Os recomendamos este interesante libro sobre la medicina hiperbárica regenerativa (en inglés)

Hyperbaric, Sensorineural Hearing Loss

Heather M. Murphy-Lavoie; Mesut Mutluoglu.

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Last Update: February 10, 2020.

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The sudden sensorineural hearing loss is defined as a hearing loss of at least 30 decibels occurring over at least three consecutive frequencies and lasting at least 3 days. A specific etiology is identified only about 10% to 15% of the time, the majority of the time this is deemed idiopathic. Possible etiologies include vascular occlusion, viral infections, labyrinthine membrane breaks, autoimmune, trauma, toxins, cochlear membrane damage, demyelinating disease, stroke, and schwannoma. The patient typically first notices symptoms upon awakening and describes an aural fullness/blockage. They may also experience tinnitus (usual), dizziness, or vertigo. There are approximately 4000 new cases in the United States annually. The spontaneous recovery rate is difficult to determine since many patients do not seek medical care but it has been reported as low as 25% and as high as 65%. In most controlled trials, the spontaneous recovery in patients receiving placebo is between 35% and 39%. Hearing loss can impose heavy social and economic burdens and significantly impair a patients quality of life. Adult-onset hearing loss is the most common cause of disability globally and the third leading cause of years of productivity lost due to disability according to the World Health Organization (WHO). Hearing aids are recommended for moderate (41 decibels to 60 decibels) and severe (61 decibels and greater) hearing loss. More than 60 treatment protocols have been described for the sudden sensorineural hearing loss, but the majority of these are not efficacious. The three most promising treatments include corticosteroids, vasodilators, and hyperbaric oxygen therapy. Of these, only hyperbaric oxygen has sufficient randomized controlled trials to have a positive meta-analysis Cochrane review.[1][2][3]

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Anatomy and Physiology
Hearing function in the inner ear is maintained by the cochlea which is known to have a high oxygen demand. Cochlear hypoxia is associated with progressive ossification, fibrosis, loss of neurons, endolymphatic hydrops, and hearing loss. Direct blood supply to the organ of Corti is minimal; oxygen must diffuse through the perilymph and cortilymph. The labyrinthine artery (internal auditory artery) is a long, slender branch off of the anterior inferior cerebellar artery (85%) or the basilar artery (15%). It accompanies the vestibulocochlear nerve through the internal acoustic meatus into the inner ear. Animal models of labyrinthine artery occlusion have shown progressive degenerative changes, fibrosis, new bone formation and hearing loss. Any pathology that results in vascular occlusion of this artery can result in hearing loss.

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