THE occurrence of widespread epidemics of paralysis caused by adulteration of food with triorthocresyl phosphate (TOCP) has encouraged numerous reports of the clinical effects and histological changes induced in the peripheral and central nervous system (CNS) in man by this chemical. Cavanagh and his associates1-3 have shown in experimental animals that the distal parts of the longest nerve fibers in the spinal cord and in the peripheral nerves show the earliest and most extensive degenerative changes. The manner in which TOCP exerts its neurotoxic effect is not known. Although initially regarded as a specific myelin poison, it is now believed that TOCP acts primarily on the neuron and that myelin disintegration is secondary to axonal destruction.3-6 It has also been shown that TOCP inhibits pseudocholinesterase activity and other esterases. What role, if any, this plays in the development of the neuropathy is not understood.7
The following report
Prineas J. Triorthocresyl Phosphate Myopathy. Arch Neurol. 1969;21(2):150–156. doi:10.1001/archneur.1969.00480140050005
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