Auswahl der wissenschaftlichen Literatur zum Thema „Central auditory deficits“

Abstract The behavioral characteristics of central auditory processing disorder (CAPD) are similar to those of other neurocognitive and communicative disorders. Differential diagnosis is used to “tease out” the auditory specific deficit. Differential intervention combines specific management strategies with specific rehabilitative procedures to minimize the impact of the CAPD and improve skills. A compelling body of research supports the use of specific types of therapeutic rehabilitation for listeners with CAPD; however, additional research is needed regarding treatment outcomes for specific auditory deficits. Single-subject case studies can provide evidence of treatment effectiveness in a clinical setting. This paper presents two cases that provide evidence that the inclusion of deficit specific auditory treatment into the overall intervention plan of students with specific central auditory processing disorder can reduce the deficit and minimize its impact in a relatively short period of time.

Background: According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, diagnosis of speech sound disorder (SSD) requires a determination that it is not the result of other congenital or acquired conditions, including hearing loss or neurological conditions that may present with similar symptomatology. Purpose: To examine peripheral and central auditory function for the purpose of determining whether a peripheral or central auditory disorder was an underlying factor or contributed to the child’s SSD. Research Design: Central auditory processing disorder clinic pediatric case reports. Study Sample: Three clinical cases are reviewed of children with diagnosed SSD who were referred for audiological evaluation by their speech–language pathologists as a result of slower than expected progress in therapy. Results: Audiological testing revealed auditory deficits involving peripheral auditory function or the central auditory nervous system. These cases demonstrate the importance of increasing awareness among professionals of the need to fully evaluate the auditory system to identify auditory deficits that could contribute to a patient’s speech sound (phonological) disorder. Conclusions: Audiological assessment in cases of suspected SSD should not be limited to pure-tone audiometry given its limitations in revealing the full range of peripheral and central auditory deficits, deficits which can compromise treatment of SSD.

Objective To investigate central auditory processing in children with unilateral stroke and to verify whether the hemisphere affected by the lesion influenced auditory competence. Method 23 children (13 male) between 7 and 16 years old were evaluated through speech-in-noise tests (auditory closure); dichotic digit test and staggered spondaic word test (selective attention); pitch pattern and duration pattern sequence tests (temporal processing) and their results were compared with control children. Auditory competence was established according to the performance in auditory analysis ability. Results Was verified similar performance between groups in auditory closure ability and pronounced deficits in selective attention and temporal processing abilities. Most children with stroke showed an impaired auditory ability in a moderate degree. Conclusion Children with stroke showed deficits in auditory processing and the degree of impairment was not related to the hemisphere affected by the lesion.

Central deafness has been linked historically to bihemispheric involvement of the temporal lobe, with more recent findings suggesting that compromise of other cortical and subcortical structures can also result in this disorder. The present investigation extends our understanding of the potential anatomical correlates to central deafness by demonstrating that bilateral involvement of an auditory structure within the midbrain can additionally result in this condition. Our subject was a 21-year-old male with a subarachnoid bleed affecting both inferior colliculi. Significant auditory deficits were noted for the middle and late auditory evoked potentials, while electrophysiologic measures of the periphery indicated normal function. The patient was enrolled in a rehabilitation program for approximately 14 weeks. Although initially unresponsive to sounds, the patient regained most of his auditory abilities during the 10 months he was followed. This case documents the range of auditory deficits that may be associated with damage to the inferior colliculi, and it profiles a hierarchical recovery of auditory function consistent with test findings.

The subject of this study was a 46-year-old female who had suffered a cerebrovascular accident (CVA). Magnetic resonance imaging revealed damage in the area of the distribution of the middle cerebral artery involving most, if not all, of the primary auditory area of the left hemisphere. No auditory problems were noted prior to the CVA; however, following the CVA, the subject reported a number of auditory difficulties. Pure-tone thresholds were normal post-CVA, and performance on speech recognition testing was good in both ears if ample time was provided between a response and the presentation of the next test item. Duration pattern, intensity discrimination, and middle latency response test results were abnormal for both ears, and right ear deficits were evident on an auditory fusion test and two dichotic speech tests (digits and rhymes). This case is significant in that it demonstrates a good correlation between damage to known key auditory regions and central auditory test results.

