Comparative study of brainstem evoked response audiometry in diabetic patients and non-diabetic subjects to assess the involvement of central auditory pathway

<p><strong>Background: </strong>Diabetes mellitus (DM) which is prevalent in world is associated with sensorineural hearing loss. Brainstem evoked response audiometry (BERA) is a simple, non-invasive procedure to detect early impairment of acoustic nerve and auditory pathway. The present study is under taken to evaluate the impact of DM on BERA parameters. Aim of the study was to compare the BERA of diabetic patients to those of age and gender matched controls to assess the involvement of central auditory pathway.</p><p><strong>Methods</strong>: A cross sectional study was conducted on 35 diabetic patients, aged 35 to 55 years, who were on treatment for at least 2 years, and 35 age and sex matched control participants, were subjected for BERA at 70,80 and 90 dB. The waveforms, absolute latency of wave I, wave III, wave V and interwave/ inter peak latency of I-III, III-V and I-V were analyzed with respect to both groups.</p><p><strong>Results</strong>: The absolute latency of wave III and wave V, interpeak/ interwave latency of I-III, interpeak/ interwave latency of I-V, III-V and absolute latency of wave V were highly significant at corresponding tested stimuli in the diabetic group compared to the control group.</p><p><strong>Conclusions</strong>: Early involvement of central auditory pathway in diabetic patients, can be detected with fair accuracy with auditory evoked potential studies; if done on a regular basis warrants meticulous glycemic control and prevents further damage.</p>

PET/CT background noise and its effect on speech recognition

Positron emission tomography (PET) has been successfully used to investigate central nervous processes, including the central auditory pathway. Unlike early water-cooled PET-scanners, novel PET/CT scanners employ air cooling and include a CT system, both of which result in higher background noise levels. In the present study, we describe the background noise generated by two state-of-the-art air-cooled PET/CT scanners. We measured speech recognition in background noise: recorded PET noise and a speech-shaped noise applied in clinical routine to subjects with normal hearing. Background noise produced by air-cooled PET/CT is considerable: 75.1 dB SPL (64.5 dB(A)) for the Philips Gemini TF64 and 76.9 dB SPL (68.4 dB(A)) for the Philips Vereos PET/CT (Philips Healthcare, The Netherlands). Subjects with normal hearing exhibited better speech recognition in recorded PET background noise compared with clinically applied speech-shaped noise. Speech recognition in both background noises correlated significantly. Background noise generated by PET/CT scanners should be considered when PET is used for the investigation of the central auditory pathway. Speech in PET noise is better than in speech-shaped noise because of the minor masking effect of the background noise of the PET/CT.

Stroke-Associated Cortical Deafness: A Systematic Review of Clinical and Radiological Characteristics

Background: Stroke is the leading cause of cortical deafness (CD), the most severe form of central hearing impairment. CD remains poorly characterized and perhaps underdiagnosed. We perform a systematic review to describe the clinical and radiological features of stroke-associated CD. Methods: PubMed and the Web of Science databases were used to identify relevant publications up to 30 June 2021 using the MeSH terms: “deafness” and “stroke”, or “hearing loss” and “stroke” or “auditory agnosia” and “stroke”. Results: We found 46 cases, caused by bilateral lesions within the central auditory pathway, mostly located within or surrounding the superior temporal lobe gyri and/or the Heschl’s gyri (30/81%). In five (13.51%) patients, CD was caused by the subcortical hemispheric and in two (0.05%) in brainstem lesions. Sensorineural hearing loss was universal. Occasionally, a misdiagnosis by peripheral or psychiatric disorders occurred. A few (20%) had clinical improvement, with a regained oral conversation or evolution to pure word deafness (36.6%). A persistent inability of oral communication occurred in 43.3%. A full recovery of conversation was restricted to patients with subcortical lesions. Conclusions: Stroke-associated CD is rare, severe and results from combinations of cortical and subcortical lesions within the central auditory pathway. The recovery of functional hearing occurs, essentially, when caused by subcortical lesions.

