathies such as GBS and MMN; (4) the simulated progressively greater degrees of axonal dysfunctions termed ALS1, ALS2 and ALS3 are specifi c indicators for the motor neuron disease ALS Type1, Tape2 and Type3; and (5) the obtained excitability properties in the simulated demyelinating neuropathies are quite different from those in the simulated ALS subtypes, because of the different fi bre electrogenesis. The results show that the abnormalities in the axonal excitability properties in the ALS1 subtype are near normal. The results also show that in the simulated hereditary, chronic and acquired demyelinating neuropathies, the slowing of action potential propagation, based on the myelin sheath dysfunctions, is larger than this, based on the progressively increased uniform axonal dysfunctions in the simulated ALS2 and ALS3 subtypes. Conversely, the abnormalities in the accommodative and adaptive processes are larger in the ALS2 and ALS3 subtypes than in the demyelinating neuropathies. The increased axonal superexcitability in the ALS2 and ALS3 subtypes leads to repetitive discharges (action potential generation) in the nodal and internodal axolemma beneath the myelin sheath along the fi bre length in response to the applied long-duration subthreshold polarizing current stimuli (accommodative processes) and to the applied long-duration suprathreshold depolarizing current stimuli (adaptive processes)"--."

genre

http://schema.org/genre

  • "Electronic books"@en

name

http://schema.org/name

  • "Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies"@en
  • "Computational neuroscience : simulated demyelinating neuropathies and neuronopathies"
  • "Computational neuroscience simulated demyelinating neuropathies and neuronopathies"
  • "Computational neuroscience simulated demyelinating neuropathies and neuronopathies"@en

workExample