Permanent Sensorineural Hearing Loss Research Articles

Altered expression of middle and inner ear cytokines in mouse otitis media

The inner ear is at risk for sensorineural hearing loss in both acute and chronic otitis media (OM), but the mechanisms underlying sensorineural hearing loss are unknown. Previous gene expression array studies have shown that cytokine genes might be upregulated in the cochleas of mice with acute and chronic OM. This finding implies that the inner ear could manifest a direct inflammatory response to OM that may cause sensorineural damage. Therefore, to better understand inner ear cytokine gene expression during OM, quantitative real-time polymerase chain reaction and immunohistochemistry were used in mouse models to evaluate middle and inner ear inflammatory and remodeling cytokines. Basic science experiment. An acute OM model was created in Balb/c mice by a transtympanic injection of Streptococcus pneumoniae in one ear; the other ear was used as a control. C3H/HeJ mice were screened for unilateral chronic OM, with the noninfected ear serving as a control. Both acute and chronic OM caused both the middle ear and inner tissues in these two mouse models to overexpress numerous cytokine genes related to tissue remodeling (tumor necrosis factor-α, bone morphogenetic proteins, fibroblast growth factors) and angiogenesis (vascular endothelial growth factor), as well as inflammatory cell proliferation (interleukin [IL]-1α,β, IL-2, IL-6). Immunohistochemistry confirmed that both the middle ear and inner ear tissues expressed these cytokines. Cochlear tissues are capable of expressing cytokine mRNA that contributes to the inflammation and remodeling that occur in association with middle ear disease. This provides a potential molecular basis for the transient and permanent sensorineural hearing loss often reported with acute and chronic OM.

Pattern of Ototoxicity in a Nigerian Teaching Hospital

Ototoxicity is a preventable cause of irreversible sensorineural hearing loss. This paper aims to highlight the pattern of ototoxicity seen in a tertiary health institution. A retrospective study of patients with ototoxicity seen over a seven year period at ENT department of Aminu Kano Teaching Hospital, Kano. Case notes were retrieved and studied. Fifty nine patients made up 37 males and 22 females were seen with 86% in the age group 20-60 years. The commonest ototoxic drugs were aminoglycosides (37.3%), loop diuretics (27.1%), antimalarials (23.7%) and traditional concoctions (11.9%). The commonest presentation from most drugs was permanent sensorineural hearing loss (50-85%). Associated comorbid conditions included "febrile illness" (475%), hypertension (30.5%), diabetes mellitus (13.6%), renal disease (5%). Follow-up was poor. Only 18 patients presented for review beyond a second hospital visit, only those with ototoxicity from antimalarials recovered hearing. There were no effective audiometric and serum drug monitoring mechanism in place before, during or after therapy with ototoxic medications. Ototoxicity is not uncommon and attempts at prevention are feeble. Increased awareness of this condition is advised. High frequency audiometric assessment, otoacoustic emission and serum drug monitoring facilities should be provided at health institutions. Caution should be exercised when prescribing ototoxic drugs in the presence of other risk factors.

Expression of candidate markers for stem/progenitor cells in the inner ears of developing and adult GFAP and nestin promoter-GFP transgenic mice

Loss of hair cells in the mammalian cochlea leads to permanent sensori-neural hearing loss. Hair cells degenerate and their places are taken by phalangeal scars formed by non-sensory supporting cells. Current data indicate that early postnatal post-mitotic supporting cells can proliferate and differentiate into hair cell-like cells in culture.In this study, we used GFAP and nestin promoter-GFP transgenic mice in combination with other stem cell markers to characterize supporting cell subtypes in the postnatal day-3 (P3) and adult organs of Corti with potential stem/progenitor cell phenotype.In P3 organ of Corti, we show GFAP-GFP signal in all the supporting cell subtypes while the nestin-GFP was restricted to the supporting cells in the inner hair cell area. At this stage, GFAP and selected stem/progenitor markers displayed overlapping expression pattern in the supporting cell population.In the adult, GFAP expression is down-regulated from the supporting cells in the outer hair cell area and nestin expression is down-regulated in the supporting cells of the inner hair cell area. Sox2 and Jagged1 expression is maintained in the mature supporting cells, while Abcg2 was down-regulated in these cells. In contrast, GFAP and Abcg2 expression was up-regulated in the inner sulcus limbal cells outside the mature organ of Corti’s area. Using quantitative reverse transcription-PCR, we found a decrease in transcripts for Jagged1 and Sox2 in adult cochleae. Our findings suggest that the loss of regenerative capacity of the adult organ of Corti is related to down-regulation of stem/progenitor key-markers from the mature supporting cells.

