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Normally if an audiologist can see a hearing loss shift between entrance and exit exams and a low incidence of occupational noise exposure they will render an opinion. If there is a Whisper Test, they should do an opinion because the Whisper Test is not scientifically based. They should state that these are the most cutting edge studies that look at hearing loss by leading researchers. The VA is behind the power curve on this issue citing old outdated studies that do not look at noise injury inside the ear. “Exposure to lots of loud noise when you are young does lead to accelerated age-related hearing loss later in life,” Wang says, “indicating that the damage from noise early in life continues to have deleterious effects over time.” She believes this may be due to lost connections between hair cells and Spiral Gagnlions (SGNs) that [b]never recover[/b]. AHRF Researchers Believe Damage From Noise Occurs Long Before Hearing Loss Is Perceived: http://american-hearing.org/ahref-news/noise-damage/ Actual Study: http://www.jneurosci.org/content/31/21/7938.full Power Point by Sharon Kujawa, PhD on the damage that happens inside the ear; very educational: http://tinyurl.com/ma76tks Very interesting that the 2nd slide shows two service members on an aircraft carrier deck. The following statement is no longer true when cited in the rating decision according to the above study and presentation: "Therefore, audiologists have no scientific basis for concluding that delayed onset hearing losses exist.” Here is more recent study dated 2014 cited at the bottom of the 2011 study: http://www.jneurosci.org/content/34/39/13110.abstract piral ganglion neurons (SGNs) receive input from cochlear hair cells and project from the cochlea to the cochlear nucleus. After destruction of hair cells with aminoglycoside antibiotics or noise SGNs gradually die. It has been assumed that SGN death is attributable to loss of neurotrophic factors (NTFs) derived from hair cells or supporting cells in the organ of Corti (OC). We used quantitative PCR (qPCR) to assay NTF expression—neurotrophin-3 (NT-3), BDNF, GDNF, neurturin, artemin, and CNTF—in the OC and cochlear nucleus at various ages from postnatal day 0 (P0) to P90 in control hearing and neonatally deafened rats. NT-3, neurturin, and CNTF were most abundant in the postnatal hearing OC; CNTF and neurturin most abundant in the cochlear nucleus. In the OC, NT-3 and CNTF showed a postnatal increase in expression approximately concomitant with hearing onset. In rats deafened by daily kanamycin injections (from P8 to P16), surviving inner hair cells were evident at P16 but absent by P19, with most postsynaptic boutons lost before P16. NT-3 and CNTF, which normally increase postnatally, had significantly reduced expression in the OC of deafened rats, although CNTF was expressed throughout the time that SGNs were dying. In contrast, neurturin expression was constant, unaffected by deafening or by age. CNTF and neurturin expression in the cochlear nucleus was unaffected by deafening or age. Thus, NTFs other than NT-3 are available to SGNs even as they are dying after deafening, apparently conflicting with the hypothesis that SGN death is attributable to lack of NTFs. This is an older Power Point by Sharon Kujawa, PhD, but it really gives you some excellent illustrations on the visible damage that happens inside the ear: http://tinyurl.com/ke4jmxb