OBJECTIVES: To assess the cognitive impairment in patients with type 2 diabetes mellitus (T2DM) using mismatch negativity (MMN) and to explore the relationship between cognitive impairment and diabetic peripheral neuropathy (DPN). METHODS: Sixty-six T2DM patients and 40 healthy controls were included. For each participant, mini-mental state examination (MMSE) was applied to assess the general cognitive function and MMN was elicited. T2DM patients were divided into two subgroups: subgroup DPN-, patients without DPN; subgroup DPN+, patients with DPN. The MMSE scores, MMN amplitudes and latencies were compared between the T2DM group and the control group using univariate analysis of variance procedures, and also among the controls, subgroup DPN- and subgroup DPN+. Pearson's correlation coefficients (r) were used to analyze potential confounding clinical factors associated with MMN. RESULTS: T2DM patients had significantly lower MMSE scores compared with controls (23.25 ± 2.86 vs. 27.15 ± 1.83; P < 0.01), whereas those of the two subgroups were not significantly different. Both subgroup DPN+ and DPN- had longer latencies and lower amplitudes of MMN than the controls. The latencies of MMN were significantly longer in subgroup DPN+ compared with subgroup DPN-. The latency of MMN was positively correlated with the duration of the disease. CONCLUSION: Cognitive decline exists in patients with T2DM irrespective of the presence of DPN. Patients with DPN may have more severe cognitive dysfunction than those without DPN. MMN may be a promising tool for evaluating cognitive function.
OBJECTIVES: To assess the cognitive impairment in patients with type 2 diabetes mellitus (T2DM) using mismatch negativity (MMN) and to explore the relationship between cognitive impairment and diabetic peripheral neuropathy (DPN). METHODS: Sixty-six T2DM patients and 40 healthy controls were included. For each participant, mini-mental state examination (MMSE) was applied to assess the general cognitive function and MMN was elicited. T2DM patients were divided into two subgroups: subgroup DPN-, patients without DPN; subgroup DPN+, patients with DPN. The MMSE scores, MMN amplitudes and latencies were compared between the T2DM group and the control group using univariate analysis of variance procedures, and also among the controls, subgroup DPN- and subgroup DPN+. Pearson's correlation coefficients (r) were used to analyze potential confounding clinical factors associated with MMN. RESULTS: T2DM patients had significantly lower MMSE scores compared with controls (23.25 ± 2.86 vs. 27.15 ± 1.83; P < 0.01), whereas those of the two subgroups were not significantly different. Both subgroup DPN+ and DPN- had longer latencies and lower amplitudes of MMN than the controls. The latencies of MMN were significantly longer in subgroup DPN+ compared with subgroup DPN-. The latency of MMN was positively correlated with the duration of the disease. CONCLUSION: Cognitive decline exists in patients with T2DM irrespective of the presence of DPN. Patients with DPN may have more severe cognitive dysfunction than those without DPN. MMN may be a promising tool for evaluating cognitive function.