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PubMedDate not supplied

Factors influencing collagen-induced autoimmune ear disease.

In 1981, the authors described a type II collagen-induced autoimmune ear disease (CIAED) model. The purpose of this study was to gather further evidence that this is a sound animal model to use in evaluating inner ear diseases. The temporal bone lesions of CIAED in Lewis and Wistar rats were characterized by the presence of sensorineural hearing loss with mild atrophy of the organ of Corti and spiral ganglion degeneration, vestibular dysfunction with vacuolar degeneration of the crista ampullaris, otospongiosis-like lesions in the tympanic annules, cochlear vasculitis, and eustachian tube disease. Both cellular and humoral immune responses to type II collagen were demonstrated. The induction of ear lesions depends on many factors. In general, animals immunized with antigens in complete Freund's adjuvant showed relatively more severe lesions than animals immunized with antigens in incomplete Freund's adjuvant, but the duration of the immunization seems to be a more important factor in reproducing severe lesions. The strain and the source of the animals are also important factors in autoimmune inner ear diseases, as is the condition of the host animals. Subclinical or clinical mycoplasma infection in the rat markedly reduced the incidence and severity of lesions in type II collagen-induced arthritis. Many researchers did not consider sialoductal adenovirus, widely present among laboratory rats, a lesion-producing factor in rats. Although many factors influence the induction and severity of CIAED, these animal models provide an excellent new avenue of inner ear research.

Animals↗
PubMed1989

Hereditary vestibulo-cochlear dysfunction and vascular disorders.

A family is described with a progressive autosomal dominant vestibulocochlear dysfunction resulting in a Dandy syndrome, head movement dependent oscillopsia and hearing loss. The history was negative for other neurological or otological diseases (including infectious diseases) or use of neuro-ototoxic drugs, except for a high incidence of vascular disorders (hypertension, stroke, and heart infarction).

Adult↗
PubMed1991

Vestibulocochlear dysfunction in a patient with rheumatoid disease and vasculitis.

The case is described of a patient with rheumatoid disease and evidence of vasculitis who developed acute vestibuloauditory dysfunction resulting in total deafness, which was assumed to be secondary to a vasculitic process affecting the vestibulocochlear nerve. Treatment of the underlying vasculitic process, despite effecting a general improvement of the patient's rheumatoid disease, did not significantly improve the auditory dysfunction.

Cochlea↗
PubMed1985

[Cochleo-vestibular attacks of viral origin].

The viral etiology of some cochlear or vestibular lesions is well documented. Concerning the cochlear congenital lesions, the cytomegalovirus is becoming the main etiologic factor, while the rubella vaccination has shown its efficiency in the United States. The acquired hearing or vestibular diseases were briefly reviewed as well as the pathology and their therapeutic considerations.

Cochlea↗
PubMed1987

[Functioning of the pituitary-adrenal system during the vestibulo-vegetative syndrome and administration of dalargin and nalorphine].

Changes in ACTH, cortisol, beta-endorphin have been investigated during vestibulo-vegetative syndrome (VVS) and injections of dalargin (leu-enkephalin analog) and nalorphine (agonist-antagonist of opioid receptors) in 9 volunteers with low level vestibulo-vegetative stability. Cumulative coriolis acceleration test during rotations on a special chair was used for VVS modelling. Dalargin (1-4 mg), nalorphine (5 mg) and placebo (NaCl solution) were injected intravenously 5-15 min before rotation. A significant increase in ACTH, cortisol and beta-endorphin plasma levels has been observed. Mean positive linear correlation (r greater than +0.6) between ACTH and beta-endorphin and ACTH and cortisol was noted immediately after the test only when dalargin was injected. It is suggested that in VVS there develops a hormonal conflict, i. e. an adequate hormonal release is disturbed.

Autonomic Nervous System Diseases↗
PubMed1994

Perilymphatic fistula.

