ABSTRACT
Clinical immunologic and electroneuromyographic examination covered patients with vibration disease. Registered- demyelination disorders on lower and upper limbs in vibration disease patients were associated with neurochemical changes in special neural structures (OBM, S-100 protein, DNA, AH-R, DA-R, Ser-R, GAMK-R). Direct proof of demyelination disorders in vibration disease patients are reliable correlation between levels of antibodies to OBM and conduction velocity in distal part of median nerve, in ulnar nerve from elbow bend and lower third of arm, and ulnar residual latency. Diagnosed relations between levels of antibodies to regulatory proteins in nervous tissue (antibodies to OBM and to S-100 protein), neurotransmitters (antibodies to AH-R, DA-R, Ser-R, GAMK-R) and functional parameters of nervous system prove important role of autoimmune reactions in vibration disease pathogenesis.
Subject(s)
Autoimmunity , Demyelinating Diseases , Median Nerve , Nerve Tissue Proteins/immunology , Ulnar Nerve , Vibration/adverse effects , Autoantibodies/blood , Demyelinating Diseases/diagnosis , Demyelinating Diseases/etiology , Extremities/innervation , Humans , Male , Median Nerve/immunology , Median Nerve/pathology , Median Nerve/physiopathology , Middle Aged , Peripheral Nervous System Diseases/diagnosis , Peripheral Nervous System Diseases/etiology , Peripheral Nervous System Diseases/immunology , Peripheral Nervous System Diseases/physiopathology , Ulnar Nerve/immunology , Ulnar Nerve/pathology , Ulnar Nerve/physiopathologyABSTRACT
Intravenous immunoglobulin (IVIg) infusions may provide clinical benefits in multifocal motor neuropathy (MMN) and chronic inflammatory demyelinating polyneuropathy (CIDP). The short delay in the clinical response to IVIg therapy is not consistent with a process of remyelination or axonal regeneration. We assessed whether or not the efficacy of IVIg infusions in MMN and CIDP could reflect changes in axonal membrane properties and nerve excitability. Ulnar motor nerve excitability was studied before and after three to five consecutive days of IVIg infusions (0.4 g/kg/day) in 10 patients with MMN, 10 patients with CIDP, and 10 neurological controls (CTRLs). Excitability recovery cycle, stimulus-response and strength-duration properties were investigated. The recovery cycle parameters (absolute and relative refractory period durations, refractoriness and supernormality) were similar in all groups and did not change after IVIg infusions. At baseline, patients with CIDP, but not with MMN, showed a reduced strength-duration time constant (chronaxie) and increased rheobase when compared to CTRLs. After IVIg infusions, strength-duration time constant remained stable in CTRLs, but decreased in patients with MMN or CIDP. Rheobase increased in the three groups after treatment. The decreased strength-duration time constant after IVIg infusions in patients with MMN or CIDP could reflect a reduction of persistent Na(+) current, able to limit intraaxonal Na(+) accumulation and then to produce neuroprotective effects. However, this could also reflect compensatory mechanisms that did not directly underlie the therapeutic effect. Whatever the underlying process, this result revealed that IVIgs were able to produce early nerve excitability changes.
