An X-ray fluorescence microscopic analysis of the tissue surrounding the multi-channel cochlear implant electrode array.

OBJECTIVES: The aim of this study was to analyse the tissue surrounding the University of Melbourne's (UOMs) multi-channel cochlear implant electrode array and cochlear limited replacements, after long-term implantations. In particular, it aimed to identify the particulate material in the fibrous tissue capsule of the arrays implanted in 1978, 1983, and 1998, by using the Australian Synchrotron for X-ray fluorescence microscopy (XFM) to reveal the characteristic spectrum of metal, in particular platinum. This also helped to determine its format and chemical state. Tissue was retrieved following the recipient's death in 2007. METHODS: Tissue was fixed and sections taken across the UOM and Cochlear Corporation (CI-22 and CI-24) electrode tracks. These were stained with Masson's trichrome. The Australian Synchrotron enabled XFM to accurately identify platinum from its characteristic fluorescence spectrum. RESULTS: There was a fibrous tissue capsule (about 100-µm thick) and small regions of calcification around the UOM and CI-22 arrays, but a thinner capsule (40-60-µm thick) around CI-24, and a greater degree of calcification. Dark particulate matter was observed within macrophages and especially in fibrous tissue in proximity to the UOM and CI-22 arrays. This was identified as platinum using X-ray fluorescence. There was also diffusion of platinum into the tissue surrounding the UOM and CI-22 electrodes and fine particles had penetrated the spiral ligament. DISCUSSION: The larger particulate matter in the tissue around the UOM and CI-22 arrays suggested that it had flaked off in the manufacturing of the UOM electrodes. The more diffuse spread of platinum in the tissue around the UOM and CI-22 electrodes was likely due to electrolysis, probably from charge imbalance with the bipolar pulses from the UOM implant. This did not occur with the Cochlear CI-24 device. Furthermore, the widespread fine particles of platinum could have also been due to corrosion, especially from the UOM electrodes.

Biomedical studies on temporal bones of the first multi-channel cochlear implant patient at the University of Melbourne.

OBJECTIVE: To analyse the temporal bones and implant of the first University of Melbourne's (UOM) patient (MC-1) to receive the multi-channel cochlear prosthesis. METHODS: The left cochlea was implanted with the prototype multi-channel cochlear prosthesis on 1 August 1978, and the Cochlear versions CI-22 and CI-24 on 22 June 1983 and 10 November 1998, respectively. MC-1 died in 2007. RESULTS: Plain X-rays of the temporal bones showed that after the CI-22 had been explanted seven electrode bands remained in situ. Micro-CT scans also revealed a partially united fracture transecting the left implanted and right control cochleae. Histology indicated a total loss of the organ of Corti on both sides, and a tear of the left basilar membrane. In addition, there was a dense fibrous capsule with heterotopic bone surrounding one proximal band of the CI-22 array that restricted its removal. This pathology was associated with dark particulate material within macrophages, probably due to the release of platinum from the electrode bands. Scanning electron microscopy (SEM) showed possible corrosion of platinum and surface roughening. Three-dimensional reconstruction of the cochlear histology demonstrated the position of the electrode tracts (C1-22 and CI-24) in relation to the spiral ganglion, which showed 85-90% loss of ganglion cells. DISCUSSION AND CONCLUSIONS: This study confirms our first histopathological findings that our first free-fitting banded electrode array produced moderate trauma to the cochlea when inserted around the scala tympani of the basal turn. The difficulty in extraction was most likely due to one band being surrounded by an unusually large amount of fibrous tissue and bone, with an electrode band caught due to surface irregularities. Some surface corrosion and a small degree of platinum deposition in the tissue may also help explain the outcome for this long-term cochlear implantation.

Decreased phosphatidylethanolamine binding protein expression correlates with Abeta accumulation in the Tg2576 mouse model of Alzheimer's disease.

Phosphatidylethanolamine binding protein (PEBP) is a multifunctional protein, with proposed roles as the precursor protein of hippocampal cholinergic neurostimulating peptide (HCNP), and as the Raf kinase inhibitor protein (RKIP). Previous studies have demonstrated a decrease in PEBP mRNA in CA1 region of AD hippocampus. The current study demonstrates that PEBP is decreased in the hippocampus of 11 month Tg2576 mice, in the absence of change in mRNA levels compared to non-transgenic littermates. The level of PEBP in transgenic mouse hippocampus significantly decreases at 11 months (a time point when Abeta begins accumulating) and 15 months (when Abeta plaques have formed). There was a significant correlation between decreased PEBP expression and accumulation of Abeta. Immunohistochemical studies on Tg2576 and AD brain sections demonstrate that PEBP immunoreactivities are present at the periphery of dense multicore Abeta plaques, and in selective astrocytes, primarily surrounding plaques. These findings suggest that PEBP expression may be influenced by accumulation of Abeta. Down-regulation of PEBP may result in lower levels of HCNP or altered coordination of signal transduction pathways that may contribute to neuronal dysfunction and pathogenesis in AD.