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IDPN NEUROPATHY IN THE CAT: COEXISTENCE OF PROXIMAL AND DISTAL AXONAL SWELLINGS
Author(s) -
GRIFFIN JOHN W.,
GOLD BRUCE G.,
CORK LINDA C.,
PRICE DONALD L.,
LOWNDES HERBERT E.
Publication year - 1982
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1982.tb00304.x
Subject(s) - wallerian degeneration , axon , neurofilament , anatomy , medicine , sciatic nerve , pathological , axonal degeneration , peripheral neuropathy , pathology , endocrinology , immunohistochemistry , diabetes mellitus
Griffin J.W., Gold B.G., Cork L.C., Price D.L. & Lowndes H.E. 1982 Neuropathology and Applied Neurobiology 8, 351–36 IDPN neuropathy in the cat: coexistence of proximal and distal axonal swellings Administration of β, β'‐iminodipropionitrile (IDPN) to rodents has previously been shown to produce neurofilament‐filled axonal swellings in the proximal regions of motor and sensory nerve fibers. Because of the distinctive distribution of these swellings, IDPN has been classed as a proximal axonopathy and thereby distinguished from other disorders in which similar axonal swellings occur in the distal parts of the axon (distal axonopathies). This report describes the pathology in the peripheral nerves of cats which received intermittent injections of IDPN and calls attention to two previously undescribed pathological changes. First, in addition to the typical proximal swellings associated with IDPN, these animals developed numerous axonal swellings within the distal branches of the sciatic nerve. Distal swellings were present as early as 23 days after initiation of intoxication, indicating that they formed locally (rather than developing in the proximal axon and undergoing transport into the distal regions). The second finding was Wallerian‐like degeneration within the affected nerve branches. These changes in the distal sciatic nerve and its branches closely resembled the pathology of the distal axonopathies produced by agents such as the neurotoxic hexacarbons and carbon disulfide. The pathological similarities suggest that IDPN may share with these agents pathogenetic mechanisms to an extent not previously suspected.