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Handb Clin Neurol. 2014;126:109-22. doi: 10.1016/B978-0-444-53480-4.00009-6.

Glucose intolerance, metabolic syndrome, and neuropathy.

Author information

1
Imaging and Neurosciences Center, University of Utah, Salt Lake City, UT, USA.
2
Department of Neurology, University of Utah, Salt Lake City, UT, USA.
3
Department of Neurology, University of Utah, Salt Lake City, UT, USA; Department of Anesthesiology, University of Utah, Salt Lake City, UT, USA. Electronic address: gordon.smith@hsc.utah.edu.

Abstract

There is increasing evidence that impaired glucose tolerance (IGT) or metabolic syndrome may result in peripheral nerve injury, although the exact relationship between the conditions is still being characterized. There is animal model, epidemiologic, and clinical evidence to suggest a pathophysiologic relationship between neuropathy and metabolic syndrome, along with its components including obesity, dyslipidemia, and insulin resistance. IGT and metabolic syndrome are associated with subclinical nerve damage or are typically painful and sensory predominant, although autonomic involvement may also occur. Because there is often preferential small fiber injury and nerve conduction studies may be relatively insensitive, skin biopsy with assessment of intraepidermal nerve fiber density is often used to confirm the diagnosis. Treatment of metabolic syndrome and IGT-associated neuropathies should include diet and exercise counseling, maintenance of normoglycemia, and targeted pharmacologic therapy for modifiable risk factors. Further research is required to fully elucidate the complex pathophysiology, as well as identify optimal diagnostic and treatment approaches.

KEYWORDS:

Impaired glucose tolerance; exercise; metabolic syndrome; nerve injury; obesity; peripheral neuropathy; pre-diabetes

[Indexed for MEDLINE]

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