IMPROVE CLINICAL OUTCOMES FOR COCHLEAR IMPLANT RECIPIENTS BY MIMICING THE VIABLE COCHLEAR ENVIRONMENT TO INDUCE NEURAL STEM CELLS TO DIFFERENTIATE INTO AUDITORY NEURONS

To the Editor: We read with interest the article by Hu et al. (1). They suggest that chronic electrical stimulation and/or neurotrophic growth factor can stimulate neurite outgrowth from implanted neurons, although based on electrical auditory brainstem response measurement, these interventions did not induce functional connections to the central auditory pathway. Hearing loss is a major challenge for modern medicine. The loss of inner hair cells in mammals causes a permanent sensorineural hearing loss and initiates a wave of secondary degeneration of auditory neurons, the target neurons of the cochlear implant. The cochlear sensory epithelium in mammals does not regenerate after severe injury. Cochlear implants to restore some hearing after neurosensory hearing loss are the only therapy for these people. Greater numbers of auditory neurons are likely to result in improved clinical outcomes for cochlear implant recipients. Neural stem cells (NSCs) are promising candidates for cochlear cell-based therapy. The finding that olfactory precursor cells of the adult mouse can be converted into hair cells in vitro (2) promise a bright future of NSCs-based treatment. Several investigators have reported evidence for NSC transplantation for the treatment of inner ear diseases. Although implanted NSCs can survive, migrate throughout the cochlea, and express markers of hair cells, supporting cells, and spiral ganglion cells with morphologic and immunohistochemical evidence (3) without physiological information may just indicate the possibility of hair cells but is unable to imply the existence of functional hair cells. Undifferentiated adult NSCs survived for a limited time in the inner ear of rats and guinea pigs, perhaps owing to a lack of essential growth factors, thus emphasizing the importance of environmental cues for survival and differentiation of NSCs (4). The developing cochlear environment plays an important role in regulating differentiation in vivo. Auditory supporting cells provide essential trophic support to auditory hair cells during development (5,6) in the form of the neurotrophins, namely, brain-derived neurotrophic factor and Neurotrophin 3. The expression gradient of these neurotrophins in the cochlea is not static and is hypothesized to be reversed between embryonic development and adulthood (7). Given the complexity of cellular signaling pathways in developing cochlear, this environment is often difficult to mimic completely in vitro. Coculture models provide a method to study differentiation under controlled conditions, with the advantage of being able to replicate some tissue-derived signaling, and have previously been used to successfully direct the differentiation of NSCs into neurons, photoreceptor cells, and hepatocytes and to promote cell survival and expansion in vitro (8). Recent evidence showed that NSCs cultured from the olfactory neuroepithelium of the adult rat exhibit the ability to differentiate into neurons and astrocytes, indicating the multipotentiality of this cell population (9), and NSCs from the olfactory neuroepithelium were capable of differentiating into cells with morphologic and immunohistochemical properties similar to those of adult spiral ganglions (10). Other studies have successfully differentiated stem cells into auditory cell marker-positive cells in vitro (11-13). Given all these considerations, we hypothesized that cocultures would provide an excellent starting point, and the present research was an attempt to, by providing the developing cochlear environment with established coculture model in vitro, induce the differentiation of NSCs toward auditory neurons. Tao Xue, M.D. Li Qiao, M.D. Jian-hua Qiu, M.D. Lian-jun Lu, M.D. Ding-jun Zha, M.D. Fu-quan Chen, M.D. Department of Otolaryngology Xijing Hospital The Fourth Military Medical University Xi'an, PR China

