Auditory Brainstem Latency Research Articles

Auditory Brainstem Response Differences in Diabetic and Non-diabetic Veterans

A number of studies have found statistically significant delays in auditory brainstem latencies of patients with diabetes compared with non-diabetic controls. However, the mechanisms ascribed as responsible for the latency differences between diabetic and non-diabetic patients vary among studies, and the latency differences, while significant, are small. In this 5-year prospective study, auditory brainstem response testing was conducted with 416 non-diabetic and 375 diabetic veterans from the Portland Veterans Affairs Medical Center as part of a larger study. Patients with diabetes had significantly delayed latencies of Wave III and V in the right ear and significantly prolonged interpeak I-III and I-V latencies in both ears. Stimulus polarity difference yielded slightly different results. None of the diabetes-related clinical characteristics were associated with the latency differences between the subject groups after accounting for hearing loss and age. Effect size was calculated and clinical significance of these differences is discussed.

Frequency specificity of the human auditory brainstem and middle latency responses to brief tones. I. High-pass noise masking.

This study investigated the frequency specificity of the auditory brainstem (ABR) and middle latency (MLR) responses to 500- and 2000-Hz brief tones using high-pass noise masking. Stimuli were linear- (2-1-2 cycles) and exact-Blackman- (5 cycles) gated tones presented at 80 dB peak-to-peak equivalent (ppe) SPL. Cochlear contributions to ABR wave V-V' and MLR wave Na-Pa were assessed by the effects of high-pass noise masking on response amplitudes and latencies. The high-pass noise results demonstrate that the ABR and the MLR to the 80 dB ppe SPL brief tones show good frequency and place specificity. Changes in ABR or MLR amplitude and latency with high-pass noise masking did not occur as the masker cutoff was decreased from 2 to 3 octaves above the stimulus nominal frequency until it was within one-half octave of this frequency, below which amplitudes rapidly decreased (500- and 2000-Hz tones) and latencies increased (500-Hz tones). No significant differences existed in the frequency specificity of the ABR versus MLR, or in these evoked potentials to exact-Blackman- versus linear-gated tones.

Effect of stimulus level and frequency on ABR and MLR binaural interaction in human neonates

Auditory brainstem (ABR) and middle latency (MLR) responses were evoked by click and tone-burst stimuli from human neonates. Electrophysiologic evidence of binaural interaction was measured by subtracting waveforms obtained for binaural stimulus conditions from waveforms obtained for the sum of right ear monaural and left ear monaural stimulus conditions. The effects of stimulus level and stimulus frequency on binaural interaction were evaluated by measuring the number, latency and amplitude of components found in the derived binaural interaction waveform, that is, binaural interaction components (BIC). BICs were more prevalent in the latency range of ABRs than for MLRs. Click and tonal stimuli were equally effective for deriving ABR-BICs, while tone-bursts were somewhat less effective than clicks for deriving MLR-BICs. Stimulus-response dependencies for ABR and MLR component latencies were apparent in monaural, binaural and binaural interaction waveforms. Normalized amplitudes for BICs showed that low-frequency tone-burst stimuli resulted in the largest values compared to click and high-frequency tonal stimuli. Comparison of these results with published results from adults demonstrated immaturity of binaural interaction in neonates.

Improvement of metabolic control does not normalize auditory brainstem latencies in subjects with insulin-dependent diabetes mellitus

Introduction: In our previous study (Am J Otolaryngol 14:413–418, 1993), we reported that prolonged auditory brainstem response latencies are associated with microvascular complications and the duration of diabetes in patients with insulin-dependent diabetes mellitus (IDDM). To investigate whether short-term improvement in metabolic control also affects ABR-responses, we compared ABR-latencies in subjects with IDDM before and after intensified insulin and diet therapy. Materials and Methods: Auditory brainstem latencies were measured in 13 subjects with IDDM (mean age: 25 years) before and after intensified insulin and diet therapy. The acoustic stimulus was a half sine wave with a duration of 0.250 millisecond and a frequency of 2,000 Hz. The stimulus was presented monaurally with fixed polarity through shielded headphones TDH-39 at repetition rate of 10 Hz and at 90 dB hearing level. All subjects had normal hearing ability. Glycated hemoglobin A,c (GHbA,c), blood glucose immediately before ABR-measurements, and mean blood glucose during 24 hours before auditory studies were measured before and after intensified therapy. Results: During intensified insulin therapy, GHbA,c improved significantly ( P < .05) in study subjects. However, no changes were observed in ABR-latencies. We also studied those 10 patients whose blood glucose improved during intensified insulin therapy. Although blood glucose was significantly lower ( P < .01) after intensified insulin therapy compared with that at baseline, no changes were observed between ABR-latencies at baseline and follow-up. Conclusion: ABR-latencies were not affected by improvement in metabolic control in patients with IDDM. Our finding suggests that delayed ABR-latencies found in patients with IDDM are not caused by poor metabolic control of diabetes but rather by other mechanisms, for example, microvascular complications.

