Facial nerve stimulation (FNS) after cochlear implant activation is a well-known side effect, with an incidence rate raging between 1% and 14.9%. Some causes of deafness have been associated with a higher incidence of this entity, however, there is still no consensus regarding its pathophysiological mechanisms. Although FNS can be solved with changes in speech processor programming, in some cases this can lead to a decrease in performance. The aim of this work was to review the epidemiologic, clinical aspects, and performance results in a group of FNS after cochlear implantation. It was conducted a retrospective chart review of 448 adult patients, all implanted between 1985 and 2016. Speech perception tests results were statistically analysed, using non-parametric tests. We registered a group of 13 patients with FNS, contributing to a prevalence of 2.9%. The causes of hearing loss in this group varied between otosclerosis, Menière's disease, head trauma, and idiopathic cause. Six cases were managed by changing the programming strategy and the other seven required the deactivation of the affected electrodes. Statistical evaluation showed no statistically significant difference between the performance results of the groups with and without FNS. In this series, the overall incidence of FNS was consistent with the literature. Our study supports the current idea that FNS can frequently be eliminated by changing programming strategies or deactivating the involved electrodes, without affecting the implant's performance.

Background It has become clear that healthcare workers are at high risk, and otolaryngology has been theorized to be among the highest risk specialties for coronavirus disease 2019 (COVID‐19). The purpose of this study was to detail the international impact of COVID‐19 among otolaryngologists, and to identify instructional cases. Methods Country representatives of the Young Otolaryngologists–International Federation of Otolaryngologic Societies (YO‐IFOS) surveyed otolaryngologists through various channels. Nationwide surveys were distributed in 19 countries. The gray literature and social media channels were searched to identify reported deaths of otolaryngologists from COVID‐19. Results A total of 361 otolaryngologists were identified to have had COVID‐19, and data for 325 surgeons was available for analysis. The age range was 25 to 84 years, with one‐half under the age of 44 years. There were 24 deaths in the study period, with 83% over age 55 years. Source of infection was likely clinical activity in 175 (54%) cases. Prolonged exposure to a colleague was the source for 37 (11%) surgeons. Six instructional cases were identified where infections occurred during the performance of aerosol‐generating operations (tracheostomy, mastoidectomy, epistaxis control, dacryocystorhinostomy, and translabyrinthine resection). In 3 of these cases, multiple operating room attendees were infected, and in 2, the surgeon succumbed to complications of COVID‐19. Conclusion The etiology of reported cases within the otolaryngology community appear to stem equally from clinical activity and community spread. Multiple procedures performed by otolaryngologists are aerosol‐generating procedures (AGPs) and great care should be taken to protect the surgical team before, during, and after these operations.

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Stroke is a leading cause of death and disability worldwide. Stroke prevention, early diagnosis, and efficient acute treatment are priorities to successfully impact stroke death and disability. Fluid biomarkers may improve stroke differential diagnostic, patient stratification for acute treatment, and post‐stroke individualized rehabilitation. In the present work, we characterized the use of stroke animal models in fluid biomarker research through a systematic review of PubMed and Scopus databases, followed by a literature review on the translation to the human stroke care setting and future perspectives in the field. We found increasing numbers of publications but with limited translation to the clinic. Animal studies are very heterogeneous, do not account for several human features present in stroke, and, importantly, only a minority of such studies used human cohorts to validate biomarker findings. Clinical studies have found appealing candidates, both protein and circulating nucleic acids, to contribute to a more personalized stroke care pathway. Still, brain tissue complexity and the fact that different brain pathologies share lesion biomarkers make this task challenging due to biomarker low specificity. Moreover, the study design and lack of validation cohorts may have precluded a formal integration of biomarkers in different steps of stroke diagnosis and treatment. To overcome such issues, recent pivotal studies on biomarker dynamics in individual patients are providing added value to diagnosis and anticipating patients' early prognosis. Presently, the most consistent protein biomarkers for stroke diagnosis and short‐ and long‐term prognosis are associated with tissue damage at neuronal (TAU), axonal (NFL), or astroglial (GFAP and S100β) levels. Most promising nucleic acids are microRNAs (miR), due to their stability in plasma and ease of access. Still, clinical validation and standardized quantitation place them a step behind compared protein as stroke biomarkers. Ultimately, the definition of clinically relevant biomarker panels and optimization of fast and sensitive biomarker measurements in the blood, together with their combination with clinical and neuroimaging data, will pave the way toward personalized stroke care.

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Background Corticobasal degeneration (CBD) may have a rapidly progressive (RP) clinical course, mimicking other neurological conditions. Objectives To describe a neuropathologically proven case of RP‐CBD in a patient initially diagnosed with immune‐mediated brainstem encephalitis. Methods Retrospective data collection from electronic records and authorized video material. Results A 51‐year‐old man presented with bilateral ptosis, diplopia, and dysphagia. The diagnostic workup was negative for myasthenic syndromes. He progressively developed cognitive dysfunction with frontal release signs and asymmetric parkinsonism. Cerebrospinal fluid evaluation revealed 4 leukocytes/uL, 0.32 g/L proteins, 0.85 g/L glucose, and absent oligoclonal bands. Weakly positive anti‐PNMA2 (Ma2/Ta) antibodies were present, and magnetic resonance imaging showed a T2 hyperintensity involving the midbrain and pons. Based on these features, the diagnosis of immune‐mediated brainstem encephalitis was considered. The patient did not improve after several cycles of methylprednisolone, intravenous immunoglobulin, and plasma exchange. At 1 year after onset, he developed horizontal and vertical gaze limitation and worsening of the parkinsonism and cognitive dysfunction. By age 53, he was severely disabled, requiring percutaneous gastrostomy for feeding. Anti‐IgLON5 was negative. He fulfilled the clinical criteria for probable progressive supranuclear palsy. He died from pneumonia at age 54. The neuropathological examination revealed a 4‐repeat tauopathy with features of CBD with extensive involvement of the brainstem. Conclusions RP‐CBD may resemble brainstem encephalitis. The severity of brainstem and upper spinal cord pathology in the postmortem examination correlated with the clinical and imaging features.

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