Abstract
Purpose
Vestibular system is critical for maintaining balance. This study aimed to determine the function of the saccule of the otolith organ in adults with type 1 diabetes (T1D) using cervical vestibular evoked myogenic potential (cVEMP) and its independently associated demographic, clinical and laboratory variables.
Method
This case-control cross-sectional study included 60 patients (male = 15; female = 45) and 30 healthy adults. They underwent cVEMP.
Results
Patients had mean age of 30.63 ± 4.20 years and duration of illness of 14.68 ± 3.65 years. More than 50% had frequent diabetic ketoacidosis (DKA), 30% had frequent hypoglycaemic attack, 35% had comorbid hyperlipidaemia, and 40% had peripheral neuropathy. Dizziness was reported in 30%. Compared to controls, 40% of patients had significantly delayed absolute latencies of P1 and N1 (p = 0.01) either unilateral or bilateral and 80% had reduced P1-N1 amplitudes (p = 0.001). Higher frequencies of abnormalities were present bilaterally. Asymmetry ratio (AR) was reported in 25%. Patients with longer duration of diabetes (>5 year), dizziness, HbA1c (>7%), frequent DKA or hypoglycaemic attacks and peripheral neuropathy had significantly prolonged P1 and N1 latencies and reduced P1-N1 amplitudes compared to those with shorter duration of diabetes, without dizziness, with HbA1c% ≤7%, low frequency of DKA hypoglycaemic attacks and those without peripheral neuropathy. Multiple regression analysis showed that presence of delayed P1 latencies and reduced P1-N1 amplitudes were significantly correlated with duration of diabetes > 5 years [OR = 3.60 (95%CI = 1.80–6.44), p = 0.01; OR = 4.56 (95%CI = 2.80–7.80), p = 0.01] and HbA1c levels >7% [OR = 5.26(95%CI = 3.83–8.05), p = 0.001; OR = 4.55(95%CI = 2.45–8.55), p = 0.001].
Conclusion
The dysfunctions of the saccule of otolith organ and/or its pathway are prevalent in adults with T1D and correlated with duration and severity of diabetes. Therefore, optimal control of glycemic control is essential.
Keywords:
Disclosure statement
No potential conflict of interest was reported by the author(s).
Figure 3. Representative cVEMP waveforms: (A) A patient with normal P1 (RT = 15.33 ms; LT = 15.08 ms) and N1 (RT = 21.75; ms; LT = 21.76 ms) latencies, reduced amplitude on the RT side (43.82 µV) and normal on the LT (92.51 µV). AR is 35.71%. (B) A patient with normal P1 (RT = 15.25 ms; LT = 14.67 ms) and N1 (RT = 20.67; ms; LT = 22.67 ms) latencies, reduced amplitude on the LT side (20.39 µV) and normal on the RT (90.73 µV). AR is 63.30%. (C) A patient with longer RT P1 (RT = 18.08 ms; LT = 13.00 ms) and RT N1 (RT = 24.25; ms; LT = 22.75 ms) latencies and normal amplitudes (RT: = 71.17 µV; LT = 69.95 µV). AR is 0.86%. (D) A healthy subject with normal P1 (RT = 14.00 ms; LT = 14.60 ms) and N1 (RT = 20.03 ms; LT = 22.33 ms) latencies and amplitudes (RT = 102.18 µV; LT = 84.11 µV). AR is 9.70%.
![Figure 3. Representative cVEMP waveforms: (A) A patient with normal P1 (RT = 15.33 ms; LT = 15.08 ms) and N1 (RT = 21.75; ms; LT = 21.76 ms) latencies, reduced amplitude on the RT side (43.82 µV) and normal on the LT (92.51 µV). AR is 35.71%. (B) A patient with normal P1 (RT = 15.25 ms; LT = 14.67 ms) and N1 (RT = 20.67; ms; LT = 22.67 ms) latencies, reduced amplitude on the LT side (20.39 µV) and normal on the RT (90.73 µV). AR is 63.30%. (C) A patient with longer RT P1 (RT = 18.08 ms; LT = 13.00 ms) and RT N1 (RT = 24.25; ms; LT = 22.75 ms) latencies and normal amplitudes (RT: = 71.17 µV; LT = 69.95 µV). AR is 0.86%. (D) A healthy subject with normal P1 (RT = 14.00 ms; LT = 14.60 ms) and N1 (RT = 20.03 ms; LT = 22.33 ms) latencies and amplitudes (RT = 102.18 µV; LT = 84.11 µV). AR is 9.70%.](/cms/asset/2ccba225-280b-45b2-9887-bf0e75f936b6/ihbc_a_2142380_f0003_b.jpg)