Central Auditory Pathway Research Articles

Choice of test stimulus matters for pitch matching performance: Comparison between pure tone and narrow band noise

Chronic tinnitus, a symptom of high prevalence, is a persistent hearing sensation in the absence of an external sound source. Recent electrophysiological studies indicate that tinnitus generation is to a high degree the result of maladaptive plasticity in the central auditory pathway. The pitch of the tinnitus sensation can be assessed by performing a pitch matching procedure. In the most frequent “tonal tinnitus” type pure tones are used as test stimuli. However, in the case of tonal tinnitus not a single malfunctioning neuron, but rather a population of neighbouring neurons is involved in the generation process of tinnitus and patients typically perceive their tinnitus as a sound having a prominent centre frequency with some spectral extent. Thus, the question arises, why not to use narrow band noise (NBN) instead of pure tones as test stimuli in pitch matching procedures? To investigate this, we first evaluated the pitch matching performance of healthy subjects. In a recursive two alternative choice testing, driven by a computer based automated procedure, the subjects were asked to match the pitch of two sounds. In a crosswise design, NBNs and pure tones were used both as target and as test stimuli. We were able to show that across all four possible combinations the pitch matching performance was least favourable when a sinusoidal sound had to be matched to an NBN target. Even though matching two sinusoidal sounds results in the lowest error, considering that the tinnitus percept typically includes some spectral extent, an NBN should be preferably used as a test stimulus against a pure tone.

Peripheral and Central Auditory Findings in Individuals with Williams Syndrome

Introduction: Williams syndrome (WS) is a rare neurodevelopment genetic condition. The syndrome may present manifestations associated with the central nervous system, hearing, and language. It is possible, as well, to observe an alteration in the central auditory system, which can be diagnosed through long-latency auditory evoked potential (LLAEP).
 Objective: The aim of this study was to describe and analyze the results obtained by peripheral and central auditory evaluation on individuals with WS, verifying if there is a relationship between audiological findings and gender, age and ear side.
 Methods: This is a cross-sectional study in which 14 individuals with WS were evaluated. The exams performed consisted of pure tone audiometry, vocal audiometry, acoustic immittance measures, LLAEP, and cognitive potential.
 Results: The sample was composed of patients from 4 to 18 years old, with a mean age of 11.6 years old (±5.3), being 9 males (64.3%) and 5 females (35.7%). We mainly verified mild to moderate degree (40-44%) of sensorineural auditory loss (35.7-42.9%), type A tympanometric curve (57.1-64.3%), and absent acoustic reflexes (57.1%). As for central auditory evaluation, the subjects showed latency delay in all of the LLAEP components. Moreover, it was evidenced a statistically significant difference when comparing ears for amplitude on cognitive potential evaluation (p = 0.032), observing higher values at the left ear. It was also observed an inverse association between age and P1 wave latency both on the right (p = 0.006) and on the left ear (p = 0.022), and this result can be related to the nervous system maturational process of the WS individuals.
 Conclusion: There are few studies investigating the central auditory pathway on WS in literature. The present study contributes to the extension of the knowledge about the central involvement of the auditory phenotype in the syndrome. However, considering the sample size, more studies are suggested to confirm these findings.

Sensory deafferentation modulates and redistributes neurocan in the rat auditory brainstem.

