Peripheral neuropathy is an important complication of diabetes mellitus. However, neuropathological changes in diabetic neuropathy with axonal degeneration or segmental demyelination are still unclear. By using a newly developing electrodiagnostic method of single fiber electromyography (SFEMG) with a computer-aided program, mean jitter value and muscle fiber density were measured in extensor digitorum communis (EDC) and anterior tibial (AT) muscles from 36 diabetic patients with neuropathy (group 1) and 12 patients without neuropathy (group Ⅱ) proved by nerve conduction study. The results showed an increased mean jitter value, fiber density and abnormal percentage both in EDC and AT muscles in group 1 and II diabetic patients comparing to the normal controls. These findings suggest an impaired or immatured neuromuscular junctions and an evidence of reinnervation through axonal sprouting in the diabetic patients either with or without nerve conduction abnormalities. In conclusion, the changes of axonal degeneration and reinnervation are the main pathophysiological mechanism of diabetic neuropathy, and the SFEMG is more sensitive than routine nerve conduction study in the diagnosis of diabetic neuropathy
Peripheral neuropathy is an important complication of diabetes mellitus. However, neuropathological changes in diabetic neuropathy with axonal degeneration or segmental demyelination are still unclear. By using a newly developing electrodiagnostic method of single fiber electromyography (SFEMG) with a computer-aided program, mean jitter value and muscle fiber density were measured in extensor digitorum communis (EDC) and anterior tibial (AT) muscles from 36 diabetic patients with neuropathy (group 1) and 12 patients without neuropathy (group Ⅱ) proved by nerve conduction study. The results showed an increased mean jitter value, fiber density and abnormal percentage both in EDC and AT muscles in group 1 and II diabetic patients comparing to the normal controls. These findings suggest an impaired or immatured neuromuscular junctions and an evidence of reinnervation through axonal sprouting in the diabetic patients either with or without nerve conduction abnormalities. In conclusion, the changes of axonal degeneration and reinnervation are the main pathophysiological mechanism of diabetic neuropathy, and the SFEMG is more sensitive than routine nerve conduction study in the diagnosis of diabetic neuropathy
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