Perilymph fistula is recognized as a clinically significant problem in certain patients. Owing to its lack of specific symptoms, diagnosis is difficult and depends upon a combination of historical data, physical findings, and test results. Early treatment is initiated in patients with overwhelming evidence of perilymph fistula, in order to ameliorate vestibular symptoms and preserve auditory function. Patients with subtle symptoms, however, should not be overlooked, because they will also benefit from the treatment of this disease.

Fistula↗
PubMed2004

Acoustic responses of vestibular afferents in a model of superior canal dehiscence.

HYPOTHESIS: Afferents innervating the superior semicircular canal are rendered especially sensitive to acoustic stimulation when there is a dehiscence of the superior canal. Other vestibular end organs are also more sensitive to acoustic stimulation. BACKGROUND: Dehiscence of the superior semicircular canal is associated with vertigo and nystagmus caused by loud sounds (Tullio phenomenon) or changes in middle ear or intracranial pressures. The mechanisms by which acoustic stimuli act on the vestibular end organs are unclear. The nystagmus caused by acoustic stimuli generally aligns with the affected superior canal. METHODS: Responses to acoustic stimuli in the superior vestibular nerves of anesthetized chinchillas were recorded before and after fenestration of the superior canal. RESULTS: Two acoustic response patterns were seen: rapid phase locking and slow tonic changes in firing rate. Phasic responses principally occurred in irregular afferents and tonic responses in regular afferents. Afferents from all of the vestibular end organs encountered could respond to acoustic stimuli, even before fenestration. However, fenestration lowered the thresholds for acoustic stimulation in superior canal afferents with phasic responses and increased the magnitude of tonic responses. CONCLUSIONS: Superior canal dehiscence may render the irregular afferents innervating the superior canal particularly sensitive to loud sounds. Rapid phase-locking responses may explain the short latency of nystagmus seen in patients with superior canal dehiscence syndrome. The mechanisms by which acoustic stimuli activate the vestibular end organs may differ from the damped endolymph motion associated with head acceleration.

Acoustic Stimulation↗
PubMed1986

[Acute loss of vestibular function: an emergency for patient and physician].

The dramatic symptomatology of sudden loss of vestibular function alarms the patient and the physician who is consulted in an emergency situation. The continuous vertigo is often accompanied by marked autonomic symptomatology, so that heart and cerebral diseases as well as acute intoxication are often primarily diagnosed. The differential diagnosis, clinical features, course of the disease and treatment are presented in this study of 54 patients treated in our department between 1980 and 1985. Aetiology and pathogenesis are discussed on the basis of the literature.

Acute Disease↗
PubMed2004

Typical and atypical Cogan's syndrome: 32 cases and review of the literature.

OBJECTIVE: To report our experience on a multicentre series of 32 patients with either typical or atypical Cogan's syndrome, to combine our results with a detailed review of the literature, and to compare the clinical manifestations of typical and atypical Cogan's syndrome. METHODS: Patients were identified from a survey conducted with physicians affiliated to the French National Society for Internal Medicine, and were classified into typical or atypical Cogan's syndrome according to the Haynes criteria. Clinical data were collected in a standardized manner. A comprehensive literature review using the Medline database and the reference lists of identified articles was performed. RESULTS: Seventeen patients had typical Cogan's syndrome and 15 had atypical Cogan's syndrome. Apart from non-syphilitic interstitial keratitis, the ocular manifestations of patients with atypical Cogan's syndrome were mainly uveitis and episcleritis. All but one patient presented with Ménière-like syndrome, and at the end of follow-up 11 were deaf and 19 additional patients had developed a significant decrease in auditory acuity. Twenty-five patients (78%) developed systemic manifestations, including aortitis in four. Comparison of typical and atypical Cogan's syndrome showed that some systemic manifestations were more common in atypical Cogan's syndrome, but these differences may be explained by reporting bias in the literature. CONCLUSION: Differences regarding the associated systemic manifestations of typical and atypical Cogan's syndrome may reflect reporting bias in the literature. However, the diversity of the ocular and audiovestibular manifestations and the acceptable lengthy delay between the two types of involvement in atypical Cogan's syndrome should make one cautious before accepting this diagnosis as the diagnosis may mimic various other systemic diseases.

Adolescent↗