Inferior colliculus responses to dual-site intralamina stimulation in the ventral cochlear nucleus.

A major limitation of the present auditory brainstem implant (ABI) is its inability to access the tonotopic organization of the ventral cochlear nucleus (VCN). A previous study by our group indicated that stimulation of single sites within a given VCN frequency region did not always elicit frequency-specific responses within the central nucleus of the inferior colliculus (CIC) and in some cases did not elicit a response at all. For this study, we hypothesized that sequential stimulation (with a short interpulse delay of 320 μsec) of two VCN sites in similar frequency regions would enhance responsiveness in CIC neurons.

An in vivo investigation of first spike latencies in the inferior colliculus in response to multichannel penetrating auditory brainstem implant stimulation.

The cochlear nucleus (CN) is the first auditory processing site within the brain and the target location of the auditory brainstem implant (ABI), which provides speech perception to patients who cannot benefit from a cochlear implant (CI). Although there is variance between ABI recipient speech performance outcomes, performance is typically low compared to CI recipients. Temporal aspects of neural firing such as first spike latency (FSL) are thought to code for many speech features; however, no studies have investigated FSL from CN stimulation.

Acute cochlear nucleus compression alters tuning properties of inferior colliculus neurons.

Auditory brainstem implants (ABI) have been used in neurofibromatosis type 2 (NF2) patients in an attempt to restore hearing sensation, with limited clinical success. Factors associated with poor clinical outcomes for NF2 ABI patients include larger tumour size, longer duration of hearing loss, and brainstem distortion and/or deformation caused by tumours that compress the brainstem. The present study investigated changes in tuning properties of inferior colliculus (IC) neurons following compression of the contralateral cochlear nucleus (CN).

Creutzfeldt-Jakob disease: Australian surveillance update to March 2007.

From October 1993, prospective, national surveillance of the rare class of neurodegenerative diseases known as transmissible spongiform encephalopathies (TSEs) has been performed by the Australian National Creutzfeldt-Jakob Disease Registry. Surveillance of TSEs prior to October 1993, involved the retrospective ascertainment of TSE cases from 1970 to 1993. In this report, surveillance data for 2006 are presented in detail and compared to cumulative national TSE ascertainment as well as international experience.

Creutzfeldt-Jakob disease: Australian surveillance update to December 2005.

Australia-wide prospective surveillance of human transmissible spongiform encephalopathies (TSEs) has been conducted by the Australian National Creutzfeldt-Jakob Disease Registry (ANCJDR) since October 1993. In addition, the Registry retrospectively ascertained TSE cases within Australia from 1970. Referrals of all suspect cases of human prion diseases or TSEs are investigated by the ANCJDR and include Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome, fatal familial insomnia and variant CJD.

Precocious terminal differentiation of premigratory limb muscle precursor cells requires positive signalling.

The timing of myogenic differentiation of hypaxial muscle precursor cells in the somite lags behind that of epaxial precursors. Two hypotheses have been proposed to explain this delay. One attributes the delay to the presence of negative-acting signals from the lateral plate mesoderm adjacent to the hypaxial muscle precursor cells located in the ventrolateral lip of the somitic dermomyotome (Pourquié et al.