Abstract
The peripheral nerve pathology is described in experimental fetal alcohol syndrome. The marked retraction and shrinkage of axons with vacuolar spaces in the periaxonal area are the striking features. The direct toxicity of ethanol or its metabolites on the nerve fibers is considered to be the cause for pathological changes. Additional biochemical factors, pyridoxal phosphate dependent enzyme-depletion in the genesis of nerve damage, is proposed.
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