IntroductionCochlear ablation causing sensory deafferentation (SD) of the cochlear nucleus triggers complex re‐arrangements in the cellular and molecular communication networks of the adult mammalian central auditory system. Participation of the extracellular matrix (ECM) in these processes is not well understood.MethodsWe investigated consequences of unilateral SD for the expression and distribution of the chondroitin sulfate proteoglycans, neurocan (Ncan) and aggrecan (Agg), alongside various plasticity markers in the auditory brainstem of the adult rat using immunohistochemical techniques.ResultsIn the deafferented ventral cochlear nucleus (VCN), Ncan expression increased massively within 3 postoperative days (POD), but rapidly decreased thereafter. Agg showed a similar but less pronounced progression. Decrease in Ncan was spatially and temporally related to the re‐innervation of VCN documented by the emergence of growth‐associated protein Gap43 contained in nerve fibers and presynaptic boutons. Concurrently, astrocytes grew and expressed matrix metalloproteinase‐2 (MMP2), an enzyme known to emerge only under re‐innervation of VCN. MMP2 is capable of cleaving both Ncan and Agg when released. A transient modulation of the ECM in the central inferior colliculus on the side opposite to SD occurred by POD1. Modulations of glutamatergic synapses and Gap43 expression were detected, reflecting state changes of the surrounding tissue induced by transsynaptic effects of SD.ConclusionsThe ECM variously participates in adaptive responses to sudden deafness by SD on several levels along the central auditory pathway, with a striking spatial and temporal relationship of Ncan modulation to astrocytic activation and to synaptogenesis.

Strengthening of the Efferent Olivocochlear System Leads to Synaptic Dysfunction and Tonotopy Disruption of a Central Auditory Nucleus.

The auditory system in many mammals is immature at birth but precisely organized in adults. Spontaneous activity in the inner ear plays a critical role in guiding this maturation process. This is shaped by an efferent pathway that descends from the brainstem and makes transient direct synaptic contacts with inner hair cells. In this work, we used an α9 cholinergic nicotinic receptor knock-in mouse model (of either sex) with enhanced medial efferent activity (Chrna9L9'T, L9'T) to further understand the role of the olivocochlear system in the correct establishment of auditory circuits. Wave III of auditory brainstem responses (which represents synchronized activity of synapses within the superior olivary complex) was smaller in L9'T mice, suggesting a central dysfunction. The mechanism underlying this functional alteration was analyzed in brain slices containing the medial nucleus of the trapezoid body (MNTB), where neurons are topographically organized along a mediolateral (ML) axis. The topographic organization of MNTB physiological properties observed in wildtype (WT) was abolished in L9'T mice. Additionally, electrophysiological recordings in slices indicated MNTB synaptic alterations. In vivo multielectrode recordings showed that the overall level of MNTB activity was reduced in the L9'T The present results indicate that the transient cochlear efferent innervation to inner hair cells during the critical period before the onset of hearing is involved in the refinement of topographic maps as well as in setting the properties of synaptic transmission at a central auditory nucleus.SIGNIFICANCE STATEMENT Cochlear inner hair cells of altricial mammals display spontaneous electrical activity before hearing onset. The pattern and firing rate of these cells are crucial for the correct maturation of the central auditory pathway. A descending efferent innervation from the CNS contacts the hair cells during this developmental window. The present work shows that genetic enhancement of efferent function disrupts the orderly topographic distribution of biophysical and synaptic properties in the auditory brainstem and causes severe synaptic dysfunction. This work adds to the notion that the transient efferent innervation to the cochlea is necessary for the correct establishment of the central auditory circuitry.

Measuring the middle-ear reflex: A quantitative method to assess effects of industrial solvents on central auditory pathways

Volatile organic solvents are frequently present in industrial atmospheres. Their lipophilic properties mean they quickly reach the brain following inhalation. Acute exposure to some solvents perturbs the middle ear reflex, which could jeopardize cochlear protection against loud noises. As the physiological mechanisms involved in this protective reflex are highly complex, in vivo rodent models are required to allow rapid and reliable identification of any adverse effects of solvents on the middle ear reflex (MER).In this study, MER amplitude was measured in anesthetized Brown-Norway rats by monitoring the decrease in distortion product otoacoustic emissions (DPOAEs) caused by a contralateral stimulation. Our screening test consisted in measuring the impact of inhalation of solvent vapors at 3000 ppm for 15 min on the MER amplitude. We had previously studied a selection of aromatic solvents with this model; here, we extended the analysis to volatile compounds from other chemical families. The results obtained shed light on the mechanisms involved in the interactions between solvents and their neuronal targets. Thus, benzene and chlorobenzene had the greatest effect on MER (≥ + 1.8 dB), followed by a group composed of toluene, styrene, p-xylene, m-xylene, tetrachloroethylene and cyclohexane, which had a moderate effect on the MER (between + 0.3 and + 0.7 dB). Finally, trichloroethylene, n-hexane, methyl-ethyl-ketone, acetone, o-xylene, and ethylbenzene had no effect on the MER.Thus, the effect of solvents on the MER is not simply linked to their lipophilicity, rather it depends on specific interactions with neuronal targets. These interactions appear to be governed by the compound's chemical structure, e.g. the presence of an aromatic ring and its steric hindrance. In addition, perturbation of the MER by a solvent is independent of its toxic effects on cochlear cells. As the MER plays a protective role against exposure to high-intensity noises, these findings could have a significant impact in terms of prevention for subjects exposed to both noise and solvents.

