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ISSN: Print -2349-0977, Online - 2349-4387

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Year : 2018  |  Volume : 4  |  Issue : 4  |  Page : 217-220

Clinical significance of brainstem evoked response audiometry in patients with diabetes mellitus

Department of E.N.T, Safdarjung Hospital and Vardhman Mahavir Medical College, New Delhi, India

Date of Web Publication29-Oct-2018

Correspondence Address:
Shantanu Mandal
Safdarjung Hospital and Vardhman Mahavir Medical College, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/astrocyte.astrocyte_11_18

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Background: Brainstem evoked response audiotry (BERA) is an objective, noninvasive, electrodiagnostic test that not only evaluates the functional integrity of the subcortical auditory pathway but also provides topodiagnosis of hearing loss. Diabetes mellitus (DM) causes pathophysiological changes in multiple organ systems. The brainstem auditory response represents a simple procedure to detect both acoustic nerve and central nervous system pathway damage. The objective of this study 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. Aims and Objectives: To compare the auditory brainstem responses (ABRs) of diabetic patients to those of age and sex-matched controls with respect to absolute latencies of waves I, III, and V. Materials and Methods: This study included 30 diabetic patients who were symptomatic for more than 2 years and 30 age and sex-matched control participants. The waveforms in ABRs were recorded and analyzed in each diabetic patient and control participant. Results: The mean absolute latency of wave I was found to be significantly increased in both ears at 90, 70, and 50 dB in diabetic patients compared to the control group, whereas the mean absolute latencies of wave III was significantly increased at 50 dB in both ears and at 70 dB in the right ear. In diabetic patients, the mean absolute latencies of wave V were significantly increased compared to control participants at 90 dB in both ears and at 70 and 50 dB in the left ear.

Keywords: Brainstem evoked response audiometry, diabetes mellitus, neuropathy, sensorineural hearing loss

How to cite this article:
Gupta A, Mandal S. Clinical significance of brainstem evoked response audiometry in patients with diabetes mellitus. Astrocyte 2018;4:217-20

How to cite this URL:
Gupta A, Mandal S. Clinical significance of brainstem evoked response audiometry in patients with diabetes mellitus. Astrocyte [serial online] 2018 [cited 2019 Nov 19];4:217-20. Available from: http://www.astrocyte.in/text.asp?2018/4/4/217/244292

  Introduction Top

Diabetes mellitus (DM) is recognized as a group of heterogeneous disorders with common elements of hyperglycemia and glucose intolerance caused by insulin deficiency, impaired effectiveness of insulin action, or both.[1] India is currently the global den of diabetes with the number of diabetic people expected to reach 79.4 million by 2030.[2] The increased morbidity and mortality in diabetics is mainly caused by long-term micro and macrovascular complications affecting the eyes, kidneys, heart, and nerves.[3] There has been a persistent concern regarding hearing loss in diabetics as extensive evidence suggests that deafness might represent a complication of type 2 diabetes mellitus (T2DM).[4],[5] The typical hearing impairment described in diabetics is a bilateral sensorineural hearing loss occurring as a result of neuropathy.[6] Clinically overt neuropathy manifests only after many years of onset of diabetes, but it can be detected much earlier with the help of electrophysiological tests.[7] Brainstem evoked response audiometry (BERA) are recorded from the ear and vertex in response to brief auditory stimulation. They assess the conduction through the auditory pathway upto the midbrain. BERA comprises five or more waves occurring within 10 ms of the acoustic stimulus. The clinical utility of BERA has been established in the assessment of hearing in uncooperative patients, children, and patients with brainstem disorders.[8] The working hypothesis in most BERA studies assigned waves I, II, III, IV, and V to the segment of the auditory nerve closest to the cochlea, cochlear nucleus, superior olivary complex, lateral lemniscus, and inferior colliculus, respectively.[9] Many studies have evaluated the association of BERA abnormalities and T2DM, but with variable results.[10],[11] There is also a lack of adequate data on BERA changes in diabetics in India, mainly because very few studies have been reported. The present study was conducted to assess the BERA abnormalities in females with T2DM, and to study the correlation of the observed abnormalities with the duration of diabetes and fasting blood glucose levels.

In our study, BERA recordings were done on patients who had diabetes for different lengths of time to determine how much the disease had affected their auditory pathways as well as to evaluate the electrodiagnostic role of BERA in assessing diabetic neuropathy at different stages. The results were compared to those of nondiabetic control participants who had no hearing impairment.

