The recovery cycles reflect the adaptive processes in nerve excitable structures. In order to expand our studies of the adaptive processes, these recovery cycles are compared in previously simulated by us demyelinating neuropathies such as Charcot-Marie-Tooth disease type 1A (CMT1A), chronic inflammatory demyelinating polyneuropathy (CIDP), CIDP subtypes, Guillain-Barre Syndrome (GBS), multifocal motor neuropathy (MMN) and neuronopathies such as amyotrophic lateral sclerosis (ALS) with three progressively greater degrees termed Type 1, Type 2, Type 3. Using our multi-layered model of human motor nerve fibre, the calculated recovery cycles are presented as in the simulated normal case and in the mentioned diseases. The increased super excitability periods of the axonal excitability, recovered to the end of the investigated 100 ms cycles, are characteristic for the simulated demyelinating neuropathies and ALS Type 1. The abnormally increased super excitability periods of the axonal excitability, which is not recovered to the end of the cycles, are characteristic for ALS Type 2 and Type 3. These axonal super excitabilities lead to blockage of each applied third (testing) stimulus in the recovery cycle of ALS Type 2 and to blockage of each applied second (testing) stimulus in the recovery cycle of ALS Type 3 as a result of repetitive firing caused by the applied preceding stimulus (i. e. by the applied first (conditioning) and second (testing) stimuli in ALS Type 3 and ALS Type 2). The present study shows that the recovery cycle abnormalities in the simulated demyelinating neuropathies are quite different from those in ALS because of the different fibre electrogenesis.
Scripta Scientifica Medica 2012; 44(2): 59-63.
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