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PubMed1994

Mondini dysplasia and congenital cytomegalovirus infection.

We report a case of bilateral temporal bone anomalies in a child with symptomatic congenital cytomegalovirus infection and severe, bilateral sensorineural hearing loss identified at 3 months of age. High-resolution temporal bone computed tomography (HRCT) revealed bilateral findings of a short, malformed cochlea lacking an interscalar septum, a short and wide internal auditory canal, and an enlarged vestibular aqueduct, features diagnostic of bilateral Mondini dysplasia. To determine the importance of this observation, we completed HRCT in five additional children between 7 months and 9 years of age who had evidence of symptomatic congenital cytomegalovirus infection. One child with profound sensorineural hearing loss had severe bilateral temporal bone dysplasia with a small cochlea lacking an interscalar septum, an abnormal vestibule, and a large cochlear aqueduct. Of the remaining four children, hearing thresholds ranged from normal to profoundly decreased, but their HRCT scans were normal to visual inspection. When inner ear dimensions of these temporal bones were compared with norms established by Pappas and coworkers, however, seven of the eight ears had short cochleas and narrow lateral semicircular canals, and three ears had short or narrow vestibules. These results indicate that congenital cytomegalovirus infection may cause anomalies or growth disturbances of the temporal bone.

Child↗
PubMed1995

Normal variations of the temporal bone on high-resolution CT: their incidence and clinical significance.

We evaluated normal variations of the temporal bone on high-resolution computed tomograms (HR-CTs) and investigated their incidence. HR-CTs of the temporal bones of 325 patients were retrospectively reviewed. Six groups of variants, which were considered important for presurgical planning, were evaluated on HR-CTs. These included: (1) an incomplete bony covering of a high-positioned jugular bulb; (2) severe asymmetry of the jugular foramen; (3) an anteriorly located sigmoid sinus; (4) a deep sinus tympani; (5) a large internal auditory canal; and (6) a large cochlear aqueduct. The frequency of the variations were as follows: (1) 2.4%; (2) 4.0%; (3) 1.6%; (4) 5.9%; (5) 2.3%; and (6) 3.0%. Bilateral involvement with variation (4), (5) and (6) was frequently seen. Normal anatomical variations of the temporal bone are therefore not rare and awareness of the possible variants is necessary before surgery of the inner ear, middle ear and posterior fossa.

Adolescent↗
PubMed1983

Meniere's disease 1978-1982.

Over 250 reports concerning or related to Meniere's disease, published in English from 1978 through 1982, are summarized. Reports have been classified into the categories of incidence of occurrence, analysis and reporting results, pathophysiology, etiologic theories, diagnostic methods, medical management, and surgical procedures. Major emphases in reporting from 1978 though 1982 have been in the areas of pathophysiologic studies, expansion of diagnostic procedures, and the use of sac decompression and neurectomy procedures. This literature review reveals the continuing disagreement regarding the pathophysiology of Meniere's disease and the resultant continued controversies in its management.

Animals↗
PubMed2000

Effects of cerebrospinal fluid loss on hearing.

There is a direct communication between the cerebrospinal fluid (CSF) and the perilymph through the cochlear aqueduct (CA). Perilymph depletion due to perilymphatic fistulas has been demonstrated to influence inner ear function, with signs and symptoms similar in many ways to those of Meniere's disease. A leakage of CSF could also theoretically affect the inner ear. The present study was conducted to investigate whether hearing was affected in patients submitted to a leakage of CSF and, if so, to what extent, in which frequency range, which time course and incidence. The study comprised 126 patients who were exposed to different surgical procedures that involved puncture or incision of the dura, and a control group of 32 patients without such leakage. Hearing was reversibly affected only in patients with leak of CSF. The size of the hearing loss, the number of affected patients and the number of frequencies involved increased with increasing amount of CSF lost. Changes in the constituent cochlear fluids due to a transitory reduction in the CSF and the perilymphatic volume with a compensatory endolymphatic expansion may be responsible for the observed findings.

Auditory Threshold↗
PubMed2006

Pneumococcal meningitis: development of a new animal model.