Hair Cell Regeneration

Hair Cell Regeneration

Therapeutic effect of edaravone on inner ear barotrauma in the guinea pig

Inner ear barotrauma (IEB) that is caused by acute pressure changes can often lead to permanent severe sensorineural hearing loss (SNHL). However, the mechanism that causes IEB is still unknown. In the current study, we assessed the involvement of reactive oxygen species (ROS) in IEB and the therapeutic effect of 3-methyl 1-phenyl-2-pyrazolin-5-one (edaravone), which is a free radical scavenger. To create the IEB model, guinea pigs were subjected to quick pressure changes that resulted in acute SNHL. The animals were then divided into two groups, an edaravone-treated IEB group and a non-treated IEB group that only received normal saline. Immunohistochemical analyses for 8-hydroxy-2-deoxyguanosine (8-OHdG) and 4-hydroxy-2-nonenal (4-HNE) were performed to examine the amount of oxidative DNA damage and lipid peroxidation that occurred in guinea pig cochlea. To assess the curative efficacy of edaravone, auditory brainstem response (ABR) testing was performed to evaluate auditory function. Strong immunoreactivities against 8-OHdG and 4-HNE were observed in the inner ear tissues of the non-treated IEB group. Lesser amounts of immunoreactivity were observed in the same region of the edaravone-treated IEB group as compared to the non-treated IEB group. Furthermore, ABR measurement revealed that there was a faster improvement in the threshold shift for the edaravone-treated IEB group as compared to that of the non-treated IEB group. At the final 7-week time point, the threshold shift for the edaravone-treated IEB group was significantly smaller as compared to the non-treated IEB group. These results strongly suggest that ROS is produced in the cochlea in response to acute pressure changes and that ROS plays an important role in the pathophysiology of IEB. Furthermore, edaravone treatment had a therapeutic effect on IEB-induced acute SNHL and thus, edaravone might possibly be able to be used as a therapeutic treatment for IEB.

Role of Pneumococcal Proteins in Sensorineural Hearing Loss Due to Otitis Media

Two Streptococcus pneumoniae proteins, pneumococcal surface protein A (PspA) and pneumolysin (Ply), have functional and histopathologic effects on the inner ear. Temporary or permanent sensorineural hearing loss is known to be a sequela of pneumococcal otitis media. Several pneumococcal proteins such as PspA and Ply have been shown to contribute to the pathogenesis of the middle ear; however, effects of these proteins on the inner ear and hearing loss are unknown. Middle ears of chinchillas were inoculated with either wild-type S. pneumoniae or its mutants, deficient in PspA or Ply proteins. After 28 days, auditory brainstem response of animals was tested, and their bullae were processed for histopathologic analysis by light microscopy. Twenty-eight days after instillation of 20 colony-forming units of wild-type pneumococci, auditory brainstem response test showed threshold changes of 10 to 15 dB for 4 to 32 kHz and more than 20 dB for 1 to 2 kHz. No significant hearing loss was observed after instillation of the same or even higher doses of isogenic S. pneumoniae mutants of PspA or Ply proteins, or saline injection, after the same period. Histologic analysis showed no fluid, inflammatory cells, or bacteria in the middle ear, indicating that hearing loss was sensorineural. Inner ear morphology showed pathologic changes in the stria vascularis, suggesting it as the target of otitis media-induced damage, which may lead to sensorineural hearing loss. The virulence PspA and Ply proteins of S. pneumoniae affect the inner ear and auditory function.

