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Assessing Paediatric Development in Psychiatry
Published in Cathy Laver-Bradbury, Margaret J.J. Thompson, Christopher Gale, Christine M. Hooper, Child and Adolescent Mental Health, 2021
Receptive hair cells located in the centre of the coiled cochlear apparatus are sensitive to sounds of low frequency, whereas the proximal hair cells detect sounds of higher frequencies. This information is relayed to the two primary cortical areas responsible for analysis of basic sound information, auditory I and II, via the inferior colliculus and the medial geniculate nucleus of thalamus. Cells within both the thalamus and the cortical areas associated with hearing organise these inputs in such a way that they have an accurate spatial representation of the location from which the sound originated.
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?
Ernesto
Published in Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner, The Integrated Nervous System, 2017
Walter J. Hendelman, Peter Humphreys, Christopher R. Skinner
The upwardly projecting fibers synapse in the midbrain (the inferior colliculi, at the lower midbrain level), where some auditory processing occurs. The auditory pathway then travels upwards to a specific relay nucleus of the thalamus, the medial geniculate nucleus, after which it arrives at the cortex along the transverse gyri of Heschl, located along the superior part of the temporal lobe, within the lateral fissure (see Figures 1.10, 6.1 and 13.3). Sound frequency (pitch) is preserved throughout the pathway up to and including the primary auditory cortex, where there is tonotopic localization. Adjacent areas of the cortex are association areas for sound interpretation, including the nearby Wernicke’s area (in the dominant hemisphere, as discussed in Chapter 1).
Evaluating Auditory Pathway by Electrical Auditory Middle Latency Response and Postoperative Hearing Rehabilitation
Published in Journal of Investigative Surgery, 2019
Bin Wang, Keli Cao, Chaogang Wei, Zhiqiang Gao, Huan Li
Since the waveform of auditory brainstem response is identified, the response recorded in the far-field of auditory cortex at 10–100 ms after stimulus onset are called AMLR.2 The neural sources of AMLR are different from those of auditory brainstem response, and the waveform usually has 5 peaks, which are labeled as Po, Na, Pa, Nb and Pb. Current evidence suggests the putative generator sites of AMLR include the primary auditory cortex, midbrain reticular formation, nonspecific nuclei in the hypothalamus and the medial geniculate nucleus.3 Pa wave is believed to be generated from the primary auditory cortex and Na wave is from the subcortical structures.3 The average threshold value of AMLR we recorded using Bio-logic brand auditory evoked potential measurement system in normal hearing subjects was 12.5 ± 8.6 dB nHL, comparable with the value (10.5 ± 7.7 dB nHL) reported from the literature.4 The activity from thalamus to cortex in adults by artificial cochlear device was recorded by Firszt et al.5 Similar EMLR waveforms was reported in an 8.5 years old child with cochlear implant.6 A systematical study evoked potentials, and described the waveforms and thresholds of EMLR in detail, including stimulating between electrodes 4 and 10 of a 24 Nucleus implant with a pulse width of 50 µsec at 7 pulses per second.7 The actual behavioral threshold of this patient under the same condition was 190 Nucleus clinical units, and as depicted the threshold of EMLR was also 190 clinical units, which is more comparable than that of EABR or nerve response telemetry (NRT).
Sleep duration is associated with auditory radiation microstructure
Published in Neurological Research, 2020
Toshikazu Ikuta, Taylor E. Stansberry, Rebecca O. Lowe
It remains unclear which constituents of neural pathways are and are not involved in sleep and hearing interaction, although neuronal firing in the auditory cortex of animal models proved to be altered by manipulating the sleep cycle [6]. One of these neural pathways, the auditory radiation, is the final part of the pathway from the cochlea to the cerebral cortex, connecting the medial geniculate nucleus and the primary auditory cortex. The auditory radiation, if damaged, could cause cortical deafness and loss of vestibular and somatosensory sensations [7]. However, it is not clear whether this particular neural pathway is associated with sleep.
Association between hearing loss and hereditary ATTR amyloidosis
Published in Amyloid, 2019
Sophie Bartier, Diane Bodez, Mounira Kharoubi, Aziz Guellich, Florence Canouï-Poitrine, Véronique Chatelin, André Coste, Thibaud Damy, Emilie Béquignon
Contrary to the study of Omata et al. [22], our results suggest than amyloid deposits could be not only in cochlear hair cells but also in other anatomical levels of auditory system such as middle ear (tendons, muscles, ossicles), cochleo-vestibular nerve and central nervous system. There are many places in the auditory pathways where amyloid has been identified [7,22], and this provides a large number of hypotheses for future researchers to test. Neuropathies related to ATTRv deposits are very well known. Large non-myelinated and small myelinated fibers are affected and lost. Amyloid deposits’ toxicity has been proven by histological studies on nerve biopsies, showing amyloid infiltration of the endoneurium, endoneural and epineural arterioles and atrophy of Schwann cells [24]. It is also possible that amyloid infiltration could be responsible for central auditory damages. Central nervous system ATTRv amyloidosis is well documented: ATTRv deposition can be found in the media and adventitia of medium- and small-sized arteries, arterioles, and veins of the cortex and the leptomeningeas [5]. Comparison with Alzheimer’s disease could be useful. It has recently been reported that Alzheimer’s disease could be linked to severe auditory impairment. It could be related to central neurodegenerative processes in primary auditory cortex [25]. Autopsy studies have shown neuronal degeneration in inferior colliculus and medial geniculate nucleus (responsible for auditory signal transmission) due to amyloid plaques [26]. We could therefore infer that there is a similar toxicity of amyloid depositions in neuronal structures. In future research, brain and temporal bone MRI will be of great help to investigate potential sensorineural processes (cochleovestibular nerve enhancement for example).