The link between Brain and Hearing system

2020 ◽  
Vol 12 (4) ◽  
pp. 114-117
Author(s):  
Alireza Bina

There are some studies which confirmed that dysfunction in Central Nervous System(CNS) may cause a malfunction in the Peripheral Auditory system (Cochlea_ Auditory Nerve, Auditory Neuropathy), but the question is could Brain Disorder without any lesion in the Cochlea and/or Auditory nerve cause Sensorineural Hearing Loss? It means that the Audiogram shows that the patient suffers from sensorineural hearing loss but the site of the lesion is neither Sensory nor Neural while Brain may be involved in charge of this. And if the answer is yes then could we hear with our Brain and without Cochlea and /or Auditory nerve? We deal with this subject in this paper by: Otosclerosis and Meniere’s disease and The Brain Involvement. Hearing Loss following dysfunction in the Central Auditory and/or central non auditory system. Auditory Brainstem Implant in Patients who suffer from Neurofibromatosis Type two compare to Non Tumor cases, Mondini Syndrome, Michel aplasia. Possible role of Utricle and Saccule in Auditory (Hearing) System We propose a new Hypothesis that the External Ear Canal is not the only input of Auditory Signals, Sounds could transfer by our eyes and skin to the Cerebral Cortex and approach to the Cochlea (Backward Auditory input pathway of Sounds).

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xi Gu ◽  
Daqi Wang ◽  
Zhijiao Xu ◽  
Jinghan Wang ◽  
Luo Guo ◽  
...  

Abstract Background Aging, noise, infection, and ototoxic drugs are the major causes of human acquired sensorineural hearing loss, but treatment options are limited. CRISPR/Cas9 technology has tremendous potential to become a new therapeutic modality for acquired non-inherited sensorineural hearing loss. Here, we develop CRISPR/Cas9 strategies to prevent aminoglycoside-induced deafness, a common type of acquired non-inherited sensorineural hearing loss, via disrupting the Htra2 gene in the inner ear which is involved in apoptosis but has not been investigated in cochlear hair cell protection. Results The results indicate that adeno-associated virus (AAV)-mediated delivery of CRISPR/SpCas9 system ameliorates neomycin-induced apoptosis, promotes hair cell survival, and significantly improves hearing function in neomycin-treated mice. The protective effect of the AAV–CRISPR/Cas9 system in vivo is sustained up to 8 weeks after neomycin exposure. For more efficient delivery of the whole CRISPR/Cas9 system, we also explore the AAV–CRISPR/SaCas9 system to prevent neomycin-induced deafness. The in vivo editing efficiency of the SaCas9 system is 1.73% on average. We observed significant improvement in auditory brainstem response thresholds in the injected ears compared with the non-injected ears. At 4 weeks after neomycin exposure, the protective effect of the AAV–CRISPR/SaCas9 system is still obvious, with the improvement in auditory brainstem response threshold up to 50 dB at 8 kHz. Conclusions These findings demonstrate the safe and effective prevention of aminoglycoside-induced deafness via Htra2 gene editing and support further development of the CRISPR/Cas9 technology in the treatment of non-inherited hearing loss as well as other non-inherited diseases.


2018 ◽  
Vol 132 (11) ◽  
pp. 1039-1041 ◽  
Author(s):  
J Suzuki ◽  
Y Takanashi ◽  
A Koyama ◽  
Y Katori

AbstractObjectivesSodium bromate is a strong oxidant, and bromate intoxication can cause irreversible severe-to-profound sensorineural hearing loss. This paper reports the first case in the English literature of bromate-induced hearing loss with hearing recovery measured by formal audiological assessment.Case reportA 72-year-old woman was admitted to hospital with complaints of profound hearing loss, nausea, diarrhoea and anuria after bromate ingestion in a suicide attempt. On admission, pure tone audiometry and auditory brainstem responses showed profound bilateral deafness. Under the diagnosis of bromate-induced acute renal failure and sensorineural hearing loss, continuous haemodiafiltration was performed. When dialysis was discontinued, pure tone audiometry and auditory brainstem responses showed partial threshold recovery from profound deafness.ConclusionSevere-to-profound sensorineural hearing loss is a common symptom of bromate intoxication. Bromate-induced hearing loss may be partially treated, and early application of continuous haemodiafiltration might be useful as a treatment for this intractable condition.


2019 ◽  
Vol 39 (35) ◽  
pp. 6879-6887 ◽  
Author(s):  
Kenneth S. Henry ◽  
Mark Sayles ◽  
Ann E. Hickox ◽  
Michael G. Heinz

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 927 ◽  
Author(s):  
M Charles Liberman

The classic view of sensorineural hearing loss has been that the primary damage targets are hair cells and that auditory nerve loss is typically secondary to hair cell degeneration. Recent work has challenged that view. In noise-induced hearing loss, exposures causing only reversible threshold shifts (and no hair cell loss) nevertheless cause permanent loss of >50% of the synaptic connections between hair cells and the auditory nerve. Similarly, in age-related hearing loss, degeneration of cochlear synapses precedes both hair cell loss and threshold elevation. This primary neural degeneration has remained a “hidden hearing loss” for two reasons: 1) the neuronal cell bodies survive for years despite loss of synaptic connection with hair cells, and 2) the degeneration is selective for auditory nerve fibers with high thresholds. Although not required for threshold detection when quiet, these high-threshold fibers are critical for hearing in noisy environments. Research suggests that primary neural degeneration is an important contributor to the perceptual handicap in sensorineural hearing loss, and it may be key to the generation of tinnitus and other associated perceptual anomalies. In cases where the hair cells survive, neurotrophin therapies can elicit neurite outgrowth from surviving auditory neurons and re-establishment of their peripheral synapses; thus, treatments may be on the horizon.


2017 ◽  
Vol 345 ◽  
pp. 79-87 ◽  
Author(s):  
Steven Kroon ◽  
Dyan Ramekers ◽  
Emma M. Smeets ◽  
Ferry G.J. Hendriksen ◽  
Sjaak F.L. Klis ◽  
...  

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