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Cortical Deafness (Plus Other Central Hearing Disorders)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
What makes cortical deafness so rare is that it requires brain damage to large parts of both sides of the brain (Graham et al., 1980). Specifically, damage to parts of both of the auditory cortices located in the temporal lobes. One fun fact about the way that the brain is wired is that incoming sound wave information from both ears is shared with both auditory cortices. Therefore, a person who has damage to just one auditory cortex will not experience cortical deafness, and may not show significant impairments to hearing at all (Polster & Rose, 1998). Because the auditory cortices are located far away from one another, the typical person who develops cortical deafness first has a stroke in one auditory cortex, and then later has another stroke in the other one (Brody et al., 2013).
Pleasurable emotional response to music: A case of neurodegenerative generalized auditory agnosia
Published in Howard J. Rosen, Robert W. Levenson, Neurocase, 2020
Brandy R. Matthews, Chiung-Chih Chang, Mary De May, John Engstrom, Bruce L. Miller
A brief review of the nosology of auditory agnosia is pertinent to our description of this patient. Generalized auditory agnosia refers to a rare condition in which subjects demonstrate impairment in the ability to recognize sounds in spite of adequate hearing as measured by standard audiometry (Mendez, 2001). Bitemporal cortical lesions have been reported as the neuroanatomic substrate of the condition, most frequently as the result of cerebrovascular disease (Vignolo, 2003), but also in association with neurodegeneration (Pinard et al., 2002), herpes encephalitis (Kaga et al., 2003), and traumatic brain injury (Hattiangadi et al., 2005). Lesions with a similar distribution involving the primary auditory cortex (BA 41) and auditory association cortex (BA 42 & 22) bilaterally may also result in cortical deafness, a distinct condition that yields an abnormal pure tone audiogram and therefore impairs the perception of sounds preceding the assignment of their meanings (Mendez & Geehan, 1988; Szirmai et al., 2003).
Joseph LeDoux (b. 1949)
Published in Andrew P. Wickens, Key Thinkers in Neuroscience, 2018
To begin, LeDoux traced the sensory neural pathway by which the tone elicited the behavioural fear response. This was relatively straightforward as the pathways from the ears to the brain were well known, with the auditory nerve projecting to the brain stem’s cochlear nucleus and inferior colliculus of the midbrain. From here, sound information reaches the primary auditory cortex (located in the temporal lobe) via the medial geniculate nucleus of the thalamus.1 LeDoux then set about identifying the important parts of this system for fear conditioning. One area to be lesioned was the auditory cortex – an operation that did not impair the fear response to the tone. He then destroyed the next lower station, the medial geniculate nucleus – a lesion that now impaired the rat’s ability to learn the conditioning procedure, with the tone and shock pairings having little effect on blood pressure or the elicitation of freezing.2 Clearly, this part of the thalamus was crucial for learning about fearful events, although it also raised a difficult question: if the tone stimulus was not reaching the auditory cortex, then where in the brain was it going?
The applications of targeted delivery for gene therapies in hearing loss
Published in Journal of Drug Targeting, 2023
Melissa Jones, Bozica Kovacevic, Corina Mihaela Ionescu, Susbin Raj Wagle, Christina Quintas, Elaine Y. M. Wong, Momir Mikov, Armin Mooranian, Hani Al-Salami
Sensorineural hearing loss is described as involving the inner ear and auditory cortex via neural pathways, impacting both children and adults. In terms of children, sensorineural hearing loss may be either hereditary or non-hereditary in nature [29]. One category within the classification of sensorineural hearing loss is sudden sensorineural hearing loss, which is defined as a sudden impairment in hearing, which is typically a result of alternative factors such as trauma or systemic infections. Often, no direct cause can be linked, with such termed idiopathic sudden sensorineural hearing loss [30]. This hearing loss subcategory is also prevalent in children, noted often as being viral or idiopathic [31]. Histologically, sensorineural hearing loss is most commonly depicted by cochlea sensory cells being lost or damaged, often via trauma or the use of drugs [32]. There are wide indications that a multitude of cells located in the cochlea, and, more specifically the organ of Corti, are involved in hearing loss, and will be explored further in this review.
Gap detection responses modelled using the Hill equation in adults with well-controlled HIV
Published in International Journal of Audiology, 2023
Christopher E. Niemczak, Christopher Cox, Gevorg Grigoryan, Gayle Springer, Abigail M. Fellows, Peter Torre, Howard J. Hoffman, Jay C. Buckey, Michael W. Plankey
While peripheral mechanisms in the cochlea encode temporal aspects of sound, the auditory cortex also contributes to auditory temporal processing (Eggermont 2000; Rupp et al. 2002). For example, Bertoli, Smurzynski, and Probst (2002) compared psychoacoustic gap detection thresholds with auditory electrophysiological responses evoked by varying gap durations. They found evident mismatch negativity responses when a silent gap within a 1.0-kHz sinusoid was approximately 9 ms as compared with behavioural gap detection thresholds at approximately 6 ms in the same listeners. Additionally, Rupp, Gutschalk et al. (2002) found evidence from neuromagnetic recording of middle latency responses that showed the primary auditory cortex can resolve gaps as small as 3 ms. While the differences in results were most likely due to different recording techniques, it is evident that the primary auditory cortex plays a central role in auditory temporal processing.
Virtual reality for tinnitus management: a randomized controlled trial
Published in International Journal of Audiology, 2022
Aniruddha K. Deshpande, Ishan Bhatt, Chanapong Rojanaworarit
The present study documented the effect of ST + VR intervention on tinnitus loudness and TFI scores. The underlying neurobiological mechanisms responsible for mediating the VR effect on tinnitus outcomes remain largely elusive. Tinnitus is associated with peripheral and central auditory structures (e.g. Henry et al. 2014). Auditory deafferentation caused due to ageing, noise, and ototoxic agents are known to induce hyperactivity in the central auditory structures (Vanneste and De Ridder 2016; Weisz et al. 2006). Tinnitus is associated with the tonotopic reorganisation of the auditory cortex – a consequence that may arise from the abnormal increase in the central gain and auditory deafferentation (e.g. Auerbach, Rodrigues, and Salvi 2014). Non-auditory structures, such as the anterior cingulate cortex, dorsal lateral prefrontal cortex, insula, orbitofrontal cortex, parahippocampus, and posterior cingulate cortex are also associated with tinnitus (Vanneste and De Ridder 2012). The complex interaction between cortical and subcortical networks (both auditory and non-auditory areas) might produce a clinical representation of tinnitus (e.g. Haider et al. 2018).