Schwann cells revert to non‐myelinating phenotypes in the deafened rat cochlea

Loss of sensory hair cells within the cochlea results in a permanent sensorineural hearing loss and initiates the gradual degeneration of spiral ganglion neurons (SGNs) - the primary afferent neurons of the cochlea. While these neurons are normally myelinated via Schwann cells, loss of myelin occurs as a precursor to neural degeneration. However, the relationship between demyelination and the status of Schwann cells in deafness is not well understood. We used a marker of peripheral myelin (myelin protein zero; P0) and a marker of Schwann cells (S100) to determine the temporal sequence of myelin and Schwann cell loss as a function of duration of deafness. Rat pups were systemically deafened for periods ranging from 2 weeks to greater than 6 months by co-administration of frusemide and gentamicin. Cochleae were cryosectioned and quantitative immunohistochemistry used to determine the extent of P0 and S100 labelling within the peripheral processes, SGN soma and their central processes within the modiolus. SGN density was also determined for each cochlear turn. P0 labelling decreased throughout the cochlea with increasing duration of deafness. The reduction in P0 labelling occurred at a faster rate than the SGN loss. In contrast, S100 labelling was not significantly reduced compared with age-matched controls in any cochlear region until 6 months post-deafening. These results suggest that Schwann cells may revert to non-myelinating phenotypes in response to deafness and exhibit greater survival traits than SGNs. The potential clinical significance of these findings for cochlear implants is discussed.

An outbreak of Streptococcus suis in Chengdu, China

To the Editor: In the summer of 2005, 30 patients were admitted to the isolation ward of our hospital, whose disease met the Chinese Center for Disease Control and Prevention (CDC) case definition of Streptococcus suis (S. suis) infection (1). As a result, it confirmed that S. suis serotype 2 was the causative agents of this outbreak and the isolates carried genes for all of the known virulence-associated factors (2,3), which is indistinguishable from the isolates that caused the earlier 1998 outbreak in Jiangsu, China (2). The patients exclusively came from China's southwestern province of Sichuan. The epidemic outbreak first happened in Ziyang and Neijiang, and later spread to 10 cities including Chengdu, capital city of Sichuan (4). Eleven of 30 were laboratory confirmed, and 19 met the clinical diagnosis. According to the proposed classification (1), 30 patients were divided into four groups: the common type, the shock type, the meningitis type and the complex type. The demographic data and clinical characteristics of those patients were listed in Table 1. Out of the 30 patients with swine S. suis infection, two (6.7%) died. Finally, there were 11 of 28 patients alive with permanent sensorineural hearing loss. We reported 30 of 215 cases (more than one-seventh) on the largest known zoonotic outbreak of S. suis (5). Epidemiologically, all cases of human disease in this outbreak in Chengdu were linked to exposure to infected pigs, part of whom were possibly transmitted directly through broken skin. Antibiotics, such as cephalosporins, were effective. The low percentage of death in Chengdu in comparison with outbreak in other places of Sichuan province (6.67% vs. 19.46%, p = 0.066) may resulted from improved health facility and medical care. In conclusion, our results suggest that the law of prohibiting slaughtering, eating, selling and transporting deceased or sick pigs should be strictly enforced, and surveillance systems should be established to alert farmers and the general public in response to human S. suis outbreak especially in rural China.

Evaluation of individuals with known or suspected noise damage to hearing

The diagnosis of hearing impairment due to noise damage is based on the assessment of the type and level of exposure to noise, the patient's medical history, and a clinical and audiometric evaluation. The risk for developing hearing loss increases substantially when the equivalent sound pressure levels of noise exceed 80dB(A). Very high exposures (above 100dB(A)), usually to impulse noise (e.g. fireworks), can result in acoustic trauma. In this case, sensorineural hearing loss develops immediately after exposure and is frequently accompanied by tinnitus. It can be unilateral or asymmetrical, and temporary (temporary threshold shift – TTS) or permanent (permanent threshold shift – PTS). Noise-induced hearing loss (NIHL) that develops after prolonged occupational exposures to relatively moderate levels of noise (85–100dB(A)) is a bilateral, symmetrical, or almost symmetrical, and permanent sensorineural hearing loss progressing slowly over the years of employment. The most dynamic rise in PTS can be seen du...

