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Computational neuroscience : simulated demyelinating neuropathies and neuronopathies

Author: Diana I Stephanova; Bozhidar Dimitrov Kolev
Publisher: Boca Raton : CRC Press, 2013.
Edition/Format:   eBook : Document : EnglishView all editions and formats
Summary:
"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  Read more...
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Genre/Form: Electronic books
Additional Physical Format: Print version:
Stephanova, Diana Ivanova.
Computational neuroscience.
Boca Raton : CRC Press, 2013
(DLC) 2012036915
(OCoLC)809027668
Material Type: Document, Internet resource
Document Type: Internet Resource, Computer File
All Authors / Contributors: Diana I Stephanova; Bozhidar Dimitrov Kolev
ISBN: 9781466578364 146657836X
OCLC Number: 844924363
Description: 1 online resource (x, 136 pages) : illustrations
Contents: I. Nerve fibres --
II. Models and methods for investigation of the human motor nerve fibre --
III. Simulated demyelinating neuropathies and neuropathies --
IV. Effect of myelin sheath aqueous layers on the excitability properties of simulated hereditary and chronic demyelinating neuropathies.
Responsibility: Diana Ivanova Stephanova, Institute of Biophysics and Biomedical Engineering, Bulgarian Academy of Sciences, Sofia, Bulgaria and Bozhidar Dimitrov Kolev, Institute of Population and Human Studies, Bulgarian Academy of Sciences, Sofia, Bulgaria.
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Abstract:

"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)"--

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