Long-term administration of vasopressin can cause Ménière's disease in mice.

CONCLUSION: A new murine model of Ménière's disease has been developed, based on long-term administration of vasopressin. Induction of vestibular dysfunction in the present animal model can cause additional stress, by reducing inner ear blood flow. Latanoprost, a selective agonist for the FP prostanoid receptor, may become a new remedy for Ménière's disease. OBJECTIVE: The purpose of this study was to develop a more suitable animal model, with a closer resemblance to the pathophysiological process in Ménière's disease. METHODS: Adult CBA/J or ICR mice were treated by subcutaneous injection of vasopressin for 5 days up to 8 weeks. Morphological analyses were performed of the cochlea, vestibular end organs and endolymphatic sac. The effect of latanoprost on the development of endolymphatic hydrops was also examined. RESULTS: All experimental animals showed mild to moderate endolymphatic hydrops, increasing in severity as the vasopressin treatment was prolonged. Animals treated with vasopressin for 8 weeks showed severe endolymphatic hydrops with partial loss of outer hair cells and spiral ganglion cells. These animals also had a reversible vestibular dysfunction following intratympanic injection of epinephrine. Latanoprost inhibited the development of endolymphatic hydrops caused by vasopressin.

Morphological and functional changes in a new animal model of Ménière's disease.

The purpose of this study was to clarify the underlying mechanism of vertiginous attacks in Ménière's disease (MD) while obtaining insight into water homeostasis in the inner ear using a new animal model. We conducted both histopathological and functional assessment of the vestibular system in the guinea-pig. In the first experiment, all animals were maintained 1 or 4 weeks after electrocauterization of the endolymphatic sac of the left ear and were given either saline or desmopressin (vasopressin type 2 receptor agonist). The temporal bones from both ears were harvested and the extent of endolymphatic hydrops was quantitatively assessed. In the second experiment, either 1 or 4 weeks after surgery, animals were assessed for balance disorders and nystagmus after the administration of saline or desmopressin. In the first experiment, the proportion of endolymphatic space in the cochlea and the saccule was significantly greater in ears that survived for 4 weeks after surgery and were given desmopressin compared with other groups. In the second experiment, all animals that underwent surgery and were given desmopressin showed spontaneous nystagmus and balance disorder, whereas all animals that had surgery but without desmopressin administration were asymptomatic. Our animal model induced severe endolymphatic hydrops in the cochlea and the saccule, and showed episodes of balance disorder along with spontaneous nystagmus. These findings suggest that administration of desmopressin can exacerbate endolymphatic hydrops because of acute V2 (vasopressin type 2 receptor)-mediated effects, and, when combined with endolymphathic sac dysfunction, can cause temporary vestibular abnormalities that are similar to the vertiginous attacks in patients with MD.

Vestibulotoxicity as a consequence of systemically administered tobramycin in cystic fibrosis patients.

CONCLUSION: The reported prevalence of vestibulotoxicity (30.4%) in cystic fibrosis (CF) patients supports vestibulotoxicity screening in CF patients during or after tobramycin exposure. Prospective longitudinal investigation is required for a more specific evidence-based proposal. OBJECTIVE: To investigate the prevalence of tobramycin-induced vestibulotoxicity in CF patients, as it had not been investigated before. PATIENTS AND METHODS: In this observational cohort study, 23 CF patient volunteers from the Haga Teaching Hospital Adult CF centre who had been exposed to at least one treatment with systemically administered tobramycin were included. Subjective feelings of dizziness were measured using validated questionnaires and vestibular symptoms were assessed by physical examination. Electronystagmography (ENG) with caloric irrigation was used as the gold standard. RESULTS: Peripheral vestibular loss was found in seven patients (7/23 = 30.4%). Central vestibular loss was found in one patient. Analysis of the 19 completed questionnaires showed that 12 patients (12/19 = 63.2%) did not experience dizziness and 3 patients (3/19 = 15/8%) experienced specific vestibular symptoms. The results of the questionnaire could not predict the results of ENG with caloric irrigation. Physical examination showed no abnormalities in any patients. No age- or dose-related predictive factors were found.

A new animal model for Ménière's disease.

CONCLUSION: A new murine model for the study of Ménière's disease has been developed by treatment with both lipopolysaccharide (LPS) and aldosterone. Induction of vestibular dysfunction in the hydropic animal model may entail additional stress such as reduced inner ear blood flow, and sudden acute changes in endolymph volume and/or pressure. OBJECTIVE: The purpose of this study was to develop a more suitable animal model, showing closer resemblance to the pathophysiological process in Ménière's disease. MATERIALS AND METHODS: Adult CBA/J mice were treated by intratympanic injection of LPS, intraperitoneal injection of aldosterone, or injection of both LPS and aldosterone. Morphological analyses were performed in the cochlea and endolymphatic sac. RESULTS: All experimental animals showed mild to moderate endolymphatic hydrops. Those treated with both LPS and aldosterone showed reversible vestibular dysfunction after the intratympanic injection of epinephrine.

Acute cochleovestibular toxicity due to topical application of potassium iodide.

We present a case report of a patient who suffered from an acute cochleovestibular deficit after topical application of potassium iodide solution into the left ear. Although the vestibular symptoms progressively disappeared, severe sensorineural hearing loss persisted after treatment with hyperbaric oxygen therapy and intravenous administration of corticosteroids and vasodilating agents. The mechanisms of ototoxicity after topical application of solutions are discussed with emphasis on the particular features of the present case: a patulous Eustachian tube syndrome and the presence of a tympanostomy tube in the left ear.

Carbamazepine-induced sensorineural hearing loss.

Carbamazepine is a commonly prescribed anticonvulsant medication that affects various levels of the nervous system. We report a case of temporary sensorineural hearing loss in a patient after overdosing with 36 g of carbamazepine. Six days after the overdose, the patient complained of bilateral hearing loss and tinnitus. Audiograms revealed a 30- to 40-dB sensorineural hearing loss bilaterally. Another audiogram 2 weeks later showed a complete recovery in both ears accompanied by a clinical resolution in audiovestibular symptoms. Carbamazepine is used to treat partial and generalized seizures, trigeminal neuralgia, and bipolar illness. Adverse effects are not common but most frequently include dizziness, drowziness, nausea, and skin rashes; rare complications are agranulocytosis, bradycardia, and heart block. Documented hearing loss as a side effect of carbamazepine has not been reported, to our knowledge.

[Side effects of drugs on the equilibrium]. / Nebenwirkungen von Medikamenten auf das Gleichgewicht.

Side effects of drugs on the vestibular system may occur when a drug is injected too fast during chronic application of drugs after discontinuation of drugs Dizziness due to ototoxic drugs is rare because of the symmetric influence on the vestibular system. The oculomotor system most often is found being reversible or irreversible damaged by chronic drug effects especially from barbiturates, psychopharmacologic drugs, anticonvulsives and some antiarrhythmics, whereas the vestibular organs and their pathways usually remain unaffected except from ototoxic drugs. An isolated oculomotor disfunction therefore could be an indication for a drug side effect.