tory-evoked responses and evoked otoacoustic emissions were measured in 48 normally hear- ing IDDM patients and in age- and sex-matched nondiabetic ...
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Cochlear Dysfunction in IDDM Patients With Subclinical Peripheral Neuropathy MAURO A.S. D I LEO, MD WALTER DI NARDO, MD STEFANIA CERCONE, MD AMEDEO CIERVO, MD
MAURO LO MONACO, MD ALDO V. GRECO, MD GAETANO PALUDETTI, MD GIOVANNI GHIRLANDA, MD
OBJECTIVE — To investigate the function of the auditory pathway from the cochlea to the auditory cortex in subjects with IDDM. RESEARCH DESIGN A N D 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; middlelatency 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; Scheffe 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.
O
ver the past decade, there has been growing interest in the evaluation of human auditory function in diabetes. An early hearing impairment in diabetes is still a matter of controversy (1,2), since hearing loss is considered a nontypical symptom of this disease. The need for tests able to detect central auditory dysfunctions is increasingly recognized. Several tests (3) have proven useful in the recording of auditory evoked
potentials, but so far, direct noninvasive measures of neural activation at all levels of the auditory pathway have not been carried out in diabetic patients. Brain stem auditory evoked potentials that represent noninvasive procedures for monitoring central nervous system involvement in diabetes (4) include auditory brain stem responses (ABRs), middle-latency responses (MLRs), and long-latency responses (LLRs) (5,6). ABRs are mainly
From the Departments of Internal and Geriatric Medicine (M.A.S.D.L., S.C., A.VG., G.G.), Otorhinolaryngology (WD.N., G.P), and Neurology (A.C., M.L.M.), 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. Received for publication 10 July 1996 and accepted in revised form 26 November 1996. ABR, auditory brain stem response; CNS, central nervous system; EOAE, evoked otoacoustic emission; LLR, long-latency response; MLR, middle-latency response; MNC, motor nerve conduction; NCV, nerve conduction velocity; SNC, sensory nerve conduction; SPL, sound pressure level.
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generated in structures along the auditory lemniscal pathway, while MLRs are thought to be generated in the auditory areas of the temporal lobe, although midbrain sources have not yet been ruled out. LLRs are thought to be generated, at least partially, in primary and associative auditory cortices. A comprehensive understanding of the nervous pathways originating from the cochlea provides a physiopathological basis for the use of evoked otoacoustic emissions (EOAEs) as a clinical test of hearing. EOAEs can be recorded in the outer ear canal and give objective information about preneural, mechanical elements of the cochlear function (7,8). EOAEs appear to be a general property of the human peripheral auditory system. In the past years, conflicting reports have appeared of a possible impairment of the central nervous system (CNS) in diabetic patients (9-16). Such studies support the conclusion that central subclinical neuropathy may have the same critical role as peripheral neuropathy in the pathogenesis of hearing loss in diabetes. The aim of this study was to evaluate the function of peripheral and central auditory pathway in order to detect signs of subclinical neuropathy in subjects with IDDM. Possible correlations between auditory function and nerve conduction velocity (NCV) at peroneal and sural nerves and the relationship between auditory evoked responses and NCVs, metabolic control, and duration of disease have been investigated.
RESEARCH DESIGN AND METHODS — The control group consisted of 43 healthy normally hearing subjects (22 men aged 27.9 ± 6.4 years and 21 women aged 28.4 ± 6.8 years). Subjects with a history of ototoxicity, noise exposure, or previous ear diseases were excluded from the study. The clinical population consisted of 48 normally hearing IDDM patients (aged 28 ± 6 years) with diabetes duration of 13 ± 6.3 years. Informed consent was obtained from each subject. Methods Stereofundus photography and fluorescein angiography were performed on each patient. DIABETES CARE, VOLUME 20, NUMBER 5, MAY
1997
Di Leo and Associates
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