Graeme Clark Collection
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ItemMeningitis after cochlear implantation: the risk is low, and preventive measures can reduce this further( 2007)Since the 1980s, more than 80 000 people have received cochlear implants worldwide. These implants are designed to enable people who are severely or profoundly deaf to experience sound and speech. Since 1990, implantation has become standard treatment for people who cannot communicate effectively despite well fitted hearing aids. Children who are deaf when they are born can perceive sound and learn to speak if they receive cochlear implants at a young age (ideally under 18 months). The use of cochlear implants has been thought to be safe. But since 2002 the number of patients with meningitis related to cochlear implantation has increased worldwide. Mortality and neurological complications after meningitis are high. We need to investigate the reasons for this and look at measures to reduce them.
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ItemThreshold shift: effects of cochlear implantation on the risk of pneumococcal meningitis( 2007)Unavailable due to copyright.
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ItemEffects of inner ear trauma on the risk of pneumococcal meningitis( 2007)Objective: To examine the risk of pneumococcal meningitis in healthy rats that received a severe surgical trauma to the modiolus and osseous spiral lamina or the standard insertion technique for acute cochlear implantation. Design: Interventional animal studies. Subjects: Fifty-four otologically normal adult Hooded- Wistar rats. Interventions: Fifty-four rats (18 of which received a cochleostomy alone; 18, a cochleostomy and acute cochlear implantation using standard surgical techniques; and 18, a cochleostomy followed by severe inner ear trauma) were infected 4 weeks after surgery with Streptococcus pneumoniae via 3 different routes (hematogenous, middle ear, and inner ear) to represent all potential routes of bacterial infection from the upper respiratory tract to the meninges in cochlear implant recipients with meningitis. Results: Severe trauma to the osseous spiral lamina and modiolus increased the risk of pneumococcal meningitis when the bacteria were given via the middle or inner ear (Fisher exact test, P<.05). However, the risk of meningitis did not change when the bacteria were given via the hematogenous route. Acute electrode insertion did not alter the risk of subsequent pneumococcal meningitis for any route of infection. Conclusions: Severe inner ear surgical trauma to the osseous spiral lamina and modiolus can increase the risk of pneumococcal meningitis. Therefore, every effort should be made to ensure that cochlear implant design and insertion technique cause minimal trauma to the bony structures of the inner ear to reduce the risk of pneumococcalmeningitis.
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ItemAssessment of the protective effect of pneumococcal vaccination in preventing meningitis after cochlear implantation( 2007)Objectives: To examine if a 23-valent pneumococcal capsular polysaccharide vaccine (PPV23) reduces the risk of meningitis in healthy rats after cochlear implantation. Design: Interventional animal study. Interventions: Thirty-six rats (18 immunized and 18 unimmunized) received cochlear implantations and were then infected with Streptococcus pneumoniae via 3 different routes (hematogenous, middle ear, and inner ear) in numbers sufficient to induce meningitis. Results: The rats with implants that received PPV23 were protected from meningitis when the bacteria were delivered via the hematogenous and middle-ear routes (Fisher exact test P<.05). However, the protective effect of the vaccine in the rats with implants was only moderate when the bacteria were inoculated directly into the inner ear. Conclusions: Our animal model clearly demonstrates that immunization can protect healthy rats with a cochlear implant from meningitis caused by a vaccine-covered serotype. This finding supports the notion that all current and future implant recipients should be vaccinated against S pneumoniae.
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ItemHistopathology of the binaural cochlear implant subject [Abstract]( 2001)Binaural hearing improves speech reception in noise, and is necessary for sound localisation. Normal hearing subjects use both interaural time, and intensity, differences to localise sound. This study investigates why sound localisation in bilateral cochlear implantees is insensitive to interaural time differences (Hoesel 1993). We looked for evidence of neural degeneration in the auditory brainstem involved in binaural sound localisation, since this may have degraded the neural circuitry required to accurately code interaural time delays. Method: The brainstem of a bilateral cochlear implantee was prepared for light microscopy by embedding it in paraffin, sectioning at 10 mm and staining sections with thionine or Luxol fast blue (LFB). The histological sections were digitised with NIH Image and 3-dimensional reconstructions made of the cochlear nucleus (CN) and superior olivary complex (SOC) with AnalysePC. Within the CN and the SOC, cell number and size were estimated by the physical dissector technique following thionine staining, and myelination of the nerve fibres was estimated using the optical density method following LFB staining. Results: A reduction in cell size (from thionine staining) and myelination (from LFB staining) was seen in both the CN and the SOC. Conclusions: These finding are consistent with neural degeneration within the auditory pathways. This may have lead to a degradation of the neural circuitry required to accurately detect interaural time delays.