Changes in auditory thalamus neural firing patterns after acoustic trauma in rats

Tinnitus is an abnormal phantom perception associated with cochlear trauma, and is thought to cause changes in the rates and patterns of firing neurons in the central auditory pathway. Recent studies have suggested a key role for the auditory thalamus, the medial geniculate nucleus (MGN), in the generation of tinnitus as it may serve a gating function for information en route to cortex. Dysfunctional gating would lead to abnormal activity reaching cortex and hence inappropriate perception, tinnitus, would occur. In this study we compared spontaneous MGN firing rates and burst firing parameters in Wistar rats with and without behavioural evidence of tinnitus following an acoustic trauma. Data were also compared with animals subjected to sham surgery and at an early time-point (2 weeks) after acoustic trauma. Acoustic trauma resulted in a temporary but not a permanent threshold loss and no differences were found in spontaneous firing rate between any of the groups. However, acoustic trauma, whether resulting in tinnitus or not, was accompanied by a significant decrease in the percentage of neurons showing burst firing. In bursting neurons, the number of spikes occurring in a burst and the number of burst per minutes was also significantly reduced compared to the sham group. Our results show that in our rat model without permanent threshold loss, elevated spontaneous firing rates are not associated with acoustic trauma and/or tinnitus and that burst firing parameters are associated with acoustic trauma but are not a neural signature for tinnitus.

Noise-induced hearing loss alters hippocampal glucocorticoid receptor expression in rats

Although the effects of intense noise exposure on the peripheral and central auditory pathway have been well characterized, its effects on non-classical auditory structures in the brain, such as the hippocampus, are less well understood. Previously, we demonstrated that noise-induced hearing loss causes a significant long-term reduction in hippocampal neurogenesis and cell proliferation. Given the known suppressive effects of stress hormones on neurogenesis, the goal of the present study was to determine if activation of the stress response is an underlying mechanism for the long-term reduction in hippocampal neurogenesis observed following noise trauma. To accomplish this, we monitored basal and reactive blood plasma levels of the stress hormone corticosterone in rats for ten weeks following acoustic trauma, and quantified changes in hippocampal glucocorticoid and mineralocorticoid receptors. Our results indicate that long-term auditory deprivation does not cause a persistent increase in basal or reactive stress hormone levels in the weeks following noise exposure. Instead, we observed a greater decline in reactive corticosterone release in noise-exposed rats between the first and tenth week of sampling compared to control rats. We also observed a significant increase in hippocampal glucocorticoid receptor expression which may cause greater hippocampal sensitivity to circulating glucocorticoid levels and result in glucocorticoid-induced suppression of neurogenesis, as well as increased feedback inhibition on the HPA axis. No change in mineralocorticoid receptor expression was observed between control and noise exposed rats. These results highlight the adverse effect of intense noise exposure and auditory deprivation on the hippocampus.

