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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 20  |  Issue : 4  |  Page : 199-202

Evaluation of auditory brain-stem evoked response in middle: Aged type 2 diabetes mellitus with normal hearing subjects


Department of ENT, Audiology and Speech Language Pathology Unit, Pt. J. N. M. Medical College, Ayush Health Science University, Raipur, Chhattisgarh, India

Date of Web Publication13-Dec-2014

Correspondence Address:
Debadatta Mahallik
Department of ENT, Audiology and Speech Language Pathology Unit, Pt. J. N. M. Medical College, Ayush Health Science University, Raipur 492 001, Chhattisgarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-7749.146939

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  Abstract 

Background: Diabetes mellitus (DM) is commonly metabolic disorders of carbohydrate in which blood glucose levels are abnormally high due to relative or absolute insulin deficiency. In addition, it is characterized by abnormal metabolism of fat, protein resulting from insulin deficit or insulin action, or both. There are two broad categories of DM are designated as type 1 and type 2. Type 2 diabetes is due to predominantly insulin resistance with relative insulin deficiency noninsulin-dependent DM. Type 2 diabetes is much more common than insulin-dependent DM. Objectives: The aim of this study was to assess, if there is any abnormality in neural conduction in auditory brain-stem pathway in type 2 DM patients having normal hearing sensitivity when compared to age-matched healthy populations. Materials and Methods: This study included middle - aged 25 subjects having normal hearing with diabetes type 2 mellitus. All were submitted to the full audiological history taking, otological examination, basic audiological evaluation and auditory brain-stem response audiometry which was recorded in both ears, followed by calculation of the absolute latencies of wave I, III and V, as well as interpeak latencies I-III, III-V, I-V. Results: Type 2 DM patients showed significant prolonged absolute latencies of I, III (P = 0.001) and interpeak latencies I-III, III-V and I-V in left ear (P = 0.001) and absolute latencies of I, V (P = 0.001), interpeak latencies III-V was statistically significant in right ear. Conclusions: The prolonged absolute latencies and interpeak latencies suggests abnormal neural firing synchronization or in the transmission in the auditory pathways in normal hearing type 2 diabetes mellitus patients.

Keywords: Brainstem evoked response audiometry, Neural conduction, Type 2 diabetes mellitus


How to cite this article:
Mahallik D, Sahu P, Mishra R. Evaluation of auditory brain-stem evoked response in middle: Aged type 2 diabetes mellitus with normal hearing subjects. Indian J Otol 2014;20:199-202

How to cite this URL:
Mahallik D, Sahu P, Mishra R. Evaluation of auditory brain-stem evoked response in middle: Aged type 2 diabetes mellitus with normal hearing subjects. Indian J Otol [serial online] 2014 [cited 2020 Feb 21];20:199-202. Available from: http://www.indianjotol.org/text.asp?2014/20/4/199/146939


  Introduction Top


Diabetes mellitus (DM) is common metabolic disorders of carbohydrate in which blood glucose levels are abnormally high due to relative or absolute insulin deficiency. In addition, it is characterized by abnormal metabolism of fat, protein resulting from insulin deficit or insulin action, or both. There are two broad categories of DM are designated as type 1 and type 2. Type 2 diabetes is due to predominantly insulin resistance with relative insulin deficiency noninsulin-dependent DM. Type 2 diabetes is much more common than insulin-dependent DM was discovered by chance. [1] Diffused thickening of the basilar membrane, also seen in vascular endothelium, is one of the most clinical morphologic findings in DM, and that is referred to as diabetic microangiopathy. Though the pathogenesis of this morphologic disorder is yet not conformed but it is directly related to hyperglycaemia. [2],[3],[4] In diabetic mellitus, there is involvement of the smaller vessels in the inner ear that leads to hypoxia and thus leading to hearing loss. [5],[6],[7],[8] Some of other reports show the lack of relation between diabetes and hearing loss. [9]

