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A few studies have reported a variety of nonspecific histological lesions in patients with IgA monoclonal gammopathies and polyneuropathy. In our case, using electron microscopy, we observed widenings of the myelin lamellae identical to those commonly described in IgM neuropathies with anti-myelin-associated glycoprotein activity. Using immunoelectron microscopy, we demonstrated a direct involvement of IgA in myelin lesions. The search for a direct link between monoclonal dysglobulinemia, regardless of type, and polyneuropathy is important and may influence treatment.

There is a lack of agreement regarding the potential for peripheral nerve cells with short axons to regenerate and innervate the terminal end organs of nerve cells with long axons. We designed a study to evaluate experimentally the possibility of neurons to reconstitute much longer axonal segments. Twenty Wistar rats were used. The brachial plexus was isolated and the radial nerve transected immediately after its origin. The proximal end of the axillary nerve (previously cut) then was coapted tot he distal stump of the radial nerve. In 10 other rats, the cut radial nerve was simply recoapted to itself without involvement of the axillary nerve; these animals served as controls. Finally, in 10 rats, nerves were cut without repair to evaluate the degenerative changes. After 90 days, the distal part of the radial nerve was examined by light microscopy, calculating the number and area of regenerated axons. We also checked the motor end-plates of reinnervated muscles. In the nerve-transferred group, good axonal regeneration with good reinnervation of the muscles was seen. In this way, we have experimentally demonstrated a plasticity of regeneration in peripheral nerves. This suggests that the surgeon may use nerves connected to proximal muscles to neurotize avulsed nerves of distal muscles.