Purpose A growing body of evidence suggests that military service members and military veterans are at risk for deficits in central auditory processing. Risk factors include exposure to blast, neurotrauma, hazardous noise, and ototoxicants. We overview these risk factors and comorbidities, address implications for clinical assessment and care of central auditory processing deficits in service members and veterans, and specify knowledge gaps that warrant research. Method We reviewed the literature to identify studies of risk factors, assessment, and care of central auditory processing deficits in service members and veterans. We also assessed the current state of the science for knowledge gaps that warrant additional study. This literature review describes key findings relating to military risk factors and clinical considerations for the assessment and care of those exposed. Conclusions Central auditory processing deficits are associated with exposure to known military risk factors. Research is needed to characterize mechanisms, sources of variance, and differential diagnosis in this population. Existing best practices do not explicitly consider confounds faced by military personnel. Assessment and rehabilitation strategies that account for these challenges are needed. Finally, investment is critical to ensure that Veterans Affairs and Department of Defense clinical staff are informed, trained, and equipped to implement effective patient care. Infographic https://doi.org/10.23641/asha.12071232

This case study involves a 41-year-old female who had sustained a mild traumatic brain injury during a horseback riding accident. The patient was seen for medical and neuropsychological testing following this incident and was referred to a speech-language pathologist for rehabilitative services. At 13 months posttrauma, the patient, who was frustrated by a lack of significant progress, requested an audiologic work-up. Results of testing conducted at this time revealed normal peripheral hearing and significant central auditory deficits. Based on these findings, an auditory rehabilitation program was developed and implemented. The components of this patient's rehabilitation program are reviewed, and the posttherapy improvements noted in her auditory functions are detailed. The case is important in that it demonstrates (1) that auditory deficits can be a sequel to minor head injury, (2) that these deficits are often subtle and may not be detected unless central auditory testing is conducted, and (3) that these deficits may be amenable to remediation.

Many individuals with central auditory nervous system (CANS) pathology/disorder report a variety of auditory symptoms with difficulty hearing in noise being one of the most common complaints (Chermak and Musiek, 1992) Interestingly, there seems to be a paucity of information in the literature on lateralized hearing loss symptoms in patients with central auditory disorders. Reported here is a case where the patient reported auditory symptoms, specifically hearing loss that was lateralized distinctly to the right ear. This ear was contralateral to a stroke that involved the left hemisphere with neural compromise limited primarily to the left Heschl's gyrus. Although the patient reported other hearing difficulties, the lateralized symptom of right-sided hearing loss seemed to be the most noticed. While the pure-tone audiogram was totally disassociated from the right ear auditory symptoms, central auditory tests revealed a marked and consistent right ear deficit, which was consistent with the site of lesion. It is rare that a relatively small lesion in Heschl's gyrus results in the perception of hearing loss so specifically localized to the right ear. It is also of interest that a patient with definite complaints of hearing loss would yield a normal, highly symmetrical pure-tone audiogram. The triad of patient symptoms, anatomy of the lesion, and central auditory test findings in this case are discussed, and theories as to possible underlying mechanisms for the patient's auditory deficits are provided.