HumanStreptococcus suisMeningitis in the United States

To the Editor: Streptococcus suis commonly causes meningitis in swine. Human infection is infrequent and is typically manifested as meningitis, frequently followed by permanent sensorineural hearing loss. Most cases have occurred in Southeast Asia. A recent outbreak in China resulted in substantial morbidity and mortality. The World Health Organization reports that nearly all those affected were farmers or butchers who had been either killing sick pigs or handling their meat. Transmission may occur through breaks in the skin.1 We report a case of human S. suis infection in the United States. A 59-year-old, previously healthy male farmer presented with a . . .

Mechanisms of hair cell death and protection

Sensory hair cells are mechanotransducers of the inner ear that are essential for hearing and balance. Hair cell death commonly occurs following acoustic trauma or exposure to ototoxins, such as the aminoglycoside antibiotics and the antineoplastic agent cisplatin. Loss of these inner ear sensory cells can lead to permanent sensorineural hearing loss, balance disturbance, or both. Currently, the only effective clinical intervention is prevention from exposure to known ototoxic insults. To help improve therapeutic strategies, a better understanding of the molecular mechanisms underlying hair cell degeneration is required. Current knowledge of these cell death mechanisms and potential therapeutic targets are discussed in this review. Studies have shown that caspase-9 and caspase-3 are key mediators of hair cell death induced by noise, aminoglycosides, and cisplatin. The Bcl-2 family consists of a group of proapoptotic and antiapoptotic molecules that act upstream of and regulate caspase activation. Recent studies have shed light on the roles of molecules acting more upstream, including mitogen-activated protein kinases and p53. The mechanisms of sensory hair cell degeneration in response to different ototoxic stimuli share a final common pathway: caspase activation. Inhibition of caspases prevents or delays hair cell death and may preserve hearing/balance function. Inhibition of mitogen-activated protein kinases protects against noise-induced and aminoglycoside-induced but not cisplatin-induced hair cell death, which suggests divergent upstream regulatory mechanisms.

Evaluation of the Austrian Newborn Hearing Screening Program

Universal Neonatal Hearing Screening (UNHS) has been gradually implemented since the mid-nineties in Austrian maternity wards and neonatal intensive care units. This study evaluated the effect of UNHS on reducing age at identification as well as age of intervention for children with congenital and perinatal sensorineural hearing impairment. This was a retrospective analysis of clinical data of 394 Austrian children diagnosed with an at least mild degree (> 20 dB hearing level) of permanent sensorineural hearing loss. Age at identification and age at intervention were compared between children who underwent UNHS ('with UNHS') and those who did not undergo UNHS ('without UNHS'). The median of age of identification was 37.6 months in children without UNHS, and 3.9 months in children with UNHS. By six months of age, 69% of hearing-impaired children who underwent UNHS, were identified but only 6% of those without UNHS. At one year, the corresponding percentages are 80% and 12%, respectively. In children without UNHS, the degree of hearing loss was the most predictive factor of age at identification (median of age at diagnosis for profound hearing loss: 15 months; severe: 26 months; moderate: 52 months; mild: 73 months). In children with UNHS, age of identification was unrelated to degree of hearing loss (medians between 3.7 and 4.4 months). In the majority of children intervention began within one month after diagnosis, regardless of whether or not the child was identified by UNHS. UNHS greatly increases the proportion of children whose hearing impairment is diagnosed before six months of age. However, in some 20% of children, hearing impairment was diagnosed later than one year of age, despite having failed the screening. Additionally, data from this study suggest that about 15% of childhood hearing losses manifest themselves after the hearing screening period. Efforts are thus required for the early detection of these children as well.

Auditory hair cell replacement and hearing improvement by Atoh1 gene therapy in deaf mammals

In the mammalian auditory system, sensory cell loss resulting from aging, ototoxic drugs, infections, overstimulation and other causes is irreversible and leads to permanent sensorineural hearing loss. To restore hearing, it is necessary to generate new functional hair cells. One potential way to regenerate hair cells is to induce a phenotypic transdifferentiation of nonsensory cells that remain in the deaf cochlea. Here we report that Atoh1, a gene also known as Math1 encoding a basic helix-loop-helix transcription factor and key regulator of hair cell development, induces regeneration of hair cells and substantially improves hearing thresholds in the mature deaf inner ear after delivery to nonsensory cells through adenovectors. This is the first demonstration of cellular and functional repair in the organ of Corti of a mature deaf mammal. The data suggest a new therapeutic approach based on expressing crucial developmental genes for cellular and functional restoration in the damaged auditory epithelium and other sensory systems.

