Author(s): G. Rekha1, G. S. Prema2, O. Padmini3

Diabetes mellitus is the most common metabolic disorder affecting majority of population. It is estimated that over 400 million people throughout the world have diabetes. It has progressed to be a pandemic from an epidemic causing morbidity and mortality in the population. Among the many complications of diabetes, diabetic neuropathies contribute majorly to the morbidity associated with the disease. Axonal conduction is affected by elevated levels of protein kinase c causing neuronal ischemia; decreased cellular myoinositol affecting sodium potassium ATPase pump leads to decreased nerve conduction; Somatosensory Evoked Potentials (SSEPs) reflect the activity of somatosensory pathways mediated through the dorsal columns of the spinal cord and the specific somatosensory cortex. Recording of Somatosensory Evoked Potentials in diabetics is done to assess the sensory involvement of spinal cord. Presence of SEPs provides clear evidence for axonal continuity and by using different stimulation sites, the rate of regeneration can be determined. Both onset and peak latencies of all SEP components are prolonged in patients with diabetes. Present study is done to compare somatosensory evoked potentials in diabetics and normal subjects. MATERIALS AND METHODS: The present study was undertaken at the Upgraded Department of Physiology, Osmania Medical College, Koti, Hyderabad. The study was conducted on subjects, both male and female in the age group of 45 to 55 years, suffering from type II diabetes excluding other neurological disorders. Non-invasive method of estimation of nerve conduction studies using SFEMG/EP— Electromyography or evoked potential system (Nicolet systems—USA) using surface electrodes with automated computerized monitor attached with printer is used. RESULTS: ANOVA showed statistically significant N9 latency (right & left sides). Latencies of all the components of SSEPs were more significant than amplitudes in Diabetic patients multiple linear regression analysis showed statistically significant values for N9 latency, N13 latency, P25 latency, N20 amplitude and P25 amplitude. DISCUSSION: Conductive function in the central as well as peripheral somatosensory pathways is affected earlier in diabetes. Increased oxidative stress and mitochondrial dysfunction in diabetic neurons cause nerve dysfunction and decreased neuronal regenerative capacity in sensory, motor and autonomic neurons. In our study significant prolongation of latencies was observed in sensory nerves in diabetic individuals when compared to normals. Multiple regression analysis of N9, N13 & P25 latencies showed significant ‘F’ values (F value>l). Similar attempts can aid future studies to predict the risk before the onset of diabetic neuropathy.

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