The Spatial Release of Cognitive Load in Cocktail Party Is Determined by the Relative Levels of the Talkers

Abstract

In a multi-talker situation, spatial separation between talkers reduces cognitive processing load: this is the “spatial release of cognitive load”. The present study investigated the role played by the relative levels of the talkers on this spatial release of cognitive load. During the experiment, participants had to report the speech emitted by a target talker in the presence of a concurrent masker talker. The spatial separation (0° and 120° angular distance in azimuth) and the relative levels of the talkers (adverse, intermediate, and favorable target-to-masker ratio) were manipulated. The cognitive load was assessed with a prefrontal functional near-infrared spectroscopy. Data from 14 young normal-hearing listeners revealed that the target-to-masker ratio had a direct impact on the spatial release of cognitive load. Spatial separation significantly reduced the prefrontal activity only for the intermediate target-to-masker ratio and had no effect on prefrontal activity for the favorable and the adverse target-to-masker ratios. Therefore, the relative levels of the talkers might be a key point to determine the spatial release of cognitive load and more specifically the prefrontal activity induced by spatial cues in multi-talker situations.

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Remission of Tinnitus

Tinnitus is a condition in which sufferers hear sounds without anything that might be causing the sound. It often manifests as a high pitched whine or ringing in the ears, but some sufferers hear a lower sound like a background growl or rumble. Some even report a sensation like a barely-heard conversation that can’t be made out. Whatever form it takes, it is usually unpleasant to deal with.

Side effects of tinnitus are varied and frustrating. A common effect is to be kept awake by the constant perception of sound. As the house gets quiet when you go to bed, it’s easier to notice the sound. Knowing that the sound can keep you up also causes anxiety in some sufferers; they know they’re going to have to deal with the sound, and feel helpless to deal with it.

Remission of Tinnitus

There are unfortunately not many treatment options that can help deal with tinnitus or put it into remission. Many doctors have observed that tinnitus will go into remission on its own, but if it has not done so within two years of manifesting, it is likely permanent. Spontaneous remission like this is usually observed in tinnitus caused as a side-effect of loud noises such as explosions.

Medical Options

Some medicines can produce a temporary remission of tinnitus symptoms. Benzodiazepan medicines such as clonozepam and alprazolam have shown an effect in about half of the patients who take them for tinnitus symptoms. The problem is, these medications have a strong effect on the nervous system; in fact, they are anti-anxiety medications used to treat serious mood disorders and conditions. They have the potential to be addictive. To make the news even better, going off the medication usually brings back the tinnitus at a stronger level than before the medicine was prescribed.

Distracting Sounds

While the remission of tinnitus might sound like it’s too much to hope for, there are some techniques that can help. Tinnitus is the perception of sound in the absence of a cause. Some patients find that providing a distraction sound can help. For example, an audiobook, white noise generator, or podcast could be played on a soft setting at bedtime, and the brain will listen to it and temporarily forget to pay attention to the tinnitus.

Ultimately, a doctor can probably help you diagnose the condition of tinnitus, but the remission of tinnitus is not something that is easily achieved.

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Problemas del lenguaje en niños con parálisis cerebral

Publication date: Available online 17 January 2017
Source:Revista de Logopedia, Foniatría y Audiología
Author(s): Remedios Rivera Velázquez, Antoinette Hawayek González, Rubén Román Ramos, Ignacio Méndez Ramírez, Luis Rodríguez Fernández
La parálisis cerebral es una lesión no progresiva en las estructuras cerebrales que genera un trastorno del movimiento y de la postura. Estas lesiones también pueden afectar otras áreas responsables del desarrollo del lenguaje, tales como el sistema del habla, el sistema lingüístico o el procesamiento léxico, además de conllevar otras comorbilidades en diversas áreas.Objetivo. Constatar el desarrollo del sistema lingüístico mediante la longitud media de los enunciados verbales y analizar el desempeño del procesamiento léxico que presentaron 142 niños mexicanos con parálisis cerebral cuyas edades comprendían de los 7 a los 13 años.Material y métodosMediante una elicitación de datos controlados la población debían nombrar 107 entidades clasificadas en 12 campos semánticos y contar el cuento Frog, Where are you? («Dónde está la ranita») siguiendo las imágenes de la historia para comprobar su longitud media de los enunciados verbales.ResultsSolo el 16.9% de estos niños lograron nombrar más de 50 imágenes y contar el cuento que se les había mostrado. La longitud media de los enunciados verbales solo correspondió con la edad cronológica de un solo niño; el resto estuvo por debajo de lo esperado. El 83.1% de los 142 niños con parálisis cerebral evaluados no lograron emitir más de 10 palabras en ambas elicitaciones.Cerebral palsy is a non-progressive lesion in the brain structures that generates a disorder of movement and posture. These lesions can also affect other areas responsible for the language development system such as speech, linguistic or lexical retrieval system, as well as leading to other comorbidities in various areas.ObjectiveTo observe the development of the language system using the Mean Length of Utterance and an analysis of the lexical retrieval presented in 142 Mexican children with cerebral palsy with ages ranging from 7 to 13 years.Material and methodsUsing controlled data elicitation, the children with Cerebral Palsy were to name 107 entities (images) classified into 12 semantic fields and tell a story about «Frog, Where are you?», following the images of the story in order to check the Mean Length of Utterances.ResultsOnly 16.9% of these children were able to name more than 50 images that were shown and tell a story. The Mean Length of Utterance only corresponded with the chronological age in just one child, with the rest being lower than expected. The vast majority (83.1%) of the 142 children with palsy cerebral assessed did not exceed 10 words.



