Nonsynaptic clusters of postsynaptic proteins have been documented; however, their role remains elusive. We monitored the trafficking of several candidate proteins implicated in synaptogenesis, when nonsynaptic clusters of scaffold proteins are most abundant. We find a protein complex consisting of two populations that differ in their content, mobility, and involvement in synapse formation. One subpopulation is mobile and relies on actin transport for delivery to nascent and existing synapses. These mobile clusters contain the scaffolding proteins PSD-95, GKAP, and Shank. A proportion of mobile clusters that exhibits slow movement and travels short distances contains neuroligin-1. The second group consists of stationary nonsynaptic scaffold complexes that mainly contain neuroligin-1, can recruit synaptophysin-containing axonal transport vesicles, and are readily transformed to functional presynaptic contacts that recycle the vital dye FM 4-64. These results postulate a mechanism whereby preformed scaffold protein complexes serve as predetermined postsynaptic hotspots for establishment of new functional excitatory synapses.

Benign paroxysmal positional vertigo (BPPV) is a peripheral vestibular disorder that manifests as sudden, short-lived episodes of vertigo elicited by specific head movements. BPPV is one of the most common causes of dizziness or vertigo, and almost 10% of the elderly population experiences BPPV. It is often self-limiting but can become chronic and recurrent with considerable effects on a person's quality of life. Most cases result from the migration of free-floating canalith particles into the posterior (more commonly) or horizontal (less commonly) semicircular canals, rendering them sensitive to gravity. Diagnosis of BPPV is based on a suggestive history and physical examination, and other tests are not normally required. Repositioning maneuvers are highly efficacious in resolving BPPV. Medications are not an effective treatment option. Posterior canal occlusion surgery is highly effective and is reserved for intractable and severe cases.KEYWORDS: BPV, BPPV, benign paroxysmal positional vertigo management, benign paroxysmal positional vertigo treatment, benign paroxysmal positional vertigo diagnosis Learning Objectives: As a result of this activity, the participant will be able to (1) describe the aspects of diagnosing benign paroxysmal positional vertigo including taking an effective dizziness history and performing and interpreting a Dix-Hallpike maneuver and lateral supine head turn, (2) describe a three-position particle repositioning maneuver and identify the referral criteria appropriate for tertiary center dizziness clinics.Benign paroxysmal positional vertigo (BPPV) is a common cause of dizziness or vertigo. It is a peripheral vestibular disorder that manifests as sudden, short-lived episodes of vertigo precipitated by certain head movements. BPPV can have considerable effects on a person's quality of life, at times causing significant anxiety and fear of a sinister illness.

Objectives: To compare the circulating microRNA (miRNA) expression profiles between sudden sensory neural hearing loss (SSNHL) patients and age-matched normal hearing controls.Study Design: Prospective cohort multi-center study. Methods: Patients presenting within 28 days of onset of SSNHL were prospectively recruited along with contemporaneous age-matched controls. Pooled sera of four patient (n = 09, mean age = 53.0 years; 07, 55.0; 10, 52.9; 10, 51.6) and two control (09, 51.2 and 03, 50.0) groups were assessed using a TaqMan Low Density Array. The patients' sera were also divided into two pools, untreated (04, 57.7) and treated (32, 52.6) for additional analysis. miRNA expression level was derived from cycle threshold (Ct) values normalized to a global mean. Inter-group mean Ct differences with fold changes ≥2.0 and ≤0.5 at P < .05 were considered significant. Bioinformatic databases were used to identify putative target mRNAs or validated genes and their functional annotations.Results: Thirty-six SSNHL patients (mean age 53.0 AE standard deviation (SD) 15.2 years) and 12 controls (50.9 AE 11.9) were studied. Eight miRNAs hsa-miR-590-5p/ -186-5p/ -195-5p/ -140-3p/ -128-3p/ -132-3p/ -375-3p, and -30a-3p were identified as significantly differentially expressed in SSNHL patients. Most of these miRNAs were abundantly identified in the nervous system and the putative target messenger RNAs (mRNAs) were enriched in signaling pathways such as phosphatidyl inositol 3 kinase/protein Kinase B (PI3K/Akt), Ras and mitogen-activated protein kinase (MAPK).Conclusion: These findings suggest the possible cellular signaling pathways that underlie the disruption of auditory signal transmission in SSNHL.

The Sound Sense™ hearing conservation program improved earplug use practices in elementary school children in the short and long term. The development, implementation and evaluation of a community-based health promotion project around hearing loss can serve as a tremendous opportunity for students to develop their knowledge and skills in health advocacy.

Bilateral Ménière's disease can be challenging to diagnose via clinical suspicion and pure-tone audiometry alone. Therefore, adjunctive diagnostic tools including electrocochleography, vestibular-evoked myogenic potential, and intratympanic gadolinium-based contrast agent MRI are of even greater value, and may predict progression to bilaterality - allowing better optimization of treatment. Ablative treatments are relatively contraindicated due to the risks of bilateral vestibular and cochlear hypofunction. Nonablative treatments such as the Meniett device, intratympanic steroids, and endolymphatic sac surgery appear to be efficacious, and useful alternatives after conservative measures fail. Systemic aminoglycoside therapy is reserved for only the most severe and intractable cases.