International Neuropsychiatric Disease Journal

Abstract

Background: Individuals with elevated glycosylated hemoglobin (HbA1c) have a higher rate of microvascular complications, especially peripheral neuropathy.

Objective: To  find the relation  between  elevated   (HbA1c) and the  occurrence of  peripheral  nerve dysfunction in prediabetic individuals and to find  the role of the  inflammatory marker as,  C-Reactive  Protein (CRP),  in  the  development  of  Diabetic Peripheral Neuropathy (DPN).

Methods: Screening was done for 80 pre-diabetic individuals and 40 control subjects presenting to the internal medicine clinics,  Mansoura University Hospital; Egypt, from August 2014 to July 2015. The pre-diabetic individuals (HBA1c: 6.0-6.5%)   and a control group of 40 subjects with HbA1c < 6%. All subjects underwent neurological examination, nerve conduction study of both peroneal and sural nerves, and measurement of HbA1c and CRP.

Results: The sural nerve Sensory Nerve Action Potential (SNAP) amplitude was significantly lower in pre-diabetics than in control group. Compound Muscle Action Potential (CMAP) of the peroneal nerve was lower significantly in pre-diabetics with subclinical neuropathy in comparison to controls. The peroneal and sural nerve amplitudes were significantly correlated to CRP, but not to HbA1c.

Conclusion: Axonal subclinical neuropathy occurs significantly more in pre-diabetics than in normal (control) individuals. The CRP is significantly correlated with the presence of the axonal subclinical neuropathy which indicates an underlying inflammatory role.