GBS vs. Acute Transverse Myelitis diagnosis

  On 3/25/98 I posted a question asking about clinical signs/tests which neurologists use to distinguish between GBS and acute transverse myelitis (mylopathy).  I did receive a clear response from one of the doctors, but he was apparently interrupted and never got to the EMG results part. My Babinski signs were positive (I had upturned toes), had a high cell count as well as high protein count in my spinal tap, had rapid onset of weakness followed within days by total leg paralysis and loss of urinary/bowel functions, and preceeded by three months of lower back parasthesias.  I also had preserved reflexes.
  The preserved reflexes and upturned toes indicate acute transverse myelitis ( I did have spinal cord, nerve roots AND peripheral nerve involvement/demylination). My neurologist says its NOT GBS because of the three months of preceeeding parasthesias, but also NOT acute transverse myelitis because of the involvement of the peripheral nerves.  I now can walk fairly well using a single tip cane, have residual "tightness" in leg muscles, "hot feet" (no pain), and am scheduled for another EMG in three weeks.  What does the above sound like?  What should the EMG show if I have GBS vs. acute transverse myelitis.  My neurologist had diagnosed me as "myleopathy" and "polyradiculoneuropathy" which are really descriptive terms.  He also says I may have CIDP or MS, although this was a one-time occurrance.  I also was found to have pernicious anemia and a B12 deficiency (of less than one year) due to gastroplasty in 1996. I seem to have a little of everything, central, root and peripheral nerve involvement. ???  Your help gratefully appreciated!  Hope this time whoever answers gets to finish! ;-)
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Apologies for the previous response which did not upload completely,
The presence of a Babinski response and preserved reflexes makes this
more likely to be a spinal cord disease than a peripheral nerve disease,
reflexes are absent in GBS.
The descriptive terms you mention may be the only labels possible since
an inflammatory process does not always respect neat anatomoical boundaries.
The clinical picture suggests to me that this is a predominantly spinal cord process.
I am unclear as to how to express the EMG  results other than to say that
are there clear cut and classical findings on EMG in GBS, evidence of demyelination,
conduction block, absent F responses, the EMG findings in tramsverse
myelitis are less classical but the disorders should be easy to differentiate.