Hearing Noise Notch

If you believe that you have tinnitus, the first thing that you need to do is to get an evaluation from a doctor. He or she will be able to do a full physical exam to determine the extent of your tinnitus and make sure that it isn’t the result of a tumor or some other underlying physical condition. From there, you can use a hearing noise notch to reduce your symptoms.

What’s a Hearing Noise Notch?

Those who have tinnitus are going to have different volumes and frequencies that they hear even when no sound is present. The first step is to determine your tinnitus volume and create a notch in that frequency. Next, a software program will create sounds based on that volume that you need to listen to for at least an hour a day. You can listen to your hearing noise notch whenever it is convenient for you.

When Should You Listen to Your Notch?

Make sure that you listen to your notch at different times of the day to help reduce your sensitivity to different volumes and frequencies. For instance, if you listen to audio for 90 minutes a day, you should listen for a few minutes before breakfast, at lunch and then at some point before you go to bed at night. It is important that you listen at a reasonable volume to ensure that you don’t actually make your tinnitus worse.

What Happens If Symptoms Don’t Improve or Get Worse?

It is perfectly normal for the volume or frequency of your tinnitus to change during the course of your treatment. If this happens, make sure to talk to your doctor as soon as possible. Your doctor will examine you again to make sure that there are no new physical issues that may have caused the change. Then, you will once again go through the process of detecting your tinnitus volume and altering treatment to account for it.

Tinnitus can be a frustrating condition to live with. Even in a perfectly quiet environment, you may hear a ringing noise that won’t go away even when you are trying to sleep. While you may adjust to it over time, it can also have a profound impact on your life. With notch treatment, you can decrease the volume of your tinnitus, which will help you live a better quality of life now and into the future.

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Detecting Hearing Loss, Vertigo Via Blood Tests

On the one hand, the ability to detect inner-ear proteins as biomarkers of hearing loss and vestibular dysfunction from blood samples is very promising, but on the other, how hard is it to get the more primary care physicians to refer for a hearing test?

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Auditory Thalamic Circuits and GABAA Receptor Function: Putative Mechanisms in Tinnitus Pathology

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Donald M. Caspary, Daniel A. Llano
Tinnitus is defined as a phantom sound (ringing in the ears), and can significantly reduce the quality of life for those who suffer its effects. Ten to fifteen percent of the general adult population report symptoms of tinnitus with 1-2% reporting that tinnitus negatively impacts their quality of life. Noise exposure is the most common cause of tinnitus and the military environment presents many challenging high-noise situations. Military noise levels can be so intense that standard hearing protection is not adequate. Recent studies suggest a role for inhibitory neurotransmitter dysfunction in response to noise-induced peripheral deafferentation as a key element in the pathology of tinnitus. The auditory thalamus, or medial geniculate body (MGB), is an obligate auditory brain center in a unique position to gate the percept of sound as it projects to auditory cortex and to limbic structures. Both areas are thought to be involved in those individuals most impacted by tinnitus. For MGB, opposing hypotheses have posited either a tinnitus-related pathologic decrease or pathologic increase in GABAergic inhibition. In sensory thalamus, GABA mediates fast synaptic inhibition via synaptic GABAA receptors (GABAARs) as well as a persistent tonic inhibition via high-affinity extrasynaptic GABAARs and slow synaptic inhibition via GABABRs. Down-regulation of inhibitory neurotransmission, related to partial peripheral deafferentation, is consistently presented as partially underpinning neuronal hyperactivity seen in animal models of tinnitus. This maladaptive plasticity/Gain Control Theory of tinnitus pathology (see Auerbach et al., 2014; Richardson et al., 2012) is characterized by reduced inhibition associated with increased spontaneous and abnormal neuronal activity, including bursting and increased synchrony throughout much of the central auditory pathway. A competing hypothesis suggests that maladaptive oscillations between the MGB and auditory cortex, thalamocortical dysrhythmia, predicts tinnitus pathology (De Ridder et al., 2015). These unusual oscillations/rhythms reflect net increased tonic inhibition in a subset of thalamocortical projection neurons resulting in abnormal bursting. Hyperpolarizing de-inactivation of t-type Ca2+ channels switches thalamocortical projection neurons into burst mode. Thalamocortical dysrhythmia originating in sensory thalamus has been postulated to underpin neuropathies including tinnitus and chronic pain. Here we review the relationship between noise-induced tinnitus and altered inhibition in the MGB.