HYPOTHESIS: The rat is a suitable animal to establish a model for the study of pneumococcal meningitis postcochlear implantation. BACKGROUND: There has been an increase in the number of cases of cochlear implant-related meningitis. The most common organism identified was Streptococcus pneumoniae. Whether cochlear implantation increases the risk of pneumococcal meningitis in healthy subjects without other risk factors remains to be determined. Previous animal studies do not focus on the pathogenesis and risk of pneumococcal meningitis postimplantation and are based on relatively small animal numbers, making it difficult to assess the cause-and-effect relationship. There is, therefore, a need to develop a new animal model allowing direct examination of the pathogenesis of meningitis in the presence of a cochlear implant. METHODS: Eighteen nonimplanted rats were infected with 1 x 10 and 1 x 10 colony-forming units (CFU) of a clinical isolate of S. pneumoniae via three different inoculation routes (middle ear, inner ear, and i.p.) to examine for evidence of meningitis during 24 hours. Six implanted rats were infected with the highest amount of bacteria possible for each route of inoculation (4 x 10 CFU i.p., 3 x 10 CFU middle ear, and 1 x 10 CFU inner ear) to examine for evidence of meningitis with the presence of an implant. The histological pattern of cochlear infections for each of the three different inoculating routes were examined. RESULTS: Pneumococcal meningitis was evident in all 6 implanted animals for each of the three different routes of inoculation. Once in the inner ear, bacteria were found to enter the central nervous system via either the cochlear aqueduct or canaliculi perforantes of the osseous spiral lamina, reaching the perineural and perivascular space then the internal acoustic meatus. The rate, extent, and pattern of infection within the cochleae depended on the route of inoculation. Finally, there was no evidence of pneumococcal meningitis observed in 18 nonimplanted rats inoculated at a lower concentration of S. pneumoniae when observed for 24 hours postinoculation. CONCLUSION: Meningitis in implanted rats after inoculation with a clinical isolate of S. pneumoniae is possible via all three potential routes of infection via the upper respiratory tract. The lack of meningitis observed in the 18 nonimplanted rats suggests that longer postinoculation monitoring periods are required to ensure whether or not meningitis will develop. Based on this work, we have developed a new animal model that will allow quantitative risk assessment of meningitis postcochlear implantation, and the assessment of the efficacy of potential interventional strategies in future studies.

Animals↗
PubMed1979

Delayed meningitis following stapes surgery.

Perilymphatic fistulae, developing even years after stapedectomy, open a communication between the perilymph and middle ear. These fistulae constitute a potential pathway for flora of the middle ear to invade the subarachnoid space by way of the cochlear aqueduct. Our patient developed pneumococcal meningitis 14 months after stapedectomy. The history of stapedectomy in a patient with meningitis is an indication for reexploration+ion of the operative site. The appearance of fistula symptoms in patients who have had stapedectomy indicates a high risk for development of intracranial infection.

Ear, Middle↗
PubMed2004

Effects of central nervous system residua on cochlear implant results in children deafened by meningitis.

BACKGROUND: This study explored factors associated with speech recognition outcomes in postmeningitic deafness (PMD). The results of cochlear implantation may vary in children with PMD because of sequelae that extend beyond the auditory periphery. OBJECTIVE: To determine which factors might be most determinative of outcome of cochlear implantation in children with PMD. DESIGN: Retrospective chart review. SETTING: A referral center for pediatric cochlear implantation and rehabilitation. SUBJECTS: Thirty children with cochlear implants who were deafened by meningitis were matched with subjects who were deafened by other causes based on the age at diagnosis, age at cochlear implantation, age at which hearing aids were first used, and method of communication used at home or in the classroom. MAIN OUTCOME MEASURE: Speech perception performance within the first 2 years after cochlear implantation and its relationship with presurgical cognitive measures and medical history. RESULTS: There was no difference in the overall cognitive or postoperative speech perception performance between the children with PMD and those deafened by other causes. The presence of postmeningitic hydrocephalus, however, posed greater challenges to the rehabilitation process, as indicated by significantly smaller gains in speech perception and a predilection for behavioral problems. By comparison, cochlear scarring and incomplete electrode insertion had no impact on speech perception results. CONCLUSIONS: Although the results demonstrated no significant delay in cognitive or speech perception performance in the PMD group, central nervous system residua, when present, can impede the acquisition of speech perception with a cochlear implant. Central effects associated with PMD may thus impact language learning potential; cognitive and behavioral therapy should be considered in rehabilitative planning and in establishing expectations of outcome.

Child↗
PubMed1975

Trisomy 18. A temporal bone report.

Since Edwards first described the trisomy 17-18 syndrome in 1960, the findings in the temporal bones of only four patients with this condition have been reported. They varied widely, ranging from a normal temporal bone, to severe malformations of both the middle and inner ear structures. This study describes the temporal bone findings in a patient with this syndrome. Many of the abnormalities described previously were present as well as the following unreported findings: complete bony atresia of the external canal, an aberrant tensor tympani muscle that did not insert into the malleus but rather attached to a dehiscent area in the Fallopian canal, wide short utricular and saccular ducts, and a widely patent cochlear aqueduct. There was also a developmental arrest of the membranous structures within the cochlea that probably occurred during the 12th week of fetal life.

