scholarly journals Invoking the influence of emotion in central auditory processing to improve the treatment of speech impairments

2021 ◽  
Vol 42 (12) ◽  
pp. 1325-1332
Author(s):  
Safa Alqudah ◽  
Maha Zaitoun ◽  
Sara Alqudah
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Joseph P. Pillion

Deficits in central auditory processing may occur in a variety of clinical conditions including traumatic brain injury, neurodegenerative disease, auditory neuropathy/dyssynchrony syndrome, neurological disorders associated with aging, and aphasia. Deficits in central auditory processing of a more subtle nature have also been studied extensively in neurodevelopmental disorders in children with learning disabilities, ADD, and developmental language disorders. Illustrative cases are reviewed demonstrating the use of an audiological test battery in patients with auditory neuropathy/dyssynchrony syndrome, bilateral lesions to the inferior colliculi, and bilateral lesions to the temporal lobes. Electrophysiological tests of auditory function were utilized to define the locus of dysfunction at neural levels ranging from the auditory nerve, midbrain, and cortical levels.


Author(s):  
Anna Rasmus ◽  
Aleksandra Błachnio

Background: Language communication, which is one of the basic forms of building and maintaining interpersonal relationships, deteriorates in elder age. One of the probable causes is a decline in auditory functioning, including auditory central processing. The aim of the present study is to evaluate the profile of central auditory processing disorders in the elderly as well as the relationship between these disorders and the perception of emotional and linguistic prosody. Methods: The Right Hemisphere Language Battery (RHLB-PL), and the Brain-Boy Universal Professional (BUP) were used. Results: There are statistically significant relationships between emotional prosody and: spatial hearing (r(18) = 0.46, p = 0.04); the time of the reaction (r(18) = 0.49, p = 0.03); recognizing the frequency pattern (r(18) = 0.49, p = 0.03 (4); and recognizing the duration pattern (r(18) = 0.45, p = 0.05. There are statistically significant correlations between linguistic prosody and: pitch discrimination (r(18) = 0.5, p = 0.02); recognition of the frequency pattern (r(18) = 0.55, p = 0.01); recognition of the temporal pattern; and emotional prosody (r(18) = 0.58, p = 0.01). Conclusions: The analysis of the disturbed components of auditory central processing among the tested samples showed a reduction in the functions related to frequency differentiation, the recognition of the temporal pattern, the process of discriminating between important sounds, and the speed of reaction. De-automation of the basic functions of auditory central processing, which we observe in older age, lowers the perception of both emotional and linguistic prosody, thus reducing the quality of communication in older people.


Author(s):  
Nadja Cristina Furtado Back ◽  
Ana Chrystina de Souza Crippa ◽  
Tatiana Izabelle Jaworski de Sá Riechi ◽  
Liliane Desgualdo Pereira

Abstract Introduction Nowadays, there is no consensus on whether central auditory processing disorder is a primary or a secondary deficit to other cognitive deficits. A better understanding of the association between cognitive functions and central auditory skills may help elucidate this dilemma. Objective To investigate possible associations between auditory abilities and cognitive functions in schoolchildren. Methods Fifty-eight schoolchildren, aged between 8 years and 0 months old and 11 years and 11 months old, who underwent the following tests: masking level difference, gaps in noise, pitch pattern sequence test, dichotic digits test, sustained auditory attention ability test, Wechsler intelligence scale for children – IV, junior Hayling test, five digits test, and behavior rating inventory of executive function. Results Significant correlations were found between the hearing ability of temporal resolution and executive functions, temporal ordering/sequencing, binaural integration and separation, and sustained auditory attention, operational memory, inhibitory control, and cognitive flexibility; binaural integration was also associated with intelligence. The statistically significant positive correlation found between the ability of binaural interaction and the components of emotional control and behavior regulation of the behavior rating inventory of executive function was unexpected. Conclusion The associations identified reinforce the complexity of the tasks involved in the evaluation of central auditory processing and the need for multidisciplinary evaluation for the differential diagnosis of auditory processing disorder. Confirmation of the presence or absence of comorbidities between different disorders allows directing the therapeutic behaviors and reducing the impact of possible auditory and/or cognitive deficits in the different daily life situations of children.


2005 ◽  
Vol 14 (2) ◽  
pp. 112-123 ◽  
Author(s):  
Anthony T. Cacace ◽  
Dennis J. McFarland

Purpose: This article argues for the use of modality specificity as a unifying framework by which to conceptualize and diagnose central auditory processing disorder (CAPD). The intent is to generate dialogue and critical discussion in this area of study. Method: Research in the cognitive, behavioral, and neural sciences that relates to the concept of modality specificity was reviewed and synthesized. Results: Modality specificity has a long history as an organizing construct within a diverse collection of mainstream scientific disciplines. The principle of modality specificity was contrasted with the unimodal inclusive framework, which holds that auditory tests alone are sufficient to make the CAPD diagnosis. Evidence from a large body of data demonstrated that the unimodal framework was unable to delineate modality-specific processes from more generalized dysfunction; it lacked discriminant validity and resulted in an incomplete assessment. Consequently, any hypothetical model resulting from incomplete assessments or potential therapies that are based on indeterminate diagnoses are themselves questionable, and caution should be used in their application. Conclusions: Improving specificity of diagnosis is an imperative core issue to the area of CAPD. Without specificity, the concept has little explanatory power. Because of serious flaws in concept and design, the unimodal inclusive framework should be abandoned in favor of a more valid approach that uses modality specificity.


2018 ◽  
Vol 29 (8) ◽  
pp. 3294-3304 ◽  
Author(s):  
Xia Liu ◽  
Fanfan Wei ◽  
Yuan Cheng ◽  
Yifan Zhang ◽  
Guoqiang Jia ◽  
...  

Abstract Lead (Pb) causes significant adverse effects on the developing brain, resulting in cognitive and learning disabilities in children. The process by which lead produces these negative changes is largely unknown. The fact that children with these syndromes also show deficits in central auditory processing, however, indicates a speculative but disturbing relationship between lead-exposure, impaired auditory processing, and behavioral dysfunction. Here we studied in rats the changes in cortical spatial tuning impacted by early lead-exposure and their potential restoration to normal by auditory training. We found animals that were exposed to lead early in life displayed significant behavioral impairments compared with naïve controls while conducting the sound-azimuth discrimination task. Lead-exposure also degraded the sound-azimuth selectivity of neurons in the primary auditory cortex. Subsequent sound-azimuth discrimination training, however, restored to nearly normal the lead-degraded cortical azimuth selectivity. This reversal of cortical spatial fidelity was paralleled by changes in cortical expression of certain excitatory and inhibitory neurotransmitter receptor subunits. These results in a rodent model demonstrate the persisting neurotoxic effects of early lead-exposure on behavioral and cortical neuronal processing of spatial information of sound. They also indicate that attention-demanding auditory training may remediate lead-induced cortical neurological deficits even after these deficits have occurred.


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