In diabetic mellitus, the auditory system shows some histological changes, such as:

  1. Decrease the number of ciliated cells, atrophy of spiral ganglian, demyelination in 8 th nerve, degenerative starts in lower and upper brain-stem.
  2. Hemorrhages in endolymph and perilymph.
  3. Microangiopathic changes with periodic acid-Schiff deposition in stria vascularis, internal auditory artery, spiral ligaments, and nutrient vessels of the auditory nerve. [7]


Auditory brain-stem evoked response audiometry is used to evaluate the performance of the auditory pathway from the inner ear to brain-stem having seven waves in auditory brain-stem-evoked responses, [9] however only waves I, II, and V are recorded reliably enough to be routinely used in clinical applications. Initially auditory brain-stem response (ABR) audiometry was applied to study diabetics type 1 patient [10] and most evident fact seen was the prolongation of wave III, [11] but there were also studies that showed no significant difference among healthy and diabetic patients for ABR peaks. [12]

Due to the high prevalence of diabetes in Indian population and also due to the complication in from of hearing loss and other adverse effect by it, the present study aimed to determine any abnormality in neural conduction in the auditory pathway in type 2 DM patients with normal hearing sensitivity through by brain-stem evoked response audiometry.


  Materials And Methods Top


Subject selection criteria

Inclusion criteria

Twenty-five normal hearing healthy subject with age range of 25-45 years where mean age was 37.72 years (standard deviation [SD]: ±6.64) were kept in the control group and whereas 25 normal hearing subject with a history of DM type 2 since > 5 years with age range 25-45, mean age 36.64 years (SD: ±3.51) were placed in the experimental group. All were diagnosed as having type 2 DM in the department of medicine and endocrinology.

Exclusion criteria

Patients were excluded if they had any history of hearing loss, ear discharge, tinnitus, head injury, neurological deficit, and cerebrovascular accident, history of noise exposure in past, history of drug intake known to cause central neuropathy such as reserpine, alpha methyl dopa, phenytoin or nitrofurantoin.

Diabetic patients were grouped into two groups:

1. First group consisted of 25 subjects with type 2 DM.

2. Second group consisted of 25 ages and sex matched control subjects for comparison.

All patients selected for this study were suffering type 2 DM > 5 years and well controlled blood sugar level for at least 2 months prior to testing. For all patients, tuning fork tests were performed at all fundamental series from 250 Hz to 1024 Hz, otoscopy and conventional pure-tone audiometry (Interacoustic, Denmark AC 40) with TDH 39 earphone at all frequencies from (250, 500, 1000, 2000, 4000, 8000 Hz) both air-conduction and bone-conduction were executed in sound proof room for each ear. The threshold of pure-tone at any frequency > 20 dB HL was excluded. Intelligent hearing system instrument was used for recording of auditory brain-stem response [Table 1].
Table 1: Acquisition and stimulus parameters used in ABR

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  Results Top


In pure-tone audiometry, the hearing thresholds at all frequencies for all groups were normal (according to Goodman's classifications) [Table 2].
Table 2: Hearing threshold in pure - tone audiometry

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In ABR, the absolute and interpeak latencies of wave I, III, V and I-III, III-V, I-V were identified separately for each right and left ear for each patient. Different values were taken for the right as well as left ear. Wave morphology was normal in all groups.