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Endothelin-1 Mediated Induction of Extracellular Matrix Genes in Strial Marginal Cells Underlies Strial Pathology in Alport Mice

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Daniel T. Meehan, Duane Delimont, Brianna Dufek, Marisa Zallocchi, Grady Phillips, Michael Anne Gratton, Dominic Cosgrove
Alport syndrome, a type IV collagen disorder, manifests as glomerular disease associated with hearing loss with thickening of the glomerular and strial capillary basement membranes (SCBMs). We have identified a role for endothelin-1 (ET-1) activation of endothelin A receptors (ETARs) in glomerular pathogenesis. Here we explore whether ET-1 plays a role in strial pathology. Wild type (WT) and Alport mice were treated with the ETAR antagonist, sitaxentan. The stria vascularis was analyzed for SCBM thickness and for extracellular matrix (ECM) proteins. Additional WT and Alport mice were exposed to noise or hypoxia and the stria analyzed for hypoxia-related and ECM genes. A strial marginal cell line cultured under hypoxic conditions, or stimulated with ET-1 was analyzed for expression of hypoxia-related and ECM transcripts. Noise exposure resulted in significantly elevated ABR thresholds in Alport mice relative to wild type littermates. Alport stria showed elevated expression of collagen α1(IV), laminin α2, and laminin α5 proteins relative to WT. SCBM thickening and elevated ECM protein expression was ameliorated by ETAR blockade. Stria from normoxic Alport mice and hypoxic WT mice showed upregulation of hypoxia-related, ECM, and ET-1 transcripts. Both ET-1 stimulation and hypoxia up-regulated ECM transcripts in cultured marginal cells. We conclude that ET-1 mediated activation of ETARs on strial marginal cells results in elevated expression of ECM genes and thickening of the SCBMs in Alport mice. SCBM thickening results in hypoxic stress further elevating ECM and ET-1 gene expression, exacerbating strial pathology.



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Auditory Thalamic Circuits and GABAA Receptor Function: Putative Mechanisms in Tinnitus Pathology

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Donald M. Caspary, Daniel A. Llano
Tinnitus is defined as a phantom sound (ringing in the ears), and can significantly reduce the quality of life for those who suffer its effects. Ten to fifteen percent of the general adult population report symptoms of tinnitus with 1-2% reporting that tinnitus negatively impacts their quality of life. Noise exposure is the most common cause of tinnitus and the military environment presents many challenging high-noise situations. Military noise levels can be so intense that standard hearing protection is not adequate. Recent studies suggest a role for inhibitory neurotransmitter dysfunction in response to noise-induced peripheral deafferentation as a key element in the pathology of tinnitus. The auditory thalamus, or medial geniculate body (MGB), is an obligate auditory brain center in a unique position to gate the percept of sound as it projects to auditory cortex and to limbic structures. Both areas are thought to be involved in those individuals most impacted by tinnitus. For MGB, opposing hypotheses have posited either a tinnitus-related pathologic decrease or pathologic increase in GABAergic inhibition. In sensory thalamus, GABA mediates fast synaptic inhibition via synaptic GABAA receptors (GABAARs) as well as a persistent tonic inhibition via high-affinity extrasynaptic GABAARs and slow synaptic inhibition via GABABRs. Down-regulation of inhibitory neurotransmission, related to partial peripheral deafferentation, is consistently presented as partially underpinning neuronal hyperactivity seen in animal models of tinnitus. This maladaptive plasticity/Gain Control Theory of tinnitus pathology (see Auerbach et al., 2014; Richardson et al., 2012) is characterized by reduced inhibition associated with increased spontaneous and abnormal neuronal activity, including bursting and increased synchrony throughout much of the central auditory pathway. A competing hypothesis suggests that maladaptive oscillations between the MGB and auditory cortex, thalamocortical dysrhythmia, predicts tinnitus pathology (De Ridder et al., 2015). These unusual oscillations/rhythms reflect net increased tonic inhibition in a subset of thalamocortical projection neurons resulting in abnormal bursting. Hyperpolarizing de-inactivation of t-type Ca2+ channels switches thalamocortical projection neurons into burst mode. Thalamocortical dysrhythmia originating in sensory thalamus has been postulated to underpin neuropathies including tinnitus and chronic pain. Here we review the relationship between noise-induced tinnitus and altered inhibition in the MGB.



