1998; Dietrich et al 2001; Lockwood et al 2002; Moller 2003)

1998; Dietrich et al. 2001; Lockwood et al. 2002; Moller 2003). Such data brought support for a cochlear origin for tinnitus but alternative possibilities have been raised. Thus, it is unclear whether hyperactivity along the auditory pathway is a direct consequence

of cochlear cell damage or results from hyperactivity in Inhibitors,research,lifescience,medical other neuronal pathways (Shore et al. 2008) and it has been argued that an auditory map reorganization, cannot satisfactorily explain the emergence of tinnitus perception (Weisz et al. 2005). Additionally, not all available data fit with an exclusive role of cochlear damages. Several studies have shown that hearing loss, which is directly related to cochlear cell damage, is not a clear http://www.selleckchem.com/products/SB-431542.html predictor of the occurrence Inhibitors,research,lifescience,medical and severity of tinnitus, despite the fact that tinnitus is more prevalent in subjects with hearing loss (Jastreboff and Hazell 2004; Verret et al. 2005; Nottet et al. 2006). Besides cochlear damage, other factors, such as somatosensory disturbances may be involved in tinnitus (Levine 1999, 2003; Sanchez et al. 2002; Levine et al. 2007).

However, evidence for a somatosensory origin has been lacking in the case of AAT tinnitus. Tinnitus has also been proposed to be analogous to phantom pain (Tonndorf Inhibitors,research,lifescience,medical 1987; Moller 1997; Folmer Inhibitors,research,lifescience,medical et al. 2001; De Ridder et al. 2007). Patients with severe tinnitus actually share similar emotional disturbances proposed to be similar to chronic pain sufferers (Axelsson and Ringdahl 1989; Heller 2003). Finally, an influence of

anxiety/mood states on noise-induced tinnitus onset after noise exposure has been also demonstrated (Job et al. 2004), suggesting a role for the autonomous sympathetic system (Hoehn–Saric and McLeod 1988; Critchley et al. Inhibitors,research,lifescience,medical 2004). Very recently parasympathetic stimulation in rats has demonstrated to abolish the tinnitus-like signal in conditioned animals when coupled to simultaneous auditory stimulation (Engineer et al. 2011). Could AAT tinnitus be a proprioceptive illusion? Tinnitus is defined as an illusory percept. In osteoarticular and muscle systems, illusory percepts can be triggered by GBA3 activation of the fusimotor systems (Goodwin et al. 1972; Roll et al. 1989). In limb muscles, for instance, low-frequency vibration applied to a specific muscle tendons activate muscle spindle endings via the fusimotor system and induce illusory sensation of specific gesture(Calvin–Figuiere et al. 1999). Interestingly, the induction of kinesthetic illusions generates hyperactivations in the precentral gyrus (BA 6), inferior parietal lobule (BA 40), and cingulate cortex (BA 32, BA 24) (Romaiguere et al. 2003), which we also find hyperactive in AAT subjects.

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