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Permanent Hearing Loss (permanent + hearing_loss)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Morphological Correlates of Acute and Permanent Hearing Loss During Experimental Pneumococcal Meningitis

BRAIN PATHOLOGY, Issue 2 2003
Matthias Klein
In patients with acute bacterial meningitis, hearing loss can be transient but is often permanent. The mechanisms underlying meningitis-associated hearing loss are not fully understood. Therefore, we investigated the morphological correlates of hearing loss in a rat model of pneumococcal meningitis. Transcutaneous intracisternal injection of Streptococcus pneumoniae resulted in a dose-dependent hearing loss (determined by auditory brainstem response audiometry), which was partially reversible during the acute stage. Nevertheless, a severe permanent hearing loss persisted until 2 weeks after infection. Suppurative labyrinthitis was accompanied by blood-labyrinth barrier disruption (determined by cochlear Evans blue extravasation), which correlated closely with hearing loss during the acute stage but not after recovery. Two weeks after infection, spiral ganglion neuronal density was markedly decreased and correlated with the severity of permanent hearing loss. Neuronal loss can be explained by the new finding of meningitis-associated spiral ganglion neuronal necrosis rather than apop-tosis (determined by morphology, TUNEL staining, and immunohistochemistry). [source]

Adverse perinatal conditions in hearing-impaired children in a developing country

PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2006
Bolajoko O. Olusanya
Summary Prevailing adverse perinatal conditions in developing countries have been associated with substantial mortality, but little evidence exists on their impact on permanent childhood disabilities and morbidity due to limitations in clinical investigations and medical records. This study aims to identify the possible association between parent-reported adverse perinatal conditions and permanent hearing loss, in order to establish service needs within current maternal and child health programmes. Structured questionnaires were administered to 363 parents of deaf children and 309 parents of normal-hearing children in an inner city area of Lagos, Nigeria. The parents were from all social classes. After a multivariable logistic regression analysis, birth asphyxia [OR 20.45; 95% CI 6.26, 66.85], difficult delivery [OR 8.09; 95% CI 2.76, 23.68], neonatal jaundice [OR 2.45; 95% CI 1.25, 4.79] and neonatal seizures [OR 2.30; 95% CI 1.09, 4.85] were associated with permanent hearing loss. Consanguineous marriages [OR 6.69; 95% CI 2.72, 16.46] and family history of deafness [OR 6.27; 95% CI 2.07, 18.97] also emerged as additional risk factors for permanent hearing loss. In addition, parents of children in state-owned schools for the deaf were significantly more likely to belong to higher social classes compared with normal-hearing children in mainstream state-owned schools. There is a need to incorporate services for the early detection of permanent hearing loss into current maternal and child healthcare programmes in developing countries. [source]

Enhancing Intrinsic Cochlear Stress Defenses to Reduce Noise-Induced Hearing Loss,,§

THE LARYNGOSCOPE, Issue 9 2002
Richard D. Kopke COL MC USA
Abstract Objectives/Hypothesis Oxidative stress plays a substantial role in the genesis of noise-induced cochlear injury that causes permanent hearing loss. We present the results of three different approaches to enhance intrinsic cochlear defense mechanisms against oxidative stress. This article explores, through the following set of hypotheses, some of the postulated causes of noise-induced cochlear oxidative stress (NICOS) and how noise-induced cochlear damage may be reduced pharmacologically. 1) NICOS is in part related to defects in mitochondrial bioenergetics and biogenesis. Therefore, NICOS can be reduced by acetyl-L carnitine (ALCAR), an endogenous mitochondrial membrane compound that helps maintain mitochondrial bioenergetics and biogenesis in the face of oxidative stress. 2) A contributing factor in NICOS injury is glutamate excitotoxicity, which can be reduced by antagonizing the action of cochlear N -methyl-D-aspartate (NMDA) receptors using carbamathione, which acts as a glutamate antagonist. 3) Noise-induced hearing loss (NIHL) may be characterized as a cochlear-reduced glutathione (GSH) deficiency state; therefore, strategies to enhance cochlear GSH levels may reduce noise-induced cochlear injury. The objective of this study was to document the reduction in noise-induced hearing and hair cell loss, following application of ALCAR, carbamathione, and a GSH repletion drug D-methionine (MET), to a model of noise-induced hearing loss. Study Design This was a prospective, blinded observer study using the above-listed agents as modulators of the noise-induced cochlear injury response in the species chinchilla laniger. Methods Adult chinchilla laniger had baseline-hearing thresholds determined by auditory brainstem response (ABR) recording. The animals then received injections of saline or saline plus active experimental compound starting before and continuing after a 6-hour 105 dB SPL continuous 4-kHz octave band noise exposure. ABRs were obtained immediately after noise exposure and weekly for 3 weeks. After euthanization, cochlear hair cell counts were obtained and analyzed. Results ALCAR administration reduced noise-induced threshold shifts. Three weeks after noise exposure, no threshold shift at 2 to 4 kHz and <10 dB threshold shifts were seen at 6 to 8 kHz in ALCAR-treated animals compared with 30 to 35 dB in control animals. ALCAR treatment reduced both inner and outer hair cell loss. OHC loss averaged <10% for the 4- to 10-kHz region in ALCAR-treated animals and 60% in saline-injected-noise-exposed control animals. Noise-induced threshold shifts were also reduced in carbamathione-treated animals. At 3 weeks, threshold shifts averaged 15 dB or less at all frequencies in treated animals and 30 to 35 dB in control animals. Averaged OHC losses were 30% to 40% in carbamathione-treated animals and 60% in control animals. IHC losses were 5% in the 4- to 10-kHz region in treated animals and 10% to 20% in control animals. MET administration reduced noise-induced threshold shifts. ANOVA revealed a significant difference (P <.001). Mean OHC and IHC losses were also significantly reduced (P <.001). Conclusions These data lend further support to the growing body of evidence that oxidative stress, generated in part by glutamate excitotoxicity, impaired mitochondrial function and GSH depletion causes cochlear injury induced by noise. Enhancing the cellular oxidative stress defense pathways in the cochlea eliminates noise-induced cochlear injury. The data also suggest strategies for therapeutic intervention to reduce NIHL clinically. [source]