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Endothelin-1 Mediated Induction of Extracellular Matrix Genes in Strial Marginal Cells Underlies Strial Pathology in Alport Mice

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Daniel T. Meehan, Duane Delimont, Brianna Dufek, Marisa Zallocchi, Grady Phillips, Michael Anne Gratton, Dominic Cosgrove
Alport syndrome, a type IV collagen disorder, manifests as glomerular disease associated with hearing loss with thickening of the glomerular and strial capillary basement membranes (SCBMs). We have identified a role for endothelin-1 (ET-1) activation of endothelin A receptors (ETARs) in glomerular pathogenesis. Here we explore whether ET-1 plays a role in strial pathology. Wild type (WT) and Alport mice were treated with the ETAR antagonist, sitaxentan. The stria vascularis was analyzed for SCBM thickness and for extracellular matrix (ECM) proteins. Additional WT and Alport mice were exposed to noise or hypoxia and the stria analyzed for hypoxia-related and ECM genes. A strial marginal cell line cultured under hypoxic conditions, or stimulated with ET-1 was analyzed for expression of hypoxia-related and ECM transcripts. Noise exposure resulted in significantly elevated ABR thresholds in Alport mice relative to wild type littermates. Alport stria showed elevated expression of collagen α1(IV), laminin α2, and laminin α5 proteins relative to WT. SCBM thickening and elevated ECM protein expression was ameliorated by ETAR blockade. Stria from normoxic Alport mice and hypoxic WT mice showed upregulation of hypoxia-related, ECM, and ET-1 transcripts. Both ET-1 stimulation and hypoxia up-regulated ECM transcripts in cultured marginal cells. We conclude that ET-1 mediated activation of ETARs on strial marginal cells results in elevated expression of ECM genes and thickening of the SCBMs in Alport mice. SCBM thickening results in hypoxic stress further elevating ECM and ET-1 gene expression, exacerbating strial pathology.



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Auditory Thalamic Circuits and GABAA Receptor Function: Putative Mechanisms in Tinnitus Pathology

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Donald M. Caspary, Daniel A. Llano
Tinnitus is defined as a phantom sound (ringing in the ears), and can significantly reduce the quality of life for those who suffer its effects. Ten to fifteen percent of the general adult population report symptoms of tinnitus with 1-2% reporting that tinnitus negatively impacts their quality of life. Noise exposure is the most common cause of tinnitus and the military environment presents many challenging high-noise situations. Military noise levels can be so intense that standard hearing protection is not adequate. Recent studies suggest a role for inhibitory neurotransmitter dysfunction in response to noise-induced peripheral deafferentation as a key element in the pathology of tinnitus. The auditory thalamus, or medial geniculate body (MGB), is an obligate auditory brain center in a unique position to gate the percept of sound as it projects to auditory cortex and to limbic structures. Both areas are thought to be involved in those individuals most impacted by tinnitus. For MGB, opposing hypotheses have posited either a tinnitus-related pathologic decrease or pathologic increase in GABAergic inhibition. In sensory thalamus, GABA mediates fast synaptic inhibition via synaptic GABAA receptors (GABAARs) as well as a persistent tonic inhibition via high-affinity extrasynaptic GABAARs and slow synaptic inhibition via GABABRs. Down-regulation of inhibitory neurotransmission, related to partial peripheral deafferentation, is consistently presented as partially underpinning neuronal hyperactivity seen in animal models of tinnitus. This maladaptive plasticity/Gain Control Theory of tinnitus pathology (see Auerbach et al., 2014; Richardson et al., 2012) is characterized by reduced inhibition associated with increased spontaneous and abnormal neuronal activity, including bursting and increased synchrony throughout much of the central auditory pathway. A competing hypothesis suggests that maladaptive oscillations between the MGB and auditory cortex, thalamocortical dysrhythmia, predicts tinnitus pathology (De Ridder et al., 2015). These unusual oscillations/rhythms reflect net increased tonic inhibition in a subset of thalamocortical projection neurons resulting in abnormal bursting. Hyperpolarizing de-inactivation of t-type Ca2+ channels switches thalamocortical projection neurons into burst mode. Thalamocortical dysrhythmia originating in sensory thalamus has been postulated to underpin neuropathies including tinnitus and chronic pain. Here we review the relationship between noise-induced tinnitus and altered inhibition in the MGB.



