Abstract
WHEN THE continuity of a peripheral nerve fiber is interrupted by crush or section the terminal parts of the axons immediately above and below the site of injury rapidly undergo a variety of structural and biochemical changes. These changes, which develop during the first 24 hours after injury, are characterized by swelling and distortion of the axonal stumps 1 and by the accumulation of certain enzymes, 2-11 mitochondria, and other electron dense profiles. 12-14 The mechanism responsible for these changes remains largely unexplained although many ideas have been proposed. Some authors have suggested that the accumulation of enzymes and ultrastructural particles on the proximal side of the lesion is the direct result of a damming up of axoplasmic flow due to interruption of the axonal pathway. Such a mechanism does not, however, explain the essentially similar findings on the distal side of the lesion, nor does a flow rate
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