The diabetic neuropathies.
BACKGROUND
Diabetes remains the most common cause of neuropathy in the United States and is a significant source of morbidity and mortality, accounting for substantial suffering and billions of dollars in health care expenditures each year.


RESULTS
Our insight into the pathophysiology of the diabetic neuropathies has increased considerably over the last decade. aided by advances in the basic science of diabetes itself. A wide variety of potential mechanisms for nerve injury in diabetes has been identified, including the polyol pathway of glucose metabolism, oxidative nerve injury, the deposition of advanced glycosylation end products within the nerve and the effects of vascular insufficiency, among others. Diabetic neuropathy may take a variety of clinical forms beyond the well-known distal symmetric neuropathy, many of which are often misdiagnosed or overlooked entirely, sometimes with serious consequences for the patient. Proper therapy after diagnosis is also critical and may include not only primary management, but also treatment of painful diabetic neuropathy through an expanding repertoire of increasingly effective pharmacologic agents. Though primary treatment trials have not yet provided effective therapies, ongoing and future trials offer continuing promise.


CONCLUSIONS
The diabetic neuropathies are exceedingly common, but often improperly diagnosed and incompletely treated. A proper understanding of the mechanisms underlying these diseases and the clinical recognition of their various forms is highly important as appropriate primary and symptomatic management can substantially reduce the morbidity and mortality associated with these disorders.
Gooch
Clifton
C
Electromyography Laboratory, Columbia University College of Physicians and Surgeons, Columbia Presbyterian Medical Center, 710 West 168th Street, 13th Floor, New York, NY 10032, USA. clg33@columbia.edu
Podwall
David
D
D000449:Aldehyde Reductase / Q000037:antagonists & inhibitors; D000700:Analgesics / Q000627:therapeutic use; D000928:Antidepressive Agents / Q000627:therapeutic use; D001786:Blood Glucose / Q000378:metabolism; D003929:Diabetic Neuropathies / Q000175:diagnosis / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D020932:Nerve Growth Factor / Q000378:metabolism; D011108:Polymers / Q000378:metabolism; D014652:Vascular Diseases / Q000378:metabolism / Q000473:pathology
D000700:Analgesics; D000928:Antidepressive Agents; D001786:Blood Glucose; D017127:Glycation End Products, Advanced; D007328:Insulin; D007473:Ion Channels; D011108:Polymers; C024617:polyol; D020932:Nerve Growth Factor; D000449:Aldehyde Reductase