Au cours des trois dernières décennies, l’étude des formes héréditaires de surdité par une approche génétique a permis de mieux comprendre la physiologie de la cochlée, l’organe sensoriel de l’audition. Cependant, cette approche ne permet pas d’étudier aussi efficacement les dysfonctionnements du système auditif central affectant pourtant de nombreux patients. Ces déficits auditifs centraux sont mal connus et, dans certains cas, passent même inaperçus. Ceci est probablement dû à l’atteinte cochléaire qui prive le cerveau de tout ou partie des informations acoustiques qu’il reçoit normalement. Afin d’identifier les formes génétiques de surdités pouvant associer à la fois des déficits auditifs périphériques et centraux, mon laboratoire de thèse étudie la susceptibilité des souris aux crises audiogènes. Ce sont des épilepsies réflexes en réponse à un son de forte intensité, une manifestation typique de déficits centraux. En effet, plusieurs lignées de souris mutantes pour des gènes de surdité présentent une susceptibilité aux crises audiogènes. C’est notamment le cas des souris porteuses de mutation dans les gènes Cdhr23 et Pcdh15, sourdes à l’état bi-allélique mais susceptibles aux crises audiogènes à l’état mono-allélique sans perte auditive. Il a été suggéré que ces deux gènes de surdité jouent un rôle dans le développement des interneurones inhibiteurs corticaux exprimant la parvalbumine (PV). L’objectif de ma thèse était d’une part de développer des outils permettant d’identifier facilement la présence de troubles auditifs centraux dans les modèles murins de surdité d’origine génétique, et d’autre part d’approfondir les rôles de Cdhr23 et Pcdh15 dans le système auditif central grâce à des modèles murins d’inactivation conditionnelle dans l’encéphale. J’ai tout d’abord mis au point chez la souris une méthode de mesure non invasive des potentiels évoqués auditifs corticaux, et mis en évidence que les souris perçoivent différemment des sons aversifs aux caractéristiques acoustiques particulières, qui, chez l’humain, activent un large réseau de neurones bien au-delà de ceux nécessaires à l’audition. Ces résultats permettront à l’avenir d’étudier plus finement les déficits auditifs centraux. Dans un deuxième temps, j’ai montré, grâce à des techniques d’électrophysiologie in vivo et des études psychoacoustiques chez la souris, que l’inactivation conditionnelle de Cdhr23 et Pcdh15 modifiait certaines caractéristiques spectrales et temporelles des réponses neuronales à des sons sans en modifier significativement leur perception. De plus, j’ai pu préciser le rôle de ces deux gènes dans le développement des interneurones à PV. Alors qu’une précédente étude suggérait que Cdhr23 et Pcdh15 étaient exprimés dans des neuroblastes à destination du cortex auditif, mes résultats montrent qu’ils seraient exprimés dans l’ensemble du cortex et majoritairement dans la microglie (pour Cdhr23) et dans des progéniteurs d’oligodendrocytes (pour Pcdh15), deux populations fortement liées au développement et au fonctionnement des interneurones à PV. Cdhr23 est aussi exprimé dans des neurones sous-corticaux de régions auditives, motrices et multisensorielles. Le rôle de Cdhr23 et Pcdh15 dans le développement des interneurones à PV serait donc indirect et plus complexe qu’envisagé. Il faudra par la suite prendre en compte cette nouvelle avancée pour analyser précisément les conséquences fonctionnelles de leur inactivation dans le cerveau. Ainsi, mes résultats montrent que ces deux gènes de surdité ont un rôle intrinsèque dans le système nerveux central sans être restreints aux circuits auditifs et participent probablement à de nombreux mécanismes cellulaires dont la diversité doit encore être explorée afin de mieux caractériser les déficits centraux qui pourraient exister chez des patients porteurs de mutations CDHR23 ou PCDH15
Over the past three decades, the study of hereditary forms of deafness has provided considerable insight into the molecular mechanisms of hearing, particularly those involved in the development and/or physiology of the auditory sensory organ, the cochlea. In contrast, the genetic approach has provided little information about the central auditory system although many people have central auditory dysfunctions. Central auditory deficits are poorly understood and can, in some cases, go unnoticed. This is likely as a result of cochlear damage depriving the brain of all or part of the acoustic information it would normally receive. To identify genetic forms of deafness that result in both peripheral and central hearing deficits, the Michalski research group uses the susceptibility of mice to audiogenic seizures, epileptic seizures triggered in response to loud sound, which are a manifestation of central deficits. Several strains of mice carrying mutations in deafness genes show susceptibility to audiogenic seizures in the bi-allelic state (if the deafness is not complete) or in the mono-allelic state. Through this strategy, two such genes, Cdhr23 and Pcdh15, have been identified to be involved in the establishment of cortical neurons expressing parvalbumin (PV) which serve as the primary cortical inhibitory neurons in the auditory cortex. The aim of my thesis was a) to develop tools to easily identify the presence of central auditory deficits in genetic models of deafness in mice and b) to further investigate the roles of cdhr23 and pcdh15 in the central auditory system through conditional inactivation of Cdhr23 and Pcdh15 in the mouse brain. First, I developed a non-invasive method to measure auditory cortical evoked potentials in mice and demonstrated that mice respond to certain aversive acoustic features differently to humans for which a large network of neurons (even outside the auditory system) is activated. These results will allow to study more precisely the central deficits associated with hearing impairments. Second, using in vivo electrophysiology and psychoacoustics following the conditional inactivation of Cdhr23 and Pcdh15, I could show that the spectral and temporal characteristics of neuronal responses to sounds were modified without significantly altering their perception by the mice. Furthermore, I was able to better characterise the role of these two genes in the development of PV interneurons. Although a previous study suggested that Cdhr23 and Pcdh15 were expressed in neuroblasts destined to migrate to the auditory cortex, my results show that in fact they are expressed extensively throughout the cortex with the majority in the microglia (for Cdhr23) and in oligodendrocyte progenitors (for Pcdhr15), both populations strongly associated with the development and function of PV interneurons. In addition, Cdhr23 was also found to be expressed in subcortical neuronal populations of the auditory, motor, and multisensory regions. These new advances in demonstrating the role of Cdhr23 and Pcdh15 to be more intricate and indirect than initially thought need to be considered for future investigations into the consequences of their inactivation in the brain. Thus, my results show that two deafness genes have an intrinsic role in the central nervous system without being restricted to auditory circuits and probably participate in many different cellular mechanisms that remain to be explored in order to better characterize the central deficits that might exist in patients carrying CDHR23 or PCDH15 mutations

