Embedded Files
Background
Background
The sensory receptors of the auditory system are the hair cells. They are located in the cochlea of the inner ear. They derive their name from the stereocilia that protrude from the cell. The hair cells transform the sound vibrations which arrive in the fluids of the cochlea into electrical signals that are then relayed via the auditory nerve first to the auditory brainstem, then to the thalamus and finally to the auditory cortex. (Reference: https://en.wikipedia.org/wiki/Hair_cell)
The hair cells form synaptic connections with neurons called spiral (cochlear) ganglion neurons. The axons of these neurons, or in other words these nerve fibers, called auditory nerve fibers, are forming the auditory nerve.
(References: https://en.wikipedia.org/wiki/Cochlear_nerve and https://en.wikipedia.org/wiki/Spiral_ganglion)
Tinnitus may be caused by severe or subtle damage of hair cells or auditory nerve fibers. Specifically, it may be caused:
1) By damage of hair cells, in which case there is severe hearing loss, detected by a standard audiogram,
2) By damage of auditory nerve fibers (neuronal axons forming the auditory nerve), in which case there is subtle hearing loss, not easily detected, which is experienced as loss of clarity in noisy backgrounds.
Upon these conditions, inhibitory mechanisms may be removed, triggering hyperactivity in components of the nervous system. Neuroplastic mechanisms (cf. compensatory mechanisms) may be applicable.
Hyperactivity has been reported in brainstem auditory nuclei and the auditory cortex.
It is noted that brainstem nuclei include the following: Cochlear nuclei (CN), Inferior colliculi (IC), Nuclei of the lateral lemniscus, Superior olivary complex. It is also noted that the auditory nerve enters the brainstem just below the juncture between the medulla and pons to synapse in the cochlear nuclei.
"Loss of Auditory Nerve Fibers Uncovered in Individuals with Tinnitus"
"Loss of Auditory Nerve Fibers Uncovered in Individuals with Tinnitus"
2023-11-30, Mass Eye and Ear center
"Individuals who report tinnitus" "are experiencing auditory nerve loss that is not picked up by conventional hearing tests". They also show "hyperactivity in the brainstem".
(FB) "Tinnitus may be linked to ‘hidden hearing loss’ missed on common tests, study suggests"
(FB) Mass Eye and Ear Tinnitus Clinic
(FB)
Interview de Stéphane Maison, professeur associé d’otolaryngologie à Harvard et directeur de la clinique des acouphènes de Boston.
Sur l'hypothèse qui consiste à dire que les acouphènes proviennent d'une hyperactivité du cerveau, qui comme mentionné ici, serait due aux endommagements des neurones, même difficilement détectés pour les cas des "normo-entendants".
Les scientifiques ont mesuré par enregistrement l’influx nerveux qui va de l'oreille interne jusqu'au cerveau. Ils ont déterminé qu'il y a toujours une diminution auditive, même inaperçue, en raison des dégâts des neurones (axones ou fibres).
Il faut noter que le bon fonctionnement du cerveau nécessite une équilibre entre excitation et inhibition neuronale, ce qui est rendu possible grâce aux contrôles qui sont en place entre neurones inhibiteurs et excitateurs.
Il est connu que les personnes qui ont des acouphènes ont une hyperactivité du tronc cérébrale. Il s'agit de l'endroit où se trouvent des noyaux auditifs.
Comment cela peut s'expliquer ? Il est possible que ceci reflète une suractivation des certaines neurones en raison de la disparition des neurones inhibiteurs.
On pourrait également parler d'une forme de plasticité du cerveau.
"Silencing tinnitus" - "Mettre les acouphènes en sourdine"
"Silencing tinnitus" - "Mettre les acouphènes en sourdine"
CNRS, 13-03-2024
https://lejournal.cnrs.fr/articles/mettre-les-acouphenes-en-sourdine
The role of the brainstem in tinnitus
The role of the brainstem in tinnitus
The role of the brainstem in tinnitus is cited in the presentation "Role of the Brainstem in Tinnitus". A representative slide is shown in Figure 1.
Figure 1: On the left, role of the brainstem auditory nuclei (cochlear nuclei and inferior colliculi) in tinnitus. From Role of the Brainstem in Tinnitus. On the right, the brainstem.
An important cited article is "The Relation between Perception and Brain Activity in Gaze-Evoked Tinnitus" mentions that "increased tinnitus loudness is represented by increased activity in the cochlear nucleus (CN) and IC and reduced inhibition in the auditory cortex (AC)."