Dynamic Changes of Functional Neuronal Activities Between the Auditory Pathway and Limbic Systems Contribute to Noise-Induced Tinnitus with a Normal Audiogram

Tinnitus is thought to be triggered by aberrant neural activity in the central auditory pathway and is often accompanied by comorbidities of emotional distress and anxiety, which imply maladaptive functional connectivity to limbic structures, such as the amygdala and hippocampus. Tinnitus patients with normal audiograms can also have accompanying anxiety and depression, clinically. To test the role of functional connectivity between the central auditory pathway and limbic structures in patients with tinnitus with normal audiograms, we developed a murine noise-induced tinnitus model with a temporary threshold shift (TTS). Tinnitus mice exhibited reduced auditory brainstem response wave I amplitude, and an enhanced wave IV amplitude and wave IV/I amplitude ratio, as compared with control and non-tinnitus mice. Resting-state functional magnetic resonance imaging (fMRI) was used to identify abnormal connectivity of the amygdala and hippocampus and to determine the relationship with tinnitus characteristics. We found increased fMRI responses with amplitude of low-frequency fluctuation (ALFF) in the auditory cortex and decreased ALFF in the amygdala and hippocampus at day 1, but decreased ALFF in the auditory cortex and increased ALFF in the amygdala at day 28 post-noise exposure in tinnitus mice. Decreased functional connectivity between auditory brain regions and limbic structures was demonstrated at day 28 in tinnitus mice. Therefore, aberrant neural activities in tinnitus mice with TTS involved not only the central auditory pathway, but also limbic structures, and there was maladaptive functional connectivity between the central auditory pathway and limbic structures, such as the amygdala and hippocampus.

In vivo transcranial flavoprotein autofluorescence imaging of tonotopic map reorganization in the mouse auditory cortex with impaired auditory periphery

Ototoxic-drug-induced hearing disturbances in the auditory periphery are associated with tonotopic map reorganization and neural activity modulation, as well as changes in neural correlates in the central auditory pathway, including the auditory cortex (AC). Previous studies have reported that peripheral auditory impairment induces AC plasticity that involves changes in the balance of excitatory vs. inhibitory synapses, within existing and newly forming patterns of connectivity. Although we know that such plastic changes modulate sound-evoked neural responses and the organization of tonotopic maps in the primary AC (A1), little is known about the effects of peripheral impairment on other frequency-organized AC subfields, such as the anterior auditory field (AAF) and the secondary auditory cortex (A2). Therefore, to examine ototoxic-drug-induced spatiotemporal effects on AC subfields, we measured sound-evoked neural activity in mice before and after the administration of kanamycin sulfate (1 mg/g body weight) and bumetanide (0.05 mg/g body weight), using in vivo transcranial flavoprotein autofluorescence imaging over a 4-week period. At first, ototoxic treatment gradually reduced responses driven by tone bursts with lower- (≤8 kHz) and middle- (e.g., 16 kHz) range frequencies in all AC subfields. Subsequently, response intensities in the A1 recovered to more than 78% of the pre-drug condition; however, in the AAF and A2, they remained significantly lower and were unchanged over 3 weeks. Furthermore, after drug administration, the best frequency (BF) areas of the lower (4 and 8 kHz) and higher (25 and 32 kHz) ranges in all subfields were reduced and shifted to those of a middle range (centered around 16 kHz) during the 3 weeks following drug administration. Our results also indicated that, compared with A1, BF distributions in the AAF and A2 were sharper around 16 kHz 3 weeks after drug administration. These results indicate that the ototoxic-damage-induced tonotopic map reorganizations that occurred in each of the three AC subfields were similar, but that there were subfield-dependent differences in the extent of response intensities and in the activated areas that were responsive to tone bursts with specific frequencies. Thus, by examining cortical reorganization induced by ototoxic drugs, we may contribute to the understanding of how this reorganization can be caused by peripheral damage.