Autopsy↗
PubMed1978

Congenital deafness and spontaneous CSF otorrhea.

Two patients with congenital deafness had spontaneous CSF otorrhea and recurrent bacterial meningitis. A careful workup, including tomograms, is especially important in the treatment of the closed type of CSF otorrhea. At operation of our patients, the leak was found to be at or near the oval window. The stapes was removed, and muscle was packed into the defect. The profuse flow of CSF was believed to be secondary to a wide-open cochlear aqueduct in the first case, and to an abnormal communication between the internal auditory meatus and the vestibule in the second case. These findings were the bases for the recurrent bacterial meningitis.

Adolescent↗
PubMed1978

Round window niche melanocytes and webby tissue. Possible collateral route of vascular and perilymph circulation.

Two hundred thirteen human temporal bones were studied for characteristics of the round window niche. In 163 specimens melanocytes were found within the attachments of the round window membrane and in the niche, most prominently at the level of the cochlear aqueduct opening. Sixty-two specimens demonstrated discrete webby foci within the lining of the niche, 16 of which completely or partially covered the tympanic surface of the round window membrane, unassociated with fibrous tags or adhesions, and in some cases contained congested vascular channels and melanocytes. The webby foci were sometimes associate; with melanocytes, while melanocytes were present without demonstrable webby foci. These findings may represent a collateral route of vascular or perilymph-related drainage from the inner ear.

Adolescent↗
PubMed1994

Acute Streptococcus pneumoniae meningogenic labyrinthitis. An experimental guinea pig model and literature review.

OBJECTIVE: To create an experimental model of Streptococcus pneumoniae type 3 meningogenic labyrinthitis (a leading cause of deafness) similar to that in human disease. DESIGN: Cohort analytic study of guinea pigs that were inoculated intrathecally with varying dilutions of S pneumoniae type 3; the progress of the disease was compared with that in saline solution-inoculated control animals. SUBJECTS: Healthy adult Hartley guinea pigs without clinical evidence of middle ear disease that were conveniently sampled. INTERVENTIONS: Intrathecal inoculation of 10(4) to 10(6) colony-forming units of S pneumoniae type 3 into 13 guinea pigs; signs and symptoms of meningitis/labyrinthitis were observed for 15 days and compared with those in two saline solution-inoculated control animals. MAIN OUTCOME MEASURES: Morbidity--labyrinthitis, meningitis; end point--death. RESULTS: The 10(4) to 10(6) colony-forming units of S pneumoniae type 3 caused inflammation that extended from the meninges to the inner ear via the cochlear aqueduct within 3 days after inoculation; a dose of 10(7) killed animals within 12 hours after inoculation. Three of five animals that were inoculated with a 10(6) dose died 3 days after inoculation; two of three animals that were inoculated with a 10(5) dose lived to 15 days after inoculation. One of two animals that were inoculated with a 10(4) dose did not become infected. Inflammation extended to the middle ear by round-window destruction. Reactive bone formation simulated labyrinthine osteosclerosis. Observers assessed histologic slides "blindly." CONCLUSION: Guinea pigs can survive 15 days after intrathecal inoculation of a 10(5) dose, with morphologic features similar to those in human disease. This is an effective model for this study of meningogenic labyrinthitis.

Acute Disease↗
PubMed1991

On the pathomechanism of cochlear dysfunction in experimental perilymph fistulas.

The mechanism leading to hearing impairment in perilymph fistulas was investigated in guinea pigs with perforated round window membranes (RWM) by analyzing alterations of inner ear fluid pressure, changes of auditory function following manipulations to get presumed air bubbles out of the cochlea ("positional audiometry"), and temporal bone sections. The instantaneous loss of normal positive inner ear fluid pressure after RWM perforation had no immediate effect on auditory function. Inner ear pressure was restored 4 days following RWM perforation. "Positional audiometry" was negative in guinea pigs with perforated RWM. All ears in which auditory thresholds had increased had additional iatrogenic lesions at the spiral lamina. Fistulas in the RWM per se do not affect auditory thresholds. The question of the surgical repair of fistulas was not directly addressed; it only can be concluded that there are no direct sequelae of an isolated fistula which induce auditory impairment and which could be prevented by surgical repair of the fistula.

Acoustic Stimulation↗
PubMed2000

Safety of adeno-associated virus as cochlear gene transfer vector: analysis of distant spread beyond injected cochleae.

