Objectives/Hypothesis: To clarify the time course of recovery in patients with idiopathic vocal fold paralysis. Study Design: Retrospective chart review. Methods: Medical records for all patients with idiopathic vocal fold paralysis over a 10-year period were reviewed to obtain demographic and clinical information, including onset of disease and recovery of vocal function. Stroboscopic exams of patients who recovered voice were reviewed blindly to assess return of vocal fold motion.Results: Thirty-eight of 55 patients (69%) recovered vocal function. Time course of recovery could be assessed in 34 patients who did not undergo injection augmentation. The mean time to recovery was 152.8 6 109.3 days (left, 179.8 6 111.3 days; right, 105.3 6 93.7 days; P 5.088). Two-thirds of patients recovered within 6 months. Probability of recovery declined over time. Five of 22 patients who recovered voice had return of vocal fold motion; 17 did not. The mean time to recovery did not differ between these groups (return of motion, 127.4 6 132.3 days; no return of motion, 160.1 6 105.1 days; P 5.290).Conclusions: Sixty-nine percent of patients with idiopathic vocal fold paralysis recovered vocal function, two-thirds doing so within 6 months of onset. Age, gender, laterality, use of injection augmentation did not influence recovery rate. Declining probability of recovery over time leads us to consider framework surgery after 6 months in patients with idiopathic paralysis.

The cell surface receptor dystroglycan mediates interactions between oligodendroglia and laminin-211, an extracellular matrix protein that regulates timely oligodendroglial development. However, dystroglycan's precise role in oligodendroglial development and the potential mechanisms to regulate laminindystroglycan interactions remain unknown. Here we report that oligodendroglial dystroglycan is cleaved by metalloproteinases, thereby uncoupling oligodendroglia from laminin binding. Dystroglycan cleavage is selectively stimulated by oligodendrocyte progenitor cell attachment to laminin-211, but not laminin-111 or poly-D-lysine. In addition, dystroglycan cleavage occurs most prominently in oligodendrocyte progenitor cells, with limited dystroglycan cleavage observed in differentiating oligodendrocytes. When dystroglycan cleavage is blocked by metalloproteinase inhibitors, oligodendrocyte progenitor cell proliferation is substantially decreased. Conversely, expression of the intracellular portion of cleaved dystroglycan results in increased oligodendrocyte progenitor cell proliferation, suggesting that endogenous dystroglycan cleavage may promote oligodendrocyte progenitor cell cycle progression. Intriguingly, while matrix metalloproteinase-2 and/or -9 have been reported to be responsible for dystroglycan cleavage, we find that these two metalloproteinases are neither necessary nor sufficient for cleavage of oligodendroglial dystroglycan. In summary, laminin-211 stimulates metalloproteinase-mediated dystroglycan cleavage in oligodendrocyte progenitor cells (but not in differentiated oligodendrocytes), which in turn promotes oligodendrocyte progenitor cell proliferation. This novel regulation of oligodendroglial laminin-dystroglycan interactions may have important consequences for oligodendroglial differentiation, both during development and during disease when metalloproteinase levels become elevated.

Current literature shows that there is a lower risk of femoral head collapse in patients with ONFH treated with CD combined with BMMCs when compared to CD alone; however, there is no robust evidence to determine the effect on functional outcomes. More RCTs assessing new combination therapies and using standardized outcome measures are required.

Objective To clarify the time course of recovery in patients with iatrogenic vocal fold paralysis. Study Design Retrospective chart review. Methods Medical records for all patients with iatrogenic vocal fold paralysis over a 10‐year period were reviewed to obtain demographic and clinical information, including onset of disease and recovery of vocal function. Stroboscopic exams of patients who recovered voice were reviewed blindly to assess return of vocal fold motion. Results One hundred and two patients of 114 (89%) recovered vocal function. Time to recovery could be assessed in 39 patients who did not undergo injection augmentation. The mean time to recovery was 181.8 ± 109.3 days (left: 166.4 ± 106.7 days; right: 221.8 ± 115.6 days; P value = 0.095). Patients were analyzed according to anatomical site of surgery (skull base, carotid endarterectomy, thoracic, neck and intubation); there was no significant difference in time to recovery (P value = 0.60). Twelve of the 39 patients had recovery of vocal fold motion. The mean time to vocal recovery did not differ between patients with return of motion versus no return of motion (140.6 ± 118.0 days vs. 200.1 ± 102.2 days; P value = 0.147). Conclusion Age, gender, laterality, and anatomical site of injury do not influence recovery rate in iatrogenic vocal fold paralysis. The probability of recovery decreases over time but more slowly in comparison with idiopathic vocal fold paralysis, reflecting the greater heterogeneity of injury type in the iatrogenic population. Commonly available aggregate recovery rates overstate the potential for recovery. Level of Evidence 4 Laryngoscope, 129:1159–1163, 2019