Diameters of Perikarya in Different Regions of Rat Central Nervous System after Streptomycin and Kanamycin Intoxication

Introduction: Streptomycin and Kanamycin, an aminoglycosidic antibiotic, is known to destroy the ventral cochlear nuclei of brainstem in man. Ototoxicity is well known side effect of kanamycin, the effect on central nervous system in general and central auditory pathway in particular is still unclear. Subjects and Methods: Thirty albino rats were divided into three groups I, II and III of ten animals each. Group III was control. Group I and II received Streptomycin (30mg/Kg body weight) and kanamycin (400mg/kg body weight) intramuscular injections, daily for 3 weeks. Paraffin embedded sections of cerebellum, spinal cord, dorsal cochlear nucleus, inferior colliculus nucleus and auditory cortex were stained with haematoxylin and eosin stains and perikarya measured using slide and ocular micrometres. Results: Size of cerebellar Purkinje cells increased significantly in control rats for streptomycin and kanamycin intoxicated animals respectively. Ventral horn cells of spinal cord are affected highly significantly only by streptomycin. Vestibular nucleus also showed similar results i.e. neuronal body. Neurons of dorsal cochlear nucleus is affected significantly by both the drugs i.e. streptomycin and kanamycin. Conclusion: Streptomycin causes an increase in diameter of auditory cortical cells on other hand kanamycin led to highly significant decrement in size of cells of same region. Preferential affinity and differential effects were noticed. The latter throws some clues about mechanism of action.

Morphological and neurochemical changes in GABAergic neurons of the aging human inferior colliculus

It is well known that quality of hearing decreases with increasing age due to changes in the peripheral or central auditory pathway. Along with the decrease in the number of neurons the neurotransmitter profile is also affected in the various parts of the auditory system. Particularly, changes in the inhibitory neurons in the inferior colliculus (IC) are known to affect quality of hearing with aging. To date, there is no information about the status of the inhibitory neurotransmitter GABA in the human IC during aging. We have collected and processed inferior colliculi of persons aged 11–97 years at the time of death for morphometry and immunohistochemical expression of glutamic acid decarboxylase (GAD67) and parvalbumin. We used unbiased stereology to estimate the number of cresyl-violet and immunostained neurons. Quantitative real-time PCR was used to measure the relative expression of the GAD67 mRNA. We found that the number of total, GABAergic and PV-positive neurons significantly decreased with increasing age (p < 0.05). The proportion of GAD67-ir neurons to total number of neurons was also negatively associated with increasing age (p = 0.004), but there was no change observed in the proportion of PV-ir neurons relative to GABAergic neurons (p = 0.25). Further, the fold change in the levels of GAD67 mRNA was negatively correlated to age (p = 0.024). We conclude that the poorer quality of hearing with increasing age may be due to decreased expression of inhibitory neurotransmitters and the decline in the number of inhibitory neurons in the IC.

Physiological parallels with perception

Signal detection theory (SDT) lends itself to comparison among perceptual and physiological results in humans and other animals. In physiological recordings, trial-by-trial distributions of single-unit spike counts or of event-related-potentials typically yield non-normal distributions, calling for non-parametric tests. An empirical receiver operating characteristic (ROC) curve can compare distributions of physiological measures between pairs of stimulus conditions. The area under the ROC curve is a non-parametric measure of sensitivity, yielding the proportion correct and, thence, the sensitivity index, d’. The d’ cumulated over a succession of the increasing values of a stimulus parameter provides a measure of the growth of response over that parameter range. I will present examples from several ongoing projects including: (1) studies of activation of the central auditory pathway by cochlear implants and by a penetrating auditory nerve electrode, with single-unit recordings from the inferior colliculus; (2) comparisons of spatial stream segregation among 2-alternative forced choice in humans, hold-response measures in cats, and cortical single-unit recording in cats; and (3) studies of frequency sensitivity using the auditory change complex and masked onset responses. In general, these techniques derived from SDT yield a satisfying agreement among perceptual measures and their physiological underpinnings.

