Certain clinical implications arise from these histological studies. Firstly, a neuroma cannot be expected to degenerate in the life span of the patient and is therefore a persistent problem. Because the capacity for axon sprouting is retained indefinitely, resection of neuroma is followed by a wave of regeneration which forms another neuroma. Finally, in order to prevent the formation of a neuroma, it is necessary to inhibit regeneration of the injured nerve fibers. Attempts to poison the regenerating fibers locally have been unsuccessful. Attention should now be directed toward supressing the neuron cell body which initiates and supports the regeneration process. For example, it may be feasible selectively to restrict the growth of regenerating neurons. This approach might involve immunization with a nerve growth factor antiserum or perhaps an antineuronal serum. Alternatively one could produce an antiserum to a structural component integral for axon growth such as a fibrous protein. Another possibility would be to switch off the neuron's regeneration program by introducing a repressor into the system. Such a substance would have to be picked up by the regenerating axons, transported to the neuron and there interrupt protein synthesis necessary to maintain regeneration. While these alternatives are speculative, if neuroma formation is to be prevented, it is clear that novel experimental approaches must be explored.
|Original language||English (US)|
|Number of pages||18|
|Journal||Bulletin of the NYU Hospital for Joint Diseases|
|Publication status||Published - 1974|
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