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According to the\u00a0NICD (2016),\u00a0<\/a>about 15% of the US population between the ages of 20 and 69 or\u00a026 million people have hearing loss that was probably caused by noise exposure at work or in those noisy, but fun leisure activities.\u00a0 Until recently, the thought was that most NIHL was caused by\u00a0significant damage or death of the hair cells within the cochlea.\u00a0\u00a0Rabinowitz (2000)<\/a>\u00a0summarized the typical thoughts on the pathophysiology of NIHL.\u00a0 \u00a0He felt that, \u201cSounds must exert a shearing force on the stereo cilia of the hair cells lining the basilar membrane of the cochlea. When excessive, this force can lead to cellular metabolic overload, cell damage and cell death. Noise-induced hearing loss therefore represents excessive \u201cwear and tear\u201d on the delicate inner ear structures. Once exposure to damaging noise levels is discontinued, further\u00a0significant progression of hearing loss stops. Individual susceptibility to noise-induced hearing loss varies greatly, but the reason that some persons are more resistant to it while others are more susceptible is not well understood.\u201d\u00a0\u00a0 For decades\u2019 studies from around the world have concurred with this suggestion that NIHL and age related hearing loss\u00a0have focused upon the loss of these\u00a0stereo cilia<\/a>, often called hair cells.\u00a0 While these stereo cilia are vulnerable, researchers at the\u00a0Massachusetts Eye and Ear Infirmary\u2019s\u00a0\u00a0<\/a>(MEEI)\u00a0Eaton Peabody Laboratory\u00a0<\/a>at Harvard Medical School have now shown that nerve fibers are even more vulnerable to damage from noise.<\/p>\n In the normal ear, sound waves are transmitted through the middle ear bones to the inner ear, where they cause vibrations in the sensory epithelium called the\u00a0\u201corgan of Corti.\u201d\u00a0<\/a>The organ of Corti turns this mechanical function into electrical pulse trains in the fibers of the cochlear nerve, which then carries the information to the brain for analysis of the acoustic scene.\u00a0 Dr. Charles Liberman,\u00a0Director of\u00a0MEEIs Eaton Peabody\u00a0Laboratory,\u00a0is an expert on\u00a0the peripheral auditory system.\u00a0 He\u00a0explains that,\u00a0\u201cThe organ of Corti contains two types of sensory cells:\u00a0outer and inner hair cells,\u201d\u00a0<\/a>explained Charles Liberman, director of MEEI\u2019s Eaton Peabody Laboratory.<\/p>\n \u201cThe sensory cells are called \u2018hair cells\u2019 because of the hair-like tufts of microvilla on their apical surfaces, which are called \u2018stereo cilia.\u2019 Bending the stereo cilia opens ion channels in the nerve hair cells and allows a current to flow that ultimately excites the fibers of the cochlear nerve. This is the heart of the\u00a0mechanical-to-electrical transduction process in the inner ear.\u201d<\/a><\/p>\n How did this hidden hearing loss remain \u201chidden\u201d so long?\u00a0\u00a0 Liberman felt that there are two main reasons for this,\u00a0\u201dFirst, the field of auditory neuroscience didn\u2019t appreciate until recently that you can lose up to 90 percent of your cochlear nerve fibers without a change in the ability to detect a tone in quiet,\u201d he said. \u201cTone detection in quiet is the basis of the threshold audiogram \u2014 the gold standard test of hearing function. The fact that thresholds may transiently elevate and then recover within hours or days after an acoustic overexposure doesn\u2019t mean that the inner ear has recovered.\u201d \u201cAnd\u00a0Second, the most vulnerable part of the neuron turns out to be the synapse between the nerve terminal and the hair cell, and it\u00a0happens to be difficult to see. \u201cUntil recently, they could only be seen and counted by using an electron microscope,\u201d<\/p>\n In their research, Liberman and Sharon Kujawa, Director of Audiology for MEEI stained synapses with antibodies that target molecular structures within the synapse, which allowed the\u00a0synapses<\/a>\u00a0to be seen and easily counted in a\u00a0light microscope<\/a>. This enabled them to view many synapses on hair cells in a normal ear, as well as the\u00a0greatly reduced numbers of synapses hair cells following a noise exposure<\/em>\u00a0that caused only a transient elevation of thresholds.<\/p>\n They noted that \u201ceach missing synapse represents a missing cochlear nerve that has been disconnected due to retraction of the terminal segment \u2014\u00a0it will never reconnect<\/em>.\u201d\u00a0 Liberman also indicated that, \u201cIt no longer responds to sound and, within a few months is almost certainly unwarranted,\u201d\u00a0The researchers are aware of the public health implications of their findings in that all our federal noise exposure guidelines assume that noise exposures cause only transient threshold elevation are benign and now that assumption is certainly outdated.<\/p>\n While their research was conducted on mammalian ears, mouse, guinea pig and chinchillas, there is\u00a0every reason to believe that that this same phenomenon exists in humans.\u00a0 The study has led to the possibility that maybe these synapse issues can be reversible, continuing research goes on in their laboratory on this issue.<\/p>\n Epilog:<\/p>\n Those of us that see patients each day can testify to this interesting study as we often see patients that have minimal hearing loss on the audiogram, but significant difficulty hearing, or with tinnitus.\u00a0 It is just this type of research that begins to confirm some of the clinical mysteries of hearing, hearing loss and hearing rehabilitation, seen in the clinic each day, and unexplained for decades.\u00a0<\/em><\/strong><\/p>\n![\"\"](\"https:\/\/arizonahearing.com\/wp-content\/uploads\/2016\/11\/hearing-loss-ct-scan.jpg\" "\\"hearing-loss-ct-scan\\"")
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