THE NEUROTOXIC effect of isoniazid (isonicotinic acid hydrazide, INH) has been studied experimentally for the first time by Zbinden and Studer.1 Rats proved to be very sensitive to this drug and regularly developed degeneration of peripheral nerves. Electron microscopic observations of Schlaepfer and Hager2 showed that the early stages of nerve degeneration were similar to those observed in early wallerian degeneration.
In previous investigations of human neuropathies, it was recognized that changes in motor end-plates and intramuscular nerve fibers suggesting axonal damage, together with a reactive collateral sprouting of subterminal axons, could occur in the absence of clinical signs of motor involvement and even without volumetric changes of the neurogenic type in the muscle fibers. These observations enabled us to establish the concept of latent or subclinical neuropathy on morphological ground.3,4
We found it interesting to study the isoniazide neuropathy in its early stages in an
Hildebrand J, Joffroy A, Coërs C. Myoneural Changes in Experimental Isoniazid Neuropathy: Electrophysiological and Histological Study. Arch Neurol. 1968;19(1):60–70. doi:10.1001/archneur.1968.00480010078006
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