Hearing Loss of a Central Type Secondary to Anoxic Anoxia

1976 ◽  
Vol 85 (6) ◽  
pp. 826-832 ◽  
Author(s):  
Kazumi Makishima ◽  
Roger B. Katz ◽  
James B. Snow
Keyword(s):  
Hearing Loss ◽  
Auditory Cortex ◽  
Inferior Colliculus ◽  
Guinea Pigs ◽  
Auditory Pathway ◽  
Threshold Sensitivity ◽  
Central Type ◽  
Acoustic Stimuli ◽  
Central Auditory Pathway ◽  
Relative Vulnerability

The effect of anoxic anoxia on the threshold sensitivity and amplitude of the responses from the auditory cortex, inferior colliculus and cochlea to acoustic stimuli in guinea pigs was studied. Decay of the amplitude of the responses from the auditory cortex and the inferior colliculus occurs faster and is more severe than that of the cochlea. Recovery of the amplitude of the responses is slower at the auditory cortex and the inferior colliculus than at the cochlea. Loss of auditory threshold sensitivity in anoxic anoxia is most prominent at the auditory cortex. The loss of sensitivity at the inferior colliculus is the next most severe. The loss of sensitivity at the cochlea is negligible. The relative vulnerability of the central auditory pathway to anoxic anoxia as compared to the end organ is demonstrated.

scholarly journals Changes in microRNA Expression in the Cochlear Nucleus and Inferior Colliculus after Acute Noise-Induced Hearing Loss

2020 ◽  
Vol 21 (22) ◽  
pp. 8792
Author(s):  
Sohyeon Park ◽  
Seung Hee Han ◽  
Byeong-Gon Kim ◽  
Myung-Whan Suh ◽  
Jun Ho Lee ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Inferior Colliculus ◽  
Neural Plasticity ◽  
Cochlear Nucleus ◽  
Organ Of Corti ◽  
Auditory Pathway ◽  
Noise Induced Hearing Loss ◽  
Candidate Mirnas ◽  
Central Auditory Pathway

Noise-induced hearing loss (NIHL) can lead to secondary changes that induce neural plasticity in the central auditory pathway. These changes include decreases in the number of synapses, the degeneration of auditory nerve fibers, and reorganization of the cochlear nucleus (CN) and inferior colliculus (IC) in the brain. This study investigated the role of microRNAs (miRNAs) in the neural plasticity of the central auditory pathway after acute NIHL. Male Sprague–Dawley rats were exposed to white band noise at 115 dB for 2 h, and the auditory brainstem response (ABR) and morphology of the organ of Corti were evaluated on days 1 and 3. Following noise exposure, the ABR threshold shift was significantly smaller in the day 3 group, while wave II amplitudes were significantly larger in the day 3 group compared to the day 1 group. The organ of Corti on the basal turn showed evidence of damage and the number of surviving outer hair cells was significantly lower in the basal and middle turn areas of the hearing loss groups relative to controls. Five and three candidate miRNAs for each CN and IC were selected based on microarray analysis and quantitative reverse transcription PCR (RT-qPCR). The data confirmed that even short-term acoustic stimulation can lead to changes in neuroplasticity. Further studies are needed to validate the role of these candidate miRNAs. Such miRNAs may be used in the early diagnosis and treatment of neural plasticity of the central auditory pathway after acute NIHL.

Structural Abnormalities of the Central Auditory Pathway in Infants with Nonsyndromic Cleft Lip and/or Palate

2012 ◽  
Vol 49 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Frank F. Yang ◽  
Bradley McPherson ◽  
Huang Shu ◽  
Na Xie ◽  
Kui Xiang
Keyword(s):  
Auditory Cortex ◽  
Cleft Lip ◽  
Right Hemisphere ◽  
Auditory Pathway ◽  
Normal Children ◽  
Significant Group ◽  
Structural Abnormalities ◽  
Magnetic Resonance Imaging Mri ◽  
Central Auditory Pathway ◽  
Mri Measurements

Objective To investigate possible structural abnormalities of the central auditory pathway in infants with nonsyndromic cleft lip and/or palate (NSCL/P). Participants Twenty-seven Chinese infants with NSCL/P, aged from 6 to 24 months. Intervention Morphological magnetic resonance imaging (MRI) measurements of the central auditory nervous system (CANS) in infants with NSCL/P were analyzed and compared with those of age- and sex-matched normal controls. Results No significant group differences were found in general brain measurements, including volumes of the brain stem and right hemisphere. However, infants with NSCL/P had statistically significantly smaller volumes of the left thalamus and left auditory cortex and notably decreased thickness of the left auditory cortex. Conclusion Cortical abnormalities were more marked compared with other MRI measurements. Structural CANS abnormalities in infants with NSCL/P may be located mainly in the left cerebral hemisphere. The development and maturation of the auditory cortex in infants with NSCL/P may be abnormal when compared with those of normal children.