Acoustic-reflex responses in patients with insulin-dependent diabetes mellitus

Purpose: patients with insulin-dependent diabetes mellitus (IDDM) are especially susceptible to microangiopathic complications such as nephropathy, retinopathy, and neuropathy. Microangiopathic changes are also the most important findings in histopathologic studies of the inner ear and central nervous systems in diabetic subjects. No previous studies have measured acoustic-reflex latencies (ARL) or amplitudes (ARA) in patients with IDDM. ARL and ARA reflect the function of the acoustic-reflex arch. Furthermore, possible changes in the tympanic membrane, ossicular chain, and stapedius muscle may affect the shape of acoustic-reflex. Subjects and Methods: Acoustic-reflex thresholds, latencies, and amplitudes were studied in 53 patients with IDDM and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years, using the Madsen Model ZO 73 Impedance Bridge (Madsen Electronics, Copenhagen, Denmark). Subjects with an abnormal tympanic membrane, conductive hearing loss, and known cause for hearing impairment eg, noise damage, were excluded from the study. Results: There were no differences between control and diabetic subjects in the contralateral acoustic-reflex thresholds. In contrast, patients with IDDM had longer ARLs and decreased ARAs compared with those of control subjects. ARA amplitude had linear correlation with the amplitude of tympanogram, whereas ARL had no linear correlation with auditory brainstem latencies in the same study subjects. Acoustic-reflex responses in insulin-dependent diabetic patients were not associated with the duration of diabetes, metabolic control, microangiopathy, or neuropathy. Concluslons: Prolonged ARLs and decreased ARAs in patients with insulin-dependent diabetes are probably caused more by the stiff middle ear system than disturbances in the brainstem.

Auditory brainstem latencies in type I (insulin-dependent) diabetic patients

Introduction: This study was undertaken to compare auditory brainstem response latencies in insulin-dependent diabetics, and to compare these findings with metabolic control, microangiopathy, neuropathy, and the duration of diabetes. Methods: Auditory brainstem latencies were studied in 53 type I diabetic patients and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years. Three different stimulus repetition rates (10, 30, and 50 Hz) were used. All subjects had normal hearing ability. Results: Wave V latencies were longer in diabetic patients when compared with those of control subjects at all repetition rates. At repetition rates of 10 and 50 Hz, diabetic patients had a prolonged I–V interwave latency, and at a repetition rate of 50 Hz, diabetics had a longer III–V interwave latency than control subjects. These findings indicate a central disturbance in the auditory pathway. Microvascular complications (retinopathy, nephropathy) and the duration of diabetes were associated with the prolongation of auditory brainstem latencies. In contrast, poor metabolic control (high fasting blood glucose and glycated hemoglobin A 1c) at the time of the present study was only marginally associated with prolonged auditory brainstem latencies. The changes in auditory brainstem latencies associated with diabetic neuropathy (measured with five cardiac autonomic nervous function tests) appeared simultaneously with microvascular complications and in patients with diabetes of long duration, and thus a causative role of diabetic neuropathy in the pathogenesis of prolonged auditory brainstem latencies remains unsolved. Conclusion: Delayed auditory brainstem latencies in type I diabetic patients are probably caused by the long duration of diabetes and the microvascular complications associated with it.

Maturation of auditory evoked potentials in young guinea pigs with binaural conductive hearing loss.

A reversible conductive hearing loss produced during the first 4 weeks post partum caused marked alterations in the development of click-evoked auditory brainstem (ABR) and middle latency (MLR) responses in guinea pigs. The early component PI in the ABR in controls showed adult-like latencies at the time of birth, while the later ABR components PIII and PV and all components investigated in the MLR showed postnatal development characterized by a shortened latency that persisted for the whole period of investigation. The course of the ABR latencies showed the sharpest decrease during the first 2-3 weeks of life, while that for the MLR took place during the first 5 weeks. In addition to the increased ABR thresholds and lengthened ABR latencies due to the conductive hearing loss, development of the ABR inter-peak latencies (IPL) and MLR latencies was retarded. The IPL reached control values 1 week after the end of the deprivation phase, while the delay in MLR started later (4th week) and lasted longer than did that in the ABR. These findings showed that a long-lasting postnatal conductive hearing loss does not generate sustained impairment at the level of the brainstem but can evoke longer-lasting deficiencies at higher stations of the auditory pathway.

Effect of the menstrual cycle on the auditory brainstem response.

The present study sought to determine if the gender difference in auditory brainstem (ABR) latency and peak amplitude varies systematically across the menstrual cycle. Behavioral thresholds and auditory-evoked brainstem responses to alternating click stimuli were obtained from 17 normal hearing young adults (10 female, 7 male). Absolute behavioral thresholds and ABR measurements were compared every other day over a complete menstrual cycle. Results show consistent gender differences in ABR latency, peak amplitude, and behavioral threshold of the ABR stimuli, but these differences do not vary across the menstrual cycle.