Auditory brain-stem response results of left ear for all patients with type 2 DM and control group are shown in [Table 3]. It can be concluded that diabetic patient (type 2 DM) have significantly delayed absolute latencies of I and III compared to control group (P = 0.001), but there was no significant statistical difference of wave V (P = 0.16) and the interpeak latencies between control and type 2 DM have significantly delayed (P = 0.001).
Table 3: ABR results from patients with type 2 DM and control group (in left ear)

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Auditory brain-stem response results of right ear for all patients with type 2 DM and control group are shown in [Table 4]. It can be concluded that diabetic patient (type 2 DM) have significantly delayed absolute latencies of wave I and V compared to control group (P = 0.001), but wave III was not significant (P value). For interpeak latencies there was a significant difference for wave III-V (P = 0.001), but no significant statistical difference was found between wave I-III and I-V.
Table 4: ABR results from patients with type 2 DM and control group (in right ear)

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  Discussion Top


The present study confirmed the existence of auditory organ dysfunction in relatively young type 2 DM patients even with a short duration of disease and normal hearing sensitivity. ABR findings in this study showed a significant difference between diabetic and control groups. In type 2 DM patients there were significant difference of I, III absolute latencies (P = 0.001) of left ear and I and V absolute latencies of right ear (P = 0.001), with no significant difference of absolute latency for wave V in left ear (P = 0.16) and wave III, in right ear (P = 0.796).

According to normal hearing threshold in diabetic patients, the prolongation of wave peak I could be due to a reduction of peripheral transmission time (wave I) in the auditory nerve that occurred secondary to diabetic neuropathy. [13]

In type 2 DM patients there were significant difference of interpeak I-III, III-V and I-V for left ear and inter peak latencies III-V both left and right were found significant (P = 0.001) and significant difference of I-III in left ear (P = 0.001) with insignificant difference of I-III interpeak latencies of right ear in comparison with control group. This study is supported by Fawi et al.[14] In some literature, the latencies of I-III, III-V, I-V was longer in diabetic than healthy people. [13],[15],[16] A study where ABR latency was studied on a diabetic patient found that the difference was significantly increased in absolute latencies (I, III and V) and interpeak latencies (I-III, III-V, I-V) when compared to the normal population. [17]

The delay in inter peak latencies I-III and I-V are evidence of central conduction delay in the auditory pathway of diabetics at the level of brain-stem and mid-brain. This delay in latency for wave III and V in diabetics indicates neuropathy at brain-stem and mid-brain level in the auditory pathway Fedele et al. [18]

In the present study, hearing was evaluated in type 2 DM patients. Similar studies have been conducted on type 1 DM. [13],[16],[19] They found a significant increase of absolute and interpeak latencies. Thus, it seems that regardless of type of diabetes, it can lead to hearing problem in brain-stem or in mid-brain level.

Bilateral, symmetric, gradually progressive high frequency sensori-neural hearing loss with slow onset is usually seen in patients suffering from diabetes. [20],[21] This is may be due to cochlear, retro-cochlear or both involvement. The result of this present study showed that all parameters of ABR components were delayed in comparison with healthy control groups. However, the prolongation interpeak latency of wave III-V was most pronounced among other parameters. It can be speculated that the impairment of neural at an early stage is more central than peripheral.


  Conclusion Top


Patients with type 2 DM had the findings of delay absolute latency I, III, V and interpeak latencies I-III, III-V, I-V when compared to control groups. This indicates that there is an abnormality in neural conduction in type 2 DM. A substantial delay of interpeak latency III-V shows that the diabetic neuropathy is at upper brain-stem level. These findings are similar to Durmus et al. [15],[18] It seems that ABR test should be a complementary diagnostic tool for early diagnosis of any auditory alterations and periodic evaluation in of diabetes for early intervention regarding metabolic regulations.

 
  References Top

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American diabetes association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2005;28 Suppl 1:S37-42.  Back to cited text no. 1
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2.
Robins SL, Cotran RS, Kumar V. Pathologic Basis of Disease. 3 rd ed. Philadelphia: WB Sauders Co.; 1991.  Back to cited text no. 2
    
3.
Makishima K, Tanaka K. Pathological changes of the inner ear and central auditory pathway in diabetics. Ann Otol Rhinol Laryngol 1971;80:218-28.  Back to cited text no. 3
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4.
Akinic A, Deda G, Karagol U, Tezic T. Brain stem evoked potential, visual evoked potential and nerve conduction velocity and their relation with Hb1c and beta 2 microglobulin in children with insulin dependent diabetes mellitus. The Turk J Pediatr 1994;36:279-87.  Back to cited text no. 4
    
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Kurien M, Thomas K, Bhanu TS. Hearing threshold in patients with diabetes mellitus. J Laryngol Otol 1989;103:164-8.  Back to cited text no. 5
    
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Malpas S, Blake P, Bishop R, Robinson B, Johnson R. Does autonomic neuropathy in diabetes cause hearing deficits? N Z Med J 1989;102:434-5.  Back to cited text no. 6
    
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Wackym PA, Linthicum FH Jr. Diabetes mellitus and hearing loss: Clinical and histopathologic relationships. Am J Otol 1986;7:176-82.  Back to cited text no. 7
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Krochmalska E, Lazarczyk B, Rogowski M, Rzewnicki I, Wasilewska A, Jakubczyk D. Evaluation of hearing in patients with diabetes. Otolaryngol Pol 1989;43:45-51.  Back to cited text no. 8
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Huang YM, Pan CY, Gu R, Cai XH, Yu LM, Qiu CY. Hearing impairment in diabetics. Chin Med J (Engl) 1992;105:44-8.  Back to cited text no. 9
    
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Chiappa KH. Evoked Potentials in Clinical Medicine. New York: Raven Press; 1997. p. 145-7.  Back to cited text no. 10
    
11.
Donald MW, Bird CE. Lawson JS, Letemendia FJ, Monga TN, Surridge DH, et al. Delayed auditory brainstem responses in diabetes mellitus. J Neurol Neurosurg Psychiatry 1981;44:641-4.  Back to cited text no. 11
    
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Díaz de León-Morales LV, Jáuregui-Renaud K, Garay-Sevilla ME, Hernández-Prado J, Malacara-Hernández JM. Auditory impairment in patients with type 2 diabetes mellitus. Arch Med Res 2005;36:507-10.  Back to cited text no. 12
    
13.
Bayazit Y, Yilmaz M, Kepekçi Y, Mumbuç S, Kanlikama M. Use of the auditory brainstem response testing in the clinical evaluation of the patients with diabetes mellitus. J Neurol Sci 2000;181:29-32.  Back to cited text no. 13
    
14.
Fawi GH. Khalifa GA, Kasim MA. Central and peripheral abnormalities in diabetes Mellitus. Egypt J Neurol Psychiatry Neurosurg 2005;42:209-21.  Back to cited text no. 14
    
15.
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. 15
    
16.
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. 16
    
17.
Al-Azzawi LM, Mirza KB. The usefulness of the brainstem auditory evoked potential in the early diagnosis of cranial nerve neuropathy associated with diabetes mellitus. Electromyogr Clin Neurophysiol 2004;44:387-94.  Back to cited text no. 17
    
18.
Fedele D, Martini A, Cardone C, Comacchio F, Bellavere F, Molinari G, et al. Impaired auditory brainstem-evoked responses in insulin-dependent diabetic subjects. Diabetes 1984;33:1085-9.  Back to cited text no. 18
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Konrad-Martin D, Austin DF, Griest S, McMillan GP, McDermott D, Fausti S. Diabetes-related changes in auditory brainstem responses. Laryngoscope 2010;120:150-8.  Back to cited text no. 19
    
20.
Taylor IG, Irwin J. Some audiological aspects of diabetes mellitus. J Laryngol Otol 1978;92:99-113.  Back to cited text no. 20
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21.
Carmen RE, Svihovec D, Gocka EF, Ermshar CB, Gay GC, Vanore JF, et al. Audiometric configuration as a reflection of diabetes. Am J Otol 1988;9:327-33.  Back to cited text no. 21
    



 
 
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  [Table 1], [Table 2], [Table 3], [Table 4]



 

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