Auditory event-related potentials and function of the medial olivocochlear efferent system in children with auditory processing disorders

Objective: The objectives were to investigate the function of central auditory pathways and of the medial efferent olivocochlear system (MOCS).Design: Event-related potentials (ERP) were recorded following the delivery of the stimulus /da/ in quiet and in ipsilateral, contralateral, and binaural noise conditions and correlated to the results of the auditory processing disorders (APD) diagnostic test battery. MOCS function was investigated by adding ipsilateral, contralateral, and binaural noise to transient evoked otoacoustic emission recordings. Auditory brainstem responses and pure tone audiogram were also evaluated.Study Sample: Nineteen children (7 to 12 years old) with APD were compared with 24 age-matched controls.Results: Otoacoustic emissions and ABR characteristics did not differ between groups, whereas ERP latencies were significantly longer and of higher amplitudes in APD children than in controls, in both quiet and noise conditions. The MOCS suppression was higher in APD children.Conclusions: Findings indicate that children with APD present with neural deficiencies in both challenging and nonchallenging environments with an increase in the timing of several central auditory processes correlated to their behavioural performances. Meanwhile, their modulation of the auditory periphery under noisy conditions differs from control children with higher suppression.

Recessive GM3 synthase deficiency: Natural history, biochemistry, and therapeutic frontier

GM3 synthase, encoded by ST3GAL5, initiates synthesis of all downstream cerebral gangliosides. Here, we present biochemical, functional, and natural history data from 50 individuals homozygous for a pathogenic ST3GAL5 c.862C>T founder allele (median age 8.1, range 0.7–30.5 years). GM3 and its derivatives were undetectable in plasma. Weight and head circumference were normal at birth and mean Apgar scores were 7.7 ± 2.0 (1 min) and 8.9 ± 0.5 (5 min). Somatic growth failure, progressive microcephaly, global developmental delay, visual inattentiveness, and dyskinetic movements developed within a few months of life. Infantile-onset epileptic encephalopathy was characterized by a slow, disorganized, high-voltage background, poor state transitions, absent posterior rhythm, and spike trains from multiple independent cortical foci; >90% of electrographic seizures were clinically silent. Hearing loss affected cochlea and central auditory pathways and 76% of children tested failed the newborn hearing screen. Development stagnated early in life; only 13 (26%) patients sat independently (median age 30 months), three (6%) learned to crawl, and none achieved reciprocal communication. Incessant irritability, often accompanied by insomnia, began during infancy and contributed to high parental stress. Despite catastrophic neurological dysfunction, neuroimaging showed only subtle or no destructive changes into late childhood and hospitalizations were surprisingly rare (0.2 per patient per year). Median survival was 23.5 years. Our observations corroborate findings from transgenic mice which indicate that gangliosides might have a limited role in embryonic neurodevelopment but become vital for postnatal brain growth and function. These results have critical implications for the design and implementation of ganglioside restitution therapies.

Alleviation of Tinnitus With High-Frequency Stimulation of the Dorsal Cochlear Nucleus: A Rodent Study.

Deep brain stimulation of the central auditory pathway is emerging as a promising treatment modality for tinnitus. Within this pathway, the dorsal cochlear nucleus (DCN) plays a key role in the pathophysiology of tinnitus and is believed to be a tinnitus generator. We hypothesized that high-frequency stimulation (HFS) of the DCN would influence tinnitus-related abnormal neuronal activity within the auditory pathway and hereby suppress tinnitus. To this end, we assessed the effect of HFS of the DCN in a noise-induced rat model of tinnitus. The presence of tinnitus was verified using the gap prepulse inhibition of the acoustic startle response paradigm. Hearing thresholds were determined before and after noise trauma by measuring the auditory brainstem responses. In addition, changes in neuronal activity induced by noise trauma and HFS were assessed using c-Fos immunohistochemistry in related structures. Results showed tinnitus development after noise trauma and hearing loss ipsilateral to the side exposed to noise trauma. During HFS of the DCN, tinnitus was suppressed. There was no change in c-Fos expression within the central auditory pathway after HFS. These findings suggest that DCN-HFS changes patterns of activity and results in information lesioning within the network and hereby blocking the relay of abnormal tinnitus-related neuronal activity.

