[Compensation of peripheral damage of the organ of equilibrium and its evaluation in caloric and rotation tests].
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Seventy-one patients with an unilateral caloric hypofunction were examined in order to establish the correlation with cochlear function. We divised our cases following the subjective clinical syndromes. Groupe A (12 patients) with a history of only one crise of vertigo. Groupe B (13 patients) with repeated vertiginous attacks. Groupe C (21 patients) with a positional vertigo only. Groupe D (15 patients) with rather undefinite complaints. Groupe E (7 patients) with no vertigo at all. We believe to discern the following syndromes in our cases of unilateral vestibular hypofunction: 9 cases with a history of a unique vertiginous crises could be considered as a vestibular "neuronitis" in the narrow sense of the word. One case with recidiving attacks could be considered as a neuronitis, or as a Menière without cochlear disturbances. Some cases with a positional vertigo only or with very vague complaints could be considered as a neuronitis in a large sense.
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OBJECTIVE: To define the indications for surgery in lesions of the internal auditory canal (IAC) and cerebellopontine angle (CPA) in an only hearing ear. STUDY DESIGN: Retrospective case series. SETTING: Tertiary referral center. PATIENTS: Seven patients with lesions of the IAC and CPA who were deaf on the side opposite the lesion. Five patients had vestibular schwannoma (VS), and one each had meningioma and progressive osseous stenosis of the IAC, respectively. The opposite ear was deaf from three different causes: VS (neurofibromatosis type 2 [NF2]), sudden sensorineural hearing loss, idiopathic IAC stenosis. INTERVENTION(S): Middle fossa removal of VS in five, retrosigmoid resection of meningioma in one, and middle fossa IAC osseous decompression in one. MAIN OUTCOME MEASURE: Hearing as measured on pure-tone and speech audiometry. RESULTS: Preoperative hearing was class A in four patients, class B in two, and class C in one. Postoperative hearing was class A in three patients, class B in one, class C in two, and class D in one. CONCLUSIONS: Although the vast majority of neurotologic lesions in an only hearing ear are best managed nonoperatively, in highly selected cases surgical intervention is warranted. Surgical intervention should be considered when one or more of the following circumstances is present: (1) predicted natural history of the disease is relatively rapid loss of the remaining hearing, (2) substantial brainstem compression has evolved (e.g., large acoustic neuroma), and/or (3) operative intervention may result in improvement of hearing or carries relatively low risk of hearing loss (e.g., CPA meningioma).
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The Tullio phenomenon was studied in 57 control subjects, in 7 patients with confirmed PLF and in 149 patients with different types of inner ear pathology. The subjects were exposed to low-frequency sound (LFS) with sound pressure levels ranging from 130 to 132 dB and at frequencies of 25, 50, and 63 Hz. The duration of each stimulation was 30 seconds. The postural responses were measured using a force platform and analyzed with a computer. In control subjects the LFS stimulation somewhat improved the postural stability. All patients with PLF showed significantly altered postural stability during LFS exposure. Also about 20 percent of patients with labyrinthine vertigo, patients with Menièré's disease, patients with chronic middle ear disease (with vertigo) had pathologic response to LFS. None of the patients with pure sensorineural hearing loss without vertigo responded to LFS. Post-urography with LFS loading is a new, promising tool in detection of PLF, but the specificity of the test is still unsatisfactory.
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OBJECTIVE: To establish an experimental autoimmune inner ear disease model, which could exhibit high reproducibility and be adopted for detailed immunological analysis. METHODS: Extraction of guinea pig inner ear antigens (IEAg). The inbred mice were given a single subcutaneous injection of diluted solution of pertussis and an emulsion containing equal parts of CFA and IEAg. The ABR threshold shifts were evaluated. The antibody level to IEAg in serum was detected by ELISA. Inner ear specimen were examined by light microscopy with hematoxylin and eosin staining. The infiltrated cells within cochlea were clarified with immunohistochemical techniques. RESULTS: The ABR thresholds of IEAg-sensitized animals were elevated significantly. Histological changes in cochlea were significant. Inflammatory cell infiltration was clearly observed in the cochlea of the animals following sensitization with IEAg. Degeneration of the spiral ganglion cells, which characterizes a decrease in cell numbers, and formation of endolymphatic hydrops were often seen too. Serum anti-IEAg levels after inoculation were significantly increased in the IEAg sensitised groups. Most of the infiltrated lymphocytes in scala tympani were CD4+ T cells. CONCLUSIONS: The experimental autoimmune inner ear disease can be induced by a single inoculation of IEAg-CFA emulsion and pertussis in inbred C57BL/6 mice.
Before exploratory tympanotomy, it is difficult to diagnose an idiopathic perilymph fistula (PLF) because of its variable presentations. An animal model tube-PLF on guinea pigs was established to evaluate the change of the sensitivity of the cochlea function and the value of the postural audiometry in PLF. A fine polyethylene tube (O.D. 0.6mm) was inserted into the scala tympani of the basal turn through the incised round window membrane in 10 experimental guinea pigs, and another 5 as controls. The hearing threshold (HT), action potential (AP) latency for stimulus of 105 dB SPL, difference of HT and AP latency from the test ear down to up were measured by electrocochleography (ECoG) immediately after operation and one week later. The HT, AP latency and postural audiometry showed no significant changes immediately but a significant difference one week later in HT (P less than 0.01) and postural audiometry, the AP latency also presented a significant delay (P less than 0.01). The results showed that the tube-PLF model may be a valuable method for studying chronic PLF.
A case--report is given of a patient with Cogan's syndrome in childhood. This syndrome consists of non-syphilitic interstitial keratitis and vestibuloauditory symptoms. Visual loss is rare but hearing loss is rapidly progressive. A relation to autoimmune diseases especially to panarteriitis nodosa has been suggested by a number of authors.
Our aim was to elucidate the importance of anatomical aspects in planning local therapies for inner-ear diseases. The study undertakes the anatomical evaluation, from a surgical-approach perspective, of the relationship between the false and true round-window membranes. As our design, we chose a human temporal bone dissection study, for which we used 20 fresh temporal bones. After an exploratory tympanotomy and atticotomy, we drilled the anterosuperior (promontory) edge of the round-window niche until the true round-window membrane was completely exposed. We registered the presence or absence and the extent of the false round-window membranes on the round-window niche. We found false round-window membranes obstructing the round-window niche partially or completely in five temporal bones (25%). Complete obstruction was present in one temporal bone (5%). We found mucoperiosteal folds obstructing the round-window niche partially or completely in a significant proportion of the ears. These anatomical particularities could account, at least partially, for the great variability of the results of intratympanic therapies for inner-ear diseases.