Treatment of benign positional vertigo in the elderly: a randomized trial.

OBJECTIVES/HYPOTHESIS: The objective of the study was to evaluate the efficacy of three therapeutic strategies (Semont maneuver, flunarizine, and no treatment) in patients with benign paroxysmal positional vertigo. STUDY DESIGN: Randomized prospective trial. METHODS: One hundred fifty-six consecutive patients older than 60 years of age who were affected by benign paroxysmal positional vertigo of the posterior semicircular canal were enrolled. The diagnosis was made on the basis of the history of recurrent sudden crisis of vertigo and positional-induced typical nystagmus after Dix-Hallpike positioning maneuver. Patients were randomly allocated to receive Semont liberatory maneuver (intended as a statoconia-detachment maneuver), flunarizine, or no treatment. A post-treatment negative Dix-Hallpike test result was considered as a proof of vertigo resolution. RESULTS: Cure rates with Semont maneuver were significantly higher (94.2%) than those obtained with flunarizine (57.7%) and no treatment (36.4%) (P <.001). Within a 6-month follow-up, relapse rates were lower among patients treated with Semont maneuver (3.8%) than those obtained with flunarizine (5.8%) and no treatment (21.1%). All patients with resolution of symptoms and negative Dix-Hallpike test results showed a great improvement in daily activities and quality of life (P <.001). CONCLUSION: Semont liberatory maneuver is the most successful therapy for benign paroxysmal positional vertigo and improves patients' quality of life. Diagnostic and therapeutic maneuvers are easy to perform and should be part of the medical knowledge of every general practitioner and geriatrician.

Preserved otoacoustic emissions in postparotitis profound unilateral hearing loss: a case report.

We report a case of a profound unilateral sensorineural hearing loss following epidemic parotitis, with good response of otoacoustic emissions. The patient was a 12-year-old girl who had developed a unilateral hearing impairment 2 weeks after the onset of mumps. Pure tone audiometry confirmed a profound left sensorineural hearing loss. The affected ear showed an absence of auditory brain stem responses, whereas transient evoked otoacoustic emissions and distortion product otoacoustic emissions were preserved. Epidemic parotitis virus is likely responsible for an impairment of inner hair cells, primary afferent fibers or their synapses, or a combination of these areas, and it does not seem to have a specific tropism for cochlear outer hair cells. Further follow-up will be necessary to differentiate the present case from auditory neuropathy.

Congenital aplasia of the parotid gland with omolateral cheek angioma: case report and review of the literature.

Congenital agenesis of the parotid gland is a rare entity whose etiopathogenesis is still unclear. It is usually bilateral and is sometimes associated with other developmental anomalies of the head and neck region. A case is presented in which aplasia of the right parotid gland was associated with an omolateral angioma of the cheek. The radiological diagnostic approach and a review of the literature on agenesis of the salivary glands are presented.

Hearing loss associated with 35delG mutation in Connexin-26 (GJB2) gene: audiogram analysis.

35delG is the most common mutation in the Connexin-26 gene, representing a major cause of autosomal recessive hearing loss. The aim of this study was to evaluate the relationship between the audiological phenotype and the 35delG mutation in 64 Sicilians with non-syndromic deafness. Pure-tone audiometry and a screening for 35delG mutation were performed. Audiograms were evaluated according to the classification of Liu and Xu. Thirteen homozygotes and nine heterozygotes for the investigated mutation were found. Symmetrical hearing loss was significantly (p=0.008) more common in homozygous subjects than in those without the Connexin-26 mutation. Profound-severe hypoacusia was found in 92.3 per cent of 35delG homozygous, 22.3 per cent of heterozygous and 58.7 per cent of 35delG absent patients. Residual shape audiograms were more frequent in homozygotes. A molecular analysis for the 35delG mutation should be performed in cases of symmetric, severe-profound congenital hearing loss, as a genetic cause is probable in such cases.

Expression of E-cadherin and α-catenin in T1 N0 laryngeal cancer.

AIM: To determine whether modulation of expression of cell adhesion molecules occurs in neoplastic transformation of laryngeal epithelium and to investigate their possible role in clinical outcome. MATERIALS AND METHODS: Fifty-five T1 N0 laryngeal biopsies were tested by immunohistochemistry for the E-cadherin/α-catenin adhesion complex. RESULTS: High immunohistochemical expression of E-cadherin and α-catenin was found in 18% and 53% cases, respectively. Expression of both adhesion molecules decreased according to histological grading; a significant relationship was particularly found between high E-cadherin expression and G1 cases (p=0.013). High E-cad-herin expression was statistically associated with in situ carcinoma (p=0.006). Non-statistical significance was evidenced between these adhesion molecules and tobacco use or site of occurence. Regarding clinical outcome, recurrence was associated with low expression of both adhesion molecules. CONCLUSION: E-cadherin and α-catenin down-regulation might be associated with neoplastic transformation in laryngeal tissues and might be regarded as a risk factor for clinical recurrence.