Auditory Neuropathy The term “auditory neuropathy” was coined by Starr and colleagues in 1996, but was criticised by others who felt that the pathology may be misleading and instead preferred terms such as “auditory dys-synchrony”, “auditory de-synchrony” or “auditory mismatch” – terms they believe could better identify or reflect what is happening in the auditory system (Sutton, 2004; Berlin, Li, Hood, Morlet, Rose, & Brashears, 2002). The absent or abnormal morphology at high stimulus levels evident in Auditory Brainstem Response (ABR) diagnostic testing demonstrate abnormal neural responses. While on the other hand, the otoacoustic emission testing using (distortion product otoacoustic emissions) DPOAEs demonstrate present pre-neural responses, suggesting at least a moderate hearing loss present (in DPOAE testing, one would expect to get emissions up to at least 60dB HL) (Gorga, Neely, Ohlrich, 1997). These conflicting results clearly reflect the pattern of “auditory neuropathy”, a label for a pattern of test results that is typically classified to individuals whose test results show an abnormal ABR and present OAEs. Commonly, most auditory neuropathy individuals would reflect having the presence of OAEs and/or cochlear microphonics (CM) revealing normal outer hair cell function, in conjunction with absent ABRs (Starr, Picton, Sininger, Hood, Berlin, 1996). From the literature, it appears that the site of lesion for auditory neuropathy or auditory dys-synchrony (AN/AD) has not been fully understood. On the one hand, Abdala, Sininger, & Starr (2000) mentioned that many patients with AN/AD often display a hearing disorder associated with peripheral neuropathy, denoting that the rational site of lesion, would therefore be the auditory nerve. Patients with suspecting AN/AD would also display poor speech discrimination results (Hood, et. al., 2002). Hood (1998) meanwhile, mentions that the characteristics of AN/AD seem to reflect more than a single etiology and that a number of pathologies can also produce AN/AD. Some of these pathologies, according to Rance, McKay, & Grayden (2004), include: genetics, poor status of inner hair cells (IHCs), an abnormality of the synapse between the IHCs and auditory nerve fibres, a spiral ganglion cell disorder, depleted neuronal populations in the auditory brainstem, and disruption of the synchronicity of the auditory nerve fibres or demyelisation of the auditory nerve. There has also been a noted association between hypoxia and the characteristics of AN/AD. Harrison (1998) proposed that one of the causes of scattered loss of IHCs and its central cochlear afferent connections has been associated with the extended periods of mild hypoxia, which is greatly prevalent in high risk births. Thumak (2002) further states that hypoxia occurs at the IHCs and slowly progresses to include the spiral ganglion cells, with possible continued degeneration of more central neurons in the midbrain. All patients with suspecting AN/AD should undergo cochlear microphonics (CM) assessment. As stated by Berlin, Morlet, & Hood (2003), the CM or cochlear hair cell potentials reflect the electrical activity (or external stimulus) originating from the outer and inner hair cells, and would not affect the CM in AN/AD patients. The CM can also be mistaken as the ABR, however by assessing the effects of polarity, intensity, and m