  Materials and Methods Top

This study was conducted at a tertiary health care centre between 2013 and 2015. Two groups of participants were enrolled in the study. The first group included 30 diabetic patients who had biochemically proven diabetes mellitus for more than 2 years and ranged in age from 30 to 60 years. The second group included 30 normal healthy sex-matched nondiabetic control participants also aged between 30 and 60 years. Diabetic patients were selected from the Department of Medicine and the controls were selected randomly from the general population. Informed consent was obtained from all individual participants included in the study.

Patients with histories of ear discharge, previous exposure to noise, and hearing loss before being diagnosed with diabetes were excluded, along with patients who had acute complications from diabetes, such as ketoacidosis, nonketotic hyperosmolar coma, and hypoglycemia. Patients with histories of having taken drugs that are known to cause central neuropathy, such as reserpine, alpha methyldopa, phenytoin, and nitrofurantoin, and ototoxic drugs, such as gentamycin, streptomycin, kanamycin, amikacin, and quinine, were also excluded from the study.

All patients were tested for fasting blood sugar (FBS), postprandial blood sugar (PPBS), and HbA1C. The potential for brainstem evoked response was recorded in each diabetic patient and control participants, and the resulting absolute latencies of waves I, III, and V were measured and analyzed.

  Results Top

Sixty patients were enrolled in study, 30 each in the diabetic and nondiabetic group. Patients were divided in three age groups: 30–40 years, 41–50 years, and 51–60 years. Eight patients were in the age range of 30–40 years, 13 in 41–50 years, and 9 in 51–60 years age group, and similar distribution were noted in the control group. In the diabetic group, 19 were males and 11 were females. Similar gender distributions were noted in the nondiabetic group.

All the diabetics and their age-matched controls were subjected to BERA, and the mean absolute latency of wave I, III, and V at various dB levels were recorded and tabulated [Table 1].
Table 1: The Mean Value of Absolute Latencies in Both Ears in Diabetic and Normal Subjects

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Absolute latencies at 90 dB of waves I, III, and V where there was an increase in the absolute latencies in both ears at 90 dB in waves I, III, and V in diabetic patients compared to control participants. The absolute latencies of waves I and V were increased, which was significant (P < 0.05) [Figure 1].
Figure 1: Absolute Latencies at 90 dB of Both Ear in Diabetic and Non-Diabetic Group.

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Absolute latencies at 70 dB of waves I, III, and V where there was an increase in the absolute latencies at 70 dB in waves I, III, and V in diabetic patients compared to control participants. Increased latencies were found to be significant for wave I in both ears and for waves III and V for the right and left ear, respectively [Figure 2].
Figure 2: Absolute Latencies at 70 dB of Both Ear in Diabetic and Non-Diabetic Group.

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Absolute latencies at 50 dB of waves I, III, and V where there was an increase in the absolute latencies at 50 dB in waves I, III, and V in diabetic patients compared to control participants. The P values were less than 0.05 for waves I and III for the right ear and for waves I, III, and V for the left ear, all of which were significant [Figure 3].
Figure 3: Absolute Latencies at 50 dB of Both Ear in Diabetic and Non-Diabetic Group.

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  Discussion Top

Bilateral, symmetric, and progressive high-frequency sensorineural hearing loss with gradual onset is usually seen in patients who have DM and are experiencing hearing difficulties.[12] This is probably caused by cochlear, retrocochlear, or combined cochlear-retrocochlear involvement of the acoustic nerve. The pathogenesis of hearing in diabetes, which appears to be a multifactorial process, has not been fully clarified.

The recording of electrical potentials that occurs along the auditory pathways is an objective, reliable, and noninvasive method of detecting even the subclinical involvement of neural conduction, which appears at an early stage of the disease and tends to become worse over time.[13]

Donald et al.[13] were the first to use ABR to detect the latency delays through the auditory nerve in DM patients. Since the initial use of ABRs, delays in these waves in diabetic patients have been presented in various reports, and deviations in the latency values of all ABR components have been reported (Fedelle et al.,).[14] However, Khardori et al.,[15] Virtaniemi et al.,[16] and Donald et al.[13] found latency increases that were mainly in the late components of ABRs and proposed the term “central diabetic neuropathy.”

