Differences in potentials and excitability properties in simulated cases of demyelinating neuropathies. Part II. Paranodal demyelination.
OBJECTIVE
The purpose of the present investigation is to study the potentials and axonal excitability properties in progressively greater degrees of uniform paranodal demyelination of human motor nerve fibres.


METHODS
Using our previous double cable model of human motor nerve fibre, 3 paranodally systematically demyelinated cases (termed as PSD1, PSD2 and PSD3) are simulated by an uniform paranodal resistance reduction (20, 50 and 77%) along the fibre length.


RESULTS
Considerably reduced amplitudes, prolonged durations and slowed conduction velocities are obtained for the intracellular potentials of the PSD2 and PSD3 cases. In contrast, the electrotonic potentials show abnormally greater increase in the early part of the hyperpolarizing responses. The extracellular potentials indicate increased polyphasia in the PSD3 case. The strength-duration time constants are shorter and the rheobases higher in the demyelinated cases. In the recovery cycles, the demyelinated cases have less refractoriness, greater supernormality and less late subnormality than the normal case.


CONCLUSIONS
The reduction of the paranodal seal resistance has significant effects on the potentials and axonal excitability properties of the simulated demyelinated human motor fibres. The obtained abnormalities in the potentials and excitability properties can be observed in vivo in patients with chronic inflammatory demyelinating polyneuropathy.


CONCLUSIONS
The study provides important information about the pathology of human demyelinating neuropathies.
Stephanova
D I
DI
Institute of Biophysics, Bulgarian Academy of Sciences, Sofia. dsteph@iph.bio.bas.bg
Daskalova
M
M
D003711:Demyelinating Diseases / Q000503:physiopathology*; D006801:Humans; D008564:Membrane Potentials / Q000502:physiology*; D008959:Models, Neurological; D009046:Motor Neurons / Q000473:pathology* / Q000502:physiology; D009186:Myelin Sheath / Q000473:pathology / Q000502:physiology; D009431:Neural Conduction / Q000502:physiology; D011901:Ranvier's Nodes / Q000502:physiology*