Possible Skull Base Erosion After Prolonged Frontal Sinus Stenting

Frontal sinus stenting is widely used with the goal of maintaining nasofrontal duct patency after sinus surgery. The general recommendation is to leave stents in place for 6 months; however, prolonged stenting up to 6 years has been reported with no complication. We present the first reported case of frontal sinus posterior table and skull base erosion following prolonged frontal sinus stenting. A 57-year-old female presented with chronic sinusitis and nasal obstruction. Imaging revealed pansinusitis with retained stents in each frontal sinus that were placed 8 years prior. On the right, there was an area of skull base erosion at the tip of the stent. The patient underwent functional endoscopic sinus surgery with polypectomy. The stents were removed, revealing posterior table erosion on the right side but intact mucosa. Two months after surgery, there were no signs or symptoms of cerebrospinal fluid leak or other complications. Recent literature has suggested that prolonged stenting is safe; however, this case highlights a complication with potentially serious outcomes that can result from prolonged stenting. We recommend stent removal once stable nasofrontal duct patency has been achieved. If prolonged stenting is utilized, patients should be closely monitored and consideration should be given to periodic imaging to evaluate stent position

A Novel Technique to Identify the Nerve of Origin in Head and Neck Schwannomas

Objective: Identifying the nerve of origin in head and neck schwannomas is a diagnostic challenge. Surgical management leads to a risk of permanent deficit. Accurate identification of the nerve would improve operative planning and patient counselling. Methods:: Three patients with head and neck schwannomas underwent a diagnostic procedure hypothesised to identify the nerve of origin. The masses were infiltrated with 1 per cent lidocaine solution, and the patients were observed for neurological deficits. Results:: All three patients experienced temporary loss of nerve function after lidocaine injection. Facial nerve palsy, voice changes with documented unilateral same-side vocal fold paralysis, and numbness in the distribution of the maxillary nerve (V2), respectively, led to a likely identification of the nerve of origin. Conclusion:: Injection of lidocaine into a schwannoma is a safe, in-office procedure that produces a temporary nerve deficit, which may enable accurate identification of the nerve of origin of a schwannoma. Identifying the nerve of origin enhances operative planning and patient counselling

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele