Bilateral cochlear implants (CIs) might promote development of binaural hearing required to localize sound sources and hear speech in noise for children who are deaf. These hearing skills improve in children implanted bilaterally but remain poorer than normal. We thus questioned whether the deaf and immature human auditory system is able to integrate input delivered from bilateral CIs. Using electrophysiological measures of brainstem activity that include the Binaural Difference (BD), a measure of binaural processing, we showed that a period of unilateral deprivation before bilateral CI use prolonged response latencies but that amplitudes were not significantly affected. Tonotopic organization was retained to some extent as evidenced by an elimination of the BD with large mismatches in place of stimulation between the two CIs. Smaller place mismatches did not affect BD latency or amplitude, indicating that the tonotopic organization of the auditory brainstem is underdeveloped and/or not well used by CI stimulation. Finally, BD amplitudes decreased when the intensity of bilateral stimulation became weighted to one side and this corresponded to a perceptual shift of sound away from midline toward the side of increased intensity. In summary, bilateral CI stimulation is processed by the developing human auditory brainstem leading to perceptual changes in sound location and potentially improving hearing for children who are deaf.

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The classification of central nervous system tumours has more recently been shaped by a focus on molecular pathology rather than histopathology. We re-classified 82 glial tumours according to the molecular-genetic criteria of the 2016 revision of the World Health Organization (WHO) Classification of Tumours of the Central Nervous System. Initial diagnoses and grading were based on the morphological criteria of the 2007 WHO scheme. Because of the impression of an oligodendroglial component on initial histological assessment, each tumour was tested for co-deletion of chromosomes 1p and 19q and mutations of isocitrate dehydrogenase (IDH-1 and 2) genes. Additionally, expression of proteins encoded by alpha-thalassemia X-linked mental retardation (ATRX) and TP53 genes was assessed by immunohistochemistry. We found that all but two tumours could be assigned to a specific category in the 2016 revision. The most common change in diagnosis was from oligoastrocytoma to specifically astrocytoma or oligodendroglioma. Analysis of progression free survival (PFS) for WHO grade II and III tumours showed that the objective criteria of the 2016 revision separated diffuse gliomas into three distinct molecular categories: chromosome 1p/19q co-deleted/IDH mutant, intact 1p/19q/IDH mutant and IDH wild type. No significant difference in PFS was found when comparing IDH mutant grade II and III tumours suggesting that IDH status is more informative than tumour grade. The segregation into distinct molecular sub-types that is achieved by the 2016 revision provides an objective evidence base for managing patients with grade II and III diffuse gliomas based on prognosis.