The Validity of Intraoperative Brainstem Auditory Evoked Potentials (BAEPs) for the Postoperative Hearing Impairments in Microvascular Decompression (MVD)

Background: Intraoperative brainstem auditory evoked potentials reduced the sensorineural hearing loss (SNHL) after microvascular decompression (MVD). This study was performed to evaluate the validity of BAEP parameters of latency or amplitude to SNHL. Methods: 557 patients out of 930 hemifacial spasm patients performed MVD, who were free from hearing impairment preoperatively, were enrolled in this study. Maximal changes of BAEPs wave V latency and amplitude during MVD were retrospectively sought according to postoperative SNHL. Sensitivity, specificity and positive predictability of wave V latency and amplitude were also sought according to the postoperative SNHL with a critical value of 1.0 msec prolongation and 40% decrease, respectively. Results: Wave V latency of BAEPs prolonged less in patients with normal hearing outcome (0.44 0.63 msec) than in the patients with temporary or permanent SNHL (1.23 0.56 msec, 1.33 0.33 msec). Wave V amplitude also decreased less in the patients with normal hearing outcome (5.4 15.8%) than in the patients with transient or permanent SNHL (42.8 31.7%, 60.0 34.7%). While sensitivity, specificity and predictability of prolongation of wave V latency at a value of 1.0 msec for SNHL, were 52.5%, 76.4% and 14.7%, respectively, those of decrease in the amplitude of wave V for SNHL at a value of 40% were 35.0%, 93.6% and 29.8%, respectively. Conclusions: Decrease of the amplitude of wave V seems to have higher specificity, predictability and lower sensitivity for SNHL than the prolongation of wave V latency.

Interaction between middle and inner ears in otitis media

Middle ear infection is one of the most common childhood diseases that causes inner ear pathology, resulting in hearing loss and communication disorders. The presence of sensorineural hearing loss (SNHL) in the extended high frequency range (8–20 kHz) in children with otitis media histories has been well established.Pathological changes of the cochlear lateral wall and the organ of Corti have been reported in animal models of experimental otitis media (OM). The results of inoculation of Streptococcus pneumoniae in the middle ear suggest that bacterial OM can produce damage of both outer and inner hair cells. This damage may be a significant factor in temporary and permanent SNHL associated with bacterial OM. Bacteria, bacterial products and inflammatory mediators crossing the round window membrane are known to cause structural as well as biochemical changes of inner ear tissues and lead to the functional damage of the inner ear through the disruption of inner ear homeostasis and auditory transduction syst...

Sensorineural hearing loss in postmeningitic children.