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Problemas del lenguaje en niños con parálisis cerebral

Publication date: Available online 17 January 2017
Source:Revista de Logopedia, Foniatría y Audiología
Author(s): Remedios Rivera Velázquez, Antoinette Hawayek González, Rubén Román Ramos, Ignacio Méndez Ramírez, Luis Rodríguez Fernández
La parálisis cerebral es una lesión no progresiva en las estructuras cerebrales que genera un trastorno del movimiento y de la postura. Estas lesiones también pueden afectar otras áreas responsables del desarrollo del lenguaje, tales como el sistema del habla, el sistema lingüístico o el procesamiento léxico, además de conllevar otras comorbilidades en diversas áreas.Objetivo. Constatar el desarrollo del sistema lingüístico mediante la longitud media de los enunciados verbales y analizar el desempeño del procesamiento léxico que presentaron 142 niños mexicanos con parálisis cerebral cuyas edades comprendían de los 7 a los 13 años.Material y métodosMediante una elicitación de datos controlados la población debían nombrar 107 entidades clasificadas en 12 campos semánticos y contar el cuento Frog, Where are you? («Dónde está la ranita») siguiendo las imágenes de la historia para comprobar su longitud media de los enunciados verbales.ResultsSolo el 16.9% de estos niños lograron nombrar más de 50 imágenes y contar el cuento que se les había mostrado. La longitud media de los enunciados verbales solo correspondió con la edad cronológica de un solo niño; el resto estuvo por debajo de lo esperado. El 83.1% de los 142 niños con parálisis cerebral evaluados no lograron emitir más de 10 palabras en ambas elicitaciones.Cerebral palsy is a non-progressive lesion in the brain structures that generates a disorder of movement and posture. These lesions can also affect other areas responsible for the language development system such as speech, linguistic or lexical retrieval system, as well as leading to other comorbidities in various areas.ObjectiveTo observe the development of the language system using the Mean Length of Utterance and an analysis of the lexical retrieval presented in 142 Mexican children with cerebral palsy with ages ranging from 7 to 13 years.Material and methodsUsing controlled data elicitation, the children with Cerebral Palsy were to name 107 entities (images) classified into 12 semantic fields and tell a story about «Frog, Where are you?», following the images of the story in order to check the Mean Length of Utterances.ResultsOnly 16.9% of these children were able to name more than 50 images that were shown and tell a story. The Mean Length of Utterance only corresponded with the chronological age in just one child, with the rest being lower than expected. The vast majority (83.1%) of the 142 children with palsy cerebral assessed did not exceed 10 words.



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Problemas del lenguaje en niños con parálisis cerebral

Publication date: Available online 17 January 2017
Source:Revista de Logopedia, Foniatría y Audiología
Author(s): Remedios Rivera Velázquez, Antoinette Hawayek González, Rubén Román Ramos, Ignacio Méndez Ramírez, Luis Rodríguez Fernández
La parálisis cerebral es una lesión no progresiva en las estructuras cerebrales que genera un trastorno del movimiento y de la postura. Estas lesiones también pueden afectar otras áreas responsables del desarrollo del lenguaje, tales como el sistema del habla, el sistema lingüístico o el procesamiento léxico, además de conllevar otras comorbilidades en diversas áreas.Objetivo. Constatar el desarrollo del sistema lingüístico mediante la longitud media de los enunciados verbales y analizar el desempeño del procesamiento léxico que presentaron 142 niños mexicanos con parálisis cerebral cuyas edades comprendían de los 7 a los 13 años.Material y métodosMediante una elicitación de datos controlados la población debían nombrar 107 entidades clasificadas en 12 campos semánticos y contar el cuento Frog, Where are you? («Dónde está la ranita») siguiendo las imágenes de la historia para comprobar su longitud media de los enunciados verbales.ResultsSolo el 16.9% de estos niños lograron nombrar más de 50 imágenes y contar el cuento que se les había mostrado. La longitud media de los enunciados verbales solo correspondió con la edad cronológica de un solo niño; el resto estuvo por debajo de lo esperado. El 83.1% de los 142 niños con parálisis cerebral evaluados no lograron emitir más de 10 palabras en ambas elicitaciones.Cerebral palsy is a non-progressive lesion in the brain structures that generates a disorder of movement and posture. These lesions can also affect other areas responsible for the language development system such as speech, linguistic or lexical retrieval system, as well as leading to other comorbidities in various areas.ObjectiveTo observe the development of the language system using the Mean Length of Utterance and an analysis of the lexical retrieval presented in 142 Mexican children with cerebral palsy with ages ranging from 7 to 13 years.Material and methodsUsing controlled data elicitation, the children with Cerebral Palsy were to name 107 entities (images) classified into 12 semantic fields and tell a story about «Frog, Where are you?», following the images of the story in order to check the Mean Length of Utterances.ResultsOnly 16.9% of these children were able to name more than 50 images that were shown and tell a story. The Mean Length of Utterance only corresponded with the chronological age in just one child, with the rest being lower than expected. The vast majority (83.1%) of the 142 children with palsy cerebral assessed did not exceed 10 words.



