The following chapter mainly considers trauma-related peripheral nerve lesions. It is of low importance in explaining nerve irritation or entrapment; as already mentioned, it should not influence the surgeon too much. However, we are quite frequently confronted with patient histories in which slightly damaging forces have influenced vulnerable nerve structures more as expected. We are consequently asked to find the origin and reason for this, in addition to offering explanations and a solution. The fact is that neurophysiology, which evaluates pathological nerve action velocity, needs a nerve damage as prerequisite. In Chaps.​ 5 and 6, we will go into detail and demonstrate how special kinds of slight focal nerve damage can still be related to far previously developed concepts mentioned below. Thus, the diagnostic procedure, which measures electric excitability and images the nerve pattern, has to refer to these potentially substantial nerve alterations.

In 1943, Seddon established the well-known concept of three nerve lesion degrees [1]:

Theoretically, neurapraxia offers excellent chances of regeneration; a relatively quick reformation of the myelin sheath can be expected within a few weeks following the relief from compression. In the case of axonotmesis, the regeneration will take much longer; this works via axonal regrowth into the periphery and depends on the level of lesion and sprouting distance, assuming that all damaging forces are removed. Neurotmesis, of course, remains without any chance of recovery.

In 1951, Sunderland distinguished five degrees of nerve lesion [2]: