Cochlear Dysfunction in IDDM Patients With Subclinical Peripheral Neuropathy

Mauro A S Di Leo; Walter Di Nardo; Stefania Cercone; Amedeo Ciervo; Mauro Lo Monaco; Aldo V Greco; Gaetano Paludetti; Giovanni Ghirlanda

doi:10.2337/diacare.20.5.824

Original Article

Cochlear Dysfunction in IDDM Patients With Subclinical Peripheral Neuropathy

Mauro A S Di Leo, MD,
Walter Di Nardo, MD,
Stefania Cercone, MD,
Amedeo Ciervo, MD,
Mauro Lo Monaco, MD,
Aldo V Greco, MD,
Gaetano Paludetti, MD and
Giovanni Ghirlanda, MD

Department of Internal and Geriatric Medicine, Catholic University Rome, Italy
Department of Otorhinolaryngology, Catholic University Rome, Italy
Department of Neurology, Catholic University Rome, Italy

Address correspondence and reprint requests to Mauro A.S. Di Leo, MD, Catholic University, Department of Internal Medicine, Largo A. Gemelli 8, 00168 Rome, Italy.

Diabetes Care 1997 May; 20(5): 824-828. https://doi.org/10.2337/diacare.20.5.824

Abstract

OBJECTIVE To investigate the function of the auditory pathway from the cochlea to the auditory cortex in subjects with IDDM.

RESEARCH DESIGN AND METHODS Brain stem, middle-, and long-latency auditory-evoked responses and evoked otoacoustic emissions were measured in 48 normally hearing IDDM patients and in age- and sex-matched nondiabetic subjects. Peripheral neuropathy was diagnosed by nerve conduction velocity (NCV) at the peroneal and sural nerves. Auditory brain stem responses (ABRs) reflect auditory pathway function within the brain stem; middle-latency responses (MLRs) and long-latency responses (LLRs) originate from the auditory cortex; and evoked otoacoustic emissions (EOAEs) give objective information about preneural, mechanical elements of the cochlear function.

RESULTS A subclinical peripheral neuropathy was found in 12 diabetic patients. We found higher latencies of waves I (t = 4.4, P < 0.0001), III (t = 3.7, P = 0.0004), and V (t = 2.7, P = 0.008) of ABRs in diabetic patients (I: 1.7 ± 0.13 ms; III: 3.9 ± 0.17 ms; V: 5.7 ± 0.24 ms), compared with those of the control group (I: 1.6 ± 0.13 ms; III: 3.7 ± 0.18 ms; V: 5.6 ± 0.17 ms). However, neither central transmission time (i.e., the wave interpeak I-V) nor MLRs and LLRs were found to be significantly different in diabetic and control subjects. Mean EOAE amplitude was found to be significantly reduced (F = 4.2, P = 0.02) in diabetic patients with a reduced NCV (7.6 ± 3.9 dB; Scheffé test: P = 0.03), but not in those without neuropathy (9.1 ± 4.2 dB), compared with the control group (10.8 ± 3.1 dB). No correlations were found between duration of diabetes and EOAEs or between sural NCV and peroneal NCV and metabolic control. EOAEs were not correlated with peroneal and sural NCVs.

CONCLUSIONS Our results indicate that the early preneural dysfunction of cochlear receptors causes a prolonged activation of the peripheral portion of the auditory pathway, while signal conduction along the central auditory pathway was shown to be normal in diabetes.