Type-2 diabetes mellitus and auditory brainstem response

Objective: Diabetes mellitus (DM) causes pathophysiological changes at multiple organ system. With evoked potential techniques, the brain stem auditory response represents a simple procedure to detect both acoustic nerve and central nervous system pathway damage. The objective was to find the evidence of central neuropathy in diabetes patients by analyzing brainstem audiometry electric response obtained by auditory evoked potentials, quantify the characteristic of auditory brain response in long standing diabetes and to study the utility of auditory evoked potential in detecting the type, site, and nature of lesions. Design: A total of 25 Type-2 DM [13 (52%) males and 12 (48%) females] with duration of diabetes over 5 years and aged over 30 years. The brainstem evoked response audiometry (BERA) was performed by universal smart box manual version 2.0 at 70, 80, and 90 dB. The wave latency pattern and interpeak latencies were estimated. This was compared with 25 healthy controls (17 [68%] males and 8 [32%] females). Result: In Type-2 DM, BERA study revealed that wave-III representing superior olivary complex at 80 dB had wave latency of (3.99 ± 0.24) ms P < 0.001, at 90 dB (3.92 ± 0.28) ms P < 0.001 compared with control. The latency of wave III was delayed by 0.39, 0.42, and 0.42 ms at 70, 80, and 90 dB, respectively. The absolute latency of wave V representing inferior colliculus at 70 dB (6.05 ± 0.27) ms P < 0.001, at 80 dB (5.98 ± 0.27) P < 0.001, and at 90 dB (6.02 ± 0.30) ms P < 0.002 compared with control. The latency of wave-V was delayed by 0.48, 0.47, and 0.50 ms at 70, 80, and 90 dB, respectively. Interlatencies I-III at 70 dB (2.33 ± 0.22) ms P < 0.001, at 80 dB (2.39 ± 0.26) ms P < 0.001, while at 90 dB (2.47 ± 0.25) ms P < 0.001 when compared with control. Interlatencies I-V at 70 dB (4.45 ± 0.29) ms P < 0.001 at 80 dB (4.39 ± 0.34) ms P < 0.001, and at 90 dB (4.57 ± 0.31) ms P < 0.001 compared with control. Out of 25 Type-2 DM, 13 (52%) had diabetic neuropathy, of which 12 (92%) showed abnormal BERA. In nonneuropathic [12 (48%)] only 6 (50%) showed abnormal BERA. Conclusion: Delay in absolute latencies and interpeak latencies by BERA demonstrates defect at level of brainstem and midbrain in long standing Type-2 diabetes subjects, which is more pronounced in those with neuropathy