The pathogenic basis and treatment of diabetic
polyradiculoneuropathy is a source of recent controversy as there may be two or more distinct forms of diabetic polyradiculoplexopathy. We believe that the following two categories of diabetic
polyradiculoneuropathy can be made on the basis of clinically differences: 1) the more common asymmetric, painful
polyradiculoneuropathy; and 2) the rare symmetric, painless,
polyradiculoneuropathy. The asymmetric, painful form (also known as
diabetic amyotrophy) may have an autoimmune basis, but the etiology is not clear. The natural history for
diabetic amyotrophy is spontaneous improvement. Nevertheless, various
immunotherapies (eg,
corticosteroids and
intravenous immunoglobulin (
IVIg) have been tried with subsequent improvement in symptoms. Treatment is reserved only for patients with severe ongoing
pain, given the significant side effects of these medications in those patients with diabetes.
Prednisone and
IVIg may help alleviate the
pain associated with
diabetic amyotrophy. Relief of
pain can help patients begin
physical therapy earlier, however, there are no prospective, blinded, controlled studies that demonstrate that these treatments lead to an earlier and better recovery of muscle strength compared with the natural history of the disorder. The symmetric, painless form of diabetic
polyradiculoneuropathy may in fact represent chronic inflammatory demyelinating
polyneuropathy (
CIDP) occurring in a patient with
diabetes mellitus (DM). Patients with idiopathic
CIDP may improve various immunomodulating
therapies, including
corticosteroid treatment,
plasma exchange (PE), and
IVIg. In this regard, patients with the symmetric, painless, proximal diabetic
polyradiculoneuropathy may also respond to
corticosteroids,
plasma exchange,
IVIg,
azathioprine, or
cyclophosphamide. However, as with
diabetic amyotrophy, some patients improve spontaneously without treatment. In still other patients, the neuropathy appears unresponsive to
immunotherapy. In such patients, this
polyradiculoneuropathy might be caused by metabolic dysfunction associated with DM. Unfortunately, from a clinical, laboratory, and electrophysiologic standpoint, it is impossible to distinguish the patients with a symmetric, painless diabetic
polyradiculoneuropathy who might respond to
therapy. A trial of PE can be useful in identifying patients who might have a polyradiculoplexopathy that is responsive to
immunotherapy. If patients respond to PE, they may continue to receive intermittent exchanges or be switched over to
prednisone or
IVIg.