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Test1 Essay

3199 words - 13 pages

Auditory prostheses have been treating hearing loss for decades, with the cochlear implant (CI) being able to provide sufficient temporal and spectral cues required for speech understanding (Kral and O'Donoghue 2010; Shannon et al. 1995; Zeng 2004). For people without a functional auditory nerve or an implantable cochlea, central prostheses have been implanted in the brainstem since 1979. Unfortunately, the performance of the auditory brainstem implant (ABI) has generally been less successful than the CI, particularly for patients with neurofibromatosis type II (NF2), one of the key target populations for the implant (Colletti et al. 2009; Lim et al. 2009; Schwartz et al. 2008). While some ABI patients have shown performance levels approaching that of CI patients (Colletti et al. 2012; Sennaroglu et al. 2011), continued research into central auditory implants needs to be performed in order to improve hearing perception for the majority of patients who cannot benefit from a CI.
As an alternative approach to the ABI, particularly for the NF2 population, deaf patients have been implanted with a new auditory midbrain implant (AMI) consisting of a single-shank array (20 sites) designed for stimulation along the tonotopic gradient of the central nucleus of the inferior colliculus (ICC) (Lim et al. 2009; Lim et al. 2007). While AMI stimulation can activate frequency-specific neurons and transmit spectral cues to higher auditory centers, it appears to exhibit limited temporal coding abilities (Lenarz et al. 2006; Lim and Anderson 2006; Lim et al. 2013; Lim et al. 2008; McKay et al. 2013).
Calixto et al. (2012) investigated this limited performance of the AMI by stimulating the ICC of guinea pigs with the AMI array and recording the evoked local field potentials (LFPs) in the primary auditory cortex (A1). Repeated stimulation of a single site caused refractory and suppressive neural effects, which likely resulted in the inadequate temporal coding. These negative effects could be overcome by stimulating at multiple sites within an isofrequency lamina. In addition, co-activation of sites with short delays (<5 ms) resulted in cortical activity that was enhanced beyond a linear sum of activation elicited by the individual sites. However, their interpretation of A1’s role in this enhancement effect was limited because they only analyzed LFPs in the main input layer III/IV (i.e., corresponding to thalamic input into A1). They also did not analyze spike activity in A1 because of the prevalence of antidromic field potentials from ICC stimulation that could partially mask the orthodromically activated spikes across cortical layers. As a result, they were unable to determine if this enhancement effect was solely produced within the tectothalamic pathway or if it also occurred within the thalamocortical and corticocortical pathways. Moreover, they were unable to determine whether this enhancement effect could be observed when stimulating across different ICC...

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