Myasthnic related hearing loss....

Vorsia

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:wave:Hi alldeaf i have a question to ask i know you all are not doctors you never know who might be one though..I have myasthenia gravis profound in my left ear from a baby of unknown etiology right ear was mild loss.. all my life till this year when my right ear whent into the severe to profound range,so the audiology recommended a hearing aid ...so i will be receiving one aid the end of dec,so my question is this pass week i have been noticeing.My right ear is starting to sound like profound my question is could the myasthenia garvis cause me to lose more hearing loss or is this just a prgessive loss like i was told..or could the mg make it go fast meaning the hearing loss speed up i don't know i know that... Acetyl Choline (ACH) is the main neurotransmitter of the efferent auditory stem, we know that so it can affect otoacoustic emissions.Myasthenia gravis is a autoimmune neuromuscular disease that, affects the body.. so if anyone can sent me some links.. i would love to read more i can seem to find much.... thank you ALLDAEF LOVE YOU ALLL......VORSIA SINGING OFF...
 
Irreversible cochlear damage in myasthenia... [Acta Neurol Scand. 2006] - PubMed - NCBI

abstract
OBJECTIVE:

Acetyl choline (ACh) is the main neurotransmitter of the efferent auditory system. This study is aimed to evaluate cochlear function in myasthenia gravis (MG), a neuromuscular transmission disorder caused by ACh receptor autoantibodies.
METHODS:

This prospective study included 16 myasthenic patients, tested audiologically twice, first after improvement from myasthenic crisis or acute oropharyngeal dysfunction (1 week from admission) and then 2 months later. We detected the effect of contralateral acoustic stimulation (CAS) on patients' transient and distortion product otoacoustic emissions (TEOAE and DPOAE).
RESULTS:

Compared with controls, patients reported significant reduction in overall echo response and amplitude of TEOAEs at 1-2 kHz and at 1-6 kHz of DPOAE with marked reduction at 5 kHz. In the control group, CAS produced amplitude reduction in TEOAEs and DPOAEs at 1-4 kHz. Utilizing masking effect, patients reported amplitude reduction in TEOAEs at 1.5-4 kHz while DPOAEs did not reach significant level except at 1.5 and 5 kHz. After 2 months, no changes were observed compared with early assessment.
CONCLUSIONS:

It is clear that disease progression is associated with irreversible cochlear damage. Lack of improvement in patients' emissions despite partial non-audiometric improvement in relation to receptors needs to be considered.
 
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