Association Between Hearing Handicap and Life-Space Mobility in a Patient Population.

PURPOSE: The purpose of this study was to evaluate the association between self-reported hearing handicap and life-space mobility utilizing the Life-Space Questionnaire (LSQ). Life-space mobility reflects how an individual moves through their daily physical and social environment, and the role of hearing loss in life-space mobility is not fully understood. We hypothesized that those with higher self-reported hearing handicap would be more likely to demonstrate restricted life-space mobility. METHOD: A total of 189 older adults (M age = 75.76 years, SD = 5.81) completed a mail-in survey packet including the LSQ and Hearing Handicap Inventory for the Elderly (HHIE). Participants were categorized into one of three groups ("no/none," "mild/moderate," or "severe" hearing handicap) according to HHIE total score. LSQ responses were dichotomized to either "nonrestricted/typical" or "restricted" life-space mobility groups. Logistic regression models were performed to analyze life-space mobility differences among the groups. RESULTS: Logistic regression results demonstrated no statistically significant association between hearing handicap and LSQ. CONCLUSIONS: The results of this study indicate that there is no association between self-reported hearing handicap and life-space mobility as evaluated using a mail-in version of the LSQ. This counters other studies that have demonstrated that life space is associated with chronic illness, cognitive functioning, and social and health integration.

Persistent post-COVID-19 smell loss is associated with immune cell infiltration and altered gene expression in olfactory epithelium.

SARS-CoV-2 causes profound changes in the sense of smell, including total smell loss. Although these alterations are often transient, many patients with COVID-19 exhibit olfactory dysfunction that lasts months to years. Although animal and human autopsy studies have suggested mechanisms driving acute anosmia, it remains unclear how SARS-CoV-2 causes persistent smell loss in a subset of patients. To address this question, we analyzed olfactory epithelial samples collected from 24 biopsies, including from nine patients with objectively quantified long-term smell loss after COVID-19. This biopsy-based approach revealed a diffuse infiltrate of T cells expressing interferon-γ and a shift in myeloid cell population composition, including enrichment of CD207+ dendritic cells and depletion of anti-inflammatory M2 macrophages. Despite the absence of detectable SARS-CoV-2 RNA or protein, gene expression in the barrier supporting cells of the olfactory epithelium, termed sustentacular cells, appeared to reflect a response to ongoing inflammatory signaling, which was accompanied by a reduction in the number of olfactory sensory neurons relative to olfactory epithelial sustentacular cells. These findings indicate that T cell-mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post-COVID-19 smell loss.

Persistent post-COVID-19 smell loss is associated with inflammatory infiltration and altered olfactory epithelial gene expression.

Most human subjects infected by SARS-CoV-2 report an acute alteration in their sense of smell, and more than 25% of COVID patients report lasting olfactory dysfunction. While animal studies and human autopsy tissues have suggested mechanisms underlying acute loss of smell, the pathophysiology that underlies persistent smell loss remains unclear. Here we combine objective measurements of smell loss in patients suffering from post-acute sequelae of SARS-CoV-2 infection (PASC) with single cell sequencing and histology of the olfactory epithelium (OE). This approach reveals that the OE of patients with persistent smell loss harbors a diffuse infiltrate of T cells expressing interferon-gamma; gene expression in sustentacular cells appears to reflect a response to inflammatory signaling, which is accompanied by a reduction in the number of olfactory sensory neurons relative to support cells. These data identify a persistent epithelial inflammatory process associated with PASC, and suggests mechanisms through which this T cell-mediated inflammation alters the sense of smell.

Aging-related olfactory loss is associated with olfactory stem cell transcriptional alterations in humans.

BACKGROUNDPresbyosmia, or aging-related olfactory loss, occurs in a majority of humans over age 65 years, yet remains poorly understood, with no specific treatment options. The olfactory epithelium (OE) is the peripheral organ for olfaction and is subject to acquired damage, suggesting a likely site of pathology in aging. Adult stem cells reconstitute the neuroepithelium in response to cell loss under normal conditions. In aged OE, patches of respiratory-like metaplasia have been observed histologically, consistent with a failure in normal neuroepithelial homeostasis.MethodsAccordingly, we have focused on identifying cellular and molecular changes in presbyosmic OE. The study combined psychophysical testing with olfactory mucosa biopsy analysis, single-cell RNA-Sequencing (scRNA-Seq), and culture studies.ResultsWe identified evidence for inflammation-associated changes in the OE stem cells of presbyosmic patients. The presbyosmic basal stem cells exhibited increased expression of genes involved in response to cytokines or stress or the regulation of proliferation and differentiation. Using a culture model, we found that cytokine exposure drove increased TP63, a transcription factor acting to prevent OE stem cell differentiation.ConclusionsOur data suggest aging-related inflammatory changes in OE stem cells may contribute to presbyosmia via the disruption of normal epithelial homeostasis. OE stem cells may represent a therapeutic target for restoration of olfaction.FundingNIH grants DC018371, NS121067, DC016224; Office of Physician-Scientist Development, Burroughs-Wellcome Fund Research Fellowship for Medical Students Award, Duke University School of Medicine.

Test-Retest Reliability of the Listening Self-Efficacy Questionnaire.

PURPOSE: The purpose of this study was to determine the test-retest reliability and the minimum detectable change (MDC) scores of the Listening Self-Efficacy Questionnaire (LSEQ). METHOD: A total of 77 older adults who were experienced hearing aid users were administered the LSEQ in pen-paper format on two separate occasions. They were provided the first copy of the LSEQ in the clinic to take home to complete. Those participants who completed and returned the first copy of the questionnaire were then mailed a second copy of the LSEQ to complete and return approximately 2 weeks later. The mean subscale and total scale scores from the two administrations were compared using intraclass correlation coefficients (ICCs) to determine test-retest reliability of the measure. The MDC scores, or the minimum difference between scores to demonstrate a real change in self-efficacy levels, were also calculated for each subscale and the total scale. RESULTS: The ICCs ranged from 0.786 to 0.920 for the subscale and total scale scores. The MDC scores for the subscale and total scale ranged from 14.3% to 19.1%. CONCLUSIONS: The results of this study indicate that the LSEQ has moderate to excellent test-retest reliability. The MDC scores demonstrate that the LSEQ has the potential to detect true changes in listening self-efficacy in older patients with hearing loss who use hearing aids. The LSEQ may aid clinicians in understanding listening self-efficacy in their patients and how their self-efficacy levels change with amplification.