This Article  • Full text  • PDF  • CME Course for This Article  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (8)  • Contact me when this article is cited  Related Content  • Related article  • Similar articles in this journal  Topic Collections  • Neurology, Other  • Alert me on articles by topic

Charlene Hoffman-Snyder, MSN, NP-BC; Benn E. Smith, MD; Mark A. Ross, MD; Jose Hernandez, BA; E. Peter Bosch, MD

Arch Neurol. 2006;63:1075-1079. Published online June 12, 2006 (doi: 10.1001/archneur.63.8.noc50336).

Background  An underlying cause is found in only 7% to 30% of patients with chronic idiopathic axonal polyneuropathy (CIAP). Diabetes mellitus, inherited disorders, toxin exposure, and primary amyloidosis are the most common identified causes of sensory neuropathies affecting both large and small myelinated fibers. Undiagnosed impaired fasting glucose metabolism has been associated with CIAP at a higher frequency rate than in the general population. This increased prevalence rate was identified using the 2-hour oral glucose tolerance test (2h-OGTT) and a previous version of the American Diabetes Association (ADA) guidelines.

Objectives  To determine the prevalence of abnormal fasting glucose metabolism in patients with CIAP and to compare the value of determining fasting plasma glucose levels using revised (2003) ADA criteria with the 2h-OGTT for predicting abnormal fasting glucose metabolism.

Patients  In this 24-month retrospective study, 100 consecutive patients were identified with no known cause for CIAP, including diabetes mellitus, between January 2003 and January 2005. All had both a fasting plasma glucose test and a 2h-OGTT in addition to a complete neurological examination. Neurophysiological studies, computer-assisted sensory examination, and quantitative sudomotor axonal reflex testing were used to classify CIAP into subtypes according to nerve fiber involvement.

Results  The prevalence of undiagnosed abnormal fasting glucose metabolism was found to be nearly 2-fold higher (62%) in patients with CIAP than in similar age-matched general population groups (33%). Using the 2003 revised ADA criteria, 39 patients (39%) had abnormal fasting plasma glucose metabolism (36 with impaired fasting glucose, 3 with diabetes mellitus), while the 2h-OGTT provided an even higher diagnostic rate of 62% (62 patients; P<.001) of impaired fasting glucose metabolism (38 with impaired glucose tolerance, 24 with diabetes mellitus). The abnormal glucose metabolism rates were found to be similar across the 3 subtypes (sensorimotor, pure sensory, and small-fiber neuropathy) of CIAP (P = .60, .72, and .61).

Conclusions  This study adds to emerging evidence that abnormal glucose metabolism may be a risk factor for CIAP. Even with revised (2003) ADA criteria, the 2h-OGTT provides additional diagnostic information to the health care professional in the evaluation of CIAP. Subtypes of CIAP are equally likely to have abnormal glucose metabolism.

Author Affiliations: Departments of Neurology (Ms Hoffman-Snyder and Drs Smith, Ross, and Bosch) and Biostatistics (Mr Hernandez), Mayo Clinic Scottsdale, Scottsdale, Ariz.

RELATED ARTICLE

Peripheral Neuropathy With Impaired Glucose Tolerance: A Sweet Smell of Success?
John T. Kissel
Arch Neurol. 2006;63(8):1055-1056.
EXTRACT | FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Late-onset hereditary axonal neuropathies
Bennett et al.
Neurology 2008;71:14-20.
ABSTRACT | FULL TEXT  

Prevalence of Polyneuropathy in Pre-Diabetes and Diabetes Is Associated With Abdominal Obesity and Macroangiopathy: The MONICA/KORA Augsburg Surveys S2 and S3
Ziegler et al.
Diabetes Care 2008;31:464-469.
ABSTRACT | FULL TEXT  

Peripheral Neuropathy With Impaired Glucose Tolerance: A Sweet Smell of Success?
Kissel
Arch Neurol 2006;63:1055-1056.
FULL TEXT