Please refer to the discussion paragraph starting with "The decrease of activity in the MGB and the reduced inhibition in the AC" which discusses the association of tinnitus with increased theta and decreased alpha activity of the brain as well as the locks of thalamocortical loops in theta resonance.
(MGB is characterized as “auditory thalamus”).
Brainstem evoked auditory potentials in tinnitus: A best-evidence synthesis and meta-analysis
Copyright © 2022 Jacxsens, De Pauw, Cardon, van der Wal, Jacquemin, Gilles, Michiels, Van Rompaey, Lammers and De Hertogh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.
"Tinnitus, or “ringing in the ears,” is the conscious perception of an auditory sensation in the absence of a corresponding auditory source. It is a very common symptom with a prevalence of 10–15% in an adult population (1)."
(...)
"Literature strongly suggests that the brainstem has a role in tinnitus generation and modulation, as well as in non-auditory comorbid conditions associated with tinnitus, such as neck disorders, anxiety, sleep disorders, difficulty concentrating, and depression (5). Animal studies have consistently shown disturbances in the level and patterns of spontaneous neural activity of brainstem auditory nuclei, linked with the onset of tinnitus. More specifically, these changes include increased spontaneous firing rates and bursting activity, which are both forms of hyperactivity, and increased neural synchrony (5–7). These disturbances are first found in the cochlear nucleus and inferior colliculus (8–11) and may be relayed to higher levels of the pathway (5).
On functional magnetic resonance imaging (fMRI) scans, increased resting state activity is also found in the auditory nuclei in the brainstem (12, 13). Multiple structures in the brainstem, including the cochlear nuclei and inferior colliculi, display abnormal function linked to tinnitus (12, 14, 15). It is important to remember that these brainstem structures send signals via multiple pathways to other brainstem and cortical regions, resulting in a cascade of changes directly associated with tinnitus generation (5).
Among clinical procedures to assess various levels of the auditory system, the most widely used involve auditory evoked potentials (AEPs) (16, 17). It is a technique that is used for the evaluation of neural activity in the auditory pathway, from cochlea to auditory cortex (18). AEPs are generally categorized in three classes according to their latency: short-, middle- and long-latency AEPs (Figure 1). Short-latency AEPs, often referred to as auditory brainstem responses (ABRs) (19), are scalp-recorded responses during the first 10 ms after stimulus onset. Brief acoustic stimuli, of which the “click” stimulus is used most often (20), activate the nerve fibers at the first part of the auditory pathway, from the most distal portion of the auditory nerve to the brainstem (21, 22). The generated impulses are recorded by surface electrodes placed on the scalp, forehead, and both mastoids (23). The readings consist of a sequence of up to 7 positive wave peaks, labeled with roman numerals I-VII (24). The proposed sources of waves I, III, and V of click ABR, which are the most reliably recorded waves (21), are the distal portion of the auditory nerve, the superior olivary nucleus, and the inferior colliculus, respectively (Figure 1) (25–27). The measurement of ABRs is a widely used technique in clinical practice to assess auditory function, and is especially of interest in populations that are difficult to test behaviorally, such as infants (22, 28).
Middle-latency AEPs, also referred to as middle-latency responses or MLRs, are believed to be generated in the thalamus, in subcortical regions and in the primary auditory cortex (29). MLRs consist of three positive (P0, Pa, Pb) and two negative peaks (Na, Nb) (19, 29). Long-latency AEPs are generally a product of the neocortex reflecting higher-order, cortical processing (30).
Additionally, the frequency-following response (FFR) is distinguished from other evoked potentials by precisely reflecting the neural processing of a sound's acoustic features (31, 32).
Figure 1. Schematic representation of the auditory pathway and corresponding AEP components through stimulation with a click. These components include the auditory short-latency responses or auditory brainstem responses (ABR) (waves I-VI) (blue), the auditory middle latency responses (N0-Pb) (red), and the auditory late-latency responses (N1-P3) (green). Localization of the neuronal generators of the ABR waves are also depicted. Created with BioRender.com, AEPs adapted from Burkard et al. (21), Lammers (29).
Conclusion
Conclusion
"Significantly longer latencies of ABR waves I, III, and V are shown in tinnitus patients with normal hearing compared to controls. This could be explained by a high frequency sensorineural hearing loss or other less known modulating factors such as cochlear synaptopathy or somatosensory tinnitus generators. No conclusions on possible changes at subcortical level could be drawn yet."