Durmus et al.[17] measured the delays in neural conduction along the auditory pathway in 43 diabetes patients. Their ABR recordings revealed that the absolute latencies of waves I, III, and V were significantly prolonged in the diabetes group compared to the control group (P < 0.05). Donald et al. also conducted BERA on 20 insulin-dependent diabetes patients and concluded that the latency of wave III was delayed by 0.30 ms (P < 0.05) on 70, 80, and 90 dB, and the latency of wave V by 0.45 ms (P < 0.001) on 70, 80, and 90 dB. The interpeak latency wave I–III was delayed by 0.24 ms (P < 0.01), and the interpeak latency wave I–V it was delayed by 0.35 ms (P < 0.05).[18]

In our study, the delay of the absolute latencies of waves I, III, and V in diabetic patients suggests the presence of central neuropathy both at the level of the cochlear nerve (wave I) and at the level of the auditory brainstem pathway (waves III and V). It seems clear from this study that DM causes abnormalities in the BERAs in a significant number of patients with diabetes. The delay in central neural transmission that was found in our results occurs along both the auditory nerves and higher brainstem structures.

Virtanierni et al. also found the wave V latency to be delayed in diabetes patients. The overall finding of this study seems to indicate a central disturbance of the auditory pathway, and microvascular complications and duration of diabetes were associated with prolonged latencies in the auditory brainstem.[19] Fiedele et al. recorded BERA from the scalps of 30 normoacoustic insulin-dependent diabetes patients and found that the peripheral transmission time for waves I–V was delayed.[14] Goldsher et al.[20] reported abnormal brainstem response in type-2 diabetes patients with neuropathy. Sharma et al.[21] reported the incidence of delayed wave latencies in diabetics to be 64%, 72% and 84% at 2 kHz, 4 kHz, and 6 kHz, respectively, suggesting that if brainstem evoked response audiometry is conducted at higher frequencies such as 6 kHz in diabetic patients, and the involvement of central neural axis be detected earlier. Kurien et al.[22] evaluated hearing threshold among 30 diabetes patients and demonstrated poor hearing threshold in these patients, however, theycould not demonstrate any relationship between the duration of diabetes and level of hearing loss.

Diabetic neuropathy occurs in almost 50% of the individuals with long-standing type-1 and type-2 DM. In 2007, the American Diabetes Association recommended that all individuals with diabetes be screened annually for any form of neuropathy. Although nerve conduction studies are most commonly used for screening diabetic neuropathy, BERA also seems to have good potential in this area. In the present study, we found a significant association between diabetes and BERA abnormalities, which has been supported by numerous previous studies.

Delays in the central conduction times of those with DM may be related to the neurodegenerative changes occurring in these patients. The exact mechanism of neuronal degeneration in type-2 DM is uncertain. However, as some recent studies suggest, the insulin resistance in type-2 DM not only results in compromised cell survival and metabolism and neuronal plasticity but also increases oxidative stress and neuronal apoptosis. In addition, an increase in the ceramide generation and the subsequent rise in its trafficking across the blood–brain barrier promotes further insulin resistance and neurodegenerative changes in the brains of patients with type-2 DM.

Keeping in mind the ever-increasing global prevalence of diabetes and its long-term negative impact on a person's hearing ability, it is recommended that BERA testing be carried out on diabetics with abnormal HbA1C levels and/or those with long-standing diabetes. This is the most important clinical implication of this study.

  Conclusions Top

In this study, significant differences in the absolute latencies of wave I, III, and V were seen between type-2 DM patients and healthy controls. These abnormalities were attributed to a type-2 DM-associated central auditory dysfunction. This study suggests that, if BERA study is routinely carried out in diabetic patients, the central acoustic neuropathy can be detected even in the absence of any clinically apparent hearing loss. Therefore, we highly recommend the use of BERA in diabetic patients to prevent the further progression of neuropathy. More similar studies are necessary and helpful not only for the standardization of BERA results in diabetics but also for detecting the association between BERA abnormalities and severity of diabetes with greater accuracy.

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Conflicts of interest

  • There is no external source of funding
  • There is no conflict of interests among all authors
  • Research involved human participants with all procedures were performed in studies were in accordance with the ethical standards of institutional research committee comparable with ethical standards
  • Informed consent was obtained from all individual participants included in the study

