Tinnitus And The Psychology Of Hearing Essay Example for Free

Tinnitus And The Psychology Of Hearing Essay â€Å"Tinnitus is the subjective sensation of noise—usually described as ringing, hissing, buzzing, roaring, chirping, or clicking sounds—in the ears that cannot be attributed to any external sound† (Hannan, Sami, Wareing, 2005; Lalwani, Snow, 2005). The American Tinnitus Association (2007) estimates that about 50 million Americans experience tinnitus, with men affected more than women (Lockwood, Salvi, Burkard, 2002). â€Å"Twenty-five percent of these individuals suffer from severe enough tinnitus to prompt medical consultation†. Although a relatively common condition, the mechanisms of tinnitus are as yet poorly understood (Lalwani et al, 2005; Lockwood et al, 2002). â€Å"As discussed by Lockwood and associates (2002), there are currently two schools of thought that offer contradictory explanations as to the origin of tinnitus†. On the one hand are those who forward the hypothesis that tinnitus is mainly due to a cochlear pathology, as evidenced by the high incidence of cochlear damage in individuals with tinnitus. This is countered on the other hand by those who propose a central nervous system origin of tinnitus, as implied by the observation of tinnitus in patients with complete transections of the auditory nerve (Lockwood et al, 2002). The present paper is a review of the physiology of hearing, and an attempt to correlate it with tinnitus. Hearing is a function subserved peripherally by the ears and the auditory nerve (cranial nerve VIII), and centrally by the transverse temporal gyri of the temporal lobe (Willis, 2004). These structures altogether make up the auditory system, which primarily functions in the transduction of sounds emanating from the environment. The peripheral auditory apparatus—that is, the ear—â€Å"acts as the interface between the external environment and the individual†. Sound—actually wave vibrations—enters the external auditory canal and sets the tympanic membrane in motion. This, in turn, moves the ossicles—the maleus, incus and stapes—which causes pressure changes in the fluid-filled inner ear. Clearly, from the external environment to the inner ear, sound is carried as wave vibrations, transmitted initially through solids—cartilage and bone—and later through a fluid media—the perilymph and endolymph. The efficiency of this process—a transfer of energy from air, through solids, then through fluids—is ensured by the tympanic membrane and the ossicles, which act as an impedance-matching device (Lalwani et al, 2005). From the internal ear to the central nervous system, on the other hand, sound is interpreted as gradients of electron charges across membranes. The inner ear—principally the cochlea—is a complex composed of the bony and membranous labyrinths. The bony labyrinth component of the cochlea includes several chambers, namely the scala vestibuli and the scala tympani. The scala vestibuli connects with the vestibule and the oval window, whereas the scala tympani connect with the round window. These two chambers merge at the helicotrema, located at the cochlear apex. The membranous labyrinth component of the cochlea is the scala media, which is located between the scala vestibuli and scala tympani. As mentioned previously, the inner ear is a fluid-filled structure. Specifically, the scala vestibuli and the scala tympani are filled with perilymph, which resemble cerebrospinal fluid, while the scala media is filled endolymph, which resembles intracellular fluid (Willis, 2004). Within the cochlea is located the organ of Corti, the neural apparatus responsible for sound transduction, which is composed of several thousand hair cells, the sensory receptors for sound. At the apex of each hair cell are stereocilia, and at the base are nerve fibers that belong to the cochlear division of the eighth cranial nerve. The sound wave transmitted by the middle ear case fluid movements within the bony labyrinth, and part of the hydraulic energy of these fluid movements result in displacement of the organ of Corti. The stereocilia are deformed or bent by the shear forces produced by this relative displacement. The current concept of cochlear transduction is that displacement of the tips of the stereocilia, especially if this displacement is toward the tallest cilium (Willis, 2004), allows potassium to flow into the cell, resulting in its depolarization (Lalwani et al, 2005; Ricci, Kachar, Gale, Van Netten, 2006). The influx of potassium opens calcium channels near the base of the cell, stimulating transmitter release, thought to be glutamate or aspartate (Willis, 2004; Lalwani et al, 2005; Ricci et al, 2006), and firing of the cochlear nerve fibers. This discharge is transmitted to, from peripheral to central, the dorsal and ventral cochlear nuclei, trapezoid body, superior olivary complex, lateral lemniscus, inferior colliculus, medial geniculate nucleus of the thalamus (which gives rise to the auditory radiation), and ends in the auditory cortex located in the transverse temporal gyri of the temporal lobe (Willis, 2004; Lalwani et al, 2005). The end-result of all these is the perception of sound. The subjective perception of sound that is tinnitus could theoretically originate anywhere along the length of the auditory system. However, since the sound heard of individuals suffering from tinnitus is not attributable to any external source, the origin of tinnitus could be limited to the cochlea, specifically the organ of Corti, and the central nervous sytem (Lockwood et al, 2005). Cochlear damage, specifically damage to the hair cells of the organ of Corti, was initially believed to cause tinnitus (Eggermont, 1990; Zenner Ernst, 1993). Although auditory receptor cells have been documented to regenerate and subsequently recover functionally after damage in many vertebrates (Goode, Carey, Fuchs, Rubel, 1999; Stone Rubel, 2000; Zakir Dickman, 2006), spontaneous regeneration of mammalian hair cells does not occur (Zakir et al, 2006). Damage to hair cells, especially through prolonged exposure to supraphysiologic sound levels, may result to transmission of depolarization within the hair cell, and, thus, false perception of sound in the absence of an external source of the same. In contrast to this proposition was the hypothesis forwarded by Lockwood and companions (2002), which attributes tinnitus to central nervous system defects. â€Å"They propose that hearing loss results to reorganization of the pathways in the central auditory system†, which lead to abnormal interactions between auditory and other central pathways, as is seen in neuropathic pain. An example of this phenomenon is gaze-evoked tinnitus, â€Å"where lateral eye movements fail to produce the inhibition of the auditory cortex observed in controls†. It was proposed that the absence of this phenomenon may contribute to the false perception of sounds, that is, tinnitus (Lockwood et al, 2002). It was contended that this explanation accounted for the perception of tinnitus in individuals whose auditory nerves have already been previously transected. Lockwood and associates (2002), citing from Levine (1999), also forwarded the explanation that tinnitus results from a reduction in auditory-nerve input, â€Å"which leads to disinhibition of the dorsal cochlear nucleus and an increase in spontaneous activity in the central auditory system†. This mechanism was proposed to explain tinnitus experienced by normal individuals following exposure to noise, or placement in total silence. REFERENCES American Tinnitus Association (2007). About tinnitus. Retrieved April 3, 2007, from http://www.ata.org/about_tinnitus/consumer/faq.html#1. Eggermont JJ (1990). On the pathophysiology of tinnitus: a review and a peripheral model. Hear Res, 48, 111-24. Goode CT, Carey JP, Fuchs AF, Rubel EW (1999 March). Recovery of the vestibulocolic reflex after aminoglycoside ototoxicity in domestic chickens. J Neurophysiol, 81(3), 1025-35. Hannan SA, Sami F, Wareing MJ (2005, 29 January). 10-minute consultation: tinnitus. BMJ, 330, 237. 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