The purpose of this study was to investigate the effects of aldose reductase inhibitor (ARI) on metabolic derangement and prostaglandin I2 analogue (PGI₂) on vascular lesions in diabetic neuropathy by using magnetic resonance imaging (MRI)(SIGNA 1.5-Tesla). Spin-lattice relaxa tion time (Ti value) and coefficients of variation of signal intensities of nerve (CV value), as respective indices of nerve edema and structural change in the sural nerve, were calculated in normal subjects (n=19) and patients with non-insulin-dependent diabetes mellitus (DM group)(n=92). The T₁ value of the sural nerve was significantly prolonged in the DM group indicating the presence of nerve edema under hyperglycemic conditions. Administration of ARI (Epalrestat 150mg/day, n=12) improved the nerve edema as well as motor nerve conduction velocity (MNCV). There was no difference in Ti values before and after PGI₂ treatment (Beraprost sodium 120μg/day, n=12), but MNCV significantly improved. In patients with longer T₁ values, PGI₂ normalized them. These results suggest that both metabolic and vascular factors participate in the pathogenesis of nerve edema. The CV value was significantly increased in the DM group. The CV value also increased in proportion to the progression of diabetic retinopathy and nephropathy, suggesting that increased CV values may reflect changes in endoneurial structure caused by microangiopathy. These results indicated that ARI and PGI2 can ameliorate diabetic neuropathy by improving metabolic and vascular abnormalities, and that T₁ and CV values plus MRI are useful indicators for evaluation of structural changes in diabetic neuropathy and the efficacy of treatment.