The adeno-associated virus (AAV), inoculated into the perilymph, has been shown to be an effective vector for mediating intracochlear transgene expression. The unexpected finding of transgene expression in the contralateral cochlea in previous work raised concern about dissemination of the virus from the target tissue. The current study was undertaken to assess the extent of AAV dissemination following its introduction into the inner ear. Adult male guinea pigs were injected with recombinant AAV into their left ears and sacrificed at 2 or 4 weeks. Various organs including the cochleae were harvested to characterize the presence and expression of the viral DNA. Virus DNA was detected via polymerase chain reaction in the infused and contralateral cochlea and in the cerebellum but not in any other organs, including cortex, heart, lung, liver, spleen, and kidney. Although the viral presence was established in the cerebellum, transgene expression in this organ was undetectable with either Western blot or immunohistochemistry. Transgene expression was demonstrated via immunohistochemistry in multinucleated giant cells in the bone marrow spaces adjacent to the infused and contralateral cochleae. Collectively, these results suggest potential routes for AAV dissemination from the infused cochlea via the cochlear aqueduct or by extension through the temporal bone marrow spaces. This study reinforces the need to investigate factors that mitigate viral leakage.

Animals↗
PubMed1995

Influence of myelography on the developmental curve of auditory brainstem responses and hearing loss.

Auditory threshold and auditory brainstem response studies were conducted in 50 patients before and after myelography. Analysis of amplitudes and latencies of auditory brainstem measurements demonstrated significant disorders of function of the cochlea and auditory pathway. The Jewett I wave showed a prolongation of latency from 1.92 to 1.98 ms using an average of all repetition rates. The Jewett III wave showed prolongation from 4.01 to 4.14 ms and the Jewett V wave prolongation from 6.01 to 6.16 ms. At the same time average amplitudes for Jewett III and V decreased. In most of the patients these disorders of function were found to be subclinical. However, 12 patients had changes ranging from a subjectively slight hearing loss to an audiometrically defined acute hearing loss. The reasons for these disorders could not be clarified. An open cochlear aqueduct through which perilymph can enter the subarachnoid space, leading to secondary endolymphatic hydrops, was suggested as the cause for the losses found. Changes in brainstem audiometry were also explained by changes in osmolality of inner ear fluids, leading to the development of an endolymphatic hydrops.

Adult↗
PubMed1985

A new method for noninvasive measurement of short-term cerebrospinal fluid pressure changes in humans.

Changes in cerebrospinal fluid (CSF) pressure were shown to be reflected by changes in tympanic membrane (TM) tension. Impedance audiometry measures mechanical tension on the TM and was used to detect changes during jugular vein compression in normal students. CSF and peri-lymph communicate through the cochlear aqueduct, permitting increases in CSF pressure to result in increased pressure on the stapes footplate. This is transmitted to the TM by the ossicles and detected by impedance audiometry. TM tension was also proportional to CSF pressure in cadavers, where CSF pressure was manipulated by saline injection through a lumbar puncture.

Acoustic Impedance Tests↗
PubMed1981

X-ray microanalysis of fluid spaces in the frozen cochlea.

The cochlea is quick-frozen and then opened while under liquid nitrogen to expose the scalae of all turns in the mid-modiolar section. Still under liquid nitrogen, the cochlea is transferred to the cold stage of a pre-vacuum chamber especially constructed for attachment to the scanning electron microscope. Under partial vacuum, it is moved to the cold stage in the high vacuum chamber of a field-emission scanning electron microscope. Energy dispersive X-ray analysis demonstrates the relative levels of sodium, potassium, and chlorine in the fluid spaces of the cochlea.

Animals↗
PubMed1980

Distribution of marked perilymph to the subarachnoidal space.

In guinea pigs the tympanic perilymph of the basal turn was marked with fluorescing rhodamine. In the first series one drop of a 2% solution of the dye was applied onto the round window membrane. Since the perilymphatic space was not opened, the physiologic state of the communicating fluids perilymph and CSF was maintained. The dye appeared within 3-5 min via cochlear aqueduct in the subarachnoidal space. In the dead animal the speed of distribution was significantly less. This most probably indicates a weak physiologic flow of the perilymph through the aqueduct to the subarachnoidal space in living animals. In the second series, 2 ng of lyophilized rhodamine was instilled directly into the tympanic perilymph near the round window. Though hardly any additional volume was brought into the perilymph, the distribution of the dye was distinctly greater as a sign of the considerable sensitivity of the fluid system, even by the slightest manipulation.

Animals↗