Auditory Midbrain Hypoplasia and Dysmorphology after Prenatal Valproic Acid Exposure

Prenatal exposure to the antiepileptic valproic acid (VPA) is associated with an increased risk of autism spectrum disorder (ASD) in humans and is used as an animal model of ASD. The majority of individuals with ASD exhibit adverse reactions to sensory stimuli and auditory dysfunction. Previous studies of animals exposed to VPA reveal abnormal neuronal responses to sound and mapping of sound frequency in the cerebral cortex and hyperactivation, hypoplasia and abnormal neuronal morphology in the cochlear nuclei (CN) and superior olivary complex (SOC). Herein, we examine the neuronal populations in the lateral lemniscus and inferior colliculus in animals exposed in utero to VPA. We used a combination of morphometric techniques, histochemistry and immunofluorescence to examine the nuclei of the lateral lemniscus (NLL) and the central nucleus of the inferior colliculus (CNIC). We found that the VPA exposure resulted in larger neurons in the CNIC and the dorsal nucleus of the lateral lemniscus (DNLL). However, we found that there were significantly fewer neurons throughout all nuclei examined in the auditory brainstem of VPA-exposed animals. Additionally, we found significantly fewer calbindin-immunopositive neurons in the DNLL. VPA exposure had no impact on the proportions of perineuronal nets in the NLL or CNIC. Finally, consistent with our observations in the CN and SOC, VPA exposure resulted in fewer dopaminergic terminals in the CNIC. Together, these results indicate that in utero VPA exposure significantly impacts structure and function of nearly the entire central auditory pathway.

Tinnitus and Cognition: Linked?

Tinnitus is conscious auditory perception without corresponding external stimuli resulting from neuronal activity along auditory pathway either in peripheral or central auditory system. The exact origin, pathophysiologic pathway and its treatment is still under exploration. The main risk factor is hearing loss, but can occur in patients with normal hearing. Auditory brainstem response test helps to objectify this subjective complaint and aid in locating its origin. P300 is late latency auditory evoked potential, objective marker of cognitive potential. The purpose of our study was to ascertain any significant difference in P300 latency and amplitude values in cases of sensorineural hearing loss with tinnitus when compared to controls (normal hearing subjects) and also to find any correlation between severity of tinnitus and cognition. This was a case control study conducted at the department of ENT at Safdarjung Hospital, New Delhi between September 2016 to March 2018. The study comprised of one hundred and six patients, out of which fifty five patients werehaving sensorineural hearing loss with tinnitus and fifty one patients were normal hearing subjects. General medical and audiological history and examination was done. Significant increase in P300 latency and decrease in P300 amplitude was found in sensorineural hearing loss with tinnitus cases on comparing with controls. The similar pattern of P300 values was observed on increasing severity of tinnitus and degree of hearing loss. Hence, results revealed the role of cognition and involvement of central auditory pathway in tinnitus generation.

Visualization of the auditory pathway in rats with 18F-FDG PET activation studies based on different auditory stimuli and reference conditions including cochlea ablation.

Activation studies with positron emission tomography (PET) in auditory implant users explained some of the mechanisms underlying the variability of achieved speech comprehension. Since future developments of auditory implants will include studies in rodents, we aimed to inversely translate functional PET imaging to rats. In normal hearing rats, activity in auditory and non-auditory regions was studied using 18F-fluorodeoxyglucose (18F-FDG) PET with 3 different acoustic conditions: sound attenuated laboratory background, continuous white noise and rippled noise. Additionally, bilateral cochlea ablated animals were scanned. 3D image data were transferred into a stereotaxic standard space and evaluated using volume of interest (VOI) analyses and statistical parametric mapping (SPM). In normal hearing rats alongside the auditory pathway consistent activations of the nucleus cochlearis (NC), olivary complex (OC) and inferior colliculus (IC) were seen comparing stimuli with background. In this respect, no increased activation could be detected in the auditory cortex (AC), which even showed deactivation with white noise stimulation. Nevertheless, higher activity in the AC in normal hearing rats was observed for all 3 auditory conditions against the cochlea ablated status. Vice versa, in ablated status activity in the olfactory nucleus (ON) was higher compared to all auditory conditions in normal hearing rats. Our results indicate that activations can be demonstrated in normal hearing animals based on 18F-FDG PET in nuclei along the central auditory pathway with different types of noise stimuli. However, in the AC missing activation with respect to the background advises the need for more rigorous background noise attenuation for non-invasive reference conditions. Finally, our data suggest cross-modal activation of the olfactory system following cochlea ablation–underlining, that 18F-FDG PET appears to be well suited to study plasticity in rat models for cochlear implantation.

