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Results for “LABYRINTH DISEASES”

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At least 775 records · Page 43Linked to original sources
PubMed1991

Autoimmune inner ear disease: a review of basic mechanisms and clinical correlates.

Otolaryngologists have long sought to identify causes of sensorineural hearing loss that might be reversed by medical treatment. One such entity has become known as autoimmune inner ear disease. The potential improvement in auditory function in these patients subsequent to immunosuppressive therapy has created a desire in clinicians to better understand this disease. This paper begins by reviewing the basic concepts of autoimmunity. The experimental and clinical data concerning autoimmune inner ear disease are then described and analyzed. Finally, conclusions are drawn concerning our current state of understanding of this disease process.

Animals↗
PubMed1988

[Principles of conservative therapy of peripheral and central disorders of equilibrium].

Disturbance of equilibrium is a vestibular induced disturbance of orientation in space that is perceived subjectively as vertigo. Change of behaviour and specific medication is the optimal causal therapy, but symptomatic therapy is preferred in practice, using drugs that suppress different input activities or the activity of central vestibular structures. In this way a disordered flow of information is eliminated and the equilibrium is restored.

Brain↗
PubMedDate not supplied

[Cupulolithiasis].

Explore the source record for details and available documents.

Adult↗
PubMed1987

[Incidence of kidney diseases in inner ear disorders].

A retrospective study is reported based on a questionnaire sent to family doctors and otolaryngologists. Of 213 patients with various inner ear disorders, 19 were found to have renal disease. A further 19 patients were found who had abnormal laboratory and urinary tests. There was no increased frequency of renal disease compared with the normal population nor were there any differences in immunological findings. Experimental findings of renal and inner ear disorders are discussed. The serological data of the patients investigated are compared with etiological considerations of sensorineural hearing loss. This was no correlation of the clinical data with anatomical, physiological or experimental findings in the kidneys and cochlea.

Autoantibodies↗
PubMed1986

A procedure of vestibular decompensation for clinical diagnosis. I. Animal experiments.

Vestibular lesions are often so effectively compensated that their diagnosis may be difficult. Certain chemicals can decompensate the central vestibular system and thus uncover symptoms present before compensation. This study attempts to devise a procedure which can utilize such decompensation for the benefit of clinical diagnosis. Unilateral labyrinthectomies were performed in rats. Pathological movements and body positions due to the vestibular loss were compensated within about one week. Systemic application of cholinomimetic drugs (physostigmine and nicotine) led to consistent decompensation which lasted, however, too long and was accompanied by too severe side effects to be considered for clinical diagnostic purposes. Local application of these drugs into the middle ear of the healthy side were without effect. Brief inhalation of nitrous oxide (up to 79 vol.%) caused decompensation during the first four postoperative weeks but not consistently at longer survival times. Inhalation of halothane in N2O and O2 for 90 seconds caused a reliable decompensation at all times during the six month postoperative observation period. It is concluded that a brief halothane-N2O anesthesia may prove to be useful in a diagnostic search for compensated vestibular deficits.

Adaptation, Physiological↗
PubMed1987

Vestibular ototoxicity of gentamicin assessed by the recording of a short-latency vestibular-evoked response in cats.

The short-latency vestibular-evoked response (VsER) and the auditory brain stem response (ABR) were recorded with scalp electrodes in four cats before, during, and after systemic administration of gentamicin. The VsER was altered and later disappeared in three cats, and in one cat it became asymmetric, typical of a unilateral vestibular lesion. In all cats the ABR was unaffected and remained normal through the end of the experiment 4 months later. Histopathological examination of the temporal bones of three cats showed severe damage to the vestibular end-organ, particularly in the summit of the cristae, but in lesser amounts in the hair cells on the slopes of the cristae and in the maculae. In one cat, the pathological condition was greater in one ear, corresponding to the asymmetry in the VsER records. This new method of inducing and recording the VsER has been demonstrated by the present study to be an effective tool for experimentally assessing vestibular end-organ and nerve function in animal models. Furthermore, these results indicate that the VsER is generated in the vestibular labyrinth, most probably by the cristae of the semicircular canals.

Animals↗