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Umashankar, A.

Publications and source records attributed to Umashankar, A..

3 recordsLinked to original sources

Alterations in steady-state synchronisation between Acute and Chronic Tinnitus suggests reduction in both tinnitus and central gain.

The mechanism of tinnitus remains unclear as the generation and persistence of tinnitus is not widely understood. The acute tinnitus population serves as an ideal group for investigating the mechanisms behind the origin and persistence of tinnitus, from its initial onset to its subsequent chronification. One of the neural markers for measuring tinnitus such as neural synchrony or central gain is the Auditory Steady State Response (ASSR). The experiment was carried out on 39 participants with acute tinnitus (18 followed back six months post baseline), 30 with chronic tinnitus, and 27 controls. The results reveal that both cross sectionally and longitudinally, there were no significant differences in absolute amplitudes of ASSR across intensities and the slope of ASSR growth function between the groups. However, Controls tend to have an overall increase in ASSR amplitude when compared to Acute and Chronic Tinnitus which can be attributed to changes in neural synchronisation, attentional modulation, tinnitus-related distress, and diminished GABAergic inhibition coinciding with the presence of tinnitus. As there were no changes in the ASSR amplitude between Acute and Chronic Tinnitus or between Acute and Post Acute Tinnitus despite variations in distress and tinnitus loudness, we infer that auditory sensitivity/neural sensitvity is independent of the tinnitus.

neuroscience↗

Perceptual Novelty in Tinnitus a Causative Factor for its Persistence. A Stimulus Novelty Based P300 Paradigm on Acute, Chronic, and Non-Tinnitus Controls

Our understanding of tinnitus pathophysiology may be greatly advanced by understanding how the condition evolves from its initial onset or acute stage to its chronic manifestation. Such a transition likely reflects dynamic neurophysiological changes within central auditory and non-auditory networks. Previous studies have highlighted that individuals with acute tinnitus tend to have increased activity in the regions of anterior cingulate cortex, inferior parietal lobe, and insula all of which are essential in constituting the salience network. We therefore aimed at tapping into the salience network of tinnitus through a novelty based P300 paradigm in individuals with Acute, Post Acute (six months follow up since tinnitus onset) Chronic, and Controls. Participants were presented with an auditory oddball paradigm comprising three deviant types: (1) novel environmental sounds, (2) low-frequency tonal deviants, and (3) high-frequency tonal deviants, embedded within a sequence of frequent standard tones. Our results indicate a significant drop in P300 amplitude during the Post Acute stage across the three deviant stimuli, highlighting the substantial influence of the anterior cingulate cortex/salience network in possible generation of tinnitus and inferior parietal lobe in the persistence of tinnitus.

neuroscience↗

Evidence for a Transient State of Auditory Hypersensitivity During Initial Onset of Tinnitus, Evidenced by Intensity Dependence of the Auditory Evoked Potential (IDAEP)

Our understanding of tinnitus pathophysiology may be greatly advanced by understanding how the condition evolves from its initial onset or acute stage to its chronic manifestation. Such a transition likely reflects dynamic neurophysiological changes within central auditory and non-auditory networks. Our integrated model of tinnitus posits that sensory precision (sensory weighting) may be heightened during the acute stages of tinnitus to resolve degraded auditory input, but in chronic tinnitus, its role may diminish as plastic processes take over the percepts maintenance. Consequently, we hypothesize that bottom-up neural mechanisms linked to initiation of tinnitus, such as central gain and neural synchrony, are maximal around the time of tinnitus onset, but later subside by way of regression to the mean. We evaluated this hypothesis by measuring central auditory reactivity through the Intensity Dependence of Auditory Evoked Potential (IDAEP), a non-invasive index of higher-order inhibitory processing within the auditory system. A steeper IDAEP slope is associated with heightened sensory reactivity (higher sensitivity to changes in auditory stimuli), indicative of reduced central inhibition. Conversely, a shallower slope reflects greater inhibitory control. Studying a group with acute tinnitus (onset within six weeks), with a repeated assessment after six months from onset, we found an initially increased IDAEP slope in the acute stage, which had significantly reduced at follow-up, supporting our hypothesis that there is increased sensory reactivity during tinnitus onset, which need not persist in order for tinnitus to become chronic.

neuroscience↗