The Middle Latency Response: A Review of Findings in Various Central Nervous System Lesions.

The middle latency response (MLR) first came to light as an auditory evoked potential in 1958. Since then, it has aroused substantial interest and investigation by clinicians and researchers alike. In recent history, its use and popularity have dwindled in tandem with various other auditory evoked potentials in audiology. One area for which MLR research and application has been overlooked is its potential value in measuring the neural integrity of the auditory thalamocortical pathway. In a broader sense, the MLR, when combined with the auditory brain stem response, can provide information concerning the status of much of the central auditory system pathways. This review is intended to provide information concerning the MLR as a measure of central auditory function for the reader to consider. To review and synthesize the scientific literature regarding the potential value of the MLR in assessing the integrity of the central auditory system and to provide the reader an informed perspective on the value of the MLR in this regard. Information is also provided on the MLR generator sites and fundamental characteristics of this evoked potential essential to its clinical and or research application. A systematic review and synthesis of the literature focusing on the MLR and lesions of the central auditory system. Studies and individual cases were reviewed and analyzed that evidenced documented lesions of the central auditory nervous system. The authors searched and reviewed the literature (journal articles, book chapters, and books) pertaining to central auditory system lesion effects on the MLR. Although findings varied from study to study, overall, the MLR was reasonably sensitive and specific to neurological compromise of the central auditory system. This finding is consistent with the generator sites of this evoked potential. The MLR is a valuable tool for assessing the integrity of the central auditory system. It should be of interest to the clinician or researcher who focuses their attention on the function and dysfunction of the higher auditory system.

Sequential bilateral cochlear implant: results in children and adolescents

IntroductionThe use of the bilateral cochlear implants can promote the symmetrical development of the central auditory pathways, thus benefiting the development of auditory abilities and improving sound localization and the ability of auditory speech perception in situations of competitive noise. ObjectiveTo evaluate the ability of speech perception in children and adolescents using sequential bilateral cochlear implants, considering the association of these variables: age at surgery, time of device use and interval between surgeries. MethodsA total of 14 individuals between 10 and 16 years of age, who demonstrated surgical indication for the use of sequential bilateral cochlear implants as intervention in the auditory habilitation process, were assessed. The speech perception ability was assessed through sentence lists constructed in the Portuguese language, presented in two situations: in silence, with fixed intensity of 60dB SPL, and in competitive noise, with a signal-to-noise ratio of +15dB. The evaluation was performed under the following conditions: unilateral with the first activated cochlear implant, unilateral with the second activated cochlear implant and bilateral with both devices activated. ResultsThe results of the speech perception tests showed better performance in both silence and in noise for the bilateral cochlear implant condition when compared to the 1st cochlear implant and the 2nd cochlear implant alone. A worse result of speech perception was found using the 2nd cochlear implant alone. No statistically significant correlation was found between age at the surgical procedure, interval between surgeries and the time of use of the 2nd cochlear implant, and the auditory speech perception performance for all assessed conditions. The use of a hearing aid prior to the 2nd cochlear implant resulted in benefits for auditory speech perception with the 2nd cochlear implant, both in silence and in noise. ConclusionThe bilateral cochlear implant provided better speech perception in silence and in noise situations when compared to the unilateral cochlear implant, regardless of the interval between surgeries, age at the surgical procedure and the time of use of the 2nd cochlear implant. Speech perception with the 1st cochlear implant was significantly better than with the 2nd cochlear implant, both in silence and in noise. The use of the hearing aid prior to the 2nd cochlear implant influenced speech perception performance with the 2nd cochlear implant, both in silence and in noise.