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Different Phenotypes of the Two Chinese Probands with the Same c.889G>A (p.C162Y) Mutation in COCH Gene Verify Different Mechanisms Underlying Autosomal Dominant Nonsyndromic Deafness 9

by Qi Wang, Peipei Fei, Hongbo Gu, Yanmei Zhang, Xiaomei Ke, Yuhe Liu

Objectives

By analyzing the different phenotypes of two Chinese DFNA9 families with the same mutation located in the intervening region between the LCCL and vWFA domains of cochlin and testing the functional changes in the mutant cochlin, we investigated the different pathogeneses for mutations in LCCL and vWFA domains.

Methods

Targeted next-generation sequencing for deafness-related genes was used to identify the mutation in the proband in family #208. The probands of family #208 and family #32 with the same p.C162Y mutation were followed for more than 3 years to evaluate the progression of hearing loss and vestibular dysfunction using pure-tone audiometry, caloric testing, electrocochleogram, vestibular-evoked myogenic potential, and video head-impulse test. The disruption of normal cleavage to produce secreted LCCL domain fragments and the tendency to form aggregations of mutant cochlins were tested by in vitro cell experiments.

Results

The two families showed different clinical symptoms. Family #32 was identified as having early-onset, progressive sensorineural hearing loss, similar to the symptoms in DFNA9 patients with cochlin mutations in the vWFA domain. The proband of family #208 endured late-onset recurrent paroxysmal vertigo attacks and progressively deteriorating hearing, similar to symptoms in those with cochlin mutations in the LCCL domain. We therefore suggest that the disrupted cleavage of the LCCL domain fragment is likely to cause vestibular dysfunction, and aggregation of mutant cochlin caused by mutations in the vWFA domain is responsible for early-onset hearing loss. The p.C162Y mutation causes either disruption of LCCL domain fragment cleavage or aggregation of mutant cochlin, resulting in the different phenotypes in the two families.

Conclusion

This study demonstrates that DFNA9 families with the same genotype may have significantly different phenotypes. The mutation site in cochlin is related to the pathological mechanism underlying the different phenotypes.

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Different Phenotypes of the Two Chinese Probands with the Same c.889G>A (p.C162Y) Mutation in COCH Gene Verify Different Mechanisms Underlying Autosomal Dominant Nonsyndromic Deafness 9

by Qi Wang, Peipei Fei, Hongbo Gu, Yanmei Zhang, Xiaomei Ke, Yuhe Liu

Objectives

By analyzing the different phenotypes of two Chinese DFNA9 families with the same mutation located in the intervening region between the LCCL and vWFA domains of cochlin and testing the functional changes in the mutant cochlin, we investigated the different pathogeneses for mutations in LCCL and vWFA domains.

Methods

Targeted next-generation sequencing for deafness-related genes was used to identify the mutation in the proband in family #208. The probands of family #208 and family #32 with the same p.C162Y mutation were followed for more than 3 years to evaluate the progression of hearing loss and vestibular dysfunction using pure-tone audiometry, caloric testing, electrocochleogram, vestibular-evoked myogenic potential, and video head-impulse test. The disruption of normal cleavage to produce secreted LCCL domain fragments and the tendency to form aggregations of mutant cochlins were tested by in vitro cell experiments.

Results

The two families showed different clinical symptoms. Family #32 was identified as having early-onset, progressive sensorineural hearing loss, similar to the symptoms in DFNA9 patients with cochlin mutations in the vWFA domain. The proband of family #208 endured late-onset recurrent paroxysmal vertigo attacks and progressively deteriorating hearing, similar to symptoms in those with cochlin mutations in the LCCL domain. We therefore suggest that the disrupted cleavage of the LCCL domain fragment is likely to cause vestibular dysfunction, and aggregation of mutant cochlin caused by mutations in the vWFA domain is responsible for early-onset hearing loss. The p.C162Y mutation causes either disruption of LCCL domain fragment cleavage or aggregation of mutant cochlin, resulting in the different phenotypes in the two families.

Conclusion

This study demonstrates that DFNA9 families with the same genotype may have significantly different phenotypes. The mutation site in cochlin is related to the pathological mechanism underlying the different phenotypes.

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