Central hyperacusis with phonophobia in multiple sclerosis

2002 ◽  
Vol 8 (6) ◽  
pp. 505-509 ◽  
Author(s):  
H Weber ◽  
K Pfadenhauer ◽  
M Stöhr ◽  
A Rösler
Keyword(s):  
Multiple Sclerosis ◽  
Auditory Evoked Potentials ◽  
Auditory Pathway ◽  
Directional Hearing ◽  
Hearing Disorders ◽  
Brainstem Lesion ◽  
Acoustic Stimuli ◽  
Demyelinating Lesions ◽  
Magnetic Resonance Imaging Mri ◽  
Central Auditory Pathway

Hearing disorders are a well-described symptom in patients with multiple sclerosis (MS). Unilateral or bilateral hyperacusis or deafness in patients with normal sound audiometry is often attributed to demyelinating lesions in the central auditory pathway. Less known in MS is a central phonophobia, whereby acoustic stimuli provoke unpleasant and painful paresthesia and lead to the corresponding avoidance behaviour. In our comparison collective, patient 1 described acute shooting pain attacks in his right cheek, each time set off by the ringing of the telephone. Patient 2 complained of intensified, unbearable noise sensations when hearing nonlanguage acoustic stimuli. Patient 3 noticed hearing unpleasant echoes and disorders of the directional hearing. All patients had a clinical brainstem syndrome. ENT inspection, sound audiometry and stapedius reflex were normal. All three patients had pathologically changed auditory evoked potentials (AEPs) with indications of a brainstem lesion, and in magnetic resonance imaging (MRI) demyelinating lesions in the ipsilateral pons and in the central auditory pathway. The origin we presume in case 1 is an abnormal impulse conduction from the leminiscus lateralis to the central trigeminus pathway and, in the other cases, a disturbance in the central sensory modulation. All patients developed in the further course a clinically definite MS. Having excluded peripheral causes for a hyperacusis, such as, e.g., an idiopathic facial nerve palsy or myasthenia gravis, one should always consider the possibility of MS in a case of central phonophobia. Therapeutic possibilities include the giving of serotonin reuptake inhibitors or acoustic lenses for clearly definable disturbing frequencies.

Diffusion tensor imaging and MR morphometry of the central auditory pathway and auditory cortex in aging

Neuroscience ◽  
2014 ◽  
Vol 260 ◽  
pp. 87-97 ◽  
Author(s):  
O. Profant ◽  
A. Škoch ◽  
Z. Balogová ◽  
J. Tintěra ◽  
J. Hlinka ◽  
...  
Keyword(s):  
Diffusion Tensor Imaging ◽  
Auditory Cortex ◽  
Diffusion Tensor ◽  
Auditory Pathway ◽  
Central Auditory Pathway

Molecular and Structural Changes in the Cochlear Nucleus in Response to Hearing Loss

2018 ◽  
pp. 142-162
Author(s):  
Maria E. Rubio
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Structural Changes ◽  
Auditory Pathway ◽  
The United States ◽  
Cellular Mechanisms ◽  
Auditory Experience ◽  
Central Auditory Pathway ◽  
The Brain

Hearing loss is the third most common health problem in the United States. It can affect the quality of life and relationships. About 48 million Americans have lost some hearing. Age, illness, and genetics contribute to the generation of hearing loss. During development, auditory synaptic circuitries are highly plastic and able to adapt to fluctuations in auditory experience. Whether this is so for mature auditory nerve synapses and circuitries within nuclei along the central auditory pathway is less understood. Daily fluctuations in auditory experience can lead to hearing deficits, including hearing loss and/or deafness, Therefore, understanding the cellular mechanisms that occur in mature central auditory synaptic circuitries that lead and/or contribute to hearing loss is important. This chapter focuses on published studies using animal models describing structural and molecular changes that occur in the cochlear nucleus in response to hearing loss, the first gateway of sound processing in the brain.

Extralemniscal activation of auditory cortex in cats

1961 ◽  
Vol 200 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Robert Galambos ◽  
Ronald E. Myers ◽  
Guy C. Sheatz
Keyword(s):  
Auditory Cortex ◽  
Inferior Colliculus ◽  
Auditory Pathway ◽  
Complex Pattern ◽  
Evoked Activity

Unanesthetized cats exhibit a complex pattern of evoked activity at the cortex lasting up to a second or longer following click stimulation to the ear. Transection of the classical auditory pathway at the level of the brachium of the inferior colliculus does not in any significant way alter this pattern of response. Most important, the onset of the response, if affected at all by the section, is delayed only up to 2 or 3 msec. A more medial pathway of prime importance paralleling the classical auditory projection must therefore be postulated. Conduction in this extralemniscal system is completely blocked by deep barbiturate anesthesia while it is left intact by chloralose anesthesia.

Stimulation-mapping of the upper human auditory pathway

1973 ◽  
Vol 38 (3) ◽  
pp. 320-325 ◽  
Author(s):  
Ronald R. Tasker ◽  
L. W. Organ
Keyword(s):  
Electrical Stimulation ◽  
Auditory Cortex ◽  
Brain Stem ◽  
Inferior Colliculus ◽  
Primary Auditory Cortex ◽  
Auditory Pathway ◽  
Association Cortex ◽  
Content Type ◽  
Medial Geniculate ◽  
Stimulation Of

✓ Auditory hallucinations were produced by electrical stimulation of the human upper brain stem during stereotaxic operations. The responses were confined to stimulation of the inferior colliculus, brachium of the inferior colliculus, medial geniculate body, and auditory radiations. Anatomical confirmation of an auditory site was obtained in one patient. The hallucination produced was a low-pitched nonspecific auditory “paresthesia” independent of the structure stimulated, the conditions of stimulation, or sonotopic factors. The effect was identical to that reported from stimulating the primary auditory cortex, and virtually all responses were contralateral. These observations have led to the following generalizations concerning electrical stimulation of the somesthetic, auditory, vestibular, and visual pathways within the human brain stem: the hallucination induced in each is the response to comparable conditions of stimulation, is nonspecific, independent of stimulation site, confined to the primary pathway concerned, chiefly contralateral, and identical to that induced by stimulating the corresponding primary auditory cortex. No sensory responses are found in the brain stem corresponding to those from the sensory association cortex.

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