A concerted effort to tackle the global health problem posed by traumatic brain injury (TBI) is long overdue. TBI is a public health challenge of vast, but insufficiently recognised, proportions. Worldwide, more than 50 million people have a TBI each year, and it is estimated that about half the world's population will have one or more TBIs over their lifetime. TBI is the leading cause of mortality in young adults and a major cause of death and disability across all ages in all countries, with a disproportionate burden of disability and death occurring in low-income and middle-income countries (LMICs). It has been estimated that TBI costs the global economy approximately $US400 billion annually. Deficiencies in prevention, care, and research urgently need to be addressed to reduce the huge burden and societal costs of TBI. This Commission highlights priorities and provides expert recommendations for all stakeholders—policy makers, funders, health-care professionals, researchers, and patient representatives—on clinical and research strategies to reduce this growing public health problem and improve the lives of people with TBI.Additional co-authors: Endre Czeiter, Marek Czosnyka, Ramon Diaz-Arrastia, Jens P Dreier, Ann-Christine Duhaime, Ari Ercole, Thomas A van Essen, Valery L Feigin, Guoyi Gao, Joseph Giacino, Laura E Gonzalez-Lara, Russell L Gruen, Deepak Gupta, Jed A Hartings, Sean Hill, Ji-yao Jiang, Naomi Ketharanathan, Erwin J O Kompanje, Linda Lanyon, Steven Laureys, Fiona Lecky, Harvey Levin, Hester F Lingsma, Marc Maegele, Marek Majdan, Geoffrey Manley, Jill Marsteller, Luciana Mascia, Charles McFadyen, Stefania Mondello, Virginia Newcombe, Aarno Palotie, Paul M Parizel, Wilco Peul, James Piercy, Suzanne Polinder, Louis Puybasset, Todd E Rasmussen, Rolf Rossaint, Peter Smielewski, Jeannette Söderberg, Simon J Stanworth, Murray B Stein, Nicole von Steinbüchel, William Stewart, Ewout W Steyerberg, Nino Stocchetti, Anneliese Synnot, Braden Te Ao, Olli Tenovuo, Alice Theadom, Dick Tibboel, Walter Videtta, Kevin K W Wang, W Huw Williams, Kristine Yaffe for the InTBIR Participants and Investigator

In agreement with other recent reports, the utility of HLA typing in HIV patients to identify genetic factors that may confer susceptibility to drug-induced hypersensitive reaction was confirmed. A careful choice of antiretroviral therapy in susceptible individuals should significantly reduce the risk of severe hypersensitive reaction.

Purpose Optical Coherence Tomography (OCT) is a powerful instrument for helping clinicians detect and monitor glaucoma. The aim of this study was to provide a detailed mapping of the relationships between visual field (VF) sensitivities and measures of retinal structure provided by a commercial Spectral Domain (SD)-OCT system (RTvue-100 Optovue). Methods Sixty-three eyes of open angle glaucoma patients (17 males, 16 females, and mean age 71 ± 7.5 years) were included in this retrospective, observational clinical study. Thickness values for superior and inferior retina, as well as average values, were recorded for the full retina, the outer retina, the ganglion cell complex, and the peripapillary retinal nerve fiber layer (RNFL). RNFL thickness was further evaluated along eight separate sectors (temporal lower, temporal upper, superior temporal, superior nasal, nasal upper, nasal lower, inferior nasal, and inferior temporal). Point-wise correlations were then computed between each of these OCT measures and the visual sensitivities at all VF locations assessed via Humphrey 10-2 and 24-2 perimetry. Lastly, OCT data were fit to VF data to predict glaucoma stage. Results The relationship between retinal thickness and visual sensitivities reflects the known topography of the retina. Spatial correlation patterns between visual sensitivities and RNFL thickness along different sectors broadly agree with previously hypothesized structure-function maps, yet suggest that structure-function maps still require more precise characterizations. Given these relationships, we find that OCT data can predict glaucoma stage. Conclusion Ganglion cell complex and RNFL thickness measurements are highlighted as the most promising candidate metrics for glaucoma detection and monitoring.

Citation: Cappelli F, Caudano F, Marenco M, Testa V, Masala A, Sindaco D, Macrì A, Traverso CE, Iester M, Ricciarelli R. Evaluating the correlation between Alzheimer's amyloid-β peptides and glaucoma in human aqueous humor. Trans Vis Sci Tech. 2020;9(5):21, https://doi.org/10.1167/tvst.9.5.21Purpose: Recent studies suggest that glaucoma may share common pathogenic mechanisms with Alzheimer's disease. To test this hypothesis, we investigated the correlation between glaucoma and amyloid-β 42 (Aβ 42 ) concentration in human samples of aqueous humor (AH).Methods: Eighty-one candidates for cataract or glaucoma surgery were consecutively enrolled, with a median age of 77 years; of these, 32 subjects were affected by glaucoma and 49 were controls. Before surgery, each patient received an ophthalmological examination including biometry, intraocular pressure (IOP) measurement, fundus photography, and determination of the mean thickness of the ganglion cell complex (GCC) and/or retinal nerve fiber layer. During the surgical procedure, an AH sample was collected and immediately processed for total protein (TP) and Aβ 42 evaluation.Results: Aβ 42 levels were not statistically different between the glaucomatous and control samples, but a significant increase in TP concentration was found in the AH of glaucoma patients compared with controls (P = 0.02). In addition, positive correlations were observed between TP and Aβ 42 (r = 0.51; P < 0.0001), between TP and IOP (r = 0.44; P < 0.0001), and between Aβ 42 and IOP (r = 0.22; P = 0.033). Conclusions:Our results indicate that an increased protein concentration in the AH could play a role in the pathogenesis of glaucomatous disease.Translational Relevance: This study strongly supports the hypothesis that increased TP in the AH may have a pathogenic role in glaucoma. Further investigations are needed to clarify whether the protein enhancement represents a causative factor and whether it can be used as a marker of disease or as a novel therapeutic target.