[The pathogenetic mechanisms of the development of experimental allergic polyradiculoneuritis]

Biochemical, immune and morphological changes in peripheral nervous system at different stages of experimental allergic polyradiculoneuritis were studied in 102 rabbits as indicated by total lipids, cholesterol, phospholipids and their fractions, diene conjugates of spinal ganglions, cervical, thoracic and lumbosacral roots, trigeminal ganglions and nerve trunks of extremities. It was found out, that derangement of lipid metabolism in spinal ganglions and nerve roots is the primary phase in the development of the disease. Those could be seen as early as the experiment day 6. From the 8th day after the injection of antigen (myelin in complete Freund adjuvant) impairment of protective function of blood-nerve barrier took place in the form of increased vascular permeability of spinal ganglions, roots and trigeminal ganglions. Fixed antibodies, located on myelin sheath predominantly of intraganglion fibres of lumbar, cervical and thoracic segments, trigeminal ganglions, appeared after these changes. Demyelination and inflammatory infiltration began in the end of the incubation against initial clinical signs of polyneuritis in rabbits and reached its maximum at the peak of the disease.