To establish the proportion of children who develop sensorineural hearing loss after bacterial meningitis and to correlate such loss with patient factors. Retrospective case review. McMaster University Children's Hospital, a tertiary referral center. Children between the ages of 1 day and 18 years admitted to McMaster University Children's Hospital with a confirmed diagnosis of bacterial meningitis between January 1, 1991 and December 30, 2000. Audiological assessment including auditory brainstem responses and cortical electric-response audiometry or standard audiometry. The nature of sensorineural hearing loss was assessed according to the degree (mild to profound) and course (transient versus permanent). Correlations between sensorineural hearing loss and the patient's age, sex, duration of illness before admission, use of dexamethasone, concurrent neurologic complications, and types of pathogens were evaluated. Patterns of inpatient and outpatient audiological assessment were determined. Seventy-nine children had confirmed bacterial meningitis. Streptococcus pneumoniae accounted for 36.7 percent of all cases, followed-up by Neisseria meningitides (16.5%), group B Streptococcus (15.2%), and Hemophilus influenzae (13.9%). Sixty-eight (86.1%) children underwent hearing assessment, either as inpatients or after discharge. Of the remaining 11 (13.9%) in whom audiological evaluation could not be confirmed, only two made mention of a referral. As such, a nonreferral rate of 11.4 percent was identified. Abnormal auditory brainstem response findings were present in 22 cases (32.3%), with 11 cases (13.9%) of permanent sensorineural hearing loss identified. A statistically significant association between sensorineural hearing loss and Streptococcus pneumoniae was found (p < 0.001). No association between age, sex, duration of illness before admission, use of dexamethasone, and number of concurrent neurologic complications could be established. In our series, 11 children (13.9%) experienced permanent sensorineural hearing loss, consistent with previously reported rates of 5 to 35 percent within the pediatric population. Since introduction of the Hemophilus influenzae type B vaccine, Streptococcus pneumoniae has emerged as the dominant causative organism of bacterial meningitis in children. Our study additionally confirms the role of Streptococcus pneumoniae as a precipitant of sensorineural hearing loss (p < 0.001). Audiological assessment in our series (86.1%) exceeds most of the screening rates previously reported in the literature. Because of compliance problems with outpatient audiological assessment and because early identification and expedient amplification lead to better academic and language outcomes, routine inpatient audiological screening of postmeningitic children is advocated.

Communication in Noise with Acoustic and Electronic Hearing Protection Devices

The purpose of the present study was to evaluate communication ability in noise at two signal presentation levels when using acoustic and electronic hearing protection devices (HPDs). Fourteen normal hearing subjects were fitted binaurally with custom acoustic HPDs (ER-15) and custom electronic HPDs (Starkey SA T9). Probe microphone measurements were obtained on 28 ears for three experimental conditions (open ear, acoustic HPD, electronic HPD) at four input signal levels (60, 70, 80, 90 dB SPL). Also, communication in noise was evaluated for three conditions (open ear, acoustic HPD, electronic HPD) at two input signal levels (75 and 90 dB SPL) using the Hearing In Noise Test. Results indicated significantly greater attenuation as well as significantly better communication in noise for the acoustic HPD. Results also indicated that the electronic HPD failed to attenuate any input signal utilized. Although results of behavioral testing indicated that communication ability in noise was not significantly impacted by varying the signal presentation level when utilizing either HPD, a more salient finding may be that utilization of the electronic HPD may place listeners at risk for temporary or permanent sensorineural hearing loss.

Dynamics of sensorineural hearing loss after head trauma.

To estimate the temporal endpoint of permanent sensorineural hearing loss after head trauma. Retrospective observational case study. In patients with sensorineural hearing loss caused by head trauma, 1,741 ears were studied. A follow-up survey of audiograms in patients with sensorineural hearing loss after head trauma was performed for up to 4 years from the date of injury. Each patient's audiograms were compared according to a severity score that specifically classified hearing loss that was associated with acoustic trauma. Either improvement or deterioration of the early posttrauma hearing loss occurred during the first year after head trauma. Thereafter, hearing levels could be expected to remain stationary. Fluctuation in hearing after head trauma may take place within the first year after trauma, after which the associated hearing loss should be considered to be stabilized.

Current status of universal newborn hearing screening

Universal newborn hearing screening is becoming accepted as the standard of care for infants in the United States as more states create legislative screening mandates. Advances in screening technology have provided programs with efficient tools. As new universal newborn hearing screening programs are developed, information from existing programs assists in the development of increasingly better models that include diagnosis and intervention by 6 months of age. Additional information about hearing loss emerges from the thousands of newborns tested, with new prevalence figures for permanent congenital sensorineural hearing loss of 1.5 to 2.2 per 1000 live births. As with any screening program, there is continuing concern about populations who may not be detected in the process because of later onset or unique characteristics of the hearing loss. Continual vigilance on the part of the primary care provider, otolaryngologist, and audiologist is necessary to detect hearing loss in these children. This paper reviews the current status of universal newborn hearing screening.