--there's never been conclusive proof that Guillain Barre or its variants are directly transmissable through a family; as acute neuropathies, they do seem to require some sort of trigger combined with a tendency towards autoimmune disorder.

It's that last part that's tricky, as there is some evidence that certain genetic subtypes are more susceptible to autoimmunity phenomena. Some of these are farily well known, such as the human leukocyte antigen (HLA) DQ2/DQ8 associations with celiac, and the HLA_B27 associations with ankylosing spondylitis. I suspect this may have to do with certain chemical structuirng of the body that is set by genetic background--if one has bodily tissues that are structurally more similar to certain types of pathogens, the possibility of an autoimmunity set off by an entry of these pathogens increases. (Many who have gotten Guillain Barre report a prodrome of some sort of viral or bacterial bout, often with an initial Epsten-Barr Virus infection, or a bout of cytomegalovirus, or campylobacter jejuni, a gastric infection. There have also been post-inoculation reports--probably the reason so many of us debate getting flu shots each year.)

I also take it that Alan's condition was not an acute onset, but a more gradual, chronic thing.

So, what I'm saying, I suppose, is that this is probably not directly related to his mom having had Guillain Barre--but the tendency to autoimmune disorder which may have manifested that way in her may be manifesting in Alan as a chronic autoimmune neuropathy. I know Dr. Latov and his colleagues think that many, maybe most, of the "idiopathic" chronic sensory neuropathies out there that are not caused by nutrient deficiency or impaired glucose tolerance have underlying immune mechanisms, and we just haven't found the specific antibodies and/or target antigens on nerve as of yet.