Review: Neural Mechanisms of Tinnitus and Hyperacusis in Acute Drug-Induced Ototoxicity

Purpose Tinnitus and hyperacusis are debilitating conditions often associated with age-, noise-, and drug-induced hearing loss. Because of their subjective nature, the neural mechanisms that give rise to tinnitus and hyperacusis are poorly understood. Over the past few decades, considerable progress has been made in deciphering the biological bases for these disorders using animal models. Method Important advances in understanding the biological bases of tinnitus and hyperacusis have come from studies in which tinnitus and hyperacusis are consistently induced with a high dose of salicylate, the active ingredient in aspirin. Results Salicylate induced a transient hearing loss characterized by a reduction in otoacoustic emissions, a moderate cochlear threshold shift, and a large reduction in the neural output of the cochlea. As the weak cochlear neural signals were relayed up the auditory pathway, they were progressively amplified so that the suprathreshold neural responses in the auditory cortex were much larger than normal. Excessive central gain (neural amplification), presumably resulting from diminished inhibition, is believed to contribute to hyperacusis and tinnitus. Salicylate also increased corticosterone stress hormone levels. Functional imaging studies indicated that salicylate increased spontaneous activity and enhanced functional connectivity between structures in the central auditory pathway and regions of the brain associated with arousal (reticular formation), emotion (amygdala), memory/spatial navigation (hippocampus), motor planning (cerebellum), and motor control (caudate/putamen). Conclusion These results suggest that tinnitus and hyperacusis arise from aberrant neural signaling in a complex neural network that includes both auditory and nonauditory structures.

Hyperexcitability of the Nucleus Accumbens Is Involved in Noise-Induced Hyperacusis

Reduced tolerance to sound stimuli (hyperacusis) is commonly seen in tinnitus patients. Dysfunction of limbic systems, such as the nucleus accumbens (NAc), may be involved in emotional reactions to the sound stimuli in tinnitus patients. To study the functional changes in the NAc in hyperacusis, we have examined the neural activity changes of the NAc using c-Fos staining in an animal model of hyperacusis. The c-Fos staining was also examined in the medial geniculate nucleus (MGN), a central auditory pathway which has neural projections to the NAc. Postnatal rats (14 days) were exposed to loud noise (115 dB SPL, 4 hours for two consecutive days) to induce hyperacusis ( n = 4 ). Rats without noise exposure were used as the controls ( n = 4 ). After P35, rats in both groups were put in a behavioral training for sound detection. After they were trained to detect sound stimuli, their reaction time to noise bursts centered at 2 kHz (40-110 dB SPL) was measured. Rats in the noise group showed a significantly shorter reaction time than those in the control group to the noise bursts at high intensities, suggesting the noise exposure induced hyperacusis behavior. The c-Fos expressions in the NAc and the MGNs of the noise group were significantly higher than those of the control group. Our results suggested that early-age noise exposure caused hyperactivity in the NAc and the MGNs which may induce the loudness increase in these rats.

Resistance to noise-induced gap detection impairment in FVB mice is correlated with reduced neuroinflammatory response and parvalbumin-positive neuron loss

Exposure to loud noises results in neuroinflammatory responses in the central auditory pathway. Noise-induced neuroinflammation is implicated in auditory processing deficits such as impairment in gap detection. In this study, we examined whether strain differences between the FVB and C57BL/6 mice in noise-induced impairment in gap detection are correlated with strain differences in neuroinflammatory responses. We found that noise induced more robust TNF-α expression in C57BL/6 than in FVB mice. Noise-induced microglial deramification was observed in C57BL/6 mice, but not in FVB mice. Furthermore, noise exposure resulted in a reduction in parvalbumin-positive (PV+) neuron density in the C57BL/6 mice, but not in FVB mice. These results suggest that neuroinflammatory responses and loss of PV+ neurons may contribute to strain differences in noise-induced impairment in gap detection.

Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss

Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.