Central-peripheral distal axonopathy--the pathology of dying-back polyneuropathies.
Spencer PS; Schaumburg HH
Prog Neuropathol 1976 Jan; 3():253-295
The pathology of neurologic disorders known as dying back diseases was studied in-vitro and experimentally in cats and rats. Five neurotoxic chemicals were used to produce slowly developing distal neuropathies in cats or rats. These included thallium-sulfate (10031591), acrylamide (79061), n-hexane (110543), methyl-n-butyl- ketone (591786) (MBK), and 2,5-hexanedione (2935446). The course of the disease process was studied by examining tissues obtained by repeated biopsy of sensory and motor terminals and distal nerves sampled from the feet. These studies were supplemented with in- vitro studies of nerve fiber degeneration and physiologic functions of nerve tissues. When 10 milligrams per kilogram acrylamide was injected intraperitoneally in cats, the most sensitive structure was the pacinian corpuscle. A single massive dose of thallium-sulfate injected in rats produced a direct toxic effect on axonal mitochondria in both peripheral and central nervous systems. In rats administered n-hexane, MBK, or 2,5-hexanedione, degeneration began distally and spread proximally, involving peripheral nerves and central nervous system tracts. N-hexane, MBK, and 2,5- hexanedione produced giant axonal degeneration concurrently in both nervous systems. A set of consistent observations in both the experimental animals and in-vitro was that the pathologic events began in a multifocal pattern, that they involved the distal axon (but only infrequently the nerve terminal), and that the proximal foci in the affected axon were more severely damaged than the more distal regions.
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