, 2005), proper diagnosis and treatment of tinnitus are of growing concern. Despite its high prevalence, there is little consensus regarding the neurophysiological origin of tinnitus. Most researchers agree that tinnitus can be linked to changes at one or more Venetoclax nmr points along the peripheral and central auditory
pathways (Eggermont and Roberts, 2004, Jastreboff, 1990, Møller, 2003 and Rauschecker et al., 2010). Indeed, human brain imaging studies have identified tinnitus-related dysfunction in auditory areas, including the inferior colliculus (Melcher et al., 2000) and auditory cortex (Giraud et al., 1999, Lockwood et al., 1998, Plewnia et al., 2007 and Reyes et al., 2002). In addition, a link between tinnitus and reorganization of central tonotopic
maps has been suggested, based on MEG studies in humans (Mühlnickel et al., 1998, Weisz et al., 2005 and Wienbruch et al., 2006) and electrophysiological investigations of animals subjected to acoustic trauma (Eggermont and Komiya, 2000, Irvine et al., 2003 and Rajan et al., 1993). Many have proposed that these changes in the central auditory system result from damage to the auditory periphery; however, some cases of Onalespib research buy tinnitus without significant hearing loss seem to indicate that central auditory system dysfunction can stem from other etiologies, like head or neck injury (Henry et al., 2005 and Levine et al., 2003), or may reflect the limitations of standard audiometry (Weisz
et al., 2006). Conversely, peripheral hearing loss does not always lead to tinnitus (Hoffman and Reed, 2004). While it seems, therefore, that auditory system dysfunction is necessary for tinnitus to occur, it is unclear whether auditory system damage alone is sufficient to cause chronic tinnitus, or whether additional mechanisms Farnesyltransferase outside auditory-sensory regions may be involved. Clinicians have noted a relationship between tinnitus and emotional state (Dobie, 2003 and Sullivan et al., 1988), which has led some researchers to propose that the limbic system may play a role in modulating or perpetuating tinnitus (Jastreboff, 1990 and Rauschecker et al., 2010). Indeed, the lifetime incidence of clinical depression in tinnitus patients is estimated to be more than twice that of the national average (∼35% versus ∼15%, respectively; Folmer et al., 1999), and treatment regimens that include forms of cognitive-behavioral therapy have been shown to be effective for some patients (Jastreboff, 2007 and Robinson et al., 2008). However, empirical evidence of limbic system involvement in tinnitus is sparse, and these few studies that report limbic involvement implicate disparate sites: e.g., amygdala (Mirz et al., 2000 and Shulman et al., 1995), hippocampus (Landgrebe et al., 2009 and Lockwood et al., 1998), basal ganglia (Cheung and Larson, 2010 and Lowry et al., 2004), and subcallosal regions (Mühlau et al., 2006).
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