The purpose of this study was to determine whether or not children diagnosed with Attention-Deficit Hyperactivity Disorder (ADHD) or Central Auditory Processing Disorder (CAPD) can be distinguished from one another on the basis of both objective and subjective assessment of attention and behavior. First, children and adolescents diagnosed with ADHD, CAPD, and concomitant ADHD/CAPD were compared to participants with emotional problems on measures of attention/concentration, depression, anxiety, and parental reports of internalzing and externalizing behaviors. Overall, statistical analyses did not reveal significant differences between performances of children diagnosed with ADHD and those diagnosed with CAPD. However, clinical comparisons across groups of children diagnosed with ADHD, CAPD, comorbid ADHD/CAPD and Affective Disorders revealed condition-specific clinical profiles, thus providing some support for CAPD as a distinct clinical entity. Second, exploratory cluster analysis was performed to further investigate the relationship between ADHD and CAPD. This procedure lead to the identification of four distinct clusters. However, analyses of these clusters revealed no distinct pattern of performance for children diagnosed with either ADHD or CAPD. Rather, participants with these diagnoses were evenly distributed throughout the clusters. Additionally, no cluster clearly represented the expected clinical profile for a diagnosis of CAPD- namely, significant auditory attentional/processing problems in the absence of other attentional difficulties. Implications for the assessment and treatment of childhood attentional disorders are discussed and recommendations for future research provided.

