[Mechanisms of development of secondary axonal failure in diffuse and local demyelinating neuropathies]

To estimate a qualitative and quantitative effects of axonal failure on the clinical and electromyographic (EMG) picture of diffuse and local demyelination, 24 patients with Guillain-Barre syndrome (GBS), 144 with chronic inflammatory demyelinating polyneuropathy (CIDP) and 27 patients with multifocal motor neuropathy (MMN) have been studied. All the patients underwent a complex clinical neurological and EMG examination. Along with significant association between muscular hypotrophies and weakness in the majority of patients (tau=0,51; p<0,001), in some cases weakness in extremities was found in the absence of amyotrophic syndrome specifying a "functional" axonopathy due to the disturbance of ionic transport and the blockade of potassium channels. The formation of persisting conduction block in 100% of MMN cases and in up to 75% of GBS and CIDP cases revealed the additional special mechanism of axonopathy. The primary autoimmune affection of axonal membrane in a case of acute motor axonal neuropathy is described. The data obtained suggest that secondary axonal pathology underlies formation of the pathological system manifesting with failure of neurotrophic influence of the affected axons in relation to muscles and leading to neurological plastic deficiency at a level of self-supporting dysregulation pathology.