By Diana Ivanova Stephanova
''Preface Preface v vi Computational Neuroscience Simulated Demyelinating Neuropathies and Neuronopathies (PISD) are specifi c symptoms for CIDP and its subtypes; (3) the serious focal demyelinations, each one of them internodal and paranodal, paranodalinternodal (IFD and PFD, PIFD), are specifi c signs for received demyelinating neuropathies resembling GBS and MMN; (4) the simulated steadily higher levels of axonal dysfunctions termed ALS1, ALS2 and ALS3 are specifi c symptoms for the motor neuron ailment ALS Type1, Tape2 and Type3; and (5) the received excitability houses within the simulated demyelinating neuropathies are relatively diverse from these within the simulated ALS subtypes, as a result of assorted fi bre electrogenesis. the consequences exhibit that the abnormalities within the axonal excitability houses within the ALS1 subtype are close to general. the consequences additionally convey that during the simulated hereditary, power and purchased demyelinating neuropathies, the slowing of motion power propagation, in accordance with the myelin sheath dysfunctions, is greater than this, in line with the steadily elevated uniform axonal dysfunctions within the simulated ALS2 and ALS3 subtypes. Conversely, the abnormalities within the accommodative and adaptive procedures are higher within the ALS2 and ALS3 subtypes than within the demyelinating neuropathies. The elevated axonal superexcitability within the ALS2 and ALS3 subtypes ends up in repetitive discharges (action power new release) within the nodal and internodal axolemma underneath the myelin sheath alongside the fi bre size in accordance with the utilized long-duration subthreshold polarizing present stimuli (accommodative methods) and to the utilized long-duration suprathreshold depolarizing present stimuli (adaptive processes)''-- Read more...
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Additional resources for Computational Neuroscience: Simulated Demyelinating Neuropathies and Neuronopathies
A critical diagnostic feature of GBS and MMN is the demonstration of conduction block in multiple peripheral nerves on electrophysiological investigations (Kiernan et al. 2002, Kuwabara et al. 2002, Kaji 2003, Priori et al. 2005). Such a block was also demonstrated here in the IFD, PFD and PIFD cases. The simulated almost normal amplitudes and durations of action potentials and their near normal conduction velocities in the simulated ALS subtypes are in agreement with the slightly reduced velocities obtained for the almost normal action potentials recorded in patients with ALS (Sobue et al.
The latter is zero, as the resistive nodal gap is not taken into account in the model. However, the nodal transmembrane (external membrane) current (Im, in Fig. 6b), for all investigated cases, is less than the current across the nodal axolemma (Ia). This is because the longitudinal current flows through the paranodal seal resistance (Rpn) to the periaxonal space. 40 Computational Neuroscience: Simulated Demyelinating Neuropathies and Neuronopathies Fig. 6. Kinetics of the currents defining the action potential in the normal, ISD, PSD and PISD cases at node 10.
The kinetics of the currents in the ISD case is consistent with the effect of the uniformly reduced myelin lamellae along the fibre length and shows the mechanisms of the conduction slowing of action potentials obtained in simulated CMT1A. The kinetics of the currents in the PSD case is consistent with the effect of the uniformly reduced paranodal seal resistance along the fibre length and shows the mechanisms of the conduction slowing of action potentials obtained in simulated CIDP. The kinetics of the currents in the PISD case is consistent with the effect of the reduced myelin lamellae, additionally increased by reduced paranodal seal resistance along the fibre length and shows the mechanisms of the conduction slowing of action potentials obtained in heterogeneous demyelinations, such as in some CIDP subtypes.
Computational Neuroscience: Simulated Demyelinating Neuropathies and Neuronopathies by Diana Ivanova Stephanova