| Abstract: | Current Neuroscience dogma holds that transections or ablations of a segment of peripheral nerves produce:(1) Immediate loss of axonal continuity, sensory signaling, and motor control;(2) Wallerian rapid(1-3 days) degeneration of severed distal axons, muscle atrophy, and poor behavioral recovery after many months(if ever, after ablations) by slowly-regenerating(1 mm/d), proximal-stump outgrowths that must specifically reinnervate denervated targets;(3) Poor acceptance of microsutured nerve allografts, even if tissue-matched and immune-suppressed. Repair of transections/ablations by neurorrhaphy and well-specified-sequences of PEG-fusion solutions(one containing polyethylene glycol, PEG) successfully address these problems. However, conundrums and confusions regarding unorthodox and dramatic results of PEG-fusion repair in animal model systems often lead to misunderstandings. For example,(1) Axonal continuity and signaling is re-established within minutes by non-specifically PEG-fusing(connecting) severed motor and sensory axons across each lesion site, but remarkable behavioral recovery to near-unoperated levels takes several weeks;(2) Many distal stumps of inappropriately-reconnected, PEG-fused axons do not ever(Wallerian) degenerate and continuously innervate muscle fibers that undergo much less atrophy than otherwise-denervated muscle fibers;(3) Host rats do not reject PEG-fused donor nerve allografts in a non-immuno-privileged environment with no tissue matching or immunosuppression;(4) PEG fuses apposed open axonal ends or seals each shut(thereby preventing PEG-fusion), depending on the experimental protocol;(5) PEG-fusion protocols produce similar results in animal model systems and early human case studies. Hence, iconoclastic PEG-fusion data appropriately understood might provoke a re-thinking of some Neuroscience dogma and a paradigm shift in clinical treatment of peripheral nerve injuries. |