The aim of this action research was to investigate how auditory perceptual deficits affect reading in learners with disabilities. The sub-questions were: What auditory perceptual deficits learners’ experience? How do educators assist learners with auditory perceptual deficits? What instructional strategies and classroom management can educators apply to assist learners with auditory perceptual skills? The data collections comprised of an informal oral assessment, observation and anecdotal notes with fifteen participants with barriers to learning, from the English first year class, within a special needs educational setting. Data analysis and validity were supported by triangulation through informal assessment, observation, my critical friend and my own critical reflection. The support of phonologic, memory, and cohesion skills, auditory skills were the reading educational construct and strategies used as intervention in order to identify the efficacy of said interventions. Both bottom-up and top-down support strategies were used in relation to the participants’ individualised educational needs. The research results and discussion included methods to improve reading and listening skills in the classroom environment.
Inclusive Education
M. Ed. (Inclusive Education)

Auditory comprehension of language is a complex process. Even students who understand isolated words or are working to “listen carefully” may struggle to process the meaning of a message that is conveyed through speech. Such deficits in listening comprehension, when combined with normal hearing, may lead to a diagnosis of central auditory processing disorder (CAPD). This chapter will explore CAPD from the viewpoints of researchers, diagnosticians, and teachers. After discussing manifestations, diagnosis, and neurological foundations, the chapter will conclude with a focus on therapies, tools, and classroom strategies that can support the learning of students with CAPD.

Presbycusis-related tinnitus and cognitive impairment are common in the elderly and generate a massive burden on family and society. Except for age, the study explored the gender differences in the prevalence of the three diseases. We found that women have an advantage in maintaining better cognitive and auditory functions. Recent studies suggest the complex links among the three diseases. Peripheral hearing loss can affect sound coding and neural plasticity, which will lead to cognitive impairment and tinnitus. The deficits of the central nervous system, especially central auditory structures, can, in turn, cause the presbycusis. The interaction among three diseases indicated that comprehensive assessment, intervention and treatment in consideration of hearing loss, tinnitus and cognitive impairment are important to decay aging.

This chapter deals with four diseases affecting the central nervous system (CNS) for which neurologists are primarily involved as consultants. It follows the same approach as the chapters that focus on single diseases but does so more briefly. Brain tumors are estimated to have an incidence of 12/100,000 per year (Scharre, 2000). The incidence is highest in old age, peaking between 60 and 80 years of age. Almost 50% of intracranial tumors are gliomas, 10% to 15% are meningiomas, 5% to 7% are pituitary adenomas, and 5% to 6% are metastatic tumors. Brain tumors produce signs and symptoms in a variety of ways, including direct invasion, compression, hemorrhage, and edema. Motor, sensory, visual, and gait disturbances are frequent manifestations of brain tumors. In addition, headache and focal or generalized seizures are quite common. The psychiatric manifestations of brain tumors reflect their location; the type of brain damage they produce; patients’ reactions to their symptoms or diagnosis; and the effects of treatments such as steroids, chemotherapy, and radiation. Tumors in specific brain regions have been linked to specific psychiatric manifestations. Frontal lobe tumors are most closely associated with behavioral changes,sometimes referred to as the frontal lobe syndrome or executive dysfunction syndrome. Temporal lobe tumors are most closely associated with personality change, irritability, and hallucinations (especially auditory), as well as with a variety of language disorders. Patients with language disorders associated with temporal lobe tumors can experience catastrophic reactions when their deficits interfere with communication. Parietal lobe tumors typically are associated with cognitive deficits such as apraxia, neglect syndromes of the contralateral body or space, and unformed visual hallucinations such as streaks or flashes of light. When evaluating brain tumor patients with psychiatric symptoms and signs, careful evaluation and differential diagnosis are critical. In hospitalized and seriously ill patients, it is especially important to rule out delirium, particularly when the psychiatric phenomena are intermittent and vary in intensity. Serial observations and repeated mental status examinations are the basis for the diagnosis of delirium, but an electroencephalogram (EEG) is also helpful, because in most cases of delirium it reveals generalized slowing involving brain areas far from the location of the brain tumor.