Please also refer to the article "Underlying Mechanisms of Tinnitus: Review and Clinical Implication" and particularly to the section "Current Understanding".
Thalamus: the brain “relay station” transmitting signals from different brain areas to the cortex.
Thalamus: the brain “relay station” transmitting signals from different brain areas to the cortex.
Tinnitus, Parkinson's, neurogenic pain and depression lock the thalamus in low-frequencies (delta/theta) which are propagated in the entire brain.
Inhibition release mechanisms lead simultaneously in specific areas to higher frequencies (beta/gamma).
Cf. "How brief sadness may evolve into depression"
Reading notes from https://www.pnas.org/doi/10.1073/pnas.96.26.15222 and also [1]
Tinnitus is associated with ear or auditory nerve damage (peripheral auditory system damage), in which case we have “peripheral deafferentation”. In such a case, there is loss or reduction of sensory input to the brain. We may refer to a form of sensory deprivation.
As a result, reduced sensory input is presented to the thalamus.
In the absence of excitatory input, thalamic cells undergo prolonged hyperpolarization, meaning that the membrane potential becomes more negative than the resting potential.
Hyperpolarization activates specific ionic channels, the T-type calcium channels, which open at low, negative membrane potentials and allow calcium ions to enter the neuron. As a result, rapid depolarization occurs, which leads to a burst of action potentials at a rate of 4 Hz (usually 2-7 spikes), called low-threshold spike (LTS) bursts.
As the thalamus is closely connected anatomically to the cortex creating numerous thalamocortical (TC) loops, bursting thalamic relay neurons exert a rhythmic influence on TC loops in the delta/theta frequency band. Thalamocortical circuits are being locked in delta/theta low-frequencies.
Upon “recruitment of a sufficiently large number of TC loops, excess delta/theta power becomes measurable.”
As these TC loops now function in low-frequencies, they exert less collateral inhibition on neighboring modules, which are thereby overactivated in high (beta/gamma) frequencies. This event has been termed "edge effect". The concept is inspired by the effect of lateral inhibition in the retina.”
Asymmetrical inhibition relationships between high frequency areas and neighboring low frequency cortical areas lead to reduced inhibition and thus activation of the latter. (Cf. auditory cortex).
In conclusion: Theta/delta spread, beta/gamma edge and cortex reduced inhibition.
[1] https://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-11-40
Earables, the ear-wearable devices, could monitor brain health and infer cognitive state.
Earables, the ear-wearable devices, could monitor brain health and infer cognitive state.
Cognitive load increases the tiny sounds that our ears make.
In other words, it increases the amplitude of otoacoustic emissions produced by the cochlea.
Standard earbuds with an integrated microphone could record them, thus "becoming a real-time, personalized, cognitive monitor", "enhancing productivity, helping workers manage overload, or offering early warnings of brain health issues," Dr. Dang said.
Note that Dr. Duncan had said that he had created such recording from many electromagnetically targeted individuals. As TIs are interested in the detection of V2K, he would also comment that in none of the cases would the recording be similar to what TIs were describing to be hearing.
Full article: https://dl.acm.org/doi/epdf/10.1145/3714394.3756157 (Creative Commons License)
"Earable acoustic sensing offers a powerful and non-invasive modality for capturing fine-grained auditory and physiological signals directly from the ear canal, enabling continuous and context-aware monitoring of cognitive states. As earable devices become increasingly embedded in daily life, they provide a unique opportunity to sense mental effort and perceptual load in real time through auditory interactions. In this study, we present the first investigation of cognitive load inference through auditory perception using acoustic signals captured by off-the-shelf in-ear devices. We designed speech-based listening tasks to induce varying levels of cognitive load, while concurrently embedding acoustic stimuli to evoke Stimulus Frequency Otoacoustic Emission (SFOAEs) as a proxy for cochlear responsiveness. Statistical analysis revealed a significant association (p < 0.01) between increased cognitive load and changes in auditory sensitivity, with 63.2% of participants showing peak sensitivity at 3 kHz. Notably, sensitivity patterns also varied across demographic subgroups, suggesting opportunities for personalized sensing. Our findings demonstrate that earable acoustic sensing can support scalable, real-time cognitive load monitoring in natural settings, laying a foundation for future applications in augmented cognition, where everyday auditory technologies adapt to and support the user’s mental state."
Page updated
Google Sites
Report abuse