What is the key mechanism of healing in neurapraxia?

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In neurapraxia, recovery hinges on remyelination by Schwann cells, which restore the insulating myelin sheath around the preserved axon. Because the axon itself remains intact, the primary issue is impaired conduction due to demyelination, not axonal loss. Schwann cells proliferate and synthesize new myelin, re-establishing proper saltatory conduction and allowing normal nerve signals to resume as the myelin sheath is restored. This is why remyelination is the key healing mechanism here.

Others would require the axon to be damaged or severed. Axonal sprouting from the cell body happens when the axon is disrupted, leading to axonal regeneration along the path of injury. Wallerian degeneration of the distal segment occurs after axonal damage with loss of the distal axon distal to the injury. Regeneration of the entire nerve across the lesion implies a complete axonal disruption, which is not the situation in neurapraxia.