  References Top

Umegaki H. Neurodegenration in diabetes mellitus. Adv Exp Med Biol 2012;724:258-65.  Back to cited text no. 1
Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:1047-53.  Back to cited text no. 2
Girling J, Dornhorst A. Pregnancy and Diabetes Mellitus. In: Pickup JC, Williams G, editors. Textbook of Diabetes. 3rd ed. Oxford: Blackwell Publishing Company; 2003. pp 65-6.  Back to cited text no. 3
Kashyap AS, Kashyap S. Increased prevalence of impaired hearing in patients with type 2 diabetes in western India. Postgrad Med J 2000;76:38.  Back to cited text no. 4
Lerman GI, Cuevas RD, Valdes S, Enriquez L, Lobato M, Osornjo M, et al. Sensorineural hearing loss- a common finding in early onset type 2 diabetes mellitus. Endocr Pract 2012;18:549-57.  Back to cited text no. 5
Maia CA, Campos CA. Diabetes mellitus as etiological factor for hearing loss. Braz J Otorhinolaringol 2005;71:208-14.  Back to cited text no. 6
Imam M, Shehata OH. Subclinical central neuropathy in type 2 diabetes mellitus. Bull Alex Fac Med 2009;45:65-73.  Back to cited text no. 7
Misra UK, Kalita J. Brainstem auditory evoked potentials. In: Misra UK, Kalita J, editors. Clinical Neurophysiology. 2nd ed. New Delhi: Elsevier Publications; 2006. pp 329-45.  Back to cited text no. 8
Biacabe B, Chevallier JM, Avan P, Bonfils P. Functional anatomy of auditory brainstem nuclei: Application to the anatomical basis of brainstem auditory evoked potentials. Auris Nasus Larynx 2001;28:85-94.  Back to cited text no. 9
Das T, Kundu S, Mazumdar AK, Mukhopadhyay SC. Studies on central nervous system function in diabetes mellitus. J Indian Med Assoc 2001;84:86-9.  Back to cited text no. 10
Ren J, Zhao P, Chen Li, Xu A, Brown SN, Xiao X. Hearing loss in middle age subjects with type 2 diabetes mellitus. Arch Res Med 2009;40:18-23.  Back to cited text no. 11
Taylor IG, Irwin J. Some audiological aspects of diabetes mellitus. J Laryngol Otol 1978;92:99-113.  Back to cited text no. 12
Donald MW, Bird CE, Lawson JS, Letemedia FJJ, Monga TN, Sumdge DHC, et al. Delayed auditory brainstem responses in diabetes mellitus. J Neurol Neurosurg Psychiatr 1981;44:641-4.  Back to cited text no. 13
Fiedele D, Martin A, Cardone C, Comacchio F, Bellavere F, Molinari G, et al. Impaired auditory brain stem evoked response in insulin-dependent diabetic subjects. Diabetes 1984;33:1805-9.  Back to cited text no. 14
Khardori R, Soler NG, Good DC. Brainstem auditory and visual evoked potentials in type-1 (insulin-dependent) diabetic patents. Diabetologia 1986;29:362-5.  Back to cited text no. 15
Virtaniemi J, Laakso M, Karja J, Nuutinen J, Karjalainen S. Auditory brainstem latencies in type-I (insulin-dependent) diabetic patients. Am J Otolaryngol 1993;14: 413-8.  Back to cited text no. 16
Durmus C, Yetiser S, Durmus O. Auditory brainstem evoked responses in insulin-dependent (ID) and non-insulin-dependent (NID) diabetic subjects with normal hearing. Int J Audiol 2004;43:29-33.  Back to cited text no. 17
Donald MW, Erdahl DL, Surridge DH, Monga TN, Lawson JS, Bird CE, et al. Functional correlates of reduced central conduction velocity in diabetic subjects. Diabetes 1984;33:627-33.  Back to cited text no. 18
Virtaniemi J, Kuusisto J, Karjalainen L, Karjalainen S, Laakso M. Improvement of metabolic control does not normalize auditory brainstem latencies in subjects with insulin dependent diabetes mellitus. Am J Otolaryngol 1995;163:172-8.  Back to cited text no. 19
Goldsher M, Pratt H, Hassan A, Shenkav R, Eliachari I, Kanter Y. Auditory brainstem evoked potentials in insulin dependent diabetics with and without peripheral neuropathy. Acta Otolaryngol (Stockh) 1986;102:204-6.  Back to cited text no. 20
Sharma R, Gupta SC, Tyagi I, Kumar S, Mukherjee K. Brain stem evoked responses in patients with diabetes mellitus. Indian J Otolaryngol Head Neck Surg 2000;52:223-9.  Back to cited text no. 21
Kurien M, Thomas K, Bhanu S. Hearing threshold in patients with diabetes mellitus. J Laryngol Otol Rhinol 1989;80:218-88.  Back to cited text no. 22


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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