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Endothelin-1 Mediated Induction of Extracellular Matrix Genes in Strial Marginal Cells Underlies Strial Pathology in Alport Mice

Publication date: Available online 21 August 2016
Source:Hearing Research
Author(s): Daniel T. Meehan, Duane Delimont, Brianna Dufek, Marisa Zallocchi, Grady Phillips, Michael Anne Gratton, Dominic Cosgrove
Alport syndrome, a type IV collagen disorder, manifests as glomerular disease associated with hearing loss with thickening of the glomerular and strial capillary basement membranes (SCBMs). We have identified a role for endothelin-1 (ET-1) activation of endothelin A receptors (ETARs) in glomerular pathogenesis. Here we explore whether ET-1 plays a role in strial pathology. Wild type (WT) and Alport mice were treated with the ETAR antagonist, sitaxentan. The stria vascularis was analyzed for SCBM thickness and for extracellular matrix (ECM) proteins. Additional WT and Alport mice were exposed to noise or hypoxia and the stria analyzed for hypoxia-related and ECM genes. A strial marginal cell line cultured under hypoxic conditions, or stimulated with ET-1 was analyzed for expression of hypoxia-related and ECM transcripts. Noise exposure resulted in significantly elevated ABR thresholds in Alport mice relative to wild type littermates. Alport stria showed elevated expression of collagen α1(IV), laminin α2, and laminin α5 proteins relative to WT. SCBM thickening and elevated ECM protein expression was ameliorated by ETAR blockade. Stria from normoxic Alport mice and hypoxic WT mice showed upregulation of hypoxia-related, ECM, and ET-1 transcripts. Both ET-1 stimulation and hypoxia up-regulated ECM transcripts in cultured marginal cells. We conclude that ET-1 mediated activation of ETARs on strial marginal cells results in elevated expression of ECM genes and thickening of the SCBMs in Alport mice. SCBM thickening results in hypoxic stress further elevating ECM and ET-1 gene expression, exacerbating strial pathology.



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Influence of a rhythmic auditory stimulation on asymptomatic gait

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Céline Schreiber, Angélique Remacle, Frédéric Chantraine, Elizabeth Kolanowski, Florent Moissenet
The direct effects of a rhythmic auditory stimulation (RAS) on the gait of asymptomatic subjects are not clear. Previous studies only showed modifications in the gastrocnemius activity, inconsistent effects on temporal parameters, and no modification of spatial parameters. Furthermore, the influence of RAS on kinematics and kinetics has only been reported in pathological gait. The objective of this study was to perform a full comparison of gait characteristics in asymptomatic subjects at preferred and reduced walking speed between without and with RAS conditions. Spatiotemporal parameters, kinematics, kinetics and EMG signals datasets were collected for each condition. RAS conditions were obtained by asking subjects to walk on metronomic beats. 17 asymptomatic subjects were included in the study (12M/5W, 37.4±15.7years, 74.0±14.8kg, 1.77±0.09m). Comparisons between without and with RAS conditions were then performed using the Statistical Parametric Mapping method. For all combined subjects, the effect of RAS was limited whatever the walking speed. Meanwhile, global effects were observed for kinematics, kinetics and EMG at both spontaneous and reduced walking speed, which can only be explained by covariances (i.e., no effect on individual time-series). The use of RAS to impose a specific cadence matching the desired walking speed (e.g., to collect normative data) appears thus possible, as none parameters were modified individually. However, RAS should be used with caution taking into account covariances (i.e., muscle synergy or joint coordination patterns). This study has to be extended to a larger number of subjects to confirm these observations.



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Quantifying accommodation to prosthesis interventions in persons with lower limb loss

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Goeran Fiedler, Xueyi Zhang
Determining the appropriate amount of accommodation time is an important component of research protocol design in the field of limb prosthetics. Insufficiently short or excessively long accommodation periods may limit the external validity of findings and/or the economic efficiency and ethical innocuousness of a study. However, issuing general recommendations is difficult, as individual accommodation periods are affected by subject characteristics, the nature of the intervention, and possibly a number of environmental factors.We are discussing an approach to determine individual accommodation times based on the assumption that the process of becoming accustomed to a prosthetic intervention follows a similar exponential “learning curve” as many other learning processes that have been previously investigated. Initial data collected with a small subject sample gives some indication that gait cycle symmetry changes along the hypothesized curve trajectory. If those preliminary results can be confirmed it may be possible to extrapolate a subject’s eventual level of accommodation based on a small data set that is easily collected during the first twenty minutes after introducing a prosthetic intervention.



