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Results for “LABYRINTH DISEASES”

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At least 523 records · Page 29Linked to original sources
PubMed1988

Vestibular ototoxicity following intratympanic applications of chlorhexidine gluconate in the cat.

Our previous studies have shown that the disinfectant chlorhexidine gluconate (CH) has an ototoxic effect on the cochlea following its topical application in the middle ear space. The purpose of the present investigation was to demonstrate morphologically if CH also has the potential to injure the vestibular organs in the inner ear and, if so, what structures are most strongly damaged. Nine cats were used for the study. The drug dose of CH and the number of its applications to the middle ear were the same as used in our previous study to produce middle ear injuries. In the 2% CH group of cats pronounced degeneration was found in afferent nerve endings and both types of sensory cells. These nerve terminals showed edematous dilatations and contained degenerated mitochondria. Highly dark-stained degenerated mitochondria were distributed in the sensory cells and the afferent nerve terminals in the 0.05% CH group, but these degenerative changes were much less than in the 2% CH group. No otolithic crystals or synaptic vesicles could be seen in the 2% CH group. The results from this study showed that CH as a disinfectant has an ototoxic effect on the labyrinthine vestibule in which the sensory cell-nerve ending complex is affected as the main target. Even when used in dilute clinical concentrations, vestibular disturbances are a likely complication if the drug solution flows into the middle ear through a perforated eardrum.

Administration, Topical↗
PubMedDate not supplied

Perilymph fistula: a cause of auditory, vestibular, neurological and psychiatric disorder.

It is suggested that damage by mild trauma, viruses or bone disease to the otic capsule or to the membranes between the cochlea and the middle ear is common, and involved in many syndromes of obscure etiology. The clinical perilymph fistula (PF) syndrome can consist of any combination of the following: tinnitus, deafness, phonophobia, vertigo, ataxia, otalgia, facial palsy, headache, diplopia, blackouts, psychological distress. The following testable hypotheses are proposed: otitis media is due to perilymph in the middle ear, with secondary changes resulting from infection or inflammation: otosclerosis results from a slow leak in the presence of enzymes promoting bone growth: Meniere's syndrome follows reduced perilymph support for the endolymphatic system: Bell's palsy results from a perilymph provoked oedema in the bony facial nerve canal: PFs may be responsible for progressive rubella deafness, and for some cases of migraine, epilepsy, anxiety neurosis and hysteria: psychiatric sequelae of the PF syndrome predominate in the post-concussional syndrome and infantile autism: organisms can pass from the throat into the spinal fluid, causing meningitis or encephalitis. The tinnitus and vertigo are caused by random labyrinthine fluid movements, the headache and diplopia by reduced spinal fluid pressure.

Deafness↗
PubMed1996

Vestibular nerve section following previous mastoidectomy.

Vestibular neurectomy is an effective procedure in the management of vertigo due to active labyrinthine disease. Various approaches have been developed for selectively sectioning the vestibular nerve, in order to preserve serviceable hearing and avoid facial nerve injury. In patients who have a mastoid cavity, from previous surgery for chronic otitis media, the approach to the vestibular nerve has to be modified. Considerations taken into account are cavity infection, hearing status, and the presence of associated loud tinnitus. Vestibular or vestibulo-cochlear nerve section has been undertaken, by the senior author, in eight patients with a mastoid cavity from previous surgery for chronic otitis media. Translabyrinthine, retrosigmoid and middle fossa approaches have all been used; strategies for selection of each specific technique are considered, and the aetiology of post-chronic suppurative otitis media (CSOM) peripheral vestibular disease discussed.

Adult↗
PubMed1976

[Cogan's syndrome with angitis of cranial nerves, aortitis, endocarditis, and glomerulonephritis (author's transl)].

A 34-year-old woman died of left-heart failure due to combinated aortic-valve disease three years after manifestation of Cogan's syndrome characterized by sudden inner-ear deafness, loss of equilibrium, interstitial keratitis, and progressive loss of vision during pregnancy. At necropsy there was evidence of recurrent endocarditis of the aortic valves with stenosis and regurgitation, severe angitis of the thoracic aorta with marked secondary sclerosing changes as the cause of the heart failure. Angitis within the optical fasciculus and stato-acoustic nerve was the cause of the vestibular and optical defects. Primary changes in the visual and auditory cortices, the retina and inner ear were excluded as causes. There was also acute membrano-proliferative glomerulonephritis, which may have been coincidental.

Acute Disease↗
PubMed1987

Peripheral labyrinthine causes of dizziness.

A patient's complaint of dizziness must be defined specifically. Many dizzy patients do not have labyrinthine or balance system disease. The patient with dysequilibrium, on the other hand, often has a balance system disease but not necessarily a labyrinthine disorder. The patient with vertigo most likely has labyrinthine disease. Vertigo is accompanied by nystagmus, which can be identified only when the examiner specifically looks for it. Although vertigo is the classic symptom of labyrinthine disease, not all labyrinthine diseases have associated vertigo. Careful history taking, physical examination, audiometry, caloric testing, electronystagmography, and radiographic studies will identify patients with labyrinthine disorders. Treatment depends on the diagnosis. Usually it is medical, but occasionally it may be surgical. Most patients have no residual problems; a few have permanent disability.

Acute Disease↗
PubMed1981

Cochleo-saccular degeneration in one of three sisters with hereditary deafness, absent gastric motility, small bowel diverticulitis and progressive sensory neuropathy.

This is a report of cochleo-saccular degeneration found in temporal bones from a patient who had suffered from slowly progressive and total sensorineural deafness which had an inherited origin. At age 8, this patient began to complain of hearing loss, and by age 10 she was totally deaf. The patient was 1 of 3 female siblings who have suffered from an exactly identical progressive disease: deafness, absent gastric motility, small bowel diverticulitis and ulceration, and sensory neuropathy. The temporal bone pathology found in this case was the degenerative change in the cochlear duct and sacculus. No pathology was found in the utriculus and semicircular canals.

Adolescent↗
PubMed1979

Head-eye coordination in normals and in patients with vestibular disorders.

Oculomotor response in the absence of vision was examined in 8 normal subjects, 11 unilaterally labyrinthectomised patients and 2 patients with suspected bilateral canal paresis. The experiments involved (a) voluntary oscillation of the head, (b) whole body oscillation on a turntable and (c) stimulation of neck afferents by oscillation of the body with the head fixed. In the patients with unilateral lesions there was a directional preponderance of the slow phase eye velocity towards the side of the lesion which differed significantly from that of the normal population. In the patients with bilateral paresis the oculomotor response to whole body oscillation was negligible, whereas the response to voluntary head movement had a mean gain of 0.45 and at high frequency could not be suppressed when viewing a head-fixed image. The saccadic activity during voluntary head movement was similar in all subjects and was correlated with slow phase velocity.

Eye Movements↗