Directional asymmetries in vestibular reflexes have aided the diagnosis of vestibular lesions; however, potential asymmetries in vestibular perception have not been well defined. This investigation sought to measure potential asymmetries in human vestibular perception. Vestibular perception thresholds were measured in 24 healthy human subjects between the ages of 21 and 68 years. Stimuli consisted of a single cycle of sinusoidal acceleration in a single direction lasting 1 or 2 s (1 or 0.5 Hz), delivered in sway (leftright), surge (forward-backward), heave (up-down), or yaw rotation. Subject identified self-motion directions were analyzed using a forced choice technique, which permitted thresholds to be independently determined for each direction. Non-motion stimuli were presented to measure possible response bias. A significant directional asymmetry in the dynamic response occurred in 27% of conditions tested within subjects, and in at least one type of motion in 92% of subjects. Directional asymmetries were usually consistent when retested in the same subject but did not occur consistently in one direction across the population with the exception of heave at 0.5 Hz. Responses during null stimuli presentation suggested that asymmetries were not due to biased guessing. Multiple models were applied and compared to determine if sensitivities were direction specific. Using Akaike information criterion, it was found that the model with direction specific sensitivities better described the data in 86% of runs when compared with a model that used the same sensitivity for both directions. Mean thresholds for yaw were 1.3±0.9°/s at 0.5 Hz and 0.9±0.7°/s at 1 Hz and were independent of age. Thresholds for surge and sway were 1.7±0.8 cm/s at 0.5 Hz and 0.7±0.3 cm/s at 1.0 Hz for subjects G50 and were significantly higher in subjects 950 years old. Heave thresholds were higher and were independent of age.

Patients with acute olfactory disorders typically present to the otolaryngologist with both acute hyposmia and less often with anosmia. With the onset of COVID-19 we have noticed an increase in the number of patients who have presented with new onset of complete smell loss to the senior author's practice in Tehran, Iran. This anosmia and the frequency with which patients present is highly unusual. Coronaviruses have been known to cause common cold symptoms. COVID-19 infections have been described as causing more severe respiratory infections and the symptoms reported by authors from Wuhan, China have not specifically included anosmia. We describe patients who have presented during a two-week period of the COVID-19 pandemic with complete loss of sense of smell. Most had either no symptoms or mild respiratory symptoms. Many had a normal otolaryngologic exam. A relationship between COVID-19 and anosmia should be considered during the pandemic. We hypothesize that the mechanism of injury is similar to that of other coronavirus infections that cause central and peripheral neurologic deficits.

Mast cells (MCs) play a pathobiologic role in type 2 (T2) allergic inflammatory diseases of the airway, including asthma and chronic rhinosinusitis with nasal polyposis (CRSwNP). Distinct MC subsets infiltrate the airway mucosa in T2 disease, including subepithelial MCs expressing the proteases tryptase and chymase (MCTC) and epithelial MCs expressing tryptase without chymase (MCT). However, mechanisms underlying MC expansion and the transcriptional programs underlying their heterogeneity are poorly understood. Here, we use flow cytometry and single-cell RNA-sequencing (scRNA-seq) to conduct a comprehensive analysis of human MC hyperplasia in CRSwNP, a T2 cytokine–mediated inflammatory disease. We link discrete cell surface phenotypes to the distinct transcriptomes of CRSwNP MCT and MCTC, which represent polarized ends of a transcriptional gradient of nasal polyp MCs. We find a subepithelial population of CD38highCD117high MCs that is markedly expanded during T2 inflammation. These CD38highCD117high MCs exhibit an intermediate phenotype relative to the expanded MCT and MCTC subsets. CD38highCD117high MCs are distinct from circulating MC progenitors and are enriched for proliferation, which is markedly increased in CRSwNP patients with aspirin-exacerbated respiratory disease, a severe disease subset characterized by increased MC burden and elevated MC activation. We observe that MCs expressing a polyp MCT–like effector program are also found within the lung during fibrotic diseases and asthma, and further identify marked differences between MCTC in nasal polyps and skin. These results indicate that MCs display distinct inflammation-associated effector programs and suggest that in situ MC proliferation is a major component of MC hyperplasia in human T2 inflammation.