Difference between revisions of "Physiological Dynamics in Demyelinating Diseases: Unraveling Complex Relationships through Computer Modeling"

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Mild systematic and severe focal demyelination correspond to hereditary (CMT1A) and acquired (CIDP, GBS and MMN) neuropathies (Table 1). It was also found that 70% systematic demyelination is insufficient to cause symptoms and 96% is required for conduction block at a single node [18]. Thus, there is a large safety factor for focal demyelination. With their temperature-dependent version of the model of the myelinated human motor nerve fiber, Stephanova and Daskalova<ref>Stephanova D.I., Daskalova M. Electrotonic potentials in simulated chronic inflammatory demyelinating polyneuropathy at 20 °C–42 °C. J. Integr. Neurosci. 2015;27:1–18. doi: 10.1142/S0219635215500119. [PubMed] [CrossRef] [Google Scholar]</ref> showed that the electrotonic potentials in patients with CIDP are in high risk for blocking during hypo- and even mild hyperthermia and suggest mechanisms involving increased magnitude of polarizing nodal and depolarizing internodal electrotonic potentials, inward rectifier K+ and leak K+ currents increase with temperature, and the accommodation to long-lasting hyperpolarization is greater than to depolarization.
Mild systematic and severe focal demyelination correspond to hereditary (CMT1A) and acquired (CIDP, GBS and MMN) neuropathies (Table 1). It was also found that 70% systematic demyelination is insufficient to cause symptoms and 96% is required for conduction block at a single node [18]. Thus, there is a large safety factor for focal demyelination. With their temperature-dependent version of the model of the myelinated human motor nerve fiber, Stephanova and Daskalova<ref>Stephanova D.I., Daskalova M. Electrotonic potentials in simulated chronic inflammatory demyelinating polyneuropathy at 20 °C–42 °C. J. Integr. Neurosci. 2015;27:1–18. doi: 10.1142/S0219635215500119. [PubMed] [CrossRef] [Google Scholar]</ref> showed that the electrotonic potentials in patients with CIDP are in high risk for blocking during hypo- and even mild hyperthermia and suggest mechanisms involving increased magnitude of polarizing nodal and depolarizing internodal electrotonic potentials, inward rectifier K+ and leak K+ currents increase with temperature, and the accommodation to long-lasting hyperpolarization is greater than to depolarization.


Table 1
{| class="wikitable"
Table 1
|+
Correspondence between types of demyelination and diseases according to Stephanova and Dimitrov.<ref name=":3" />  
! colspan="2" |Table 1
Correspondence between types of demyelination and diseases according to Stephanova and Dimitrov.<ref name=":3" />
|-
! colspan="1" rowspan="1" |Type of Demyelination
! colspan="1" rowspan="1" |Corresponding Disease (PNS)
|-
| colspan="1" rowspan="1" |Internodal systematic demyelination (ISD)
| colspan="1" rowspan="1" |Charcot-Marie-Tooth Disease Type 1A (CMT1A)
|-
| colspan="1" rowspan="1" |Paranodal systematic demyelination (PSD)
| colspan="1" rowspan="1" |Chronic inflammatory demyelinating polyneuropathy (CIDP)
|-
| colspan="1" rowspan="1" |Paranodal + internodal demyelination (PISD)
| colspan="1" rowspan="1" |Chronic inflammatory demyelinating polyneuropathy (CIPD) subtypes
|-
| colspan="1" rowspan="1" |Internodal focal demyelination (IFD)
| colspan="1" rowspan="1" |Guillain-Barré (GBS)
|-
| colspan="1" rowspan="1" |Paranodal focal demyelination (PFD)
| colspan="1" rowspan="1" |Multifocal Motor Neuropathy (MMN)
|-
| colspan="1" rowspan="1" |Paranodal + focal demyelination (PIFD)
| colspan="1" rowspan="1" |Multifocal Motor Neuropathy (MMN)
|}


==== Simple Models and Nonlinear Dynamical Analysis ====
==== Simple Models and Nonlinear Dynamical Analysis ====
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