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Influence of a rhythmic auditory stimulation on asymptomatic gait

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Céline Schreiber, Angélique Remacle, Frédéric Chantraine, Elizabeth Kolanowski, Florent Moissenet
The direct effects of a rhythmic auditory stimulation (RAS) on the gait of asymptomatic subjects are not clear. Previous studies only showed modifications in the gastrocnemius activity, inconsistent effects on temporal parameters, and no modification of spatial parameters. Furthermore, the influence of RAS on kinematics and kinetics has only been reported in pathological gait. The objective of this study was to perform a full comparison of gait characteristics in asymptomatic subjects at preferred and reduced walking speed between without and with RAS conditions. Spatiotemporal parameters, kinematics, kinetics and EMG signals datasets were collected for each condition. RAS conditions were obtained by asking subjects to walk on metronomic beats. 17 asymptomatic subjects were included in the study (12M/5W, 37.4±15.7years, 74.0±14.8kg, 1.77±0.09m). Comparisons between without and with RAS conditions were then performed using the Statistical Parametric Mapping method. For all combined subjects, the effect of RAS was limited whatever the walking speed. Meanwhile, global effects were observed for kinematics, kinetics and EMG at both spontaneous and reduced walking speed, which can only be explained by covariances (i.e., no effect on individual time-series). The use of RAS to impose a specific cadence matching the desired walking speed (e.g., to collect normative data) appears thus possible, as none parameters were modified individually. However, RAS should be used with caution taking into account covariances (i.e., muscle synergy or joint coordination patterns). This study has to be extended to a larger number of subjects to confirm these observations.



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Quantifying accommodation to prosthesis interventions in persons with lower limb loss

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Goeran Fiedler, Xueyi Zhang
Determining the appropriate amount of accommodation time is an important component of research protocol design in the field of limb prosthetics. Insufficiently short or excessively long accommodation periods may limit the external validity of findings and/or the economic efficiency and ethical innocuousness of a study. However, issuing general recommendations is difficult, as individual accommodation periods are affected by subject characteristics, the nature of the intervention, and possibly a number of environmental factors.We are discussing an approach to determine individual accommodation times based on the assumption that the process of becoming accustomed to a prosthetic intervention follows a similar exponential “learning curve” as many other learning processes that have been previously investigated. Initial data collected with a small subject sample gives some indication that gait cycle symmetry changes along the hypothesized curve trajectory. If those preliminary results can be confirmed it may be possible to extrapolate a subject’s eventual level of accommodation based on a small data set that is easily collected during the first twenty minutes after introducing a prosthetic intervention.



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via IFTTT

Influence of a rhythmic auditory stimulation on asymptomatic gait

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Céline Schreiber, Angélique Remacle, Frédéric Chantraine, Elizabeth Kolanowski, Florent Moissenet
The direct effects of a rhythmic auditory stimulation (RAS) on the gait of asymptomatic subjects are not clear. Previous studies only showed modifications in the gastrocnemius activity, inconsistent effects on temporal parameters, and no modification of spatial parameters. Furthermore, the influence of RAS on kinematics and kinetics has only been reported in pathological gait. The objective of this study was to perform a full comparison of gait characteristics in asymptomatic subjects at preferred and reduced walking speed between without and with RAS conditions. Spatiotemporal parameters, kinematics, kinetics and EMG signals datasets were collected for each condition. RAS conditions were obtained by asking subjects to walk on metronomic beats. 17 asymptomatic subjects were included in the study (12M/5W, 37.4±15.7years, 74.0±14.8kg, 1.77±0.09m). Comparisons between without and with RAS conditions were then performed using the Statistical Parametric Mapping method. For all combined subjects, the effect of RAS was limited whatever the walking speed. Meanwhile, global effects were observed for kinematics, kinetics and EMG at both spontaneous and reduced walking speed, which can only be explained by covariances (i.e., no effect on individual time-series). The use of RAS to impose a specific cadence matching the desired walking speed (e.g., to collect normative data) appears thus possible, as none parameters were modified individually. However, RAS should be used with caution taking into account covariances (i.e., muscle synergy or joint coordination patterns). This study has to be extended to a larger number of subjects to confirm these observations.



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via IFTTT

Quantifying accommodation to prosthesis interventions in persons with lower limb loss

Publication date: October 2016
Source:Gait & Posture, Volume 50
Author(s): Goeran Fiedler, Xueyi Zhang
Determining the appropriate amount of accommodation time is an important component of research protocol design in the field of limb prosthetics. Insufficiently short or excessively long accommodation periods may limit the external validity of findings and/or the economic efficiency and ethical innocuousness of a study. However, issuing general recommendations is difficult, as individual accommodation periods are affected by subject characteristics, the nature of the intervention, and possibly a number of environmental factors.We are discussing an approach to determine individual accommodation times based on the assumption that the process of becoming accustomed to a prosthetic intervention follows a similar exponential “learning curve” as many other learning processes that have been previously investigated. Initial data collected with a small subject sample gives some indication that gait cycle symmetry changes along the hypothesized curve trajectory. If those preliminary results can be confirmed it may be possible to extrapolate a subject’s eventual level of accommodation based on a small data set that is easily collected during the first twenty minutes after introducing a prosthetic intervention.



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